Voiding dysfunction

VOIDING DYSFUNCTION

URRENT

CLINICAL UROLOGV

Eric A. Klein, SERIES EDITOR Voiding Dysfunction: Diagnosisarzd Treatment, edited by Rodney A. Appell, 2000 ~ a n a ~ e ~ofeProstate nt Cancer, edited by Eric A. Klein, 2000

VOIDING DYSFUNCTION

DUGNOSIS

Edited by

RODNEY A. APPELL, MD Chehnd Clinic Foundntion,

C h e h d OH

HUMANA PRESS TOTOWA, NEWJERSEY

0 2000 Huniana Press Inc. 999 Riverview Drive, Suite 208 Totowa, New Jersey 075 12 For additional copies, pricing for bulk purchases, and/or information about other Huinana titles, contact Huinana at the above address or at any of the following numbers: Tel: 973-256-1 699. Fax. 973-256-834 I : E-mail: humana~liiinianapr.comor visit our Website at http.//humanapress.com All rights reserved No part of this book may be reproduced. stored in a retrieval system, or transmitted in any forin or by any means. electronic, mechanical, photocopying. microfilming. recording. or otherwise without written perinission from the Publisher. All articles, comments, opinions, conclusions. or recoininendations are those of the author(s), and do not necessarily reflect the views of the publisher. Due diligence has been taken by the publishers. editors, and authors of this book to ensure the accuracy of the information published and to describe generally accepted practices. The contributors herein have carefully checked to ensure that the drug selections and dosages set forth in this text are accurate in accord with the standards accepted at the time of publication. Notwithstanding, as new research, changes i n government regulations, and knowledge froin clinical experience relating to drug therapy and drug reactions constantly occurs, the reader is advised to check the product information provided by the manufacturer of each drug for any change in dosages or for additional warnings and contraindications. This is of utmost importance when the recommended drug herein is a new or infrequently used drug. It is the responsibility of the health care provider to ascertain the Food and Drug Administration status of each drug or device used in their clinical practice. The publisher, editors, and authors are not responsible for errors or omissions or for any consequences from the application of the information presented in this book and make no warranty, express or implied. with respect to the contents in this publication. This publication is printed on acid-free paper.= ANSI 239.48- 1984 (American National Standards Institute) Permanence of Paper for Printed Library Materials. Cover design by Patricia F. Cleary. Photocopy Authorization Policy: Authorization to photocopy items for internal or personal use, or the internal or personal use of specific clients, is granted by Huniana Press Inc., provided that the base fee of US $8.00 per copy, plus US $00.25 per page, is paid directly to the Copyright Clearance Center at 233 Rosewood Drive. Danvers. M A 0 1923. For those organizations that have been granted a photocopy license from the CCC, a separate system of payment has been arranged and is acceptable to Huniana Press Inc. The fee code for users ofthe Transactional Reporting Service is [O-89603-659-6100 $8.00 + $00.251. Printed in the United States of America. 10 9 8 7 6 5 4 3 2 1 Voiding dysfunction . diagnosis and treatmededited by Rodney A. Appell p. : cm.--(Current clinical urology) Includes bibliographical references and index. ISBN 0-89603-659-6 (alk. paper) 1 . Urination disorders. I. Appell, Rodney A. 11. Series. [DNLM: 1 . Urination Disorders4iagnosis. 2 . Urination Disorders-therapy. V889 20001 RC901.75.V65 3000 6 1 6 . 6 ' 2 4 ~ 12 DNLM/DLC for Library of Congress

WJ 146

00-027599 CIP

PREFACE The purpose of Voiding Dysfunction: Diagnosis and Treatmentis to bring the reader up to date on all clinical aspects of voiding dysfunction, not just urodynamic and other evaluative techniques, but varying nuances in presentation of the individual problems that may occurduring voiding, sometimes as a manifestation of an underlying disease or disorder, and at other times because of individual patient circumstances, including the patient’s behavior or the effects of treatment for an unrelated disorder. Voiding dysfunction includes disorders of urinary storage as well as the emptying ofthe lower urinary tract. Although urinary incontinence is a huge problem worldwide as exemplified by the absolute need of the World Health Organization (WHO) to sponsor the mammoth undertaking of an international consultation on the topic in mid-1998, other voiding disorders also adversely affect the quality of the lives of the individuals afflicted. These problemsare often placed on the “back burner” with respect to basic and clinical research because they do not result in death; however, it is important to recognize that the quality of one’s life is as important as mere existence itself, as demonstrated bythe extent to which people will goto try therapies (many unproven) at tremendous expenseto make small improvements in the quality of their respective lives. Fortunately, knowledge of lowerurinary tract function and dysfunction has advanced rapidly over the last half of the 20th century from the early phase of urodynamics (a term first used in 1953 by D. M. Davis [ I ] )to the current neurological era (2). I want to express my appreciation to an excellent group of contributors to Voiding Dysfunction: Diagnosisand Treatmentfor their timely response to my request to put down onpaper, in an explicable manner, the current states ofthe art and science of voiding dysfunction. First, there is a presentation on the current background information necessary, to understand the physiology ofthe normal lowerurinary tract and howto use that information to classify the various voiding dysfunctions. This is followed by an overview the of manner in which voiding dysfunction is diagnosed, stressing the importance of individualizing the evaluation to demonstrate the voiding dysfuction. Following this, there is a comprehensive discussion of major neurological problems andtheir adverse effects on voiding fbnction. This section includes discussions of specific diseases V

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Preface

and disorders that make up the so-called “neurogenic bladder,” which is, quite obviously, not a single entity. Individual discussions include the effects of stroke, multiple sclerosis, spinal cord problems, diabetes mellitus, and lumbar disc disorders on lower urinary tract function. The next section involves dysfunction in individual patients only, with comprehensive reviews of urinary incontinence and urinary retention. Attention in the following section revolves around voiding dysfunctions unique to males: bladder outlet obstruction and postprostatectomy incontinence. The final segment covers general topics involved in newer modalities of treatment for voiding dysfunction and includes phannacologic therapy, electrical stimulation, and surgery for intractable instability-augmentation cytoplasty. I am certain readers will find Voiding Dysfiuictiorz:Diagnosis and Treatment informative, practical, and clinically relevant. Rodney A. Appell,

MD

References 1. Davis, D. M. (1953) The mechanisms of urologic disease. WB Saunders, Philadelphia. 2. Hinman, F., Jr. (1996) Urodynamics I: Foreword. Ui-01.Clin. N. i4mer-.23, xi-xii.

CONTENTS Preface.........................................................................................

v

List of Contributors ...................................................................

.ix

Part I. Introduction 1 Pathophysiologyand Classification

of Voiding Dysfunction..................................................... 3 Alan J. Wein and Eric S. Rovner 2 Voiding Dysfunction: Diagnostic Evaluation....................... 25 Victor W. ~ i t tand j ~ i c h a eFicazzola l

Part II, Neurogenic Vesico-Urethral Dysfunction 3 Cerebrovascular Accidents................................................ Serge Peter ~arinkovjcand Gopal H.Badlani

63

4 Multiple Sclerosis............................................................... Jerry G. Blaivas 5 Diagnosis and Treatment of Spinal Cord injuries and Myeloneuropathie................................................. Steven W. Sukin and Timothy B. Boone 6 Diabetic Bladder Dysfunction............................................ Howard B. Goldman and Rodney A. Appell 7 Lumbar Disc Disease....................................................... Howard B. Goldman and Rodney A. Appell

83 115

139 149

Part 111. Female Voiding Dysfunction 8 Treatment of Stress Urinary Incontinence........................ Raymond Rackley 9 Urinary Retention in Women ............................................ Roger R. Dmochowski

163 185

Part N . Male Voiding Dysfunction 10 Bladder Outlet Obstruction in Males................................. Edward F. Ikeguchi, Alexis E. Te, James Choi, and Steven A. Kaplan Vii

225

...

Contents

v111

11 Post-Prostatectomy Incontinence.....................................

247

Harriette M. Scarper0 and J. Christian Winters

Part V. Treatment Modalities 12 Clinical Pharmacology..................................................... Scott R. Serels and Rodney A, Appell 13 Treatment of Detrusor Instability with Electrical Stimulation............................................ Steven W. Siege1 14 Treatment of Detrusor instability with Augmentation Cystoplasty ........................................ Joseph M. Khoury

275

Index.....................................................................................

,326

297 315

CONTRIBUTORS RODNEY A. APPELL, MD * Section of Voiding Dysfunction and Female Urology, Department of Urology, Cleveland Clinic Foundation, Cleveland, OH GOPAL H. BADLANI, MD * Department of Urology, Long Island Jewish Medical Center, New HydePark, NY JERRY G. B L A w A s , MD * Urologic Oncology, New York Hospital-Cornell Medical Center, New York, NY TIMOTHY B. BOONE, MD, PHD * Scott Department of Urology,Baylor College of Medicine, Houston, TX JAMESCHOI,MD * Department of Urology, ColumbiaUniversityMedical Center, New York, NY ROGER R. DMOCHOWSKI, MD, FACS North Texas Center,jor Urinary Control, Fort Worth, TX MICHAEL FICAZZOLA, MD * Department of Urology,New York UniversityMedical Center, New York, NY HOWARD B. GOLDMAN, MD Department of Urology, Case Western Reserve University, Cleveland, OH EDWARD F. IKEGUCHI, MD Department of Urology, Columbia University Medical Center, New York, NY STEVEN A. KAPLAN, MD Department of Urology, Columbia University Medical Center, New York, NY h s E P n M. KHOURY, MD, SCD Division of urology, UniversityofNorth Carolina Medical Center, Chapel Hill, NC SERGE PETER MARINKOVIC, MD Department of Urology, Long Island Jewish Medical Center,New Hyde Park,NY VICTOR W. NITTI,MD * Department of Urology, New York University Medical Center, New York, NY RAYMOND RACKLEY, MD Section of Voiding Dysfunction, Department of Urology, Cleveland Clinic Foundation, Cleveland, OH ERICS. ROVNER, MD Division of Urology, Hospital of theUniversity of Pennsylvania, University of Pennsylvania School of Medicine, Philadelphia, PA HARRIETTE M. SCARPERO, MD Department of Urology, Ochsner Clinic, Louisiana State University Health Sciences Center, New Orleans, LA 9

0

0

ix

Contributol

X

SCOTT R. SERELS, MD Bladder Control Center, UrologyAssociation of Norwalk, 0

Nomvalk, CT STEVEN W. SIEGEL, MD Metropolitan Neurologic Specialists, St. Paul, MN STEVEN W. SUKIN, MD Scott Department of Urology, Baylor College o f Medicine, Houston, TX ALEXIS E. ?"E, MD * Department of Urology, Columbia University Medical Center, New York, NY ALANJ. WEIN,PHD Division of Urology, Hospital of the University of Pennsylvania, University uf Pennsylvania School ofMedicine, Philadelphia, PA J. CHRISTIAN WINTERS, MD * Department of Urology, Ochsner Clinic, Louisiana State University Health Sciences Center, New Orleans, LA 0

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INTRODUCTION

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Pathophysiology and Classification of Voiding Dysfunction Alan J. Wein, MD, and Eric S. Rovner? MD CONTENTS NORMALLOWERURINARY TRACT FUNCTION ABNORMALITIES OF FILLING/STORAGE AND EMPTYING: OVERVIEW CLASSIFICATION OF VOIDINGDYSFUNCTION REFERENCES

The lower urinary tract functions as a group of inter-related structures whose purpose is to bring about efficient and low-pressure bladder filling, low-pressure urine storage with perfect continence (in the adult), and periodic voluntary urine expulsion (in the adult), again at low pressure. A simple way of looking at the pathophysiology of all types of voiding dysfunction will be presented, followed by a discussion of various systems of classification. Consistent with the author’s philosophy and prior attempts tomakethe understanding, evaluation, and management of voiding dysfunction as logical as possible (l),a functional and practical approach will be favored.

NORMAL LOWER URINARY TRACT FUNCTION Whatever disagreements exist regarding anatomic, morphologic, physiologic, pharmacologic, and mechanical details involved in both the storage and expulsion of urine by the lower urinary tract, the From: Current Clinical Urology: Voiding Dysfunction: Diagnosis and Treatment Edited by: R. A. Appell 0 Humana Press Inc., Totowa, NJ

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Wein and Rovner

“experts” would agree on certain points (1,2,). The first is that the micturition cycle involves two relatively discrete processes: (1)bladder filling and urine storage and (2) bladder emptying. The secondis that, whatever the details involved, onecan succinctly summarize these processes from a conceptual point of view as follows. Bladder filling and urine storage require: 1. Accommodation of increasing volumes of urine at a low intravesical pressure and with appropriate sensation. 2. A bladder outlet that is closedat rest and remains so during increases in intra-abdominal pressure. 3. Absence of involuntary bladder contractions.

Bladder emptying requires:

1. A coordinated contraction of the bladder smooth musculature of adequate magnitude. 2. A concomitant lowering of resistance at the level of the smooth and striated sphincter. 3. Absence of anatomic (as opposed to functional) obstruction. The term smooth sphincter refers to a physiologic but not ananatomic sphincter, and one that is not under voluntary control (this includes the smooth musculatureof the bladder neck and proximalurethra). The striated sphincter refers to the striated musculature, which is a part of the outer wall of the urethra in both the male and female (intrinsic or intramural) and the bulky skeletal muscle group that surrounds the urethra at the level of the membranous portion of the male and the middle segment inthe female (extrinsic or extramural). The extramural portion, the classically described “external urethral sphincter’’ is under voluntary control (see refs. 3 and 4 for a detailed discussion). Any type of voiding dysfunction must result from an abnormality of one or moreof the factors previously listed. This two-phase concept of micturition, with the three components of each related either to the bladder or the outlet, provides a logical framework for a functional categorization of all types of voiding dysfunction and disorders as related primarily to fillinglstorage or to emptying (see tables 1 and 2). There are indeed some types of voiding dysfunction that represent combinations of fillinglstorage andemptying abnormalities. Within this scheme, however, these become readily understandable, and their detection and treatment can belogically described. All aspects of urodynamic and video urodynamic evaluation can be conceptualized as to exactly what they evaluate in terms of either bladder or outlet activity

Chapter 1 / Pathophysiology Classification and

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Table 1 The Functional Classification of Voiding Dyshnction

Failure to store Because of the bladder Because of the outlet Failure to empty Because of the bladder Because of the outlet

during filling/storage or emptying (see Table 3). One caneasily classify all known treatments for voiding dysfunction under the broad categories of whether they facilitate fillinghtorage or emptying and whetherthey do so by an action primarily on the bladder or on one or more of the components of the bladder outlet (see Tables 4 and 5). Finally, the individual disorders produced by various neuromuscular dysfunctions can be thought of in terms of whether they produce primarily storage or emptying abnormalities, or a combination of the two.

A ~ N O ~ I T I OF E SFILLING/STORGE AND EMPTYING: OVERVIEW The pathophysiologyof failure of the lower urinary tract to fill with or store urine adequately may be secondary to reasons related to the bladder, the outlet, or both. Hyperactivity of the bladder during filling can beexpressed as phasic involuntary contractions, as low compliance, or asa combination. Involuntary contractions are most commonlyseen in association with neurologic disease or following neurologic injury; however, they may also be associated with aging, inflammationor irritation of the bladder wall, bladder outlet obstruction, or they may be idiopathic. Decreased compliance during filling may be secondary to neurologic disease, usually at a sacral or infrasacral level, but may also result from any process that destroys the viscoelastic or elastic properties of the bladder wall. Storage failure may also occur in the absence of hyperactivity secondary to hypersensitivity or pain during filling. Irritation and inflammation can be responsible, as well as neurologic, psychologic, or idiopathic causes. The classic clinical example is interstitial cystitis. Decreased outlet resistance may result from any process that damages the innervation, structural elements, or support of the smooth or striated

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Wein and Rovner Table 2 The kpanded Functional Classification

Failure to store Because of the bladder Detrusor hyperactivity Involuntary contractions Suprasacral neurologic disease Bladder outlet obstruction Idiopathic Decreased compliance Neurologic disease Fibrosis Idiopathic Detrusor hypersensitivity Inflammatory Infectious Neurologic Psychologic Idiopathic Because of the outlet Stress incontinence Nonfunctional bladder necldproximal urethra Failure to empty Because of the bladder Neurologic Myogenic Psychogenic Idiopathic Because of the outlet Anatomic Prostatic obstruction Bladder neck contracture Urethral stricture Urethral compression Functional Smooth sphincter dyssynergia Striated sphincter dyssynergia

sphincter. This may occur with, neurologic disease or injury, surgical or other mechanical trauma, or aging. Assuming the bladder neck and proximal urethra are competent at rest, lack of a stable suburethral supportive layer (see ref. 5) seems a plausible explanation of the primary factor responsible for genuine stress urinary incontinence in the female.

Chapter 1 / Pathophysiology and Classification

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Table 3 Urodynamics Simplified" Outlet

Bladder

FILLING/STORAGE Pde,"(FCMGd) UPPfPvesb PHASE FLUOROh EMPTYING PHASE

Pde/ Pve;

(VC?V~G)~

MUPPl FLUORO" EM@

(

FLOW"

1

"This functional conceptualization of urodynamics categorizes each study as to whether it examines bladder or outlet activity during the fillinglstorage or emptying phase of micturition. In this scheme, uroflow and residual urine integrate the activity of the bladder and the outlet during the emptying phase. bTcTotal bladder (P,,,) anddetrusor (Pdet)pressuresduring a fillingcystometrogram (FCMG). dFilling cystometrogram. eDetrusor leak point pressure. fUrethral pressure profilometry. g Valsalva leak point pressure. h Fluoroscopy of outlet during fillinglstorage. a voiding cystometrogram (VCMG). "jTotal bladder and detrusor pressures during kVoiding cystometrogram. 'Micturitional urethral pressure profilometry. "Fluoroscopy of outlet during emptying. "Electromyography of periurethral striated musculature. "Flowmetry. PResidual urine.

Such failure can occur because of laxity or hypermobility, each resulting in a failure of the normal transmission of intra-abdominal pressure increases to the bladder outlet. The primary etiologic factors may be any of the causes of pelvic floor relaxation or weakness. The treatment of fillinghtorage abnormalities is directed toward inhibiting bladder contractility, decreasing sensory input, or mechanically increasing bladder capacity; or, toward increasing outlet resistance, either continuously or just during increases in intra-abdominal pressure. Absolute or relative failure to empty results from decreased bladder contractility (a decrease in magnitude or duration), increased outlet resistance, or both. Absolute or relative failure of bladder contractility

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Wein and Rovner Table 4 Therapy to Facilitate Bladder Filling and Urine Storage

Inhibiting Bladder Contractility, Decreasing Sensory Input and/or Increasing Bladder Capacity Behavioral therapy Timed bladder emptying Bladder training; biofeedback Pharmacologic therapy Anticholinergic agents Musculotropic relaxants Calcium Antagonists Potassium channel openers Prostaglandin inhibitors Beta-adrenergic agonists Alpha-adrenergic antagonists Tricyclic antidepressants Dimethyl sulfoxide (DMSO) Polysynaptic inhibitors Therapy decreasing sensory input Bladder overdistention Electrical stimulation (Reflex inhibition); Neuromodulation Acupuncture Interruption of innervation Central (subarachnoid block) Sacral rhizotomy, selective sacral rhizotomy Perivesical (peripheral bladder denervation) Augmentation cystoplasty Increasing outlet resistance Physiotherapy and biofeedback Electrical stimulation Pharmacologic therapy Alpha-adrenergic agonists Tricyclic antidepressants Beta-adrenergic antagonists, agonists Estrogens Vesicourethral suspension (Stress urinary incontinence) Nonsurgical mechanical compression Periurethral polytef injection Periurethral collagen injection Occlusive and supportive devices; urethral plugs Surgical mechanical cornpression Sling procedures Closure of the bladder outlet Artificial urinary sphincter Bladder outlet reconstruction Circumventing the problem Antidiuretic hormone-like agents Diuretics Intermittent catheterization Continuous catheterization Urinary diversion External collecting devices Absorbent products

Chapter 1 / Pathophysiology Classification. and Table 5 Therapy to Facilitate Bladder Emptying

Increasing intravesical pressure and/or bladder contractility External Compression, Valsalva maneuver Promotion or initiation of reflex contractions Trigger zones or maneuvers Bladder training, tidal drainage Pharmacologic therapy Parasympathomimetic agents Prostaglandins Blockers of inhibition Alpha-adrenergic antagonists Opioid antagonists Reduction cystoplasty Electric stimulation Directly to the bladder or spinal cord To the nerve roots Transurethral intravesical electrotherapy Decreasing outlet resistance At a site of anatomic obstruction At the level of the prostate Pharmacologic Decrease prostatic size Decrease prostatic tone Balloon dilatation Intraurethral stent Urethral stricture repair or dilatation At the level of the smooth sphincter Pharmacologic therapy Transurethral resection or incisionof the bladder neck Y-V plasty of the bladder neck Alpha-adrenergic antagonists Beta-adrenergic agonists At the level of the striated sphincter Biofeedback and psychotherapy Pharmacologic therapy Skeletal muscle relaxants Benzodiazepines Baclofen Dantrolene Surgical sphincterotomy, botulinum A toxin Urethral overdilation Urethral stent Pudendal nerve interruption Alpha-adrenergic antagonists Circumventing the problem Intermittent catheterization Continuous catheterization Urinary diversion

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Wein and Rovner

may result from temporary or permanent alteration in one or more of the neuromuscular mechanismsnecessary for initiating and maintaining a normal detrusor contraction. Inhibition of the voiding reflex in a neurologically normal individual may also occur by a reflex mechanism secondary to painful stimuli, especially from the pelvic and perineal areas-or such an inhibition may be psychogenic. Non-neurogenic causes can also include impairment of bladder smooth musclefunction, which may result from overdistention, severe infection, or fibrosis. Pathologically increased outlet resistance is generally seen in the male and is most often secondary to anatomic obstruction, but it may be secondary to a failure of coordination (relaxation) of the striated or smooth sphincter during bladder contraction. Striated sphincter dyssynergia is a common cause of functional (as opposed to fixed anatomic) obstruction in patients with neurologic disease or injury. The treatment of emptying failure generally consists of attempts to increase intravesical pressure or facilitate or stimulate the micturition reflex,to decrease outlet resistance, or both. If all else fails or the attempt is impractical, intermittent catheterization is an effective way of circumventing emptying failure.

CLASSIFICATION OF VOIDING DYSFUNCTION Thepurpose of any classification system should be to facilitate understanding and management. A good classification should serve as intellectual shorthand and should convey, in a few key words or phrases, the essence of a clinical situation. An ideal system for all types of voiding dysfunction would include or imply a number of factors: I . the conclusions reached from urodynamic testing; 2. expected clinical symptoms 3. the approximate site and type of a neurologic lesion, or lack of one.

If the various categories accurately portray pathophysiology, treatment options should then be obvious, and a treatment “menu” should be evident. Most systems of classification for voiding dysfunction were formulated to describe dysfunctions secondary to neurologic disease or injury. The ideal system should be applicable to all types of voiding dysfunction. Based upon the data obtained from the neurourologic evaluation, a given voiding dysfunction can becategorized in a number of descriptive systems. None are perfect.

Chapter 1 / Pathophysiology Classification and

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Table 6 The Bors-Comarr Classification

Sensory neuron lesion Incomplete, balanced Complete, unbalanced Motor neuron lesion Balanced Imbalanced Sensory-motor neuron lesion. Upper motor neuron lesion Complete, balanced Complete, unbalanced Incomplete, balanced Incomplete, unbalanced Lower motor neuron lesion Complete, balanced Complete, unbalanced Incomplete, balanced Incomplete, unbalanced Mixed lesion Upper somatomotor neuron, lower visceromotor neuron Lower somatomotor neuron, upper visceromotor neuron Normal somatomotor neuron, lower visceromotor neuron

Bors-Comarr ClasszJicdtion (see Table 6 and re$ 6) This classification system was deduced from clinical observation of patients with traumatic spinal cord injury. This system applies only to patients with neurologic dysfunction and considers three factors: 1. The anatomic localization of the lesion; 2. The neurologic Completeness of the lesion, and 3. Whether lower urinary tract function is “balanced” or “unbalanced.”

The latter terms are based solely on the percentage of residual urine relative to bladder capacity. “Unbalanced” implies greater than 20% residual urine in a patient with an upper motor neuron (UMN) lesion or 10% in a patient with a lower motor neuron (LMN) lesion. This relative residual urine volume was ideally meant to imply coordination (synergy) or dyssynergia of the smooth and striated sphincters during bladder contraction or attempted micturition by abdominal straining or Crede. The determination of the completeness of the lesion is made on the basis of a thorough neurologic examination. The system erroneously

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assumed that the sacral spinal cord is the primary reflex center for micturition. “LMN” implies collectively the preganglionic and postganglionic parasympathetic autonomic fibers that innervate the bladder and outlet and originate as preganglionic fibers in the sacral spinal cord. The term is used in an analogy to efferent somatic nerve fibers, such as those of the pudendal nerve, which originate in the same sacral cord segment but terminate directly on pelvic floor striated musculature without the interposition of ganglia. “UMN” is used ina similar analogy to the somatic nervous systemto describe those descending autonomic pathways above the sacral spinal cord (the origin of the motor efferent supply to the bladder). In this system, “upper motor neuron bladder” refers to the pattern of micturition that results from an injury to the suprasacral spinal cord after the period of spinal shock has passed, assuming that the sacral spinal cord and the sacral nerve roots are intact and that the pelvic and pudendal nerve reflexes are intact. Lower motor neuronbladder refers to the pattern resulting if the sacral spinal cord or sacral roots are damaged and the reflex pattern through the autonomic and somatic nerves that emanate fromthese segments is absent. This system implies that if skeletal muscle spasticity exists below the level of the lesion, the lesion is above the sacral spinal cord and is by definition an UMN lesion. This type of lesion is characterized by detrusor hyperreflexia during filling. If flaccidity of the skeletal musculature below the level of a lesion exists, an LMNlesion is assumed to exist, implying detrusor areflexia. Exceptions occur andare classified in a “mixed lesion” group characterized either by detrusor hyperreflexia with a flaccid paralysis below the level of the lesion or by detrusor areflexia with spasticity or normal skeletal muscle tone neurologically below the lesion level. The use of this system is illustrated as follows. A complete, unbalanced, UMN lesion, implies a neurologically complete lesion above the level of the sacral spinal cord that results in skeletal muscle spasticity below the level of the injury. Detrusor hyperreflexia exists during filling, but a residual urine volume of greater than 20% of the bladder capacity is left after bladder contraction, implying obstruction in the area of the bladder outlet during the hyperreflexic detrusor contraction. This obstruction is generally due to striated sphincter dyssynergia, typically occurring in patients who are paraplegic and quadriplegic with lesions between the cervical and the sacral spinal cord. Smooth sphincter dyssynergia may be seen as well in patients with spinal cord lesions above the level of T6, usually in association with autonomic hyperreflexia. An LMN lesion, complete, unbalanced, implies a neurologi-

Chapter 1 I Pathophysiology and Classification

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Table 7 The Hald-Bradley Classification

Suprasacral lesion Suprasacral spinal lesion Infrasacral lesion Peripheral autonomic neuropathy Muscular lesion

cally complete lesion at the level of the sacral spinal cord or of the sacral roots, resulting in skeletal muscle flaccidity below that level. Detrusor areflexia results, and whatever measuresthe patient may use to increase intravesical pressure during attempted voiding are not sufficient to decrease residual urine to less than 10% of bladder capacity. This classification system applies best to spinal cord injury patients with complete neurologic lesions after spinal shock has passed. It is difficult to apply to patients with multicentric neurologic disease and cannot be used at all for patients with non-neurologic disease. The system fails to reconcile the clinical and urodynamicvariability exhibited by patients who, by neurological exam alone, seem to have similar lesions. The period of spinal shock that immediately follows severe cord injury is generally associated with bladder areflexia, whatever the status of the sacral somatic reflexes. Temporary or permanent changes in bladder or outlet activity during fillinghtorage or emptying may occur secondaryto a number of factors such as chronic overdistention, infection, and reinnervation or reorganization of neural pathways following injury or disease; such changes make it impossible to always accurately predict lower urinary tract activity solely on the basis of the level of the neurologic lesion. Finally, although the terms “balanced” and “unbalanced” are helpful, in that they describe the presence or absence of a certain relative percentage of residual urine, they do not necessarily imply the true functional significance of a lesion, which depends on the potential for damage to the lower or upper urinary tracts, and also on the social and vocational disability that results.

Huld-Bradley Classzfication (see ruble 7 and ref: 7 ) This is described as a simple neurotopographic classification. A supraspinal lesion implies synergy between detrusor contraction and smooth and striated sphincters, but defective inhibition of the voiding reflex. Detrusor hyperreflexia generally occurs and sensation is usually

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preserved. However, depending on the site of the lesion, detrusor areflexia and defective sensation may be seen. A suprasacral spinal lesion is roughly equivalent to what is described as a UMN lesion in the Bors-Comarr classification. An infrasacral lesion is roughly equivalent to an LMN lesion. Peripheral autonomic neuropathyis most frequently encountered in the diabetic and is characterized by deficient bladder sensation, gradually increasing residual urine and ultimate decompensation, with loss of detrusor contractility. A muscular lesion can involve the detrusor itself, the smooth sphincter, or any portion, or all, of the striated sphincter. The resultant dysfunction is dependent on which structure is affected. Detrusor dysfunction is the most common and generally results from decompensation, following long-standing bladder outlet obstruction.

This is a primarily neurologic system basedupon a conceptualization of central nervous systemcontrol of the lower urinary tract as including four neurologic “loops.” Dysfunctions are classified according to the loop affected. Loop 1 consists of neuronal connections between the cerebral cortex and the pontine-mesencephalic micturition center; this coordinates voluntary control of the detrusor reflex. Loop 1 lesions are seen in conditions such as brain tumor, cerebrovascular accident or disease, and cerebral trophy with dementia. The final result is characteristically detrusor hyperreflexia. Loop 2 includes the intraspinal pathway of detrusor muscle afferents to the brain-stem micturition center and the motor impulses from this center to the sacral spinal cord. Loop 2 is thought to coordinate and provide for a detrusor reflex of adequate temporal duration to allow complete voiding. Partial interruption by spinal cord injury results in a detrusor reflex of low threshold and in poor emptying with residual urine. Spinal cord transection of loop 2 acutely produces detrusor areflexia and urinary retention-spinal shock. After this has passed, detrusor hyperreflexia results. Loop 3 consists of the peripheral detrusor afferent axons and their pathway in the spinal cord; these terminate by synapsing on pudendal motor neurons that ultimately innervate periurethral striated muscle. Loop 3 was thought to provide a neurologic substrate for coordinated

Chapter l / Pathophysiology and Classification

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reciprocal action of the bladder and striated sphincter. Loop 3 dysfunction could be responsible for detrusor-striated sphincter dyssynergia or involuntary sphincter relaxation. Loop 4 consists of two components. Loop 4A is the suprasacral afferent and efferent innervation of the pudendal motor neuronsto the periurethrla striated musculaturewhichsynapseonpudendalmotor neurons in Onuf's nucleus-the segmental innervation of the periurethral striated muscle. In contrast to the stimulation of detrusor afferent fibers, which produce inhibitory postsynaptic potentials in pudendal motor neurons through loop3, pudendal nerve afferents produce excitatory postsynaptic potentials in those motor neurons throughloop 4B. These provide for contraction of the periurethral striated muscle during bladder filling and urine storage. The related sensory impulses arise from musclespindles and tendon organs in the pelvic floor musculature. Loop 4 provides for volitional control of the striated sphincter. Abnormalities of the suprasacral portion result in abnormal responses of the pudendal motor neurons to bladder filling and emptying, manifested as detrusor-striated sphincter dyssynergia, and/or loss of the ability to voluntarily contract the striated sphincter. This system is sophisticated and reflects the ingenuity and neurophysiologic expertise of its originator, Dr. William Bradley. For some neurologists, this method may be an excellent way to conceptualize the neurophysiology involved, assuming that they agree on the existence and significance of all four loops. Most urologists find this system difficult to use for many types of neurogenic voiding dysfunction and not at all applicable to non-neurogenic voiding dysfunction. Urodynamically, it may be extremely difficult to test the intactness of each loop system, and multicentric and partial lesions are difficult to describe.

The Lapides Class$kation (see Table 8 and re$ S) This is a modification of a system originally proposed by McLellan (a neurologist) in 1939 (9). This remains one of the most familiar systems to urologists and non-urologists because it describes in recognizable shorthand the clinical and cystometric conditions of many types of neurogenic voiding dysfunction. A sensory neurogenic bladder results from intemption of the sensory fibers between the bladder and spinal cord or the afferent tracts to the brain. Diabetes mellitus, tabes dorsalis, and pernicious anemia are most commonly responsible. The first clinical changes are described as those

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Table 8 The Lapides Classification.

Sensory neurogenic bladder Motor paralytic bladder Uninhibited neurogenic bladder Reflex neurogenic bladder Autonomous neurogenic bladder

of impaired sensation of bladder distention. Unless voiding is initiated on a timed basis, varying degrees of bladder overdistention can result with resultant hypotonicity. With bladder decompensation, significant amounts of residual urine are found and, at this time, the cystometric curve generally demonstrates a large capacity bladder with a flat high compliance low pressure filling curve. A motor paralytic bladder results from disease processes that destroy the parasympathetic motor innervation of the bladder. Extensive pelvic surgery or trauma may produce this. Herpes zoster has been listed as a cause as well, but recent evidence suggests that the voiding dysfunction seen with herpes is more related to a problem with afferent input. The early symptoms may vary from painful urinary retention to only a relative inability to initiate and maintain normal micturition. Early cystornetric filling is normal but without a voluntary bladder contraction at capacity. Chronic overdistention and decompensation may occur in a large capacity bladder with a flat, low-pressure filling curve; a large residual urine may result. The uninhibited neurogenic bladder was described originally as resulting from injury or disease to the “corticoregulatory tract.” The sacral spinal cord was presumed to be the micturition reflex center, and this “corticoregulatory tract” was believed to exert an inhibitory influence on the sacral micturition reflex center. A destructive lesion in this tract would then result in overfacilitation or lack of inhibition of the micturition reflex. Cerebrovascular accident, brain or spinal cord tumor, Parkinson’s disease, and demyelinating disease are the most common causes in this category. The voiding dysfunction is most often characterized symptomatically by frequency, urgency, and urge incontinence. Urodynamically, onesees normal sensation with aninvoluntary bladder contraction at low filling volumes. Residual urine is characteristically low unless anatomic outlet obstruction or true smooth or striated sphincter dyssynergia occurs. The patient generally can

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initiate a bladder contraction voluntarily, but is often unable to do so during cystometry becausesufficient urine storage cannot occurbefore detrusor hyperreflexia is stimulated. Reflex neurogenic bladder describes the postspinal shock condition that exists after complete interruption of the sensory and motor pathways between the sacral spinal cord and the brain stem. Most commonly, this occurs in traumatic spinal cord injury and transverse myelitis, but may occur with extensive demyelinating disease or any process that produces significant spinal cord destruction as well. Typically, there is no bladder sensation and there is inability to initiate voluntary micturition. Incontinence without sensation generally occurs because of low volume involuntary bladder contraction. Striated sphincter dyssynergia is the rule. This type of lesion is essentially equivalent to a complete UMN lesion in the Bors-Comarr system. An autonomous neurogenicbladder results from complete motor and sensory separation of the bladder from the sacral spinal cord. This may be caused by any disease that destroys the sacral cord or causes extensive damage to the sacral roots or pelvic nerves. There is inability to voluntarily initiate micturition, no bladder reflex activity, and no specific bladder sensation. This type of bladder is equivalent to a complete LMN lesion in the Bors-Comarr system andis also the type of dysfunction seen in patients with spinal shock. This characteristic cystometric pattern is initially similar to the late stages of the motor orsensory paralytic bladder, with a marked shift to the right of the cystometric filling curve and a large bladder capacity at low intravesical pressure. However, decreased compliance may develop, secondary either to chronic inflammatory change or to the effects of denervationlcentralizationwith secondaryneuromorphologicandneuropharmacologic reorganizational changes. Emptying capacity may vary widely, depending on the ability of the patient to increase intravesical pressure and on the resistance offered during this increase by the smooth andstriated sphincters. These classic categories in their usual settings are usually easily understood and remembered, and this is why this system provides an excellent framework for teaching some fundamentals of neurogenic voiding dysfunction to students and non-urologists. Unfortunately, many patients do not exactly “fit” into one or another category. Gradations of sensory, motor, andmixed lesions occur, and the patterns produced after different types of peripheral dene~ation/defunctionalization may vary widely from those which are classically described. The system is applicable only to neuropathic dysfunction.

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Table 9 A Urodynamic Classification“ Detrusor hyperreflexia (or normoreflexia) Coordinated sphincters Striated sphincter dyssynergia Smooth sphincter dyssynergia Nonrelaxing smooth sphincter Detrusor areflexia Coordinated sphincters Nonrelaxing striated sphincter Denervated striated sphincter Nonrelaxing smooth sphincter “Adapted with permission from ref. 10.

Urodynamic Clas$cation (see Table 9 and re$ 10) Systems of classification have evolved based solely on objective urodynamic data. When exact urodynamic classification is possible, this sort of system can provide an exact description of the voiding dysfunction that occurs. If a normal or hyperreflexic detrusor exists with coordinated smooth and striated sphincter function and without anatomic obstruction, normal bladder emptying should occur. Detrusor hyperreflexia is most commonlyassociated with neurologic lesions above the sacral spinal cord. Striated sphincter dyssynergia is most commonly seen after complete suprasacral spinal cord injury, following the period of spinal shock. Smooth sphincter dyssynergia is seen most classically in autonomic hyperreflexia when it is characteristically associated with detrusor hyperreflexia and striated sphincter dyssynergia. Detrusor areflexia may besecondary to bladder muscle decompensation or to various other conditions that produce inhibition at the level of the brain-stem micturition center, the sacral spinal cord, bladder ganglia, or bladder smooth muscle. This classification system is easiest to use when detrusor hyperreflexia or normoreflexia exists. Thus, a typical T l 0 level paraplegic exhibits detrusor hyperreflexia, smooth-sphincter synergia, and striatedsphincter dyssynergia. When a voluntary or hyperreflexic contraction cannot be elicited, the system is more difficult to use, because it is not appropriate to speak of true sphincter dyssynergia in the absence of an opposing bladder contraction. There are obviously many variations and extensions of such a system. Such systems work only when total urodynamic agreement exists among classifiers. Unfortunately, there

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Table 10 The International Continence Society Classification“ Phase Voiding Phase Storage

Bladder Function Detrusor activity Normal or stable Overactive Unstable Hyperreflexic Bladder sensation Normal Increased or hypersensitive Reduced or hyposensitive Absent

Bladder Function Detrusor activity Normal Underactive Acontractile Urethral Function Normal Obstructive Overactive Mechanical

Bladder capacity Normal High Low

Compliance Normal High LOW

Urethral Function Normal Incompetent “Adapted with permission from ref. 11.

are many voiding dysfunctions that do not fit neatly into a urodynarnic classification system that is agreed upon by all “experts.” As sophisticated urodynarnic technology and understanding improve, this type of classification system may supplant some others in general use.

International Continence Society Classz;ficdtion (see Table I O and ref: I I) This is in many ways an extension of a urodynamic classification system. The storage and voiding phases of micturition are described separately, and, within each, various designations are applied to describe bladder and urethral function (11).

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Normal bladder function during fillingktorage implies no significant rises in detrusor pressure (stability). Overactive detrusor function indicates the presence of involuntary contractions. If owing to neurologic disease, the term detrusor hyperreflexia is used; if not, the phenomenon is known as detrusor instability. Bladder sensation can be categorized only in qualitative terms as indicated. Bladder capacity and compliance (A) volume/A pressure) are cystometric measurements. Normalurethral function during filling/storage indicates a positive urethral closure pressure (urethral pressure minus bladder pressure) even with increases in intra-abdominal pressure. Incompetent urethral function during filling/ storage implies urine leakage in the absence of a detrusor contraction. This may be secondaryto genuine stress incontinence, intrinsic sphincter dysfunction, or an involuntary fall in urethral pressure in the absence of a detrusor contraction. During the voiding/emptying phase of micturition, normal detrusor activity implies voiding by a voluntarily initiated, sustained contraction that also can besuppressed voluntarily. An underactive detrusor defines a contraction of inadequate magnitude or/and duration to empty the bladder with a normal time span. An acontractile detrusor is one that cannot be demonstrated to contract during urodynamic testing. Areflexia is defined as acontractility owing to an abnormality of neural control, implying the complete absence of centrally coordinated contraction. Normal urethral function during voiding indicates opening prior to micturition to allow bladder emptying. An obstructed urethra is one which contracts against a detrusor contraction or fails to open (nonrelaxation) with attempted micturition. Contraction may be owingto smooth or striated sphincter dyssynergia. Striated sphincter dyssynergia is a term that should be applied only when neurologic disease is present. A similar syndrome but without neurologic disease is called dysfunctional voiding. Mechanical obstruction is generally anatomical and caused by BPH, urethral or bladder neck stricture, scarring or compression, or, rarely, kinking of a portion of the urethra during straining. Voiding dysfunction in a classic T10 level paraplegic after spinal shock has passed would be classified as follows: 1. Storage phase: overactive hyperreflexic detrusor, absent sensation, low capacity, normal compliance, normal urethral closure function. 2. 'Voiding phase: overactive obstructive urethral function, ? normal detrusor activity (actually, hyperreflexic).

The voiding dysfunction of a stroke patient with urgency incontinencewouldmost likely be classified during storage as overactive

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hyperreflexic detrusor, normal sensation, low capacity, normal compliance, and normalurethral closure function. During voiding, the dysfunction would beclassified as normaldetrusor activity and normalurethral function, assuming that no anatomic obstruction existed.

The Functional System (see Tables I and 2) Classification of voiding dysfunction can also be formulated on a simple functional basis, describing the dysfunction in terms of whether the deficit produced is primarily one of the fillinghtorage or emptying phase of micturition (see Table 1) (1,1.2)*This type of system was proposed initially by Quesada etal. (13), and is an excellent alternative when a particular dysfunction does not readily lend itself to a generally agreedupon classification elsewhere, This simple-mindedscheme assumes only that, whatever their differences, all “experts” would agree on the two-phase concept of micturition and upon the simple overall mechanisms underlying the normality of each phase (see section on normal lower urinary tract function). Storage failure results either because of bladder or outlet abnormalities or a combination. Bladder abnormalities include involuntary bladder contractions, low compliance, and hypersensitivity. The outlet abnormalities include only an intermittent or continuous decrease in outlet resistance. Similiarly, emptying failure can occur because of bladder or outlet abnormalities or a combination of the two. The bladder side includes inadequate or unsustained bladder contractility, and the outlet side includes anatomic obstruction and sphincter(s) dyssynergia. Failure in either category generally is not absolute, but more frequently relative. Such a functional system can easily be “expanded” and made more complicated to include etiologic or specific urodynamic connotations (see Table 2). However, the simplified system is perfectly workable and avoids argument in those complex situations in which the exact etiology or urodynamic mechanism for a voiding dysfunction cannot be agreed upon. Proper useof this system for a given voiding dysfunction obviously requires a reasonably accurate notion of what the urodynamic data show. However, an exact diagnosis is not required for treatment. It should be recognized that some patients do not have only a discrete storage or emptying failure, and the existence of combination deficits must berecognized to properly utilize this system ofclassification. The

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classic T10 paraplegic after spinal shock generally exhibits a relative failure to store because of detrusor hyperreflexia and a relative failure to empty because of striated sphincter dyssynergia. With such a combination deficit, to utilize this classification system as a guide to treatment one must assume that one of the deficits is primary and that significant improvement will result from its treatment alone, or, that the voiding dysfunction can be converted primarily to a disorder either of storage or emptying by means of nonsurgical or surgical therapy. The resultant deficit can then be treated or circumvented. Using the same example, the combined deficit in a T10 paraplegic can be converted primarily to a storage failure by procedures directed at the dyssynergic striated sphincter; the resultant incontinence (secondary to detrusor hyperreflexia) can be circumvented (in a male) with an external collecting device. Alternatively, the deficit can be converted primarily to an emptying failure by pharmacologic or surgical measures designed to abolish or reduce the detrusor hyperreflexia, and the resultant emptying failure can then be circumvented with clean intermittent catheterization. Other examples of combination deficits include impaired bladder contractility with sphincter dysfunction, bladder outlet obstruction with detrusor hyperactivity, bladder outlet obstruction with sphincter malfunction, and detrusor hyperactivity with impaired contractility. One of the advantages of this functional classification is that it allows the individual the liberty of “playing” with the system to suit his or her preferences without an alteration in the basic concept of “keep it simple but accurate and informative.” For instance, one could easily substitute “overactive or oversensitive bladder” and “outlet insufficiency” for “because of the bladder” and “because of the outlet” under “failure to store” in Table 1. One could choose to subcategorize the bladder reasons for overactivity (see Table 2) in terms of neurogenic, myogenic, or anatomic etiologies and further subcategorize neurogenic in terms of increased afferent activity, decreased inhibitory control, increased sensitivity to efferent activity, and so forth. The system is flexible. An additional advantage to the functional system is that the underlying concepts can be used repeatedly to simplify many areas in neurourology. One logical extension makes urodynamics become more readily understandable (see Table 3), whereas a different type of adaptation functions especially well as a “menu” for the categorization of all the types of treatment for voiding dysfunction (see Tables 4 and 5). The major problem with the functional system is that not every voiding dysfunction can be reduced or converted primarily to a failure

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of storage or emptying. Additionally, although the functional classification of therapy that is a correlate of this scheme is entirely logical and complete, there is a danger of accepting an easy therapeutic solution and of thereby overlooking an etiology for a voiding dysfunction that is reversible at the primary level of causation. Non-neurogenic voiding dysfunctions, however, can be classified within this system, including those involving only the sensory aspect of micturition. It is obvious that no type of system is perfect. Each offers something to every clinician; although his or her level and type of training, interests, experience, and prejudices regarding the accuracy and interpretation of urodynamic data will determine a system’s usefulness. The ideal approach to a patient with voiding dysfunction continues to be a thorough neurourologic evaluation. If the clinician can classify a given patient’s voiding dysfunction in each system or can understand why this cannot be done, there is enough working knowledge to proceed with treatment. However, if the clinician is familiar with only one or two of these systems and a given patient does not fit these, and the reason is uncertain, the patient should certainly be studied further and the voiding dysfunction better characterized, at least before irreversible therapy is undertaken.

REFERENCES 1. Wein AJ. Barrett DM (1988) Voiding Firriction and Dysfimctioii: A Logical and Prnctical Approach. Chicago: Year Book Medical Publishers, Tnc. 2. Wein AJ ( 1998) Pathophysiology and categorization of voiding dysfunction. In: Walsh PC, Retik AB, Vaughan ED. Jr, Wein AJ, eds. Curnpbell’s Urology (8th ed.) Philadelphia: WB Saunders Co., pp. 917-926. 3. Zderic SA, Levin RM, Wein AJ (1996) Voiding function: relevant anatomy, physiology, pharmacology and molecular aspects. In: Gillenwater JY, Grayhack JT, Howards SS, Duckett JW, Jr, eds., Adult orid Pediatric Urology, Chicago: Year Book Medical Publishers, pp. 1159-1219. 4. Steers WD ( 1 998) Physiology and pharmacology of the bladder and urethra. In: Walsh PC, Retik AB, Vaughan ED. Jr. Wein AJ, eds., Ccinzpbell’s Uro-ology,(8th ed.), Philadelphia: WB Saunders Co., pp. 870-916. 5. DeLancey JOL (1994) Structural support of the urethra as it relates to stress urinary incontinence: the hammock hypothesis. Ail7 J Obstet Gyizecol 170:17 13. 6. Bors E. Cornarr AE (197 1) Neurological Urology. Baltimore: University Park Press. 7. Hald T, Bradley WE (1982) The Urirtai? Bladder: Neurology and Dynamics, Baltimore: Williams and Wilkins. 8. Lapides J (1 970) Neur~muscular,vesical and ureteral dysfunction. In: Campbell MF and Harrison JH, eds., Urology. Philadelphia: WB Saunders Co, pp. 13431379.

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9. McLellan FC (1939) The Neurogenic Bladder. Springfield: Charles Thomas Co.. pp. 57-70, 116-185. 10. Krane RJ, Siroky MB (1984) Classification of voiding dysfunction: Value of classification systems. In: Barrett DM. Wein AJ, eds., Controversies in NertroUrology. New York: Churchill Livingstone, pp. 223-238. 11. Abrams P. Blaivas JG. Stanton SL, Andersen JT (1990) The standardization of terminology of lower urinary tract function recommended by the International Continence Society. l i d Urogynecol J 1:45. 12. Wein AJ (1981) Classification of neurogenic voiding dysfunction. J Urol 125:605. 13. Quesada EM, Scott FB, Cardus D (1968) Functional classification of neurogenic bladder dysfunction. Arch Phys Med Relzabil 49:692.

Victor M7 Nitti, MD and Michael Ficdnnola, MD CONTENTS INTRODUCTION CLASSIFICATION OF VOIDINGDYSFUNCTION HISTORY PHYSICAL EXAMINATION LABORATORY TESTING SIMPLETESTS FOR EVALUATING VOIDINGDYSFUNCTION URODYNAMICS ENDOSCOPY URINARY TRACT IMAGING REFERENCES

INTRODUCTION Voiding dysfunction usually presents in one of two ways. The first is in the form of symptoms. Symptoms related to voiding dysfunction are broadly referred to as lower urinary tract symptoms (LUTS). LUTS have classically been divided into obstructive symptoms such as difficulty initiating a stream, decreased force of urinary stream, need to push and strain to void (stranguria), hesitancy or intermittent urine flow, and irritative symptoms such as urinary frequency, urgency, and nocturia. In addition, symptoms of incontinence and lower abdominal

From: Current Clinical Urology: Voiding Dysfunction: Diagnosis and Treatment Edited by: R. A. Appell 0 Hurnana Press Inc., Totowa, NJ

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or pelvic pain may exist. The secondway in whichvoiding dysfunction presents is in the form of urinary tract decompensation suchas incomplete bladder emptying or urinary retention, renal insufficiency, and recurrent urinary tract infections. It is possible for patients who present with urinary tract decompensation to have little or no symptoms. In the case of symptoms, evaluation and treatment are often driven by the degree of bother to the patient. In many cases, patients with mild LUTS of a minimal bother will not even bring these to the attention of their physician. However, when urinary tract decompensation is diagnosed, a more aggressive diagnostic and treatment plan must be implemented. Thereare also patients who havediseases known to effect the lower urinary tract and cause voiding dysfunction, yet do not have significant symptoms or obvious signs of decompensation.These include patients with a variety of neurological conditions such as spinal cord injuries or multiple sclerosis, or non-neurological conditions such as prior pelvic irradiation or extensive pelvic surgery. In many cases careful evaluation of the urinary tract will uncover underlying voiding dysfunction. Thus the diagnostic evaluation of voiding dysfunction will be influenced by the type anddegree of bother of symptoms, the presence of urinary tract decompensation, andcoexisting medical conditions that might affect the lower urinary tract or its treatment. In this chapter we will discuss the diagnostic evaluation of voiding dysfunction. It is important to realize that this evaluation is not the same for all patients and will be influenced by many factors, including those previously mentioned. Beforediscussing the evaluation in detail, we will first present a classification system for voiding dysfunction, which should help the clinician plan a proper diagnostic evaluation and treatment plan.

CLASSIFICATION OF VOIDING DYSFUNCTION In order to formulate a plan for the diagnostic evaluation of voiding dysfunction, an understanding of the possible causes of symptoms or urinary tract decompensation and the possible manifestations of a coexisting condition is necessary. In order to accomplish this, a practical classification of voiding dysfunction is invaluable. The functional classification system proposed andpopularized by Wein ( 1 ) is simple and practical and allows treatment options to be formulated according to classification. In simple terms, voiding dysfunction can be divided into three categories:

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1. Failure to store urine. 2. Failure to empty urine. 3. Failure to store and empty.

For example, the symptom of urinary frequency or incontinence is usually associated with dysfunction of the storage phase of micturition, whereas decreased force of stream or elevated postvoid residual are associated with dysfunction of the emptying phase. In addition, we can view voiding dysfunction in simple anatomical terms: l . Bladder dysfunction (overactive, underactive). 2. Bladder outlet dysfunction (overactive, underactive). 3. Combined bladder and outlet dysfunction. Thesetwo concepts canbecombined so that onecanimagine that a patient could present with urinary incontinence (failure to store) secondary to bladder overactivity or bladder outlet underactivity. Similarly a patient with urinary retention (failure to empty) might have anunderactive-orhypocontractile-bladder or an overactive-or obstructing-outlet. Failure to empty and failure to store as well as bladder and outlet dysfunction are not mutually exclusive conditions and can exist in multiple combinations. These very simple concepts can be applied to all types of voiding dysfunction. Therefore when evaluating voiding dysfunction, from history and physical examination to simple and comprehensive testing, keeping these concepts in mind can greatly facilitate the process.

HISTORY The patient’s history is the first step in directing the clinician toward the appropriate evaluation and treatment. It should provide the clinician with a detailed account of the precise nature of the patient’ S symptoms. It is important to remember that the history is only as accurate as the patient’s ability to describe their symptoms, therefore, some skill is required by the physician to obtain this infomation. This is especially true for patients who have difficulty communicating or those who are anxious or embarrassed about their condition. A classic illustration of this is in the study by Dioknoet al. (2) in noninstitutional elderly patients. They found that only 37% of incontinent men and 41% of incontinent women told a physician about their condition (2). The history begins with an assessment of a patient’s symptoms and their onset. Eachsymptom should be characterized as to its onset,

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frequency, duration, severity,and bother; and exacerbating or relieving factors. Itisimportanttonotewhethertheonset of thesymptom occurred after a specific event such as surgery, childbirth, menopause, or with the use of a new medication. Any prior treatments by other physicians for their symptoms and the resultant outcome should also be noted. Specific questions about childhood and adolescent voiding troubles or problems with toilet training should be asked. Patients will often presentwith one or more voiding symptoms that have been traditionally separated into irritative or obstructive in nature. Irritative voiding symptoms are common presenting complaints that may herald a number of different typesof voiding dysfunction.Urgency is defined as an intense desire tovoid secondary to an abrupt sensation of bladder discomfort or as a conditional response from the fear of urine leakage. Frequency is defined as more than seven diurnal voids and may reflectexcessive fluid intake, diuretic use, or excessive caffeine consumption. Nocturia is nighttime frequency and may be secondary to detrusor overactivity, reduced bladder capacity, or excessive fluid caffeine intake prior to bedtime. Daytime frequency without nocturia may be suggestive of timing of diuretic medications or a psychogenic component to the voiding dysfunction. Dysuria refers to the burning sensation that occurs during micturitionand implies bladder, urethral, orprostaticinflammation.Obstructivevoidingsymptomsinclude decreasedforce of urinarystream,strainingtovoid,hesitancy(the prolonged interval necessary to voluntarily initiate the urinary stream), and interruption of urinary stream. They may be present in men with bladder outlet obstruction secondary to benign prostatic enlargement or urethral stricture, or in women with pelvic organ prolapse. Abrams (3) has suggested replacing the terns obstructive and irritative symptoms with symptoms of storage (e.g., frequency, urgency, incontinence) and symptoms of voiding (hesitancy, decreased force of stream, incomplete emptying)(3).This is consistentwith the functional classification presented above and may be more useful when evaluating patients initially by history. One of the most distressing of all urinary symptomsis incontinence. When evaluating the symptomof incontinence, it is essential to query extensively about the nature and severity of the incontinence. From a conceptual standpoint, urinary incontinence can occur as a result of bladder overactivity or inadequate urethral sphincter function (or a combination of both) and these in turn can result from a variety of conditions (4).Urinary incontinence is simply defined as the involuntary

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loss of urine, however, this can be further characterized according to the information relayed by the patient: 1. Urge incontinence: The symptom is incontinenceis associated with a sudden uncontrollable desire to void. This conditionis usually due to involuntary detrusor contractions. 2. Stress incontinence: The symptom is incontinence that occurs during coughing, sneezing, physical exertion, changes in body position, or other action that causes an increase in abdominal pressure. This condition may be caused by sphincter abnormalitiesor bladder overactivity provoked by physical activity. 3. Unconscious incontinence: The symptom of incontinence is unconsciousandoccurswithoutpatientawareness of urgesorstress or increases in abdominal pressure. This condition maybecaused by bladder overactivity, sphincter abnormalities, overflow, or extraurethral causes such as a fistula or ectopic ureter. 4. Continuous leakage: The symptom is a complaint of continuous loss of urine. This may be caused by sphincter abnormalities or extraurethral causes. It is not always possible to determine the etiology of incontinence based on history alone. However, careful history taking as to the nature of the incontinence andwhen it occurs is critical in directing the diagnostic evaluation and treatment options. As previously mentioned, it is essential to determine the duration of symptoms. When symptomsare acute, or subacute, history may reveal an obvious cause of transient voiding dysfunction as amedication or acute nonurologic illness. This is demonstrated bythe mnemonic DIAPPERS developed by Resnick (5)to describe causes of transient incontinence: delerium, infection, atrophic vaginitislurethritis, pharmaceuticals, psychological, endocrine, restricted mobility, and stool impaction. Questionnaires and symptoms scores can be helpful in assessing the type of symptoms a patient has, the degree of 'bother of symptoms, and/or effect on quality of life that symptoms produce. Twosuch example arethe American UrologicAssociation Symptom Index(International Prostate Symptom Score), originally designed to assess men with LUTS secondary to benign prostatic hyperplasia (6), and the IQOL, designed to assess the impact of incontinence on quality of life (7). In cases where voiding dysfunction does not present danger to a patient, it is often the degree of bother or effect onan individual patient' S quality of life that drives evaluation and treatment decisions. Symptom scores and quality of life assessments are very useful in

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monitoring response to treatment foran individual or in clinical trials. After a thorough assessmentof a patient’s presenting symptoms, the history should then focus on related areas. There are several aspects of a patient’ S history that may be intimately related to voiding function. Sexual and bowel dysfunction are often associated with voiding dysfunction. Therefore the review of symptoms should focus on these areas including defecation (constipation, diarrhea, fecal incontinence, changes in bowel movements),sexual function, dysparunia, and pelvic pain. As neurological problems are frequently associated with voiding dysfunction, a thorough neurological history is critical, including known neurologic disease as well as symptomsthat could be related to occult neurological disease (back pain, radiculopathy, extremity numbness, tingling, or weakness, headaches, changes in eyesight, and so on). In addition to a focused history regarding LUTS andvoiding dysfunction, a thorough urological history is important. This includes a history of hematuria, urinary tract infections, sexually transmitted diseases, urolilthiasis, and urological malignancy and their treatment. The past medical history should provide information about concurrent medical diseases, obstetric and gynecologic history, past surgical history, and medication use. Many medications have profound effects on the lower urinary tract or can effect fluid mobilization and urine production and thus contribute to LUTS. Examplesof medications that may be associated with voiding dysfunction include alpha-adrenergic agonists, such as pseudoephedrine, diuretics, antidepressants, and anticholinergics. A detailed history of known neurological diseases (e.g., stroke, Parkinson’s disease, spinal cord injury, multiple sclerosis, myelodysplasia, and so on) is important because these diseases have the potential to affect bladder and sphincteric function. A history of medical diseases such as diabetes or congestive heart failure can cause LUTS by their effects on the lower urinary tract or fluid mobilization. For women with voiding dysfunction, obstetrical and gynecological history is extremely important. Pregnancy and childbirth, particularly vaginal delivery, are associated with voiding dysfunction, especially incontinence and pelvic prolapse. Thus, number of pregnancies, deliveries (including method, i.e., vaginal vs cesarean), and the onset of the symptoms in relation to these events is important. Symptoms can sometimes be related to a woman’s menstrual cycle and careful questioning in this regard should be done. A women’s hormonestatus (pre-, peri-, or postmenopausal) and the onset of symptoms with changes in status should be noted. Estrogen deficiency may cause or contribute

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to LUTS, including irritative symptoms of frequency and urgency, as well as incontinence. If the patient is postmenopausal, it is important to note whether the patient is being treated with hormone replacement therapy. Careful questioning regarding a history of endometriosis and gynecological malignancy should be performed. Prior surgery may have effects on lower urinary tract function. This includes surgery on the lower urinary tract (e.g., prostate surgery in men or incontinence surgery in women). Other pelvic surgery such as gynecological surgery or lower intestinal surgery also may affect the bladder directly or indirectly through damage to the nerve supply to the bladder or sphincter. For example, new onset total incontinence after hysterectomy raise the suspicion of a vesicovaginal fistula while urinary retention after an abdominal perineal resection of the rectum may be indicative of injury to the neural innervation of the bladder. History of pelvic radiation for treatment of pelvic malignancy (urological, gynecological, or rectal) is important as this can have a marked effect on lower urinary tract function and LUTS.

PHYSICAL FXAMINATION A complete physical exam isimportant; however, certain aspects of the examneed to beemphasized. A focused physical examination should be performed to: 1. Assess the bladder for masses and fullness; 2. Assess the external genitalia; 3. Assess the pelvic floor, including anal sphincter tone, and thoroughly

examine for supportdefects,prolapse,andotherpelvicconditions in women; 4. Assess the prostate in men; 5. Demonstrate incontinence in patients with that symptom; 6. Detect neurologic abnor~alitiesthat may contribute to voiding dysfunction.

The abdominal exam, which includes examination of the flanks, begins with inspection for scars, masses, or hernias. Examination of the back should be performedto check for scars and scoliosis which may be an indication of potential spine abnormalities that may contribute to voiding dysfunction. Suprapubic palpation is performed to determine if the patient has a distended bladder or pelvic mass. In women, a systematic examination of the vagina and pelvis is important. This is first done in lithotomy position and may be repeated

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with the patient standing. The external genitalia are first inspected followed by evaluation of the vaginal mucosa for signs of atrophic vaginitis, indicating estrogen deficiency, previous surgery, and vaginal discharge. The urethral meatus should be observed and the urethra palpated for any abnormalities. The anterior vaginal compartment is examined next. This can be aided by applying slight pressure wall with the posterior blade of a small vaginal speculum. The position of the urethra, bladder neck, and bladder can be observed at rest and with straining to evaluate support of these structures and determine the presence of urethral hypermobility and cystocele. Also with coughing and straining, the urethra should be observed for urine loss and whether that loss occurs with hypermobility . In cases of stress incontinence, a Q-tip test may be performed to determine the degree of urethral hypermobility. This is done by placing a Q-tip inside the urethra with its tip at the urethrovesical junction and observing the degree of rotation with straining. Hypermobility is defined as a resting or straining angle greater than 30" from the horizontal. The central vaginal compartment is examined next. The uterus and cervix should be evaluated at rest and with straining to determine prolapse. Bimanual examination is done to evaluate the presence of uterine, adnexal, or other pelvic masses. If the patient has had a hysterectomy, the vaginal cuff should be assessed for enterocele. This is often best accomplished by first retracting the anterior vaginal wall and then the posterior wall. Finally the posterior vaginal compartment is examined by retracting the anterior vaginal wall with the speculum blade. A large rectocele is easily identifiable. Examination for rectocele can be aided by a simultaneous rectal exam, which will also assess perineal integrity, anal sphincter tone, bulbocavernosus reflex, and rectal prolapse. If it is difficult to distinguish between a high rectocele and enterocele, simultaneous rectal and vaginal exam with the index finger and thumb may palpate the enterocele sliding above the anterior rectal wall. The pelvic examination may be repeated with the patient standing with one foot on the floor and the other on a step. This may give a more realistic assessment of the degree of prolapse. Genital examination in men should include inspection of the urethral meatus and palpation of the penile and bulbar urethra. During rectal exam, anal sphincter tone and bulbocavernosus reflex are assessed, as is the size and consistency of the prostate. A focused neurologic exam may yield important information regarding voiding dysfunction. Symptoms related to voiding dysfunction may

ChapterEvaluation 2 I Diagnostic

33

be among the earliest manifestation of nervous system disease (8). A neurologic exam should begin with an observation of the patient’s general appearance and gait. Lack of coordination, tremor, or facial asymmetry may be signs of neurologic disease. The upper and lower extremities are evaluated for gross motor coordination, strength, and sensation along dermatome distributions. The deep tendon reflexes at the knee and ankle should be assessed, as well as bulbocavernosus and perianal reflexes, including an evaluation of the muscle tone of the anal sphincter. A patient with a neurologic lesion at the sacral level may demonstrate diminished anal sphincter tone, perianal sensation, or absent bulbocavernosus reflex. Patients witha suprasacral spinal cord lesion will demonstrate spastic paralysis and hyperactive reflexes below the level of the lesion.

LABOMTORY TESTING Urine analysis is part of the standard evaluation of the patient with LUTS and voiding dysfunction. Urinalysis can screen for pyuria, bacturia hematuria, and the presence of glucosuria or proteinuria. Voiding dysfunction and LUTS can be associated with infection, malignancy, or medicalillness such asdiabetes, which can bediscovered as a result of an abnormal urine analysis. When abnormalities are found on urine analysis, further testing may be warranted such asurine culture in cases of suspected infection or urine cytology, endoscopic, and radiographic studies when microscopic hematuria is present. Blood tests are useful in select cases of voiding dysfunction. The most common tests are those that evaluate renal function, e.g., serum blood urea nitrogen and creatinine, in cases where renal insufficiency is known or suspected. In select cases, more specific blood and urine testing may be performed, but these are usually dependent onpatient history and physical as well as the results of simple tests.

SIMPLE TESTS FOR EVALUATING VOIDING DYSFUNCTION When history and physical exam alone are insufficient to make a diagnosis or institute treatment, or when more objective information

34

Nitti and Ficazzola

is desired, the clinician may start with simple tests to evaluate lower urinary tract function. These are noninvasive or minimally invasive (placement of a urethral catheter) tests that can provide information that may influence treatment or further diagnostic evaluation. The most basic of these include a voiding and intake diary, measurement of postvoid residual volume, uroflowmetry, and pad testing. Bedside or eyeball urodynamics is also a simple test and is described at the end of the section on urodynamics.

Voiding and Intake Diary A diary is an extremelyuseful way to describe the nature and quantify the severity of symptoms such as frequency, nocturia, and incontinence. It also provides a baseline to assess future treatment. A voiding and intake diary should include the time, type and amount of fluid intake, the time and amount of each void, and any associated symptoms such as incontinence, extreme urgency or pain. The diary should be done for a period of 24 h, and several days are preferred. The patient should also note how representative a particular 24-h period was of his or her normal symptoms.

Postvoid Residual The postvoid residual volume (PVR)is defined as the volume of urine remaining in the bladder immediately following voiding. It provides information on the ability of the bladder to empty as well as its functional capacity (voided volume plus PVR). Normal lower urinary tract function is usually associated with a negligible PVR; however, there is no agreement as to what an “abnormal” or clinically significant value is. Thus, elevated PVR is somewhat arbitrary. This being the case, most would agree that a PVR of greater than l00 mL is elevated, although perhaps not significant. Elevated PVR may be anindication of detrusor hypocontractility or bladder outlet obstruction and may prompt further evaluation depending on the patient and the symptoms or condition being evaluated. PVR can be measured directly by in and out urethral catherization or determinednoninvasively by ultrasonography. Portable bladder scanners based on ultrasound technology are now available to determine bladder volume.

35

ChapterEvaluation 2 / Diagnostic

maximum

'II

i

J

time to maximum tiow

I

time

I I I

Flow time

Fig. 1. Normal flow curve andpattern depicting the terminology of the International Continence Society relating to urodynarnic the description of urinary flow. Adapted with permission from ref. 8a.

Uroflowmetry The determination of urinary flow rate over time, or uroflowmetry, is a simple way to measure bladder emptying. In and of itself, a uroflow is rarely able to determine the cause of voiding dysfunction; however, in conjunction with a careful history and physical, it can provide valuable information. In addition, it is extremely useful in selecting patients for more complex urodynmic testing. Uroflow is measured by a device called a uroflowmeter. Modern uroflowmeters consist of electronic collection equipment with graphic expression of the flow rate as a function of time. Common parameters determined by uroflowmetry include (see Fig. l): l. Voided volume: Actual volume of urine voided. 2. Flow time: Time during which measurable flow occurs. 3. Total voiding time: The total time of void taking into account periods

of no flow in the patient with an i n t ~ ~ i t t e pattern. nt 4. Maximum flow rate (Qmax): The highest flow rate achieved during the voiding episode (i.e. the highest point on the curve).

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Nitti and Ficazzola

5. Time to maximal flow: The elapsed time from the beginning of voiding to the point of maximal flow. It is generally about one third of the total voided time. 6. Mean flow rate (Qave):Voided volume divided by flow time. Only interpretable if flow is continuous and uninterrupted. There is considerable overlap in flow rates between normal and abnormal patients. Qmax seems to have a greater specificity than Qavein determining abnormal voiding (9)and has become the most commonly used uroflow parameter. Urinary flow rate and Qnlax varies as a function of patient age, sex, anxiety, and voided volume. Several nomograms have been established to classify Q m a x as normal or abnormal based on Qmax and voided volume (10-12). Since Drach et al. (13) described a linear relationship between Qmax and voided volume above a voided volume of 150 mL, and a hyperbolic relationship between the two below this volume, voided volume of 150 mL has been commonly used as a minimum volume to make an accurate assessment of the uroflow. This is a major limitation in patients who do not routinely void with volumes 150 mL or greater. In addition to the parameters previously mentioned, the overall flow pattern is also important. Visual inspection of the uroflow curve can give valuable insight into the patients voiding dysfunction. A normal flow curve is a continuous, almost bell-shaped, smooth curve (Fig. 1). Interruptions or spikes and valleys in the flow may be indicative of voiding dysfunction. Intermittent flow pattern is characterized by one or more episodes of flow increasing and then decreasing and is commonly owing to abdominal straining (Fig. 2). A single uroflow measurement may not be representative for a given patient (14).Therefore, measuring multiple voiding events is a much more reliable indicator of the patient’s voiding pattern. In addition, to have a reliable uroflow measurement, the flow event must represent the patient’s usual voiding pattern. This can be simply assessed by asking the patient after completing the uroflow test if the void was representative of their typical pattern with respect to its volume and force. Abnormal flow rates and patterns are suggestive of voiding dysfunction. They may be caused by a variety of conditions, including bladder outlet obstruction, impaired detrusor contractility, or learned voiding behaviors. Although an abnormal uroflow suggests a problem, it cannot differentiate between causes or make a definitive diagnosis (15).More comprehensive urodynamic testing is needed to make a precise diagnosis. Uroflow is more cominonly utilized in men as opposed to women, probably because of the relatively high incidence of bladder outlet

ChapterEvaluation 2 I Diagnostic

37

..................................................

125 ml& FlowRate : ...................................................................

...................................................................

....................................................................

.............................. Results o f UROFL Voiding Time Flow Time Time t o max Flow Max FlowRate Ruerage Flow Rate Vo i ded Vo 1ume

T100

TQ

TQnax Qmax Qave Vcomp

S 65 42 S S 17 5.5 ml/s 2.8 ml/s m1 118

Fig. 2. Abnormal flow pattern,showinginterruptedstreamandlowQmax (5 mL/s). Adapted with permission from ref. 9.

obstruction and decreased flow in elderly men (16,17’).Again it must be emphasized that uroflow alone cannot make a diagnosis of obstruction. In males, Qtnmand voided volume normally decrease with age. Giman et al. (18) found that in a group of asymptomatic men of ages 40-79 yr, Qmax dropped from a medianof 20.3 mL/s (40-44 yr) to 11.5 mL/s (75-79 yr), and voided volumedecreased from a median of 356 to 223 mL over this same time period. Uroflow is not as frequently used for women with voiding dysfunction. Uroflow tends to be higher in normal women than it is in age-matched normal men (19). This is owing to the fact that the female urethra is short and only the voluntary part of the external urethral sphincter seems to provide any sort of outlet resistance during voiding. In women, noma1 Qmax ranges between 20-36 mL/s with a bell-shaped curve and short flow time (20).

Pad Test For patients who have the symptom of incontinence, the pad test is a method that can be usedto quantify urine loss based onthe measurement of weight gain of absorbent pads over a period of time. Several

38

Nitti and Ficazzola

different pad tests have been described, using variable periods of time (20 min to 48 h) and conditions (exercises, daily activity) (21-24). Shorter tests are usually performed with a standard bladder volume. The pad test provides a quantification of urine loss, but cannot distinguish between causes of incontinence. Pad testing is commonlyused in research and clinical trials on incontinence treatments. It may also be useful in clinical practice to assess severity of incontinence and response to treatment.

Urodynamics is the study of the transport, storage, and evacuation of urine by the urinary tract. It is comprised of a number of tests that individually or collectively can be usedto gain information about lower urinary tract function and can provide a precise diagnosis of the etiology of voiding dysfunction. However, in order to use urodynamics in a practical and effective way, it is important for the clinician to h o w when andwhy a urodynamic investigation should be performed. There are situations in whichthe information gained from history and physical exam, andsimple tests like uroflow and postvoid residual determination, is sufficient to make a clinical decision. In other cases, it is necessary to monitor physiological parameters in a morecomprehensiveand precise way. For example, sometimesa limited evaluation cannot adequately or accurately explain a patient’s symptoms, or a patient may have a medical condition known to affect the urinary tract in potentially serious and/or unpredictable ways (e.g., neurological disease). Once the decision has been made to perform urodynamics on a particular patient, it is important to consider what information is expected fromthe test (25). The simple fact that a patient has symptoms or a disorder that may affect the lower urinary tract is not sufficient to start the urodynamic evaluation. A list of problems or questions that should be solved or answered by urodynamics should be made before any testing is performed. All patients are not alike and therefore each urodynamic evaluation may be different depending on the information needed to answer the questions relevant to a particular patient. We follow three important rules before starting a urodynamic evaluation (25): 1. Decide on questions to be answered before starting 2. Design the study to answer these questions. 3. Customize the study as necessary.

a study.

ChapterEvaluation 2 / Diagnostic

39

By following these simple rules, one can maximize the chance of obtaining useful information from a study. It is also critical to have an understanding of the possible causes of a patient’s symptoms andthe urodynamic manifestations of a pre-existing condition. The functional classification previously described is particularly useful in this regard, because urodynamic testing easily classifies problems into failure to empty or failure to store and further into bladder dysfunction and/or bladder outlet dysfunction.

Midtichannel Urodynamics The various components of the urodynamic evaluation include monitoring of bladder pressure during filling (cystometrogram), monitoring of bladder pressure and simultaneous urinary flow rate during voiding (voiding pressure Bow study), and monitoringof pelvic Boor and external sphincter activity (electromyography). Usually abdominalpressure is also monitored during filling and voiding so that subtracted detrusor pressure can be determined (see Cystometrogram). In select cases, the urethral pressure can also be assessed during storage and voiding (urethral pressure profilometry). It is when these components are combined together as “multichannel urodynamics” that a most sophisticated study of the lower urinary tract is obtained.

CYSTOMETROGRAM The cystometrogram (CMG)is a measure of the bladder’s response to being filled. Normally the bladder should store increasing volumes of urine at low pressure and without involuntary contractions. CMG determines the pressure-volume relationship within the bladder and also provides a subjective measure of bladder sensation with the cooperation of the patient. Ideally, the CMG should mimic noma1 bladder filling and gives an accurate assessment of true bladder function. CMG is performed by filling the bladder at a constant rate (usually 10-100 mL/s) with fluid (normal saline or contrast media) orgas (such as carbon dioxide). Filling occurs via a catheter, which is inserted transurethrally or suprapubically. Usually there are two lumens on the catheter, one to measure pressure and one to fill the bladder. Most urodynamisists have abandoned gas cystometry because fluid is more physiologic and allows the determination more parameters. The reader is referred elsewhere for a more detailed description of the technical aspects of cystometry (26).

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Nitti and Ficazzola

Filling/storage phase

Volume

Fig. 3. Idealized normal adult cystometrogram. PhasesI, 11, and I11 occur during filling and phase IV during voiding. PhaseI reflects the bladder’s initial response to filling. Phase 11 is the tonus limb and reflects bladder pressure during the majority of the filling phase. As the vesicoelastic propertiesof the bladder reach to their limit phase, IT1 is entered where pressures begin to increase just prior phase IV, the voluntary contraction phase. (Clinically the pressure change from phases T to I1 is often imperceptible and-depending on how much the bladder is allowed to fill-phase 111 may not be appreciated as a significant pressure change.) Adapted with permission from ref. 8a.

Several parameters may be evaluated by CMG:

1. Sensation. 2. Filling pressure. 3. Presence of involuntary or unstable contractions. 4.. Compliance (filling pressure in relation to volume). 5. Capacity. 6. Control over micturition. Sensation is the part of cystometry that is truly subjective and therefore requires an alert and attentive patient and clinician. It is difficult to quantify sensation, which can vary greatly under different conditions. It may be affected by factors such as infusion rate and temperature of the filling solution as well as the level of distraction of the patient. The true value of the CMG with respect to sensation is when a symptom is mimicked and sensation can be correlated with changes in vesical pressure. Normally as the bladder fills, it maintains a relatively constant and low pressure, usually not exceeding 5-10 cm H20 above starting or baseline pressure (Fig. 3). It will store increasing volumes of urine without a significant rise in pressure. The only time the bladder should

Chapter 2 / Diagnostic Evaluation.

41

contract is during the voluntary act of voiding. However, undercertain circumstances, a bladder may contract involuntarily. Involuntary contractions may be associated with the symptoms of frequency, urgency, urge incontinence, pain, or the perception of a normal desire to void. The International Continence Society (ICs) has classified involuntary detrusor contractions into two broad categories (27):

1. Detrusor instability: involuntary contractions not associated with an underlying neurologic lesion. Detrusor instability may be caused by inflammation, infection, bladder outlet obstruction, aging, so and forth, orinmanycasesis“idiopathic.”Activitymaybespontaneousor provoked by certain movements, position, etc.ICs originally required a contraction of at least 15 cm H20 for the classification of unstable bladder.However, we feelComfortableclassifyinganyinvoluntary rise in detrusor pressure that is accompanied by an urge as detrusor instability. 2. Detrusorhyperreflexia:involuntarycontractionsassociatedwith a knownneurologiclesion.Typically,theseareuppermotorneuron lesions such as supra sacral spinal cord lesions, multiple sclerosis, or cerebrovascular accident. Detrusor instability and detrusor hyperreflexia may look identical on CMG (Fig. 4). However, instability is more likely to be phasic and of lower pressure and can more often be inhibited. Hyperreflexic contractions tend to be more numerous and of higher pressure. These are only generalizations, however, and the terms instability and hyperreflexia are strictly defined by the patient’s neurological status and not the CMG appearance of the involuntary contraction. Compliance refers to the change in volume/change in pressure and is expressed in mL/cm H20. Since the bladder is normally able to hold large volumes at low pressures it is said to be highly compliant. The spherical shape of the bladder as well as the viscoelastic properties of its components contribute to its excellent compliance allowing storage of progressive volumes of urine at low pressure. When the bladder is unable to maintain low pressure with increasing volume, compliance is decreased or impaired. This may occur when there is prolonged bladder outlet obstruction as the “overworked bladder” becomes scarred assmoothmuscle is replaced by collagen. Itcan also result from radiation, surgery on the bladder, tuberculosis, and other chronic infectious diseases, as well as other conditions that affect the size, shape, and vesicoelastic properties of the normal bladder. The measurement of compliance is important because high prolonged elevated storage pressures have been shownto have a deleterious effect on the kidneys.

42

Nitti and Ficazzola pressure cm water

Involuntary contractions

Volume ml

PHASIC INSTABILITY Detrusor instability or Destrusor hyperreflexia

Fig. 4. Involuntary detrusor contractions. Note the multiple involuntary rises in bladder pressure during filling. This could be an example of detrusor instability or hyperreflexia andthatdistinctionwouldbedetermined by theabsenceor presence of a neurological lesion.

McGuireand associates haveshown that in neurogenic bladder sustained pressures of 40 cmH20 or greater during storage can lead to upper tract damage (28). In practical terms, the concept of compliance is actually more useful than its absolute value. The calculated value of compliance (in cmH20) isprobably less important than the absolute bladder pressure during filling (Fig. 5). When bladder pressure is monitored througha transurethral or suprapubic catheter, the pressure that is recorded is actually the sum of intraabdominal pressure and the pressure generated by the detrusor itself, either through a contraction or wall tension with bladder filling, i.e., compliance. Cystometry can be performed as a single channel study where the bladder pressure (Pves) is measured and recorded during filling and storage or as a multi-channel study where abdominalpressure (Pabd) is subtracted from Pves to give the detrusor pressure (Pdet). Abdominal pressure can be recorded via a small balloon catheter that

ChapterEvaluation 2 / Diagnostic

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Fig. 5. Impaired compliance. This CMG shows a gradual loss of compliance between 40 and 280 m1 with filling pressures of 17 cm H 2 0 at 280 mL. Between 280 m1 and 330mL there is arapid rise in pressure to 41 cm H 2 0which continues to rise to 51 crnH20 until filling is stopped at 400 mL. The storage pressures occurring from 300m1 on clearly present potential danger to the kidneys, Adapted with permission from ref. 26.

is place~din the rectum or vagina. The ability to calculate subtracted detrusor pressure allows one to distinguish between a true rise in detrusor pressure and the effect of increased abdominal pressure (e.g., straining, Valsalva) (Fig. 6).

VOIDING PRESSURE FLOWSTUDY Cystometry assesses the bladder's response to filling, however, by itself tells nothing about the bladder's ability to empty. This can be determined by allowing a patient to void (voluntarily or involuntarily) during bladder pressure monitoring. When the simultaneous measurement of uroflow is added, i.e., voiding pressure-flow study, detrusor contractility as well as the resistance of the bladder outlet can be determined (Fig. 7). In fact, detrusor pressure during voiding is actually determined by the amount of outlet resistance. The more resistance,

44

Nitti and Ficazzola

a

- loo WeS

c m HZO

B

-

.. . 100

-5

cm H20

- r0m P-bd ern H20 -100 0

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em H20

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Fig. 6. Adding intra-abdominal pressure monitoring gives a better representation of the true detrusor pressure. (A) Single channel study showing multiple spikes and rises in vesical pressure (Pves). Without having simultaneous monitoring of intra-abdominal pressure, it is impossible to tell if these pressure spikes are due to a rise in detrusor or abdominal pressure. (B) Same tracing with intra-abdominal pressure monitoring added. It can now be determined that the changes in Pves are due to the changes in abdominal pressure (Pabd). When one looks at the subtracted detrusor pressure curve (Pdet), it is flat without any significant rises. Adapted with permission from ref. 26.

the more forceful the bladder will contract (29).Since any given bladder has a set bladder outlet relation, the higher the pressure, the lower the flow. Thus obstruction can be defined as relatively high pressure and low flow. In cases where contractility is impaired, the same detrusor pressure will result in a lower flow. Voiding pressure flow studies are extremely important in evaluating lower urinary tract symptoms and voiding dysfunction. For example, bladder outlet obstruction and/or impaired detrusor contractility may be directly responsible for symptoms (e.g., decreased uroflow, incomplete emptying); abnormal voiding can affect the bladder’s ability to store and result in an abnormal cystometrogram (e.g., detrusor instability or decreased compliance caused by bladder outlet obstruction). In general, one can diagnose bladder outlet obstruction when high pressure and low flow are seen on a voiding pressure flow study.

45

ChapterEvaluation 2 / Diagnostic

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Fig. 7. Normal voiding pressure-flow study in a male. During voluntary voiding on the right portion of the tracing, there is a rise in Pdet associated with flow. There is a slight decrease in Pabd during the second half of voiding, with Pabd returning to just below baseline. The uroflow curve is relatively normal with Qmax = 22 mL/s. Detrusor pressure during voiding was about 30 cm H20.

Sometimes this is obvious (Fig. S), but other times a more sophisticated analysis of the pressure flow relationship is needed. In men, several such analyses or nomograms have been described to diagnose obstruction and impaired contractility (Figs. 9 and 10) (16,30).

LEAK-POINT PRESSXJRE Leak-point pressures are used to determine the pressure at which involuntary loss of urine occurs. There are two types of leak-point pressures that can be determined and each represents the measurement of a completely different parameter and concept (31): 1. Abdominal leak-point pressure (ALPP). This pressure, also known as the Valsalva leak-point pressure, is the amount of abdominal pressure required to cause leakage of urine, in the absence of a rise in Pdet. It is a measure of the resistance of the sphincter to rises in Pabd and is

46

Nitti and Ficazzoia

6:40

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t . .i .l .l . I. I. I. I. I. I. I. I. I. . I . I . I . I . I . I . I . I . I . . 1 . 1 . i . 1 . 1 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . -

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commonly used in evaluating patients with stress incontinence (Fig. l l). There is no ‘“nomal” ALPP, because there should not be leakage when any physiologic abdominal pressure is generated. Very low leakpoint pressures are suggestive of intrinsic urethral dysfunction. 2. Bladderleak-pointpressure(BLPP).This pressure, also known as detrusor leak-pointpressure, is the amount of detrusor pressure required to cause leakage in the absence of a rise in Pabd (32). It is a measure of the resistance of the sphincter to rises in Pdet. BLPP is useful in cases of detrusor dysfunction, where storage pressures are elevated, usuallyincases of impairedcompliance(Fig. 12). The higherthe BLPP, the more resistance is provided by the sphincter and the more likely is upper tract damage. BLPP thatis 40 cm W20 or greater during storage can lead to upper tract damage (28).

ELECTROMYOGRAPHY The storage and emptying phases of the micturition cycle are affected by the perineal musculature including the striated external urethral

ChapterEvaluation 2 I Diagnostic

47

200

Pdet

Unobstructed 0 t

0

I

Flow

25

Fig. 9. The Abrams-Griffiths Nomogram. Maximumflow rate and the conesponding detrusor pressure at maximum flow are plotted against each other, with detrusor pressure in cm H 2 0 on the y-axis and uroflow rate in mL/s on the x-axis. Data used from 117 males (>55 years) evaluated for possible prostatic obstruction were to create zones on their graph representing obstructed, unobstructed and equivocal micturition. The locationof the plotted maximum flow point on the graph determines the presence or absence of obstruction or an equivocal state. (In this case the patient would be obstructed.)

sphincter. Sphincter activity can be measured during urodynamic testing either by surface electrodes (similar to those used for electrocardiogram) or by inserting needle electrodes directly into the sphincter muscle (33). When surface electrodes are used, it is actually the activity of the anal sphincter that is measured, but it is extremely rare for anal sphincter activity to be dissociated from urethral sphincter activity. Normally, external sphincter activity will increase as bladder pressure rises (e.g., with detrusor instability) as a way to protect against incontinence. Conversely, the external sphincter should relax during voiding (Fig. 13). In fact, normally, the external sphincter relaxes before a bladder contraction is initiated. Failure of the external sphincter to relax during voiding can result in lower urinary tract symptoms and dysfunction. This can be a learned behavior (dysfunctional voiding) or can occur involuntarily as a result of neurological disease (detrusorexternal sphincter-dyssynergia). Either can result in significant voiding

48

Nitti and Ficazzola

pre 17/18 TURP 19/20 post Grade:

IllN -> OIN Type: cornp r o 3 I v e

2 0 30 4 0 50

Fig. 10. Linear PURR nomogram. This nomogram developed by Schafer allows for the determination of obstruction independent of contractility. The degree of obstruction is determined by 7 zones on the pressure-flow diagram labeled 0 to VI corresponding to increasing grades of obstruction: grade 0 and I, no obstruction; grade 11, equivocal or mild obstruction; grade I11to VI, increasing severity of obstruction. The boundary between grades 2 and 3 corresponds to the boundary between equivocal and obstructed in Abranis-Griffiths nomogram. Contractility zones are also seen: ST, strong; N, normal; W, weak. Adapted with permission from ref. 30.

dysfunction as outlet resistance during voiding is increased creating a functional obstruction.

VIDEOURODYNAMICS In certain cases, multichannel urodynamic testing is unable to provide a precise diagnosis. In such cases videourodynamics may be necessary. Videourodynamics refers to the simultaneous measurement and display of urodynamic parameters with radiographic visualization of the lower urinary tract (34,35). In these cases, the bladder is filled with radiographic contrast filling during urodynamics. Because all urodynamic parameters previously mentioned are visualized simultaneously with the radiographic appearance of the lower urinary tract, the clinician can better appreciate their interrelationships and recognize artifacts. Videourodynamics is the most precise way to evaluate lower urinary

49

ChapterEvaluation 2 / Diagnostic

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tract function and disturbances in micturition. In cases of complex voiding dysfunction, videourodynamics can be invaluable (Fig. 14).

BEDSIDE CYSTOMETRICS In cases where very basic urodynamic information such as sensation, capacity, and presence of detrusor contractions (voluntary or involuntary) is desired, a very simple CMG,known as bedside or eyeball urodynamics, canbe performed without any special urodynamic equipment. The urodynamicinformation provided, although limited, is sometimes enough to aid in malung a differential diagnosis (36). Bedside cystometrics are useful when sophisticated equipment is unavailable or when standard urodynamic testing would produce unduediscomfort for a particular patient. SimpleCMGcanbedonewitha urethral catheter, catheter tip syringe, and filling solution (saline or water). Prior to starting the patient is asked to void, if possible. A standard straight

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. . . . . . . . . . . . . . . . . . . . . . . . . .I

. . . . . . . . .

Fig. 12, Urodynamic study of a child with myelomeningocele and incontinence. The patient bas poorly a compliant bladderwith Pdet rising duringfilling. Leakage was demonstrated at a Pdet of 38 cm H20, marked by the vertical line. This is the bladder leak-point pressure (BLPP).

catheter 14-18 French is introduced into the bladder and postvoid residual is measured. A Foley catheter may be used if occlusion of the bladder neck is necessary or if one is already indwelling. A catheter tip syringe (usually 60 mL) is connected to the end of the catheter after its plunger is removed. Thecatheter and attached syringe are held directly upright and the top of the syringe is usually located about 15-20 cm above the patient's bladder (Fig. 15). The bladder is then slowly filled by gravity at 50-m.L increments as water or saline is poured into the syringe. The catheter and syringe should be kept as low as possible to allow for a steady infusion. Sensations and the volumes at which they occur can be noted. If it is necessary to raise the syringe to maintain flow rate, this usually means that intravesical pressure is increasing (contraction, poor compliance, orabdominal straining). When a sudden rise in pressure occurs, fluid may be seen backing up into the syringe. This is usually indicative of an involuntary contraction and may be accompanied by an urge; however, an abrupt decrease in compliance or abdominal straining can also do this. It is

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Fig. 13. Normal electromyographyof the pelvic floor during a pressure flow study. ENIG activityduringtheinvoluntarydetrusor Notethevoluntaryincreasein contraction and the decrease in activity during voluntary voiding. Adapted with permission from ref. 33.

helpful to gently place a hand on,the patient’s abdomen and careful observe for such movement. When it is important to assess voluntary contractility, the catheter can beraised to its maximum height and with the syringe empty, the patient is asked to void. If the top of the syringe is 25 cm above the bladder and fluid is raised to that level, then at least 25 cmH20 pressure was generated. If fluid is not seen backing up into the syringe, the catheter is slowly lowered to see if there is any increase in pressure. Again, a hand should be kept on the abdomen to rule out, as best as is possible, abdominal straining. Obviously, when a detrusor contraction coexists with abdominal straining, it is extremely difficult to sort out the two.

ENDOSCOPY Cystourethroscopy has been used in the evaluation of patients with lower urinary tract symptoms andvoiding dysfunction in order to assess the bladder, the urethra, and prostate and look for extraurethral causes of incontinence.

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Fig. 14. Videourodynamic evaluationof a woman in retention with primary bladder neck obstruction. Figure shows urodynamic tracing (top line is vesical pressure, second is abdominal pressure, third is detrusor pressure and forthflow) is as well as fluoroscopic image during voiding. There is a sustained detrusor contraction no Without imaging, of >40 cm H20with no openingof the bladder neck and flow. the point of obstruction could not be localized. Adapted with permission from ref. 35.

Evaluation of the Bhdder Cystourethroscopy to assess the bladder has been used as a routine part of the evaluation of males and females with LUTS and voiding dysfunction) to rule out intravesical pathology as a potential source of symptoms (37).The bladder is examined for an intravesical lesion or process that may be causing symptoms of instability, irritability, or incontinence. However a thorough review of the literature would suggest that, in routine cases, cystourethroscopy is optional and has its greatest value in select cases (38,39). There has been particular concern that irritative symptoms may be a warning of intravesical pathology such as carcinoma of the bladder. However there is no direct diagnostic value of cystourethroscopy in a patient with anunstable bladder unless microscopic hematuriais present (40,41).This would support the routine use of cystourethroscopy for patients with irritative symptoms when clinical suspicion of an intravesical lesion is high, such as when hematuria is present or when other tests such as radiography suggest

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Fig. 15. Bedside or eyeball urodymanics. A urethral catheter is placed in the bladder and raised vertically. A syringe (without its plunger) is connected tothe is Adapted with permission fromref. 26. end of the catheter and the bladderfilled.

intravesical pathology. However, cystourethroscopy is extremely helpful and recomended in cases where symptoms cannot be explained by other more routine diagnostic testing or in patients who have failed to respond to seemingly appropriate treatment. Cystourethroscopy should be part of routine follow-up for patients whose voiding dysfunction is managed by a chronic indwelling catheter or bladder augmentation or substitution.

Evaluation o f the Fmale BhdderOutlet Endoscopic evaluation of the female bladder outlet in cases of stress incontinence has been advocated by several authors ( 4 3 3 ) .However, others have found it to be inferior to other tests such as urodynamics (44-46). Most experts would nowagree that cystourethroscopy is inadequate to judge the functional integrity of the bladder outlet and will underestimate the presence of intrinsic sphincter deficiency. Endoscopic evaluation of the female bladder outlet is also of little value in the uncomplicated patient with urge incontinence (47). In select women, cystourethroscopy to evaluate the bladder outlet can be extremelyhelpful; for example, incases of urethral trauma orforeshortening, previous

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anti-incontinence surgery, suspected intraurethral pathology (e.g., urethral diverticulum), or bladder outlet obstruction. When evaluating the female urethra, it is extremely important to use an endoscope, which allows for complete visualization of the urethra. A rigid scope with no beak (or a short beak) to allow distension of the urethra, and a narrow lens (0-30”) or a flexible scope are optimal.

Evaluation o f the Male Bhdder Outlet Lower urinary tract symptoms in men were previously thought to be caused by benign prostatic hyperplasia. However, it is now known that a variety of conditions can cause such symptoms,including bladder outlet obstruction, detrusor instability, and impaireddetrusor contractility. Cystoscopic evaluation of men with LUTS used to be routine; however, now its indications are more limited. Based on the available evidence and world literature, The World Health Organization Third International Consultation onBPHmade the following recommendation:

“Diagnostic endoscopyof the lower urinary tract isan optional test in the standard patient with symptomsof prostatism because -the outcomes of intervention are unknown, -the benefits do not outweigh the harms of the invasive study,and -the patients’ preferences are expected to be divided. However, endoscopy is recommended as a guideline at the time of surgical treatment to rule out other pathology and to assess the shape and size of the prostate which may have an impact on the treatment modality chosen. (48) ”

Cystourethroscopy has a more definitive role in men who have undergone surgical treatment of the prostatic for benign or malignant disease when anatomic causes of postoperative voiding dysfunction are suspected (e.g., bladder neck contracture or anastomotic stricture).

Extmurethrul Incontinence Endoscopy can be aninvaluable tool in the diagnosis and treatment of extraurethral incontinence due to vesicovaginal fistula and ectopic ureter. Cystourethroscopy can precisely localize a fistula site in the bladder and help plan surgical correction. Occasionally, a small fistula

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that is not seen on physical exam or by radiographic studies can be diagnosed only by cystoscopy. Incontinence owing to ectopic ureter in the female is usually diagnosed by radiographic studies. However, the exact location of the ureteral orifice in the urethra or vagina can be identified by cystourethroscopy and/or vaginoscopy. This can be extremely helpful in the planning of corrective surgery.

URINARY TRACT IMAGING In certain cases of voiding dysfunction, imaging studies, including radiography, ultrasonography, magnetic resonance, and nuclear scanning, are an important part of the evaluation. Specifically, when detrimental effects on the upper urinary tract or anatomical abnormalities of the upper and lower urinary tract are suspected, such studies can be useful. We will limit our discussion to imaging of the upper and lower urinary tract; however, there are cases where a urologic workup of voiding dysfunction may prompt radiographic investigation of the nervous system or spine (e.g., in cases of suspected neurogenic voiding dysfunction).

Upper Urinary Tract Imaging As mentioned previously, voiding dysfunction can bea cause of renal damage or deterioration of function. In 1981, McCuire and colleagues popularized the now universally accepted concept of the relationship between high bladder storage pressure and renal deterioration (28). Thus, in cases of known or suspected high storage pressures (e.g., neurogenic voiding dysfunction) or elevated postvoid residual upper urinary tract, imaging is an important and necessary part of the evaluation. Also in certain patients with incontinence, an extra-urethral cause may be suspected (e.g., ectopic ureter or urinary tract fistula). The upper tract imaging modalities most commonly used are intravenous urography (IVIJ), ultrasonography, computerized tomography (CT scan), magnetic resonance imaging (MRI), and isotope scanning. The usefulness of each individual test often depends on local expertise. Intravenous urography (IVU) is a standard radiographic examination of the upper urinary tract. Successful examination is dependent upon adequate renal function. Renal dysfunction, obstruction, congenital

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anomalies, fistula, stones, andtumors may be detected. IVU is the appropriate first study when ureteral ectopia is suspected. It is also an appropriate first imaging study when ureterovaginal fistula is suspected (49,50).Confirmationof the fistula, its size, and its exact location are often obtained with retrograde ureteropyelography. IVU can also be used to evaluate hydroureteronephrosis; however, ultrasound has become the procedure of choice for this because itis more cost-effective and does not expose the patient to intravenous contrast (see below). Ultrasonography is an excellent tool for imaging of the upper urinary tracts. It is totally noninvasive, and successful imaging of the kidneys is independent of renal function. Ultrasound can beused to assess many features of renal anatomy including renal size and growth, hydronephrosis, segmental anomalies, stones, and tumors. In the evaluation of the patient with lower urinary tract dysfunction, the detection of hydronephrosis is extremely important and may be an indication of vesicoureteral reflux or obstruction. However, no correlation exists between the degree of dilatation and the severity of obstruction. Also renal blood flow can be detected by the Doppler technique. Ultrasound is an excellent tool to follow the degree of hydronephrosis over time or inresponse to treatment. CT scanning can also provide much useful information about the anatomy of the upper urinary tract. Information can be independentof renal function; however, the addition of intravenous contrast can highlight specific anatomic characteristics (dependent on renal function). In most cases of voiding dysfunction, adequate information about renal anatomy can be obtained with ultrasonography; however, there may be select cases where CT is beneficial. MRI offers some of the same benefits as CT in the evaluation of the upper urinary tracts. It has the advantageover CT in that all planes of imaging are possible. As technology advances, MRI may play an increasing role in the evaluation of hydronephrosis and urinary tract anomalies in the future. When it is necessary to investigate functional characteristics of the upper urinary tract, nuclear isotope scanning is useful. Renography is used to examine the differential function of the two kidneys as well as how they drain. There are many physiological factors and technical pitfalls that can influence the outcome, including the choice of radionucleotide, timing of diuretic injection, state of hydration and diuresis, fullness or back pressure from the bladder, variable renal function, and compliance of the collecting system (51,52).Diuresis renography with bladder drainage may be performed when obstructive uropathy is suspected (53).

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Lower Urinary Truct Imuging When anatomical factors are considered as a possible cause of voiding dysfunction, lower urinary tract imaging can be useful. A plain radiograph of the abdomen and pelvis (KUB) can determine the presence of stones or foreign bodies, which can be contributing to LUTS and voiding dysfunction. The lower spine can also be evaluated (spina bifida occulta or sacral agenesis). A cystogram, with stress and oblique views, can beuseful in select cases of pelvic prolapse (especially when the degree of cystocele is difficult to determine on a physical exam) and stress incontinence in women to determine support defects (54). Voiding cystourethrography (VCUG) may detect abnormalities such as posterior urethral valves, urethral diverticulum, urethral stricture, or other anatomic abnormalities of the urethra. In cases where female bladder outlet obstruction is suspected the VCUC in addition to urodynamic studies is important. We prefer videourodynamics in suchcases (55);however, when not available the VCUG can be done separately. The VCUG can also determine the presence of vesicoureteral reflux. Ultrasound of the bladder has become a convenient, noninvasive way to determine postvoid residual, especially with the introduction of small portable devices made specifically for determination of bladder volume.

REFERENCES 1. Wein AJ (1981) Classificationof neurogenic voidingdysfunction.J Urol125:605607. 2. Dioho AC, Brock BM, Brown MB,et al. (1986) Prevalenceof urinary and other urologic symptoms in the non-institutionalized elderly. J Urol 136:1022-1025. 3. Abrams P(1994) New wordsfor old: lower urinary tract symptoms for prostatism. Br Med J 308:929. 4. Blaivas JG, Heritz DM (1996) Classification, diagnosticevaluation and treatment overview. In: Topics in Clinical Urology-Evaluation and Treatment of Urinary Incontinence, (Blaivas JG, ed.), New York: Igaku-Shoin, pp. 22-45. 5. Resnick NM (1994)Urinary incontinence in the elderly. Medical Grand Rounds 3:281-290. FJ, O’Leary MP,et al. (1992) The American Urological Associa6. Barry MJ, Fowler tion symptom index for benign prostatic hyperplasia. J Urol 148:1549-1557. 7. Wagner TH, Partick DL, Bavendam TG, et al. (1995) Quality of life in persons with urinary incontinence: development of a new measure. Urology 47:67-72. 8. DeJong F (1967) The Neurologic Examination. Philadelphia: W.B. Saunders. 8a. Kim YH, Boone TB (1998) Voiding pressure-flow studies. In Practical Urodynamics Nitti VW, ed., Philadelphia: WB Saunders, pp. 52-64. 9. Boone TB, Kim YH (1998) Uroflowmetry. In:Practical Urodynamics, Nitti, VW, ed., Philadelphia: W.B. Saunders, pp. 28-37.

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10. Siroky MB, Olsson CA, Krane RJ (1979) The flow rate nomogram: I. Development. J. U r d 122:665-668. 11. Haylen BT, Ashby D, SutherstJR, et al. (l 989) Maximum and average urine flow rates in normal male and female populations-the Liverpool nomograms. Brit J Ur01 64~30-38. 12. Haylen BT, Parys BT, Anyaegbunam WI, et al. (1990) Urine flow rates in male and female urodynamic patients compared with the Liverpool nomograms. Br J Urol 65:483-487. 13. Drach GW, Layton TN, Binard WJ (1979) Male peak urinary flow rate: relationships to volume voided and age. J Urol 122:210-214. 14. Barry MJ, Giman CJ, O’Leary MP, et al. (1995) Using repeated measures of symptom score, uroflowmetry and prostatic specific antigen in clinical the management of prostate disease. J Urol 153:99-103. 15. Chancellor MB, Blaivas JG, Kaplan SE, et al. (1991) Bladder outlet obstruction versusimpaireddetrusor contractility: the role of uroflow. J U r d 145:810812. 16. Abrams PH, Griffths DJ(1979)The assessment of prostatic obstruction from urodynamic measurements andfrom residual urine. Br J U r d 5 I :129-134. rates versus 17. McLoughlin J,Gill KP, Abel PD,et al. (1990) Syrnptorns versus flow urodynamics in the selection of patients for prostatectomy. Br J Urol 66:303-305. 18. Girman CJ, Panser LA, Chute CG, et al. (1993) Natura1 history of prostatism: urinary flow rates in a community-base study. J Urol 150:887-892. 19. Drach GW, Ignatoff J, Layton T (1979) Peak urinary flow rate: observations in female subjects and comparison to male subjects. J U r d 122:215-219. 20. Jorgensen JB, Jensen KM-E (1996) Uroflowmetry.Urol Clin N Am. 23:237-242. 21. Hahn I, Fall M (1991) Objective quantification of stress urinary incontinence: a short reproducible, provocative pad-test. Neurourol Urodyn 10:475-48 1. testobjective 22. Jorgensen L,Lose G, AndersenJT (1987) One hour pad-weighing for assessment of female incontinence. Obstet Gynecol 69:39-41. 23. Jorgensen L, Lose G, Thunedborg P (1987) Diagnosisof mild stress incontinence in females: 24-hour home pad test versus the 1-hour ward test. Neurourol Urodyn 6: 165-166. 24. Versi E, Anand D, Smith P, et al. (1996) Evaluation of the home pad test in the investigationof female urinary incontinence.Br J Obstet Gynecol103(2):162-167. In: Practical 25. Nitti VW, Combs AJ (1998)Urodynarnicswhenwhyandhow. Urodynamics, Nitti VW, ed., Philadelphia: WB Saunders, pp. 15-26. 26. Nitti VW (1998) Cystometry and abdominal pressure monitoring. In: Practical Urodynarnics, Nitti VW, ed., Philadelphia: W.B. Saunders, pp. 38-51. JG, Stanton SA, and Andersen JT (1988) The standardization of 27. Abrams P, Blaivas terminology of lower urinarytract function. Scand J Urol NephroZ (Suppl.) 1145. 28. McGuire EM, WoodsideJR, Borden TA (1981) Prognostic valueof urodynamic testing in myelodysplasic children. J U r d 126:205. 29. Griffiths DJ (1973) The mechanics of the urethra and of micturition. Br J U r d 451497-507. 30. Schafer W (1990) Principles and clinical application of advanced urodynarnic analysis of voiding function. Urol Clin NArn 17553-566. In: 31. Cespedes RD, McGuire EJ (1998) Leak point pressures. Practical Urodynamics, Nitti VW, ed., Philadelphia: WB Saunders, pp. 94-107. 32. McGuire EJ, Fitzpatrick CC, WanJ, et al. (1993) Clinical assessment of urethral sphincter function. J U r d 150:1452-1454.

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Practical Urodynamics, Nitti WV, ed., 33. O’DonnellPD.Electromyography.In: Philadelphia: WB Saunders, 1988 pp. 65-71. 34. Blaivas JG, Fischer DM (1981) Combined radiographic and urodynamic monitoring: advances in techniques. J Urol 125:693-694. 35. Nitti NW, Raz S (1996) Urinary retention. In: Female Urology, 2nd ed, Raz S, ed., Philadelphia: WB Saunders, pp. 197-213. S, et al.(1988)Simpleversusmultichannel 36. Ouslander J, LeachG,Abelson cystometry in the evaluation of bladder function in an incontinent geriatric population. J Urol 140:1482-1486. 37. Langmade CF, Oliver JA (1984) Simplifying the management of stress incontinence. Am J Obstet Gynecol 149:24. 38. Fischer-Rasmussen W, Hansen RI,Stage P (1986) Predicative valueof diagnostic tests in the evaluation of female urinary stress incontinence.Acta Obstet Gynecol Scand 65:291. 39. Cardoza LD, StantonSL (1980) Genuine stressincontinence and detrusorinstability-a review of 200 patients. Br J Obstet Gynecol 87:184. 40. Mundy AR (1985j The unstable bladder. Urol Clin N Am 12:317-328. 41. Duldulao IUi, DioknoAC, Mitchell B (1996): Value of urinarycytology in womenpresentingwithurge incontinence and/or irritative voiding symptoms. J Urol 157:113-116. 42. Robertson JR (1976) Urethroscopy-the neglected gynecological procedure. Clin Obstet Gynecol 19:315-340. 43. Aldridge CW Jr, Beaton JH, Nanzig RP (1978) A review of office cystoscopy and cystornetry. Am J Obstet Gynecol 131:432-437. 44. Scotti RJ, Ostergard DR, Guillaume AA, Kohatsu KE (1990) Predicative value of urethroscopycompared to urodynamicsinthe diagnosis of genuine stress incontinence. J Reprod Med 35:772-776. 45. Horbach NS, Ostergard DR (1994) Predicting intrinsic sphincter dysfunction in women with stress urinary incontinence. Obstet Gynecol 84: 188-192. of thecystoscopic 46. Govier FE, Pritchett TR, KornmanJD(1994)Correlation appearance and functional integrity of the female urethral sphincteric mechanism. Urology 44:250-253. 47. Sand PR, HillRC,OstergardDA(1987)Supineurethroscopicandstanding cystometry as screening methods for the detection of detrusor instability. Obstet Gynecol 7057-60. 48. World Health Organization Proceedings of the 3rd Consultation on Benign Prostatic Hyperplasia (BPH), Monaco, June 26-28, 1995, pp. 191-193. 49. Mandal AK, Shwma SK, Vaidyanathan S, Goswami AK (1990) Ureterovaginal fistula: summary of 18 years’ experience. Br J Urol 65:453. a report of 50. Murphy DM, Grace PA, O’Flynn JD (1982) Ureterovaginal fistula: 12 cases and review of the literature. J Urol 128:924. 51. Conway JJ (1992) “Well-tempered” diuresis renography: it’s historical development, physiological and technical pitfalls, and standardized technique protocol. Seminars Nuclear Med 22174. Frokier J (1987) 52. Hvistendahl JJ, Pedersen TS, Schmidt F, Hansen W, Djurhuus JC, The vesico-renal reflex mechanism modulates urine output during elevated bladder pressure. Scand J Urol Nephrol 186(31 suppl.): 24. 53. O’ReillyPH(1992)Diuresisrenography.Recentadvancesandrecommended protocols. Br J Urol 69:113.

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54. Shapiro R, Raz S (1983) Clinical applications of the radiographic evaluation of female incontinence. In FernaEe Urology, Raz S, ed., Philadelphia: WB Saunders, pp.123-136. 55. Nitti VW, Tu LM, Gitlin J Diagnosing bladder outlet obstruction inwomen. J UPUZ 161: 1535-1540.

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Cerebrovascular Accidents serge Peter Mdrinkovic, MD

m d Gopd H. B a d h i , MD CONTENTS INTRODUCTION CENTRAL INNERVATION OF THE LOWER URINARYTRACT AND THE PONTINE MICTURITION CENTER(PMC) INCIDENCE OF URINARY INCONTINENCE PATHOPHYSIOLOGY OF INCONTINENCE

EARLYPRESENTATION LATEPRESENTATION URODYNAMICS STUDIES HEMISPHERIC DOMINANCE AND VOIDINGDYSFUNCTION UROLOGICAL EVALUATION HISTORY TECHNICAL DIFFICULTIES INTERPRETATION OF THE STUDY SPECIFICSITUATIONS MEDICALAND SURGICAL MANAGEMENT URINARY RETENTION IN WOMEN URINARY INCONTINENCE IN MEN AND WOMEN ALTERNATIVE THERAPIES SUMMARY REFERENCES

From: Current Clinical Urology: Voiding Dysfinction: Diagnosis and Treatment Edited by: R. A. Appell 0 Hurnana Press Inc., Totowa, NJ 63

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INTRODUCTION Cerebrovascular accidents (CVA) orstroke are a common andserious neurologic event in the elderly. The residual effects can be permanent or temporaryand vary in their morbidity. Theseimpairments may include the loss of memory, vision, speech, motor function, and control of micturition. A CVA isdefined as the acute onset of a focal neurologic deficit caused by an occlusive event (i.e., cerebral emboli oratherosclerotic thrombis) or a hemorrhagic focus. Cerebrovascular accidents are the third leading cause of death in the United States ( I ) and although their incidence is still one tenth that of myocardial infarction, they result in over 30 billion dollars in annual health care costs (2). Risk factors for CVA’s include hypertension, diabetes mellitus, smoking, increased serum cholesterol level, alcohol consumption, obesity, stress, and sedentary lifestyle (3-6). Greater than 500,000 CVAs occur annually in the United States, one-third of which are fatal, one-third requiring long-term nursing care, and the remaining one-third returning home, many at their previous level of function (7). Recently, the incidence of cerebrovascular accidents in individuals over 70 years of age and their mortality have been shown to be declining (8,9). CVA can have a profound effect on genitourinary function. The voiding dysfunction can range from urinary retention to total urinary incontinence (10-14). The CVA can also result in significant sexual dysfunction, Since CVA predominantlyoccurs in the elderly population, the issue is further influenced by coexisting genitourinary dysfunction (e.g., bladder outlet obstruction in males, stress urinary incontinence (SUI) in females). Cornorbid medicalconditions can effect the genitourinary system (e.g., Diabetes mellitus, vascular dysfunction, coronary artery disease). Furthermore, changes secondaryto aging (e.g., bladder instability, change in circadian rhythm, influence of hormonal withdrawal in females, cognitive impairment), can impair function of the genitourinary tract. It is generally recognized that genitourinary dysfunction improves as the time from the onset of stroke increases. It is not precisely clear if this is owing to improvement in genitourinary function or declining disability of the patient. Urinary incontinence immediately after a stroke has also been determined to infer a poor overall prognosis (1.5,16). Wade and Hewer(16) followed 532 patients shortly after the onset of a CVA. Patients with urinary incontinence within 1 wk of CVA fared poorly, with 50% dying within 6 mo of presentation. Incontinence at 3 wk also predicted a higher risk of dying and a decreased chance of regaining mobility.

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They also found a 44% incidence of urinary incontinence and 63% of these patients showed an alteration in their level of consciousness, as compared to 1% of 300 continent patients demonstrating a similar change in level of consciousness. Taub et al. (15)reviewed 639 registered CVA patients for disability at 3 and 12 mo. Initial incontinence was found to be the best single indicator of future disability with a sensitivity and specificity of 60% and 78%. Using urinary incontinence as a good predictor of morbidity and mortality, these patients can be stratified into a high-risk group requiring more detailed and intensive medical surveillance for a potentially better outcome.

CENTRAL INNERVATION OF THE LOWER URINARY TRACT AND THE PONTINE MICTURITION CENTER (PMC) The central nervous system (CNS) has an important role in regulating the ability of the bladder to facilitate the storage and emptying of urine. These CNS functions may be divided into three specific areas: suprapontine, pontine, and spinal centers. Voiding is coordinated by the neurons of the pontine-mesencephalic gray matter or the Pontine Micturition Center (PMC) (17,18). Voiding depends onthe spinobulbospinal reflex through the PMC after receiving input from the hypothalmus, thalmus, basal ganglia cerebellum, and cerebral cortex. The input from the suprapontine center is predominantly inhibitory but may have partial facilitory action. The major inhibitory areas appear to be the cerebellum, basal ganglia, and cerebral cortex, while facilitation may be regulated by the posterior hypothalmus and anterior pons ( I 7-23). Additionally, most of the suprapontine input into the PMC is inhibitory. Interruption of this input by a cerebrovascular accident, Parkinson’s disease, or brain tumor may result in detrusor overactivity or detrusor hyperreflexia (DH). This detrusor hyperreflexia may manifest itself with symptomatic frequency, urgency, and urge incontinence. ThePMC regulates efferent stimuli to the bladder and external sphincter by its two regions, medial and lateral. The medial region regulates motor stimuli to the detrusor muscle by overseeing the communication betweenthe reticulospinal tracts and the sacral intermediolateral cells carrying the preganglionic parasympathetic neurons that innervate the bladder detrusor muscle, Electrical stimulation of the

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median region elicits a decrease in pelvic floor electromyographic (EMG) activity and urethral pressure with a concomitant increase in intravesical pressure. The lateral region regulates the corticospinal stimuli to Onuf‘s nucleus in the sacral spinal cord, which innervates the levator ani, and urethral and anal sphincters. Electrical stimulation of this area results in anincrease of urethral pressure and levator ani (EMG) activity but with only no or minimal elevation in intravesical pressure.

INCIDENCE OF URINARY INCONTINENCE The incidence of early poststroke urinary incontinence varies from 57-83% (11,26,31,32). These studies suggest that incontinence may be transitory and related to the patient’ S immobility and altered mental status. In a study of 151 patients, Borrie et al. (26) reported an initial incontinence rate of 60%.After 1mo, this incidence was reduced to 29% at 1 mo. Additionally, 66% of patients with mild incontinence at 1 mo regained continence at 3 mo. Brocklehurst et al. (32) found an initial incontinence rate of 39%. They demonstratedthat by 2 mo 55% were continent and at 6 mo this increased to 80%. However, the 2 and 3 yr follow-up data demonstrate anincidence higher than the general population. Improvement with time is impressive and should be relayed to the patient and family. Communicating this information could improve the patient’s self-image and be an encouraging factor for the future.

PATHOPHYSIOLOGY OF INCONTINENCE Frontal cortical lesions from a CVA may affect a patient’s higher cognitive functions. This may be reflected by the patient’ S inability to suppress a reflex detrusor contraction resulting in urinary incontinence. This incontinence can be owing to 1. Detrusor hyperreflexia; 2. CVA related language and cognitive impairments with normal bladder function; or 3. Overflow incontinence secondary to detrusor hyporeflexia (mediated by either neuropathies or medications) (13).

The concomitantdiagnosis of dementia and benign prostatic hyperplasia (BPH) in males andurethral incontinence in females may also contribute

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to urinary incontinence. However, it must be emphasized that incontinence in the CVA patient merits evaluation to determine its etiology.

EARLY PRESENTATION Acute urinary retention commonly occurs after a CVA. The neurophysiologic explanation for this detrusor areflexia is unknown but is referred to as cerebral shock (25). The size, location, and extent of a CVA may have a profound affect on micturition. However, acute urinary retention may not necessarily be a result of CVA but may be related to the patient’s inability to communicate their need to void, impaired consciousness, temporary overdistension of the bladder, and restricted mobility (26).Pre-existing comorbidities such as bladder outlet obstruction, diabetic cystopathy, and various medications (with anticholinergic side effects) may also be responsible for urinary retention. Prospective urodynamic studies on patients soon after unilateral CVAs demonstrated a 21% incidence of overflow incontinence because of detrusor hyporeflexia. However, a significant number of patients in this study were diabetics or patients on anticholinergic medications (13). Our urodynamic evaluation of patients soon after cerebellar infarcts have detected a high incidence of urinary retention. In contrast, cerebellectomy in an animal model (27) results in hyperreflexia rather than areflexia; thus, the role of the cerebellum in micturition is still speculative and will need more prospective clinical and animal studies for clarification.

LATE PRESENTATION The symptomsof bladder dysfunction after established CVA include frequency, urgency, and urge incontinence (11,30). These symptoms are generally a result of detrusor hyperreflexia (14,28,29,30).Tsuchida et al. (30)evaluated 39 patients urodynamically after a CVA. Themean time from CVA to urodynamic evaluation was 19 m0 (range 11 da to 13 yr). They found that 66% of the patients complained of frequency or urge incontinence and the remaining 33% had either dysuria or urinary retention. Tsuchida determined that the symptoms of urgency or frequency are related to detrusor hyperreflexia, and this may also contribute to urge incontinence.

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Table 1 Patient Urodynamic Findings on CMG and EMG Group

CMG

EMG

Normal Hyperreflexic Hy perreflexc Hyperreflexic Areflexic

Normal Normal AVCS DSD Normal

Used with permission from ref. 33.

URODYNAMICS STUDIES Published studies assessing a CVA’s affect on the bladder have largely been performed in a retrospective fashion with evaluations occurring from days to years after their initial event. Detrusor hyperreflexia has been demonstrated to be the main finding in their voiding dysfunction (12,14,28,30). Other studies have attempted to correlate the site of ischemic or hemorrhagic infarct with urodynamic findings but have been inconclusive (28). Burney et al. (33) performed a prospective study of 60 patients, correlating the site of ischemic or hemorrhagic CVA by either CaT Scan or magnetic resonance imaging (MRI) with the results from urodynamic testing. All patients were imaged within 72 hr of presentation. If a patient had a diagnostic infarct, the patient underwent a filling and voiding multichannel cystometrogram (CMG) study with a simultaneous electromyogram (EMG) recording with a needle electrode. Patients were then separated into five groups based on the results of their urodynamic testing (see Table 1). This study demonstrated that the majority of frontalparietal and internal capsular lesions caused detrusor hyperreflexia and absent volitional control of the external sphincter (AVCS). Those patients with temporo-occipital lesions had normal urodynamic studies (see Table 2). Burney et al. (33) also found that 47% of their patients were in urinary retention and overflow incontinence. Various lesions were responsible for bladder areflexia, including the frontalparietal area, internal capsule, basal ganglia, thalamus, pons, and cerebellum (see Table 2). Eighty-five percent of the hemorrhagic infarcts (17/20) exhibited an areflexic bladder, whereas only 10% (n = 4) of the ischemic CVA’s demonstrated detrusor areflexia (see Table 3). Will the type of

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Table 2 Site of CVA Correlated with Urodynamic Findings Site of lesion Group

I

Group 3

Group 4

Group 5

0 0 0 0 0

6 0 0 2 12

0 0 0 0 0 0

2

0

Frontalparietal Occipital Temporal Multifocal Internal capsule Basal2ganglia Combined Thalamus Pons Cerebellum Totals Used with

Group 2

1 1 0 2 2 0

2

3

0 0 8

3

0 0

4 4

1

0 0 0 0

0

0

2 0

24

2

2 3

0 0 0 5

6

21

permission from ref. 33.

infarct determine the type of voiding dysfunction? This has yet to be confirmed, but areflexia has been seen after large infarcts of either varieties (28,34). Electromyograms performed in the majority of poststroke patients reveal uninhibited relaxation of the external sphincter during or preceding detrusor contractions with resultant urinary incontinence (15).Interestingly, detrusor sphincter dyssynergia (DSD) is uncommon in the poststroke period (13,35).However, pseudodyssynergia, demonstrated by the voluntary contraction of the external sphincter during an involuntary detrusor contraction, may bemorecommonlyobservedin the recovery phaseand should not be misinterpreted as DSD (36,37). Because of these confounding clinical possibilities, we recommend that there be close supervision of all urodynamic data and clinical symptoms by the urologist during a urodynamic study. Table 3 Type of CVA and Urodynamic Findings Type of CVA

Hemorrhagic (n = 20) Ischemic ( n 2= 40) Totals ( n = 60)

Group I

1

7

Group 2

17 4

8

Used with permission from ref. 33.

0 1

2

Group 3

Group 4

Group 5

1 23 24

5

21

4

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Table 4 Urodynamic Results with Right Hemiplegia No of patients

13 males

Average age Capacity No hyperreflexia No areflexia No normal

77 yr 288 mL

6 2 5

11 females 84 yr 317 mL 6 3 2

Used with permission from ref. 12.

HEMISPHERIC DOMINANCE AND VOIDING DYSFUNCTJON Hemisphericdominance has been well-established for language, whereas the temporal lobe has been linked to musical aptitude. Patients who have experienced a right hemispheric CVA have been known to incur more sexual dysfunction (38).In 1980, Khan etal. (14)postulated that patients after nondominant CVAs wereless likely to have urinary incontinence. If so, what effects would a dominant hemisphericstroke have on voiding? We retrospectively evaluated 44 symptomatic patients admitted to a rehabilitation unit after a stroke (12,33). The mean patient age was 81.2 yr and the time from CVAto urodynamic evaluation ranged from 1-12 mo. Tables 4 and 5 demonstrate their urodynamic findings with right hemiplegia or left hemiplegia. Both results were similar and we concluded that, as with many other studies (14,28)there was nosignificant difference in bladder dysfunction with dominant and nondominant hemispheric W A S .

Table 5 Urodynamic Results with Lek Hemiplegia No of patients

Average age Capacity No hyperreflexia No areflexia No normal Used with permission from ref. 12.

14 males 78 yr

210 mL 6

0 8

6 females 86 yr 416 mL 2

4 0

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UROLOGICAL EVALUATION The 1990s have seen the implementation of a multidisciplinary approach to the evaluation of the strokes (39). Neurologist, internist, and psychiatrist play key roles, whereas the urologist is consulted as needed. Our knowledge of voiding dysfunction in stroke patients largely comes from the evaluation of only symptomatic patients. In most instances, urological evaluation begins when the patient is transferred from an acute-care facility to a rehabilitation or a stroke unit. Like any other disease, process assessment begins with a history predating the stroke and proceeds with a laboratory and specialized tests such as a urodynamic evaluation and endoscopy. There are often problems related to the evaluation of the elderly. These can be broadly categorized into four areas: 1. Obtaining an adequate history; 2. Technical difficulty with doing studies in the elderly; 3. Interpreting a urodynarnicstudy(Whatisincidental due toaging? What is abnormal?); and 4. Multiple coexisting etiologies in a single patient.

When urodynamics are indicated, the best approach is to begin with simple screening urodynamics (uroflow and simple cystometry) then proceed to complex urodynarnics (multichannel urodynamics or video urodynamics), as needed. However, keep in mind that the evaluation and the extent to which it is carried out depend not only on the likely diagnosis, but also on the patient’s comorbid conditions, level of functioning, and the wishes of the patient and/or his or her family.

HISTORY Diagnosis largely depends on the history of symptoms. The elderly have been known to underreport their problems, especially when it is related to urinary incontinence. Interviewing the patient may not provide you with sufficient information on which to base a diagnosis. This is often compounded in those patients with dominant hemispheric CVAs with aphasia and those with dementia. Interviewing the caregiver (spouse, relative, or nurse’ S aide) may be necessary to provide additional information. A questionnaire given to the family, along with a voiding chart that is brought back on the second visit, is very helpful to assess ingested fluid and functional bladder capacity. The first visit is used

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to rule out reversible causes of incontinence such as infection, stool impaction, medications, and so forth. Targeted questions related to symptoms are helpful in relation to symptoms suchas urinary frequency. It is prudent to ask if the frequency is associated with high or low volume, whether it is day or night, and if it is associated with any symptoms of dysuria. Selective nocturia in the elderly can be caused by increased urinary output during the night due to loss of circadian rhythm, and/or peripheral pooling of fluid, which is mobilized with recumbency. Moreimportantly, nocturia can be owing simplyto a poor sleep pattern. A patient’s prescription and often-overlooked over-thecounter medications may have urological implications. In the physical examination, specific attention should be detailed to the mobility, visual acuity, hand coordination, and mental status of the patient in addition to the focused urological exam, including a digital rectal exam pelvic floor assessment in females, and prostatic evaluation in males. A regional neurological examination allows assessment of the ability to isolate the pelvic floor and voluntary contraction of the same. A voided urine analysis for infection and hematuriafollows. If hematura is present appropriate assessment with cytology, intravenous pyelogramand endoscopy should be considered.

TECHNICAL DIFFICULTIES There are several technical difficulties in doing urodynamics in the elderly, and the studies are tailored to individual patients rather than a set study being done on every individual. Often the elderly have decreased mobility and therefore may not be able to stand up or use the uroflow machine. In such cases, only a supine study may be possible. Every attempt is made to have themvoid prior to the study as a postvoid residual is an important parameter in the elderly. Use of a rectal pressure balloon is often mandatory in the elderly owing to the straining and Valsalva during the cystometry. The most useful study is cystometry and should be used as a screening urodynarnics study along with a postvoid residual. If complex urodynamics is then required, it should be performed with fluoroscopy along with the measurement of several other parameters (i.e., Valsalva leak-point pressure). Electromyogram (EMG) is done in select cases as DSD is an uncommon finding in CVA. Fluoroscopy is helpful in preselecting patients for EMG.

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I N T E R P ~ T A T I O NOF THE STUDY Since uninhibited bladder contractions can occur in continent elderly patients, the significance of bladder instability alone in the presence of incontinence is unclear. The uninhibited contraction can be present independently of associated stress incontinence and/or outlet obstruction. The reported incidence of age-related uninhibited contractions is 10%in women and25-35% in men. Otherage-related changes include, as mentioned earlier, increased urine output at night, prostatic enlargement in men, and changes in the urethra in the female related to loss of hormonal support. As such, the urethral pressure profile may change in the elderly as a normal aging process rather than being an abnormal finding. Ultimately, it is better not to rely on a single parameter, but rather review the whole picture in context of the associated conditions.

SPECIFIC SITUATIONS Benign prostatic hyperplasia (BPH) and stroke are common clinical situations involving a male patient who has some degree of incontinence following CVA. In such cases, one is left to wonder if detrusor overactivity is secondary to cerebral vascular accident and/or bladder outlet obstruction. It is helpful to get a history of voiding disturbances prior to the stroke since results following prostatectomy in CVA patients report persistence of voiding disturbances and unsatisfactory bladder control. It is prudent to evaluate these patients by sophisticated urodynamic techniques. One of the parameters that helps in differentiating the two is if a flow can be obtained from the patients (patients with BPH will generally have a low flow rate). Other techniques used are measurements of micturating urethral pressure profile during the voiding contraction. This test described by Yalla et al. (40) allows one to detect the point of obstruction or to ascertain if the posterior urethra is isobaric with the bladder during voiding. This test requires the use of fluoroscopy and a special catheter. It is also helpful clinically to know the effect of anticholinergics on this hyperreflexia preoperatively as 30% of the patients with hyperreflexia may not respond to anticholinergics and postprostatectomy. These patients will be significantly incontinent. The drawback of using anticholinergics preoperatively is that the patient may end up in urinary retention. The patient and family are prepared for the same. The use of minimally invasive techniques sach

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as temporary or permanent prostatic stents (Conticath [41]and Urolume [42,43]) may also be useful in these scenarios. Diagnostic dilemma in females includes coexisting bladder hyperreflexia secondary to CVA and urethral incontinence due to sphincteric malposition and or intrinsic deficiency. Assessment of SUI can be difficult if there is low-volume bladder hyperreflexia; conversely, detrusor hypeneflexia may be missed if the leak-point pressure is low and the bladder is not filled to an adequate volume. The latter is easy to overcome by occluding the outlet with a Foley balloon and filling the bladder to assess its filling function. A low-volume detrusor hyperreflexia with a coexisting open bladder neck at rest on fluoroscopy can be a difficult problem.

MEDICAL AND SURGICAL MANAGEMENT Retention and Obstruction in Men In the poststroke period, with the onset of cerebral shock and urinary retention, the need for clean intermittent catheterization (CIC) every 4-6 h may be a useful minimally invasive therapy. As spontaneous voiding occurs and postvoid residuals consistently return to less than 100 mL, CIC can be discontinued. If CIC is not feasible owing to patient or caretaker factors, an indwelling Foley catheter can be used and changed once a month. For those patients with documented bladder outlet obstruction, new medical and surgical therapies are becoming available. For some patients, long-acting oral medications called alphal blockers such as terazosin (44) (5 or 10 mg, qd), or doxazosin (45) (4 or 8 mg, qd) can be utilized if the patient is medically stable. They selectively antagonize the alpha, receptors, which mediate prostate smooth muscle tension, improve American Urological Association Symptom Scores, increase Qmax (peak flow rate mL/s), and reduce postvoid residuals. Their efficacy is dose-dependent and dosing needs to be titrated. However, potential side effects including dizziness, fatigue, headache, postural hypotension, and may preclude its use in the elderly. Tamsulosin46(0.4 or 0.8 mg, qd) is a potent and selective alphal, antagonist and does not require dose titration. It does not have significant effect on blood pressure and may be better tolerated. On the horizon are investigational, temporary prostatic stents or catheters. The Conticath (41); (Fig. 1) bridges the space from the

Chapter 3 I Cerebrovascular Accidents

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Fig. 1. Conticath-a temporary prostatic catheter.

bladder neck through the prostate and ends proximal to the external sphincter and can be used up to 30 da. The Conticath allows for voiding with much less discomfort and there are few contraindications for its use. Additionally, for high-risk patients, a permanent prostatic stent can beutilized. The Urolume(42,43)functions similar to the temporary stent, and can be placed under local anesthetic with minimal patient discomfort. It has proven to be an effective, low-risk therapy. Less invasive endoscopic procedures such as transurethral microwave thermotherapy (477 transurethral needle ablation of the prostate (48) Holmium (49) laser, and Indigo (50,51) laser prostatectomy may prove useful in the post-CVA patient. These procedures can all be performed under local anesthetic and reduce the operative risk to the patient. However, the urologist should refrain from performinga traditional transurethral resection of the prostate in the poststroke period for 6-12 m0 because incontinence and morbidity may be increased. Lum and Marshall(34) identified several variables that can affect outcome in the postprostatectomy CVA patient. These factors can lead to an unsatisfactory outcome in upwards of 50% of the patients. The most closely correlated with poor clinical outcome (higher incidence of urinary incontinence) were agegreater than 70, worsening neurological symptoms, site of CVA (bilateral or nondominant lesions), lack of associated urinary symptoms, and prostatectomy within 1 yr of a CVA.

76Badlani

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Fig. 2. Inflow device-24F intraurethral valved catheter with intraluminal pump.

URINARY MTENTION IN WOMEN Until recently women in urinary retention secondary to detrusor hyporeflexia have the following available: clean intermittent catheterization (CIC), or chronic indwelling Foley catheter. AlthoughCIC offers excellent long-range management of urinary retention, its use in CVA is restricted by the inability of the patient to perform this procedure owingto hemiparesis or hemiplegia, unless a family member or caregiver is able to do this. Chronic indwelling Foley catheters have been the alternative. A new investigational therapy is the In-Flow device (Influence Medical Technologies, San Francisco, CA) (Fig. 2), a 24F intraurethral valved catheter with intraluminal pump fora female atonic bladder. The catheter is fixed at the bladder neck by flexible silicone fins, which open like petals of a flower inside the bladder, and by an

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external tab at the urethral meatus. To urinate, the patient or caregiver holds a small hand-held battery operated magnetic unit near the lower abdomen, close to the pubic area. This activates a valve in the catheter and drives an intraluminal pump to draw urine from the bladder at a flow rate similar to that seen in normal urination. This device may prove to be the device of choice if clinical trials comparing it to CIC are successful. 1

"

URINARY INCONTINENCE IN MEN AND WOMEN The urologist goal with the incontinent patient is to restore a socially acceptable level of urinary continence while minimizing the risks of infection. Patients with detrusor hyperreflexia can be treated with timed voiding and concomitant fluid restriction and anticholinergic medications. Outlet obstruction inmalesand detrusor hyperactivity with impaired contraction (DHIC) in males andfemales can result in urinary retention with the injudicious use of anticholinergic medications (i.e., oxybutynin, dicyclomine hydrochloride, or hyoscyamine sulfate USP). In male patients, outflow obstruction should be treated prior to addressing detrusor hyperreflexia. We recommend the periodic monitoring of postvoid residuals in DHICpatients after the initiation of anticholinergic therapy, and educating these patients about the risks of urinary retention so that the risk can be minimized. Tolterodine (52,53) is a new anticholinergic that has been recently developed and given FDA approval for 1998. It has less binding to cholinergic receptors in the salivary glands and leads to less dry mouth and discontinuation of therapy secondary to adverse affects. For women with detrusor hyperreflexia and SUI, several oral medications are available that cause increased bladder outlet resistance, such as imipramine or phenylpropanolamine hydrochloride/ guaifenesin. There are many new minimally invasive surgical procedures that can also address concomitant SUI in women. If medical and/or behavioral therapy fail in the female CVA patient with urethral incontinence, a few minimally invasive procedures are available that provide fair to excellent improvement in SUI: 1. Periurethral or transurethral collagen injection (54); 2. Urosurge, (Urosurge Inc, Coralville, CA) (Fig. 3), an investigational self-detachable balloon system that is placed at the bladder neck under endoscopic guidance similar to collagen therapy; and

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Fig. 3. Urosurge device. A self detachable balloon system for stress urinary incontinence

3. Pubovaginal sling witwwithout bone anchors and with either autologous tissue (56) (rectus fascia or fascia lata), allogenic (57) (donor cadaver fascia), or synthetic materials (polypropylene (581 or polytetrafluoroethylene 1.591).

Allogenic and synthetic materials lead to decreased operating room time and cost without sacrificing patient outcome ormorbidity as compared to autologous tissue. Our success rate and complication rate using polypropylene with bone anchors (58) has been outstanding in this patient population. It is imperative that detrusor dysfunction be addressed first before treating urethral incontinence.

ALTERNATIVE THERAPIES Sometimes all that may be necessary for incontinence therapy in the stroke patient will be simple behavioral modifications such as fluid restriction and initiating a timed voiding schedule bothdetermined from a voiding diary. Many demented patients who no longer have socially appropriate behavior may also benefit substantially from a prompted voiding schedule. Celber et al. (13) reported that 37% of

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severely handicapped (aphasia, dementia, or immobility) incontinent patients had normalfunctioning bladders. Interesting, even these debilitated patients benefited from prompted voiding schedules and fluid restriction. This method of patient management is very labor intensive and worksbest in a home environmentwith one-to-one patient attention. For patients who fail medicalhehavioral therapy and are poor surgical candidates, there are less-than-ideal alternatives. The use of a carefully supervised chronic indwelling Foley catheter may be considered, with monthly catheter changes. However, complications can occur with a Foley catheter, such as increased detrusor hyperactivity, urinary tract infections, bladder calculi, squamous cell carcinoma of the bladder, adenocarcinoma of the bladder, urethral erosion, and fistulas. A suprapubic catheter may result in a similar complication profile to the chronic indwelling Foley and thus should also be approached with caution. Condom catheters are available but disturbing problems such as skin excoriation, maintenance of the device, and urinary tract infections may also limit their usefulness. CIC is another viable alternative therapy for those patients with overflow incontinence secondary to bladder outlet obstruction and/ or detrusor hyporeflexia. The patient or caretaker will need proper instruction, manual dexterity, and motivation to perform this minimally invasive procedure with success (60).While treatment attempts at curing a condition, management can aim at lessening the impact of voiding dysfunction and improving the quality of life.

SUMIVURY The urologist now plays an important role in the multidisciplinary evaluation of poststroke voiding dysfunction. An accurate assessment of voiding dysfunction is feasible in most patients for implementation of a logical therapeutic plan in conjunction with other caregivers. His or her role can help improve patient self-esteem, and quality of life, and reducemorbidity through anaccurate diagnosis and implementation of noninvasive or minimally invasive therapies.

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Disorders and Stroke. McDowell FM, Caplan LR,eds., Bethesda, MD: National Institute of Neurological and Communicative Disorders and Stroke, pp. 1-34. 2. Yatsu FM, Grotta JC, Villar-Cordova C (1997) In: Cerebrovascular Disorders in Scientijc American Medicine, v01 4, Dale DC, Fedeman DD, eds., New York, NY: Scientific American Inc, pp. 1-12. 3. Gorelick PB (1995) Stroke prevention. Arch Neurol 52:347-52. 4. Love BB, Biller J, Jones MP, et al. (1990) Cigarette smoking: a risk factor for cerebral infarction in young adults. Arch Neurol 47:693-697. 5. SHEP Cooperative Research Group (1993)Prevention of stroke by antihypertensive drug treatment in older persons with isolated systolic hypertension. JAMA 265:3255-3258. 6. Toni D, De Michele M, Fiorelli M, et al. (1994) Influence of hyperglycemia on infarct size and clinical outcome of acute ischemicstroke patients with intracranial arterial occlusion. J Neurol Sci 123:129-13 1. 7. Heart and Stroke Facts Statistics (1993) American Heart Association, Dallas, TX. 8. May DS, Kittner SJ (1994) Use of Medicare clairns data to estimate national trends in stroke incidence, 1985-1991. Stroke 25:2343-2346. 9. Klag MJ, Whelton PK, Seider AJ (1989) Decline in US stroke mortality, demographic trends and antihypertensive treatment. Stroke 20: 14-21. 10. Gross JC (1990) Bladder dysfunction after a stroke: it’s not always inevitable. J Gerontologic Nursing 16:20-23. 11. Arunabh MB, Badlani GH (1993) Urologic problems cerebrovascular in accidents. Problems Urol 7:41-53. 12. Badlani GH, Vohara S, Motola JA (1991) Detrusor behavior in-patients with dominant hemispheric strokes. Neurourol Urodyn 10:119-121. 13. Gelber DA, Good DC, Laven LJ, et al. (1993) Causes of urinary incontinence after acute hemispheric stroke. Stroke 24:378-382. 14. Khan Z, Hertanu J, Yang WC, et al. (1980) Predictive correlationof urodynamic dysfunction and brain injury after cerebrovascular accident. J Urol 126:86-88. 15. Taub NA, Wolfe CD, RichardsonE, et al. (1994) Predicting the disability of firsttime stroke sufferers at one year. 12-month follow-up of a population-basedcohort in Southeast England. Stroke 25:352-357. 16. Wade DT, Hewer RL (1978) Outlook after an acute stroke: Urinary incontinence andloss of consciousnesscomparedin 532 patients. Quart J Med 56:601608. 17. Carlsson CA (1978)The supraspinal control of the urinary bladder. Acta Phamzacol Toxicol 43(Supp 2):8-12. 18. DeGroat WC, Steers WD (1990) Autonomic regulation of the urinary bladder and sexual organs. In: Loewy AD, Spyer KM, eds., Central Regulation of the Autonomic Functions. London: Oxford University Press, pp. 3 13-333. 19. Bradley WE, T i m GW, Scott FB (1974) Innervation of the detrusor muscle and urethra. UroZ Clin N Am 1:3-27. 20. Bradley WE, Sundin T (1982) The physiology and pharmacology of the urinary tract dysfunction. Clin Neuropharmacol 5:131-158. 21 Bhatia NN, Bradley WE (1983) Neuroanatomy and physiology: innervation of the urinary tract. In: Raz S, ed., Female Urology, Philadelphia: WB Saunders, pp. 12-32. 22. Tang PC (1955)Levels of the brainstem and diencephaloncontrolling micturition reflex. J Neurophysiol 18:583-595. a

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areas 23. Tang PC, Ruch TC (1956) Localization of brainstemanddiencephalic controlling the micturition reflex. J Comp Neurol 106:213-231. 24. Nathan PW (1976) The central nervous connections of the bladder. In: Williams DI, Chisholm CD, eds., Scientijic Foundations of Urology, v01 2, Chicago, IL: Year Book Medical Publishers, pp. 51-58. 25. Hald T, BradleyWE(1982) The nervous control of theurinarybladder.In: Hald T, Bradley WE, eds., The Urinary Bladder: Neurology and Urodynamics, Baltimore, MD: Williams and Wilkens, pp. 48-51. 26. Borrie M, Campbell A, Caradoc-Davies TH, et al. (1986) Urinary incontinence after stroke: a prospective study. Age Aging 15:177-18 1. 27. Nishizawa 0,Ebina K, Sugaya K, et al. (1989)Effect of cerebellectomy on reflex micturition in the decerebrate dog as determined by urodynamic evaluation. Urol IntE 44:152-154. 28. Khan 2,Starer P, Yang WC,et al. (1990) Analysisof voiding disorders in patients with cerebrovascular accidents. Urology 35:265-270. 29. Motola JA, Mascarenas B, Badlani GH (1988)Cerebrovascularaccidents: urodynamic and neuroanatomical findings. J Urol 139:512A. 0,et al. (1983) Urodynamicstudies on hemiplegic 30. Tsuchida S, Noto H, Yamaguchi patients after cerebrovascular accident. Urology 2 1:315-3 18. 31. Adams M, Baron M,Caston MA (1966) Urinary incontinence in the acute phase of cerebrovascular accident. Nurse Res 15:lOO-105. 32. Brocklehurst JC, Andrews K, Richards B, et al. (1985) Incidence and correlates of incontinence in strokes patients. J Am Geriatr Soe 33:540-542. 33. Burney T, Senapati M, Desai S, et al. (1996) Effects of cerebrovascular accident on micturition. Uro Clinics N Am 23:483-486. 34. Lum SK, Marshall VR (1982) Results of prostatectomy in patients following a cerebrovascular accident. Br J Urol 54:186-189. 35. Motola JA, Badlani GH (1990) Cerebrovascular accidents, urological effects and management. Clin Geriatr Med 6:55-58. 36. Blaivas JG (1982) The neurophysiology of micturition: a clinical study of 550 patients. J Urol 127:958-963. 37. Wein A,Barrett DM (1982)Etiologic possibilitiesof increased pelvic floor electromyography activity during cystometry. J Urol 127:949-952. 38. Coslett HB, Heilman KM (1986) Male sexual function: impairment after right hemisphere stroke. Arch Neurol 43: 1036-1039. 39. Coletta EM, Murphy JB (1994)Physical and functional assessment of the elderly stroke patient. Am Fam Physician 49:1777-1785. 40. Yalla S, Blute R, Waters W, et al. (1980) Urodynamic evaluation of prostatic enlargementswithmicturitional vesicourethral static pressure profiles. J Urol 125~685-689. 41. Lightner DJ, BarrettDM, Schmidt R, et al.(1998) Conticath: a simplenew catheter designed for continence and volitional voiding past the obstructed urethra. J Urol 159:303. 42. Oesterling JE, Epstein H. (1993) North America Urolume Study Group. J Urol 149:10. 43. Corujo M, Badlani GH (1998) Uncommon complications of permanent stents. J Endo 12:385-388. 44, Lepor H, Auerbach S, Puvas-Baez A, et al. (1992) A randomized multicenter placebo controlled study of the efficacy and safety of terazosin in the treatment of benign prostatic hyperplasia. J Urol 148:1467-70.

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45. Gillenwater JY, ConnRL, Chrysant SG,et al. (1995) Doxazosinfor the treatment of benign prostatic hyperplasia in-patients with mild to moderate essential hypertension: A double blind,placebocontrolled dose response multicenter study. J Urol 154:110-1 14. 46. Lepor H, The Tamsulosin Investigator Group (1995)Clinical evaluation of tamsulosin, a prostate selective alpha,, antagonist. J Urol 153:274A. 47. Sravodimosk D, Goldfischer E, Klima W, et al. (1998) Transurethral microwave thermotherapy for management of benign prostatic hyperplasia: A single-institution experience. Urology 51:1008-1011. 48. Beduschi M, OesterlingJ (1998) Transurethral needle ablationof the prostate: A minimally invasive treatment for symptomatic benign prostatichyperplasia.Mayo Clin Proc 73:696-701. 49. Gilling P, Cass C, Cresswell M (3996) The use of the Holmium laser in the treatment of benign prostatic hyperplasia. J Endo 10:459-461. 50. IssaMM,TownsendM,JimineVK,Miller LE, Anastasia K (1998) A new technique of intraprostatic fiber placementto minimize thermal injury to prostatic urothelium during indigo interstitiallaser thermal therapy. Urology 5 l(1):105-1 10. 51. Martov A, Kilchukov 2,Gushchin B (1998) Long-term follow-up in interstitial laser coagulation in BPH treatment. J Endo 12(Supp 1):195. 52. Hills CJ, Winter SA, Balfour JA (1998) Tolterodine. Drugs 55(6):813-820. 53. Abrams P, Freeman R, Anderstrom C, Mattiasson A (1998) Tolterodine, a new antimuscarinic agent: as effective but better tolerated than oxybutyninin-patients with an overactive bladder. Br J Urol 81(6):801-810. 54. Stanton S, Monga AK (1997) Incontinence in elderlywomen: is periurethral collagen an advance? Br J Obstet Gynaecol 104(2):154-157. 55. Appell R (1998) Techniques and results in the implementation of the artificial urinary sphincter in women with type I11 stress urinary incontinence by a vaginal approach. Neurourol Urodynamics 7:613-617. 56. Marinkovic S, Mian H, Evankovich M,et al. (1998) Burch versus the pubovaginal sling. Inti Urogynecol J 8:260-265. 57. Wright EJ,Iselin CE, WebsterG (1998) Pubovaginal sling using cadaveric allograft fascia lata for the treatment of intrinsic sphincter deficiency. J Urol 159(Supp 1):215. 58. Hom D,Desautel MG, Lumerman 5, et al. (1998) Pubovaginal sling using polypropylene mesh and Vesica bone anchors. Urology 5 1:708-7 13. 59. Barbailias GA, Liatsikos EN, Athanasopoulos A (1997) Goretex sling urethral suspension in Type 3 female urinary incontinence:clinical results and urodynamic changes. Intl Urogynecol J 8:344--50. 60. Rosen N, Ravalli R (1990) Intermittent self-catherization. Clinic Geriatr Med 61101-107.

CONTENTS INTRODUCTION NEUROPHYSIOLOGY OF MICTURITION VIDEOURODYNAMICS TREATMENT OVERVIEW TRANSVAGINAL DENERVATION (INGELMANN-SUNDBERG PROCEDURE) SUBTRIGONAL PHENOL AND ALCOHOL INJECTIONS DETRUSOR MYOTOMY, BLADDER TRANSECTION AND CYSTOLYSIS DETRUSOR MYECTOMY (BLADDER AUTO-AUGMENTATION) AUGMENTATION CYSTOPLASTY & (WITH WITHOUT CONTINENT CATHETERIZABLE ABDOMINAL STOMA) AND CONTINENTURINARY DIVERSION SUMMARY REFERENCES

INTRODUCTION Multiple sclerosis is a chronic demyelinating disease with a variable clinical course. It is most common in the third to fifth decades of life and has a female to male ratio of about 3: 1. In North America and Europe, the incidence is approximately 10 new cases per 100,000 population between the ages of 20 to 50. The majority of patients have mild neurologic abnormalities, which tend to exacerbate and remit over time. The most severe cases are characterized by chronic progression, From: Current Clinical Urology: Voiding Dysfunction: Diagnosis and Treatment Edited by: R. A. Appell 0 Humana Press Inc., Totowa, NJ 83

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which may ultimately lead to quadriplegia. The clinical course is classified as acute, progressive, chronic, and benign ( I ) . The etiology of multiple sclerosis is unknown, but the prevailing theory suggests that it is an autoimmune disorder (1,2). From a pathologic standpoint it is characterized by focal inflammatory and demyelinating lesions scattered throughout the nervous system (3).The demyelinating plaques have a predilection for the white matter of the cervical spinal cord, particularly the posterior and lateral columns (4,5). Since these are the pathways that subserve vesical and urethral function ( 6 4 , bladder symptoms are prominent in the majority of patients (9-14). Bladder symptoms and urodynamic findings are subject to the same exacerbations and remissions as the underlying disease process. Some studies have reported that there is no correlation between bladder symptoms andeither the duration of illness or ageof the patient. However, others have shown a correlation between urinary symptoms and duration of disease and that as the disease progresses, urologic symptoms become common, eventually affecting at least 50% of men and 80% of women. In a series of 212 multiple sclerosis (MS) patients screened at a university clinic, Koldewijn et al. found that urologic symptoms correlated with the degree of disability, but not duration of disease (15). Over half of the patients with a Kurtzke score of greater than four suffered from urinary storage symptoms. Previously, it had been thought that urinary tract complications led to a high incidence of deaths in multiple sclerosis, ranging from 21-55% (16,17). At autopsy, Samellaset al. found that at autopsy, 55% of patients had hydronephrosis, or pyelonephritis that had directly contributed to their death (17). Leibowitz et al. on the other hand, reported that only 5% of deaths in MS patients were attributed to urologic complications (18). Withdevelopment of sophisticated urodynamic testing, modern therapeutic interventions and morecareful monitoring, urologic causes of death has decreased dramatically. However, the morbidity of lower urinary tract disorders, particularly incontinence, is still great. In a prospective study, Blaivas found that those who develop urologic complications were either women withsevere incontinence who were managed with indwelling catheters or men who had DESD. Women who developedDESD did not seem to be at nearly so high a risk (19). Lower urinary tract symptoms in patients afflicted with multiple sclerosis are usually attributed to the underlying condition, yet this is not necessarily the case. Nonneurogenic urologic disorders such as cystitis, urolithiasis, bladder and prostate cancer, and benign prostatic

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hypertrophy are probably as commonin these patients as in the general population and require the same End of diagnostic evaluation. Once these urologic conditions are excluded, the diagnosis is best accomplished when there is a clear understanding of the underlying pathophysiology. This, in turn, requires knowledge about the neurophysiology of micturition and the effect of specific neurologic lesions on normal physiology.

NEUROPHYSIOLOGY OF MICTURITION Normal voiding is accomplished by activation of the “micturition reflex.” This is a coordinated event characterized by relaxation of the striated urethral sphincter, contraction of the detrusor, opening of the vesical neck andurethra and the onset of urine flow (20). The micturition reflex is integrated in the pontine micturition center, which is located in the rostral brain stem (20,21,22). Interruption of the neural pathways connecting the “pontine micturition center” to the “sacral micturition center” usually results in detrusor external sphincter dyssynergia (23,20,24). Detrusor external sphincter dyssynergia is characterized by simultaneous involuntary contractions of the detrusor and the external sphincter. The involuntary detrusor contractions cause incontinence; the involuntary sphincter contractions result in bladder outlet obstruction. Detrusorexternal sphincter dyssynergia is commonly seen in patients with spinal cord involvement because of the demyelinating plaques, which are the hallmark of multiple sclerosis. Patients with untreated detrusorexternal sphincter dyssynergia are at high risk for developing urologic complications such as vesicoureteral reflux, hydronephrosis, urolithiasis, and urosepsis (19). When the neurologic lesion is above the pons, the “micturition reflex” is intact andwhen micturition is affected it is usually characterized by loss of voluntary control. This is usually manifest as detrusor hyperreflexia, but losing awareness of bladder events or concern about the consequences of incontinence are also common. Althoughthese patients are usually incontinent, they are at little risk for developing urologic complications unless they are treated with an indwelling vesical catheter, or have other urologic abnormalities. Neurologic lesions that interfere with the sacral reflex arcs are less common. These lesions result in various combinations of detrusor areflexia, intrinsic sphincter deficiency, and paralysis of the striated urethral sphincter.

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Symptoms Lower urinary tract symptoms may be classified as storage symptoms, emptying symptoms or mixed storage, and emptying(25). Storage symptoms include urinary frequency, urgency, incontinence, nocturia, and pain. Emptying symptoms include hesitancy, difficulty starting, weak stream, and a feeling of incomplete bladder emptying. About three fourths of patients with multiple sclerosis complain primarily of storage symptoms. The remainder has emptying or mixed symptoms. Many studies have found that there is no correlation between urologic symptoms, neurologic findings, and urodynamic findings. Blaivas performed prospective urodynamic study in 67 consecutive patients with MS and urinary bladder symptoms (19). Treatment was individualized on the basis of the underlying pathophysiology andconsisted of intermittent catheterization (21%), observation (27%), surgical (12%), drugs (g%), voiding training (6%),and external condom drainage (6%).In 18 patients (27%), lesser forms of treatment were unsuccessful, and indwelling vesical catheters were required. Symptoms correlated poorly with urodynamic findings, and treatment based on symptoms alone would have been ineffective in over half the patients. It is interesting to note that both voiding symptoms as well as urodynamic findings often changes overthe course of time. Wheeler and coworkers noted that 55% of patients had different urodynamic findings after repeat examination (26). Blaivas and associates found 15% of patients had markedlydifferent urodynamic findings upon repeat studies (11).Voiding dysfunction has also been documented in asymptomatic patients with MS. Bemelmans et al. evaluated 27 patients with no urologic complaints and a definite diagnosis of multiple sclerosis (mean duration of diagnosis-5 yr) (27). Fifty-two percent (14/27) had urodynamic abnormalities and 50% required urologic follow-up and therapeutic intervention.

Diagnostic Evaluation As always, evaluation begins with a history and physical examination. Urinary tract infection (UTI) is common is MS, andfor this reason, UTI should be excluded by urinalysis before further evaluation commences.

Urologic History The history begins with a detailed account of the precise nature of the patient’s symptoms. Each symptom should be characterized and

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quantified as accurately as possible. When more than one symptom is present, the patient’s assessment of the relative severity of each should be noted. The patient should be asked howoften he/she urinates during the day and night and how long helshe can comfortably wait between urinations. It should be determined why he/she voids as often as he/ she does. Is it because of a severe urge or is it merely out of convenience or an attempt to prevent incontinence? The severity of incontinence should be graded. Does the patient lose a few drops or saturate his/ her outer clothing? Are protective pads worn? Do they become saturated? How often are they changed? Is the patient aware of the act of incontinence or does he/she just find hidherself wet? Is there a sense of urgency first? If so, how long can micturition be postponed? Does urge incontinence occur? Does stress incontinence occur during coughing, sneezing, rising from a sitting to standing position, or only during heavy physical exercise? If the incontinence is associated with stress, is urine lost only for an instant during the stress or is there uncontrollable voiding? Is the incontinence positional? Does it ever occur in the lying or sitting positions? Is there difficulty initiating the stream requiring pushing or straining to start? Is the stream weak or interrupted? Is there postvoid dribbling? Has the patient ever been in urinary retention? In order to document the nature and severity of urinary incontinence, a micturition diary and pad test are most useful. Conceptually, a pad test will provide a semi-objective measurement of urine loss over a given period of time. Anumber of pad tests havebeen described (28,29), but none has met with widespread approval, mainly because of poor test-retest validation (30,31). The simplest pad test can be done by having the patient change his or her pads every 6 h for one representative 24 h period while he or she is taking Pyridium. The amount of staining on the pads is a rough estimate of the severity of the incontinence. Alternatively, the pads can be weighed and the total weight, minus the weight of an unused pad recorded in the patient’S record as an estimate of the volume of urine loss (1 gm approximately equals 1 mL,of urine). We believe the pad test is very useful and recommend that, once completed, the patient simply be asked to state how representative it was. To this end, the patient is asked to rate the day, on a scale of 1-10, with respect to how bad the incontinence was on the day that the pad test was recorded. The main purpose of these tests is to grossly quantitate the relative severity of the incontinence, so that it can be determined whether the symptoms are being accurately reproduced during subsequent examinations. Although there may be great variability in the actual data accumulated by these instruments,

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simply asking the patient whether or not the diary and pad test were representative of a “good” or “bad” day will usually suffice for clinical purposes.

Physical Examination The physical examination should focus on detecting anatomic and neurologic abnormalities that contribute to the patient’s symptoms. The nature of the incontinence should be determined by examining the patient with a full bladder as discussed in the following section entitled “eyeball urodynamics.”The neurourologic examination begins by observing the patient’s gait and demeanor as he first enters the office. A slight limp or lack of coordination, an abnormal speech pattern, facial asymmetry, or other abnormalities maybe subtle signs of a neurologic condition. The abdomen and flanks should be examined for masses, hernias, and a distended bladder. Rectal examination will disclose the size and consistency of the prostate. The sacral dermatomes are evaluated by assessing anal sphincter tone and control, perianal sensation, and the bulbocavernosus reflex. With a finger in the rectum, the patient is asked to squeeze as if he were in the middle of urinating and trying to stop. A lax or weakened anal sphincter or the inability to voluntarily contract and relax are signs of neurologic damage, but some patients simply don’t know ordon’t understand how to the contract these muscles, while others may be too embarrassed to comply with the instructions. The bulbocavernosus reflex is checked by suddenly squeezing the glans penis or clitoris and feeling (or seeing) the anal sphincter and perineal muscles contract. Alternatively, the reflex may be initiated by suddenly pulling the balloon of the Foley catheter against the vesical neck. The absence of this reflex in men is almost always associated with a neurologic lesion, but the reflex is not detectable in up to 30% of otherwise noma1 women (23). In men, the size and consistency of the prostate should be assessed. In women a vaginal examination should be performed with both an empty bladder (to check the pelvic organs) and a full bladder (to check for incontinence and prolapse) (33 not cited). With the bladder semifull in the lithotomy position, the patient is asked to cough or strain in an attempt to reproduce the incontinence. The degree of urethral hypermobility is assessed by the Q-tip test (34-37). The Q-tip test was devised as a method to differentiate type I stress incontinence from type I1 stress incontinence at a time when bead chain cystourethrograms were routinely used for this purpose. It is performed by inserting well

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lubricated sterile cotton tipped swab gently through the urethra into the bladder. Once in the bladder, the Q-tip is withdrawn to the point of resistance, which is at the level of the vesical neck. The resting angle from the horizontal is recorded. The patient is then asked to strain and the degree of rotation is assessed. Hypemobility is defined as a resting or straining angle of greater than 30 degrees from the horizontal and is equivalent to stress incontinence type 11, provided that incontinence is demonstrated.

Upper Urinuy l’rdct Evuluation Upper urinary tract evaluation includes measurement of serum BUN & creatinine and upper tract imaging (intravenous pyelogram (IVP), renal ultrasound, CAT scan or MRI). Renalultrasound is recommended for screening because this is the easiest, least expensive and devoidof potential complication.

Urodyndmic Evuluation There are two basic reasons for performing urodynamic investigation in patients with MS: to determine the precise etiology of the patient’s symptoms andto identify urodynamic risk factors for the development of upper urinary tract deterioration. Urodynamic risk factors include detrusorexternal sphincter dyssynergia, low bladder wall compliance, bladder outlet obstruction, and vesicoureteral reflux (1 9,3840). Urodynamic technique range from simple “eyeball urodynamics” to sophisticated multichannel synchronous v i d e o / p r e s s u r e / ~ o w ~ M ~ studies. We believe that synchronous multichannel videourodynamics offers the most comprehensive, artifact free means of arriving at a precise diagnosis and we perfom them routinely in patients with multiple sclerosis. Before starting the urodynamic study the following information should be known: 1. What symptoms are you trying to reproduce? 2. What is the functional bladder capacity (the usual voided volume based

on the voiding diary)?

3. Does the patient usually empty his or her bladder (based on examinations & measurement of postvoid residual urine)?

4. Is theuroflownormal,i.e.,isthere a likelihood of eitherurethral obstruction or impaired detrusor contractility? 5. Is urinary incontinencea complaint? If so, the natureof the incontinence

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and the severity shouldbe determined froma diary, pad test, and exam with a full bladder. 6. Is there a neurologic lesion that could cause detrusorexternal sphincter dyssynergia, detrusor hyperreflexia, or detrusor areflexia?

VIDEOURODYNAMICS Synchronous measurement and display of urodynamic parameters with radiographic visualization of the lower urinary tract videourodynamics is the most precise diagnostic tool for evaluating disturbances of micturition (41). In these studies, radiographic contrast is used as the infusant for cystometry. Depending on the level of sophistication required, other urodynamic parameters such as abdominal pressure, urethral pressure, uroflow, and sphincter electromyography may be recorded as well. There are important advantages to synchronous video/ pressure flow studies compared to conventional single channel urodynamics and to conventional cystography and voiding cystourethrography . By simultaneously measuring multiple urodynamic variables one gains a better insight into the underlying pathophysiology. Moreover, since all variables are visualized simultaneously one can better appreciate their interrelationships and identify artifacts with ease.

Common Urodynamic Patterns in MS Detrusor hyperreflexia is seen in over 50% of patients with MS ( 9 , I I ,12,42,43,44,45,46). Detrusor-external sphincter dyssynergia is found in about half or the patients with detrusor hyperreflexia (9,11,12,42,43,45,46,47). Detrusor areflexia is much less common. Most MS patients generally one of these distinct urodynamic patterns: 1. Detrusor hyperreflexia without bladder outlet obstruction (Fig. l). 2. Detrusorhyperreflexiaanddetrusor-externalsphincterdyssynergia (Figs. 2 and 3). 3. Detrusor hyperreflexia with vesical necldprostatic urethralobstruction (Fig. 4). detrusor-external sphincterdyssynergia 4. Detrusorhyperreflexiaand with vesical necldprostatic urethral obstruction (Fig. 5). 5. Detrusor areflexia and normal bladder compliance (Fig. 6). 6. Low bladder compliance.

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Fig. 1. Detrusorhyperreflexia in a 54 year old woman with exacerbating & remitting multiple sclerosis.(A) Urodynamic tracing.At a bladder volumeof 165 m1 there wasan involuntary detrusor contraction (arrow) which reached a maximum of 100 cm H20 (during sphincter contraction). Qmax = 13 ml/S and = 25 cm H20. Throughout the detrusor contraction, there was increased EMG activity as she tried to abort the detrusor contraction. When she relaxed, (at Qmax) there was complete ENIG silence. Unintubated uroflow (far right) was normal (19 ml/ S). Flow = uroflow; Pves = vesical pressure; Pabd = abdominal pressure; Pdet = detrusor pressure (Pves-Pabd); EMG = EMG of the pelvic floor (surface electrodes). (B) X-ray obtained at Qmax show a normal urethra. Courtesy of Jerry G. Blaivas, MD, with permission

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Fig. 2. Detrusor hyperreflexia and detrusor-external sphincter dyssynergia in a 56 year old woman with multiple sclerosis. (C) Urodynamic tracing. At a bladder volume of 135 cni H20 there was an involuntary detrusor contraction (arrow) which reached a maxinium of 107 cm H20 with a Qmax = 5 ml/S. Throughout the detrusor contraction, there was increased EMG activity. Flow = uroflow; Pves = vesical pressure; Pabd = abdominal pressure; Pdet = detrusor pressure (Pves-Pabd); EMG = EMG of the pelvic floor (surface electrodes). (D) X-ray obtained at the height of the detrusor contraction. The proximal urethra is dilated. The point of obstruction is the external urethral sphincter, marked by the arrow. Courtesy of J e r p G. Blaivns, MD, with permission

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Fig. 3. Detrusor hyperreflexia and detrusor-external sphincter dyssynergiaa in 53 year old paraplegic man.(A) Urodynamic tracing. Ata bladder volumeof 165 ml

there wasan involuntary detrusor contraction (arrow) which reached a maximum of l00 cm H20 with a Qmax = 5 ml/S. Throughout the detrusor contraction, there was increased EMG activity. Flow = uroflow; Pves = vesical pressure; Pabd = abdominal pressure; Pdet = detrusor pressure (Pves-Pabd); EMG = EMG of the pelvic floor (surface electrodes). (E) X-ray obtained at the height of the detrusor contraction. The proximal urethra is dilated. Theofpoint obstruction is the external arrow. Courtesy of Jerry G. BEaivas, MD, urethralsphincter,markedbythe with permission

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Fig. 4. Detrusor hyperreflexia and vesical necWprostatic urethral obstruction in a 50 year old quadriplegic man with multiple sclerosis. (A) Urodynamic tracing. At a bladder volume of 82 m1 there was an involuntary detrusor contraction = 6 ml/S. Throughout (arrow) which reached a maximum of 88 cm H20and Qmax the detrusor contraction, there was no change in EMG activity. Flow = uroflow; Pves = vesical pressure; Pabd = abdominal pressure; Pdet = detrusor pressure (Pves-Pabd); EMG = EMG of the pelvic floor (surface electrodes). (B) X-ray Courtesy of Jerry obtained at Qmax shows a diffusely narrowed prostatic urethra. G. Blaivas, MD, with permission

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Fig. 5. Detrusor hyperreflexia and detrusor-external sphincter dyssynergia with vesical neck/ prostatic urethral obstruction ina 37 year old man with multiple sclerosis.(C) Urodynamic tracing. At a bladder volume of 128 cm H20 there was an involuntary detrusor contraction (arrow) which reacheda maximum of 187 cm H20 with no flow at all. Throughout the detrusor contraction, there was increased EMG activity. At pdetmax, wasthere no contrast was visualized in the urethra, indicating both vesical neck obstruction and DESD. The fall in detrusor as the external sphincter relaxed a pressure in the middle of the detrusor contraction occurred bit and the urethra opened a bit, but the uroflow was too low to be measured by the flowmeter. Flow = uroflow; Pves= vesical pressure; Pabd = abdominal pressure; Pdet = detrusor pressure (D) X-ray obtained at the (Pves-Pabd); EMG = EMG of the pelvic floor (surface electrodes). height of the detrusor contraction. There is no visualization of the urethra at all, indicating obstruction of the prostatic urethra as well as the external sphincter. Courtesy of Jerry G. Blaivas, MD, with permission

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Fig. 6. Detrusor areflexia and normal bladder compliance in a 61 year old women filled to capacity with occult spinabifida. (A) Urodynarnic tracing. The bladder was (650 rnl) at which point she felt uncomfortably full. Pdetmax was 2 cm H20. When asked to void, she strained and the EMG activity increased. There was no detrusor contraction and no flow. Flow = uroflow; Pves = vesical pressure; Pabd= abdominal pressure; Pdet = detrusor pressure (Pves-Pabd); EMG = EMG of the pelvic floor (surface electrodes). (B) X-ray obtained at the height of straining. There is no visualization of the urethra at all and no flow. Courtesy of Jerry G. Blaivas, MD, with permission

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Fig. (DSj Low bladder complianceand vesicoureteral refluxa 48 in yearold neurologically normal man. (A) Urodynamic tracing. The bladder was filledto capacity (850 mlj at which point he felt uncomfortably full. Pdetmax during filling 50 wascm H20 and there was a steep risein detrusor pressure.When askedto void, he had a detrusor contractionto 75 cm H20, without any flow all at and nocontrast appeared in the urethra. EMG activity remained unchnaged Flow= uroflow; Pves= vesical pressure; Pabd= abdominal pressure; Pdet = detrusor pressure (Pves-Pabdj; EMG = EMG of the pelvic floor(surface electrodes).(B) X-ray obtained the at end of bladder filling (prior to detrusor the contraction) shows grade 3 vesicoureteral reflux and no contrast in theurethra. Courtesy ofJerry

G. Bluivus, MD, with permission

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TREATMENT OVERVIEW Although the ultimate goal of therapy is the restoration of normal voiding, this is usually not possible unless the neurologic abnormalities remit, or if the symptoms are caused bya coincidental urologic condition such as urinary tract infection or benign prostatic hypertrophy. The social and emotional consequences of urinary bladder symptoms, particularly incontinence, must always be weighed against the risks to the patients’ general health imposed by the proposed therapy. For example, a woman with mild, yet uncontrollable incontinence resulting from refractory detrusor hyperreflexia may be better managed with incontinence pads (which pose threat no to her health) than with anindwelling vesical catheter (which predisposes her to urinary infection). The unpredictable course of MS makes it difficult to know what to expect or howto plan for the future. If the general neurologic condition of the patient can be improved,the voiding dysfunction will generally also improve. The primary goal in managing a patient with MS is to control the symptoms and minimizing the disability (48). Treatment of each patient requires an open mind, a broad array of therapeutic strategies and the compassion and tenacity to tailor the therapeutic approach to the individual needs of the patient. Further, the potential for urologic and neurologic progression makes long-term urologic follow-up essential. We recommend that patients be followed biannually with renal and bladder ultrasound alternating with videourodynamics. The most effective treatment is predicated on a clear understanding several factors: l. The patients symptoms and how they impact on his or her daily life, 2. The physical, psychosocial and environmental milieu that the patient experiences and, finally 3. The underlying pathophysiology causing the symptoms (as determined by urodynamic studies).

From a scientific standpoint, it is the underlying pathophysiology that directs treatment, but there are a number of adjunctive therapies and considerations that for many patients are equally important. These include: l. Identifying and treating remediable causes of MS exacerbations (see

above), 2. Techniques to maximize the patient’s independence and activities of daily living, 3. Behavior modification to treat and deal with symptoms,

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4. Biofeedback and pelvic floor exercises, and 5. Absorbent pads and incontinence appliances.

Remediuble Cuwes o f MS Exucerbutions There are a number of remediable factors that can precipitate an exacerbation of MS; these should besoughtand treated whenever possible. They include urinary tract infection, fatigue, increased body temperature, skeletal spasticity, psychic or physical trauma, and emotional stress (48,49).

Mmimizing Activities o f D u i 4 Living For patients with disabilities, there are manyenvironmentaland behavioral interventions that can increase their independence andfunctionality. Some things require only common sense; others require the expertise of occupational and physical therapists, physiatrists, orthopedic surgeons, and makers of prosthetic devices. The consultation of these professionals should be sought whenever the need arises. For example, a patient with muscular weakness may benefit from sitting in a high, rather than a low chair to make it easier for him or her to rise from the sitting to standing position. The judicious use of canes and walkers should be obvious, but some patients have aversions to such aids and may need counseling. Depression, an ever present threat, should be identified and treated. Other assistive devices such as a Velcro pants zipper, a. tenodesis hand splint, a catheter with extension which will reach the toilet without having to transfer out of the wheelchair may allow a person to maintain independence and permit intermittent self catheterization which might otherwise be impractical.

Behuvior Modzjicution Behavior modification is an effective technique for ameliorating lower urinary tract symptoms, which is useful in a number of circumstances. Simple behavioral techniques, such as diary keeping, adjustment of oral intake of fluids and voiding by the clock, by decreasing the amount of urine that is in the bladder at any point in time, minimizes the likelihood of incontinence. Pelvic floor exercises, with or without biofeedback, not only has the potential to strengthen the sphincter, but also heightens the patient’s awarenessabout bladder and sphincter events. Contraction of the pelvic floor muscles and urinary sphincter

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can, in some patients, prevent momentary incontinence owing to stress and prevent or abort involuntary detrusor contractions. DDAVP, a synthetic analog of antidiuretic hormone has proven (in our unpublished experience) to be very useful in selected patients with nocturia and/or enuresis. As a general rule, by decreasing the amount of overnight urine production, the number of nocturnal voids and enuresis can be reduced. Patients are asked to keep a baseline 24 h voiding diary. On the night before their first treatment, the patient takes 0.1 mg DDAVP at bedtime and is scheduled for an office visit the next afternoon. This office visit is extremely important because complications owing to water toxicity or overhydration, when they occur, usually do so about 12 h or so after the first dose. On that visit, the patient is specifically queried about the warning signs of toxicity-headache, dizziness, nausea, vomiting, shortness of breath, mental confusion etc. Vital signs are taken and serum electrolytes are drawn. If there no signs of toxicity, the patient can be titrated up to a maximum dose of about 0.4 mg HS. Kinn treated thirteen patients with advanced MS and urge urinary incontinence with DDAVP in a double-blind crossover study (50).They demonstrated that total voided volume during the 6 h test period was reduced from 440 mL to 325 mL during treatment with DDAVP (p<0.05). Hilton in a double-blind cross-over trail of DDAVP and placebo in 16 women with MS found that nocturia was reduced from a mean of 2.55 episodes per night to 2.01 with placebo and to 1.28 with DDAVP (p<0.05) (51).

Speczjk Therapies Aimed at the Underlying Pathophysiology Although the underlying pathophysiology of lower urinary tract symptoms is best determined by urodynamic studies, many patients have other contributing factors and/or comorbidities that should be addressed to effect successful treatment. For example, urodynamic study in a women with urinary incontinence may disclose detrusorexternal sphincter dyssynergia which could be managed with anticholinergics and intermittent self catheterization, but spasticity of the hip adductors and poor hand function prevent her from catheterizing through the urethra. A practical solution is to create a continent abdominal stoma that the patient can catheterize without even having to transfer. Because of the variable course of MS, an important principle when making therapeutic decisions is to avoid irreversible or ablative surgery

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until it is absolutely clear that the voiding picture and urodynamic findings have stabilized over time, generally, a period of about 2 yr. For long term management, an indwelling catheter should only be considered as a last resort in those patients who are unable, or unwilling. to undergo continent urinary diversion or cutaneous ileo-cystostomy . In our judgement, the long term hazards of an indwelling catheter do not justify its use except in rare instances.

Detrusor Hyperreflexia The most common treatment for detrusor hyperreflexia is anticholinergic medication with or without behavior modification and intermittent catheterization as the need arises (52). Many patients on these regimens can be stable for years with a reasonable quality of life. We generally begin with a short acting medication, such as oxybutinin, in order to test the effects of a single dose. The patient is given 2.5-5 mg oxybutynin, asked to drink and evaluated by measurement of uroflow and postvoid residual urine 2-4 hours later. If he or she voids with an acceptable flow and residual urine, an anticholinergic medication is prescribed, If residual urine is unacceptable, the patient is scheduled for another session to learn intermittent self catheterization. Whether or not intermittent catheterization is used, the medication is titrated to an appropriate dosage based on the patient’s symptoms, voiding diaries and pad tests. The two most coinmon anticholinergics that we use are oxybutynin chloride (dosage is 2.5-10 ing TID or QID) and tolterodine (2 mg BID). A long acting (once a day) formulation of oxybutynin has just been approved by the FDA, but there is no clinical experience with it as of the writing of this chapter. For some patients, anticholinergics have proven most useful when taken on a PRN basis. Tricyclic antidepressants are useful as primary or adjunctive treatment. The prototype is imipramine. The usual starting dose is 10-25 mg HS which can be titrated up to a maximum of about 150 mg by increasing the dose every third day or so. In some patients the effects of tricyclics and anticholinergics are additive, and they may be used in combination. It is thought that anticholinergics and tricyclics work primarily by decreasing the frequency and amplitude of involuntary detrusor contractions. However, the warning time (from the onset of the urge to void until the iiicontinent episode) remains unchanged (52).Thus, the usefulness of these medications may be enhanced by a behavior modification

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program of timed voiding (prior to the anticipated onset of the unstable detrusor contraction).

Denervution Although denervation procedures have been used for decades in an attempt to prevent detrusor overactivity, with a few exceptions, we do not believe the long or short term success, when weighed against potential complications, warrants their use. Even when initially successful, over the long term, many patients develop low bladder compliance that proves a greater threat to their health and well being than the original condition. A great variety of techniques have been described including sacral blockade (53), dorsal rhizotomy (54), transvaginal denervation (55,561,subtrigonal injection of phenol or alcohol (57-601, cystolysis, bladder tnyotomy, and transection (61).An intrathecal baclofen infusion pump has been recently used to reduce severe spasticity resulting from neurological disease. In addition to reducing spasticity, improvement in bladder capacity and a decrease in urgency and urge incontinence has also been reported (62).Longer trials of this technique will determine if the system is reliable long-term and if tolerance develops. The use of other intrathecal pharmacological agents to inhibit the unstable bladder is a possibility for the future.

TRANSVAGINAL DENERVATION (INGELMANN-SUNDBERG PROCEDURE) In 1959, Ingelman-Sundberg described a transvaginal technique intended to accomplish partial denervation of the subtrigonal nerve supply to the bladder. He reported an 88% success rate in 34 women with urinary frequency, urgency, urge incontinence, and bladder pain. A subsequent series corroborated these results and cited a 6-15% recurrence rate in the two series (55).Several other authors cited success rates of about 50% (56). Wan and McGuire, in an abstract, reported that 72% of 62 patients were “either cured or significantly improved” at least 1 yr following surgery (63). Patient selection is of critical importance. Only those with refractory detrusor instability who respond favorably to a temporary nerve block should be considered candidates for the procedure. The nerve block is

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performed by injecting a long acting local anesthetic (1% Marcaine) beneath the trigone through a transvaginal approach. Under digital guidance, a 22 gage spinal needle is inserted into the anterior vaginal wall at the bladder neck. The needle is directed laterally toward the vaginal fornix 1 cm lateral to the cervix to a depth of about 3 cm and 5-10 mL of 1% Marcaine is injected. If the patient reports an overt clinical improvement in the 6-8 h after injection, surgery may be considered. If there is no beneficial response other options should be considered. If the patient develops significant residual urine or is unable to void after the local anesthesia, she should be warned that she has a higher than normal risk of requiring intermittent self catheterization postoperatively. The operative procedure is performed with the patient in the dorsal lithotomy position. Some surgeons perform cystourethroscopy and insert bilateral ureteral catheters to aid in the recognition of the transmural ureters andto avoid their injury during the dissection. A Foley catheter is placed transurethrally to decompress the bladder and to assist in identifying the vesical neck. A vertical midline or inverted “U” anterior vaginal incision is made from the midurethra to approx 2-4 cm proximal to the bladder neck. The anterior vaginal wallis dissected free from the urethra and bladder and a long scissors is used to dissect the soft tissue between the bladder, beneath the trigone, and the anterior vaginal wall. Care musttaken to avoid injury to the ureters at this point. In addition, it is important to confine the limits of the dissection to the lateral limits of the trigone and to be careful not to perforate the endopelvic fascia and enter the retropubic space lest stress incontinence develop postoperatively. The vaginal wall is closed with a running 2 0 chromic suture. A vaginal pack and Foley or percutaneous suprapubic cystotomy are placed and the patient is given a voiding trial the following day. Despite the encouraging results reported by the original investigators and by McGuire, transvaginal partial bladder denervation has never achieved a significant level of clinical utility and there have not been enough studies to determine its efficacy.

SUBTRIGONAL PHENOL AND ALCOHOL INJECTIONS Subtrigonal phenol injection has been employed in the treatment of patients with refractory detrusor instability and sensory urgency, but

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lack of overall efficacy and the possibility of bladder and ureteral necrosis have all but eliminated its clinical use (64,65). Most initial reports suggested that the technique was effective (66,58,64,59,65).Harris reported that 60% of patients developed an acontractile detrusor, but 30% were complicated by vesicovaginal fistula after extravesical subtrigonal injection of 50% ethanol for detrusor instability in 10 patients (67). Subtrigonal injection has fallen out of favor because of recent disappointing outcomes. McInerney in a long term follow-up of 97 patients, had only 19% long-term success, 24% short term but unsustained benefit and 57% failure (60). In addition there was a 17% complication rate: urinary retention (1 transient, 7 permanent requiring intermittent catheterization, 4 nerve palsies, erectile impotence in 1 of 9 men, and 2 bladder mucosal necrosis). Many of the phenol failures subsequently underwent augmentationcystoplasty as the definite treatment with success.

DETRUSOR MYOTOMY, BLADDER TRANSECTION AND CYSTOLYSIS Bladder transection (cystocystoplasty) was introduced for the treatment of patients with refractory detrusor instability by Turner-Warwick and Ashkenin 1967 (68).The procedureis essentially a circumferential bladder transection with immediate reconstruction. An incision was made through the full thickness of the bladder wall and perivesical tissue between a point 1 to 2 cm. lateral to each ureteral orifice. The incision through the bladder wall is then closed in 1 layer with absorbable suture (69,70). Various modifications were made involving partial versus complete bladder transection and cystolysis. In 1972 Mahony and Laferte reported on the use of multiple detrusor myotomies in the treatment of detrusor hyperreflexia refractory to pharmacological therapy (71). In cystolysis the bladder is circumferentially dissected as if a cystectomy were to be performed, but the bladder is left in place (72).Essenhigh andothers have usedthis procedure in over 100 patients and reported satisfactory results in approx 75% (69,70,73,74). In all of these procedures, the initial reports were quite encouraging. Nevertheless, none of them ever achieved widespread acceptance and no long term results have been reported. Further, even the original investigators have largely abandoned them. In our opinion, there is no role for them in current clinical practice.

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DETRUSOR MYECTOMY (BLADDER AUTO-AUGMENTATION) Detrusor myectomy was first reported by Cartwright and Snow in 1989 in pediatric patients with neurogenic bladder (75). In this procedure, the bladder is exposed through anextraperitoneal approach anda plane developed betweenthe detrusor and underlying mucosa. Detrusor muscle fibers on the anterior surface anddome of the bladder are excised being careful to leave the mucosa intact. If successful, detrusor myectomy obviates the need for enterocystoplasty with its attendant morbidity. Although initial reports, with short term follow-up have shown excellent success rates, much moreclinical data is needed before the results of this procedure can be evaluated (7576).

AUGMENTATION CYSTOPLASTY (WITH & WITHOUT CONTINENT CATHETERIZAl3LE ABDOMINAL STOMA) AND CONTINENT URINARY DIVERSION We believe that augmentation cystoplasty is the treatment of choice for MS patients with refractory detrusor hyperreflexia and/or low bladder compliance (77,78,79,80).However, it should only be considered when all conservative measures have failed in patients who are able and willing to accept permanent intermittent self catheterization should that prove necessary. A continent urinary diversion or augmentation cystoplasty with a continent abdominal stoma is especially useful for female paraplegics and quadriplegics and other patients who are physically unable to perform intermittent self catheterize through the urethra because of physical limitations. These procedures are far preferable to either urinary conduit diversions or an indwelling vesical catheter for both medical andpsychosocial reasons. From a psychosocial viewpoint, a continent abdominal stoma relieves the patient of the burden of an external urinary drainage bag. From a medical standpoint, the creation of a large capacity, low-pressure internal urinary reservoir greatly reduces the chances of urosepsis, urolithiasis, hydronephrosis, and ultimately, renal failure. Further, these procedures result in improvedself-image and sexual experiences (81). The purposeof augmentation cystoplasty is to create a urinary reservoir that permits the bladder to painlessly accept large volumes of urine at low filling pressures. If sphincter function is intact, no further

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operative procedure is necessary. However, when sphincteric incontinence is present a concomitant pubovaginalsling or a sphincter prosthesis may be required. If intermittent catheterization is not possible, a cutaneous ileo-cystostomy is a most reasonable alternative. In this procedure, a small section of terminal ileum is isolated to act as a conduit between the urinary bladder and the anterior abdominal wall; an ileal “bladder chimney.” This procedure was reported in 1957 by Cordonnier (82), but subsequently attention focused on augmentation cystoplasty and formal supravesical urinary diversion in treating those who might otherwise benefit from a bladder chimney. The creation of a bladder chimney is a major abdominal surgical endeavor, but is usually well tolerated by the patient. A twenty centimeter segment of distal ileum is isolated in standard fashion. The proximal end is spatulated widely and anastomosedto a similarly spatulated flap developed from the dome of the bladder. This wide anastomosis is required to avoid an hourglass deformity, which could impede egress of urine from the bladder. The distal end of the ileal segment is delivered to the anterior abdominal wall as the stoma of a Bricker ileal urinary conduit would be fashioned. The advantage of this procedure over standard cystectomy and ileal diversion is the avoidance of manipulation of the ureters, thereby eliminating the problems associated with uretero-intestinal anastomoses such as reflux, stenosis, devascularization, urinary extravasation, or complete anastomotic disruption. Urinary collection is achieved with a standard urostomy drainage bag, without the need for an indwelling urethral or suprapubic catheter, which wouldpredispose to chronic infection, tissue erosion, neoplasia, or calculus formation. Bladder capacity is preserved, and the gradual destruction of the bladder associated with indwelling catheters is obviated by this effective drainage procedure. Furthermore, the procedure is potentially reversible, as the bladder remains in place, with the ureters in normal anatomic position (83). If there is sphincteric incontinence, concomitant in women pubovaginal sling usually suffices; in rare instances, when there has been urethral destruction, surgical bladder neck closure may be necessary in either sex (8485).

Detrzlsor Hyperreflexia with Vesical lVech/Prostatic Urethral Obstruction In men with detrusor overactivity and prostatic obstruction, it is usually not possible with any degree of certainty to distinguish detrusor

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hyperreflexia (owing to multiple sclerosis) from detrusor instability (owing to prostatic obstruction). Logic dictates that detrusor overactivity is more likely to be because of multiple sclerosis if the patient is unaware of the involuntary detrusor contractions, cannot abort them, and is incontinent. Our experience defies this logic, and we do not believe that we can reliably make the necessary. The practical consequence of this is that we are unable to predict whether or not a man will be incontinent after transurethral incision or resection. Accordingly, if this form of therapy is chosen, it must be done so with informed consent andcontingency plans formanaging postoperative urinary incontinence because of persistent detrusor overactivity.

Detrusor Hyperreflexia With Detrusor-External Sphincter Dyssynergia Patients with detrusor hyperreflexia and DESD are at higher risk for upper urinary tract damage, stones, and urosepsis than the other two patterns (19,86). Further, when treated with anticholinergics they are more likely to develop urinary retention and require intermittent catheterization. For practical purposes, though, treatment is pretty much the same as outlined above. The most common treatment is anticholinergics and intermittent catheterization. In men, if intermittent catheterization is not an option, external sphincterotomy or an urethral stent may be considered. However, such destructive procedures should only be considered when there is no reasonable hope for neurologic regression and after more conservative therapies have been unsuccessful or are not possible. Different surgical techniques have been usedfor external sphincterotomy, using electrocautery, laser or a special urethrotome to incise one or more positions through the sphincter (87-91). Anatomically, the bulk of the striated sphincter is anteromedial, while the neurovascular bundles are lateral to the membranous urethra. Incisions at the three and nine o’clock endoscopic positions are associated with injury to the neurovascular bundles of the corporal bodies and reduced potency. The 12 o’clock sphincterotomy, described by Madersbacher et al. (87), and Yalla et al. (91)is the method of choice, because incision at this site decreases the risk of significant arterial hemorrhage and erectile dysfunction. Hemorrhage associated with the 12 o’clock incision usually emanates from venous structures, and abates spontaneously with catheter placement. Complications of conventional external sphincterotomy include a reoperation rate of from 12-26%, hemorrhage requiring blood trans-

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fusion in 5-23%, and erectile dysfunction in from 2.8 to 64% of patients (88,90,92,93).Several minimally invasive surgical alternatives to traditional sphincterotomy have beenrecently developed - laser sphincterotomy and sphincter stent placement.

Laser Sphincterotomy External sphincter ablation using the contact Nd:YAG (Neodymium: Yittrium Aluminum Garnet) laser permits carbonization as well as vaporization of tissue. Because of the near infra-red wavelengths used, minimal laser energy produces approx 4 mm of penetration. per pass. Encouraging laser sphincter results, with over 1 yr of follow-up, have recently become available (89).

The Sphincter Stent Endoluminal urethral stent prostheses have recently been used as an alternative treatment for DESD. Several intraurethral stents are currently available, but only the UroLumeTM (American Medical Systems, Minnetonka, MN) has been systematically tested in the membranous urethral for the treatment of DESD. The Multicenter North American Trial data of 153 patients treated with the sphincter stent has shown promising results (94).The efficacy of the stent prosthesis approximates that of external sphincter destruction, with much less morbidity.

D e m o r Hyperreflexia with Detrusor-External Sphincter Dyssynergia and Vesical NeckIProstatic Urethral Obstruction These patients are treated essentially the same as those with DESD except that, if external sphincterotomy or a urethral stent is used, the prostatic obstruction must be addressed at the sarne time. This can be accomplished by transurethral resection or incision of the prostate or by placing the stent through boththe proximal urethral obstruction and the membranous urethra.

Detrusor Areflexia Intermittent self catheterization is the simplest and most effective means of managing patients with detrusor areflexia. Over time, though, some of these patients develop low bladder compliance or detrusor hyperreflexia that requires a change in management (95,15). There is

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no proven pharmacologic therapy for detrusor areflexia. Bethanechol chloride is, in our experience, ineffective for the treatment of detrusor areflexia. Although bethanechol can raise intravesical pressure, this does not imply that coordinated voiding occurs. In fact, urethral pressure also increases with bethanechol medications. Therefore the use of bethanechol in detrusor hyperreflexia does not make any sense, and its use in detrusor hyperreflexia with DESD is dangerous and is contraindicated. In patients who cannot be managed by intermittent catheterization, the only alternatives to anindwelling catheter are cutaneous urinary conduit diversion and cutaneous ileocystotomy.

Concarrent Stress Incontinence In some patients with MS, particularly those with conus medullaris lesions, there is weakness and denervation of the pelvic floor striated sphincter muscles leading to sphincteric incontinence (95,96). Others have sphincteric incontinence because of anatomic abnormalities unrelated to MS. In either case, there are many effective surgical treatments for sphincteric incontinence. However, because of the unpredictable nature of MS, there is probably a higher incidence of urinary retention and incontinence owing to detrusor overactivity in these patients. Because of this, it seems prudent to offer periurethral collagen injections as primary treatment. This serves a dual purpose-it offers the possibility of effective treatment, and it may serve as a proxy for the effects of surgical treatment.

Lower urinary tract symptoms in patients afflicted with MS are very common. In general, treatment should be predicated on a clear understanding of the underlying pathophysiology, and for most patients, this means that urodynamic studies should be part of the evaluation. Because of the unpredictable course of MS, therapy should commence with the least invasive. Ablative or irreversible surgery should be reserved for patients with stable or progressive disease who have no reasonable hope for recovery in whom conservative therapy has failed. Most patients with exacerbating and remitting forms of MS will continue in that pattern for long periods of time; these patients are best managed conservatively for as long as possible.

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REFERENCES 1. McFarlin DE, McFarland HF (1982) Multiple Sclerosis, NEJM, 307:1183-1188. 2. Poser, CM (1981) Multiple Sclerosis, A Critical Update, Eur Neurol 20:394 3. MacDonald W1 (l 974) Pathophysiology in multiplesclerosis. Brain 97: 179-196. 4. Fog T (1950) Topographic distribution of plaques in the spinal cord in multiple sclerosis. Arch Neurol Psychiatry 63:382. 5. Oppenheimer DR (1978) The cervical cord in multiple sclerosis. Neuropathol App Neurobiol4:151. 6. Barrington FJF (1933) The localization of the paths serving micturition in the spinal cord of the cat. Brain 56126. 7. Nathan PW, Smith NC (195 1) The centripetal pathway from the bladder and urethra within the spinal cord. J Neurol Neurosurg Psychiatry 14:262. 8. Nathan PW, Smith NC (1958) The centrifugal pathway for micturition with the spinal cord. J Neurol Neurosurg Psychiatry 21:177. 9. Anderson JT, Bradley WE (1976) Abnormalities of detrusor and sphincter function in multiple sclerosis. Br J UroE 48:193. 10. Awad SA, Gajewski JB, Sogbein SK, Murray TJ, Field CA (1984) Relationship between neurological and urological status in patients with multiple sclerosis. J Urol 132:499-502. 11. Blaivas JG, BhimaniG, Labib KEl (1979) Vesicourethral dysfunctionin multiple sclerosis. J Urol 122:342-347. 12. Blaivas JG (1980) Management of bladder dysfunction in multiple sclerosis. Neurology 30:12- 18. 13. Miller H, Simpson CA, YeatesWE( (1965) Bladder dysfunction in multiple sclerosis. Br Med J 1:1265. 14. Piazza DH, Diokno AC (1979) Review of neurogenic bladderin multiple sclerosis. Urology 14:33. 15. Koldewijn EL, HommesOR, Lemmens WAJG, DebruyneM J , Van Kerrebroeck PEV (1995) Relationship between lower urinarytract abnormalities and disease related parameters in multiple sclerosis. J Urol 154:169--173. 16. Rheinhold M (1950) Prognosis in disseminated sclerosis. Br Med J 1:160. 17. Samellas W, Rubin B (1965) Managementof upper urinarytract complications in multiple sclerosis by means of urinary diversion toan ileal conduit. J Urol 93:548. 18. Leibowitz U, Kahana E, Jacobsen SG, Alter M (1972) The cause of death in multiple sclerosis. In: Leibowitz U, ed. Progress in Multiple Sclerosis: Research and Treatment. New York, NY: Academic Press, 196. 19. Blaivas JG, BarbaliasCA (1984) Detrusor-externalsphincter dyssynergia in men with multiple sclerosis: an ominous urologic condition. J U r d 131:91-4. 20. Blaivas JG (1982) The neurophysiology of micturition: a clinical study of 550 patients. J Urol 127:958. 21. Bradley WE, Conway CJ (1966) Bladder representation in the pontine mesencephalic reticular formation. Exp Neurol 16:237. C, Nadelhaft I (1979) 22. DeGroat WC, BoothAM,KrierJ,MilnerRJ,Morgan Neural control of the urinary bladder and large intestine. In: McBroods C, Koizumi K, Sato A, eds. Integrative Functions of the Autonomic Nervous System, Amsterdam, the Netherlands, Elsevier, Chap. 4. 23. Blaivas JG, Sinha HP, Zayed AAH, LabibKB (1981) Detrusorexternal sphincter dyssynergia, J Urol 125:541.

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24. McGuire EJ, Brady S (1979) Detrusor-sphincter dyssynergia. J Urol 121:774. 25. WeinAJ (1981) Classification of neurogenic voiding dysfunction. J Urol 125: 605. 26. Wheeler JS, Siroky MB, Pavlakis AJ, et al. (1983) The changing neurourologic pattern of multiple sclerosis. J Urol 130:123. 27. Bemelmans BLH,H o m e s OR, Van Kenebroeck PEV, Lemmens WAJG, Doesburg WH, Debruyne FMJ (1991) Evidence for early lower urinary tract dysfunction in clinically silent multiple sclerosis. J Urol 145:1219-1224. SL, Andersen JT (1988) Standardizationof lower 28. Abrams PH, Blaivas JG, Stanton urinary tract function. Neurourol Urodynam 29:458. 29. Hahn I, Fall M (1991) Objective quantification of stress urinary incontinence: A short, reproducible, provocative pad-test. Neurourol Urodynam 10:475. 30. Christensen SJ, Colstrup H, Hertz JB, et al. (1986) Inter- and intra-departmental variations of the perineal pad weighing test. Neurourol Urodynam 5:23. 31. Lose G, Gammelgaard J, Jorgensen TJ (1986) The one-hour pad weighing test: Reproducibility and the correlation between the test result, start volume in the bladder and the diuresis. Neurourol Urodynam 5:17. 32. Blaivas JG, Sinha HP, Zayed AAH, LabibKB (1981) Detrusorexternal sphincter dyssynergia: a detailed EMG study. J Urol 545. versus repair of vesicovagi33. Blaivas JG, Hertitz DM, Romanzi LJ (1995) Early late nal fistulas: Vaginal and abdominal approaches. J Urol 153:1110. 34. Bergman A, Bhatia NN (1987) Urodynamic appraisal of the Marshall-Marchetti test in women with stress urinary incontinence. Urology 29:458. 35. Crystle C, Charme L, Copeland W (1971) Q-tip test in stress urinary incontinence. Obstet Gynecol 38:313. 36. Montz FJ, Stanton SL (1986) Q-tip test in female urinary incontinence. Obstet Gynecol 67:259. 37. Walters MD, Diaz K (1987) A study of continent and incontinent women. Obstet Gynecol 70(2):208. 38. Ghoneim GM, Bloom DA, McGuire EJ, Stewar KL, (1989) Bladder compliance in meningomyelocele children. J Urol 141:1404. 39. McGuire EJ, WoodsideJR, Borden TA, Weiss RM (1981) The prognostic significance of urodynamic testing in myelodysplastic patients. J Urol 125:205. 40. Zoubek J, McGuire EJ, Noff F, Delancey JOL (1989) Late occurence of urinary tract damage inpatients successfully treated with radiation for cervical carcinoma. J Urol 141:1347. 41. Blaivas JH, Chancellor M (1996) Atlasof Urodynamics, Williams & Wilkins, Baltimore. 42. Bradley WE, Logothetis JL, Timm GW (1973) Cystometric and sphincter abnormalities in multiple sclerosis. Neurology 23: l 131. 43. Goldstein I, Siroky MB, Sax DS, Krane RJ (1982) Neurourologic abnormalities in multiple sclerosis. J Urol 128:541-545. 44. Philip T, Read DJ, Higson RH (1981) The urodynamiccharacteristics of multiple sclerosis. Br J Urol 53:672. 45. Piazza DH, Diokno AC (1979) Reviewof neurogenic bladderin multiple sclerosis. Urology 14:33. 46. Summers JL (1978) Neurogenic bladder in the woman with multiple sclerosis. J Urol 120:555. 47. Ketelaer,1977.

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48. Schneitzer L (1978) Rehabilitation of patients with multiple sclerosis. Arch Phv Men Rehnbil 59:430. 49. Poser CM (1 980) Exacerbation, activity. and progression in multiple sclerosis. Arch Neiirol 37:47I . 50. Kinn AC, Larsson PO (1990) Desmopressin: A new principle for symptomatic treatment of urgency and incontinence in patients with multiple sclerosis. Scnizd J Urol Nephrol 24: 109-1 12. 51. Hilton P, Hertogs K, Stanton SL (1983) The use of Desmopressin (DDAVP) for nocturia in women with multiple sclerosis. J Nertro Nezrroszrrg Psvdz 46:854855. 52. Wein, AJ, Nigro. DA (1996) Pharinacologic Therapy of Urinary Incontinence, Ch 3, in Evaluation and Treatment of Urinary Incontinence, Jerry G. Blaivas, ed.. Igaku-Shoin, New York, pp. 46-68. 53. Alloussi S. Loew F, Mast GJ, Wolf D (1984) Treatment of detrusor instability of the urinary bladder by selective sacral blockade. Br J Urol 56:464. 54. Rockswold GL, Bradley WE (1978) The use of sacral nerve block in the evaluation and treatment of neurologic bladder disease. J Urol 18:415-417. 55. Ingelman-Sundberg A ( 1978)Partial bladder denervation for detrusor dyssynergia. Clin Obstet Gyriecol 21 :797-805. 56. Hodgkinson CP, Drukker BH (1 977) Intravesical nerve resection for detrusor dyssynergia. Act0 Obstet Gynecol Scnricl 56:401. 57. Blackford HN, Murrary K, Stephenson TP. Mundy AR (1982)Results of transvesical infiltration of the pelvic plexuses with phenol in 1 16 patients. Br J Urol56:647649. 58. Blackford HN, Murray K, Stephenson TP, et al. (1984) Results of transvesical infiltration of the pelvic plexuses with phenol in 116 patients. Br J Urol56:647649. 59. Cameron-Strange A, Millard RJ ( 1988) Management of refractory motor urge incontinence by transvesical phenol injection. Br J Urol 62:323. 60. McInerney PD, Vanner TF. Matenhelia S, Stephenson TP (1 99 1) Assessment of the long-term results of subtrigonal phenolisation. Brit J Urology 67:586-587. 61. Freiha FS, Stamey TA (1980) Cystolysis: A procedure for the selective denervation of the bladder. J Urol 123:360. 62. Nanninga JB, Frost F and Penn R (1989) Effect of intrathecal baclofen on bladder and sphincter function. J UroZ 142101-105. 63. Wan J, McGuire EJ. Wang SC, Cerny JC, Hodgkinson CP (1991) IngelmanSundberg denervation for detrusor instability. J Urol 145:Abstract #8 1. 64. Parkhouse HF, Gilpin SA, Gosling JA, et al. (1987) Quantitative study of phenol as a neurolytic agent in the urinary bladder. Br J Urol 60:410-412. 65. Wall LL, Stanton SL (1989) Transvesical phenol injection of pelvic plexuses in females with refractory urge incontinence. Br J Urol 63:465. 66. Ewing R, Bultitude MT. Shuttleworth KED (1982) Subtrigonal phenol injection for urge incontinence secondary to detrusor instability in female. Br J Urol54:689692. 67. Harris RG. Constantinou CE, Stanley TA (1 988) Extravesical subtrigonal injection of 50 per cent ethanol for detrusor instability. J Urol 140:111-1 16. 68. Turner-Warwick RT, Ashen MH (1967) The functional results of partial. subtotal and total cystoplasty with special reference to ureterocaecocystoplasty. selective sphincterotomy and cystocystoplasty. Br J Urol 39:3.

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69. Mundy AR (1980)Bladdertransection for urgeincontinenceassociatedwith detrusor instability. Br J U r d 52:480-483. 70. Mundy AR (1982) The surgical treatment of urge incontinence of urine. J U r d 128:481-483. 71. Mahony DT, Laferte RD (1972) Studies of enuresis. IV. Multiple detrusor myotomy-a new operation for the rehabilitation of severe detrusor hypertrophy and hypercontractility. J Urol 107:1064. 72. Hindmarsh JR, Essenhigh SM, Yeates WK (1977) Bladder transection for adult enuresis. Br J Urol 49:515. 73. Essenhigh DM, Yeates WK (1973) Transection of the bladder with particular reference to enuresis. Brit J Urol 45:299. 74. Janknegt RA, Moonen WA and SchrinemachersLMH (1979) Transection of the bladder as a method of treatment in adult enuresis nocturna. Brit J Urol 51:275. 75. Cartwright PC, Snow BW (1989)Bladder autoaugmentation: earlyclinical experience. J Urol 142:505. 76. Cartwright PC, Snow BW (1995) Bladder autoaugmentation. Adv in Urol 8:273. 77. Sidi AA, Reinberg Y, Gonzalez R (1986) Influency of segment of configuration of the outcome of augmentation enterocystoplasty.J Urol 136:1201-1204. 78. Luangkhot R, Peng BCH, Blaivas JG (1991) Ileocystoplastyfor the management of the refractory neurogenicbladder: Surgical technique and urodynamic findings. J Urol 145:1340. 79. Linder A, Leach GE, Raz S (1983) Augmentation cystoplastyin the treatment of neurogenic bladder dysfunction. J U r d 129:1007. 80. Smith RB, Van Cangh P, Skinner DG, Kaufmann JJ, Goodwin WE (1977) Augmentation enterocystoplasty: A critical review. J U r d 118:35. 81. Moreno et al. (1995). 82. Cordonnier JJ (1957) Ileocystostomyfor neurogenic bladder. J U r d 78:605-610. 83. Rivas DA, KarasickS, Chancellor MB (1995) Cutaneous ileocystostomy (bladder chimney) for the treatment of severe neurogenic vesical dysfunction. Paraplegia, in press. 84. Wan J, McGuire EJ (1990) Augmentation cystoplasty and closure of the urethra for the destroyed lower urinary tract. J Am Paraplegia Soc 13:40-45. 85. Zimmern PE, Hadley HR, Leach GE, Raz S (1985) Transvaginal closure of the bladder neck and placement of a suprapubic catheter for destroyed urethra after long-term indwelling catheterization. J Urol 134:554-557. 86. McGuire EJ, Savastano JA (1984) Urodynamic findings and clinical status following vesical denervation proceduresfor control of incontinence. J Urol132:87-88. 87. Madersbacher H,Scott FB (1976) The twelve o’clocksphincterotomy:Technique, indications, results, Paraplegia 13:261-267. 88. Perkash I (1976)Modifiedapproachtosphincterotomyin spinal cordinjury patients: indications, technique, and results in 32 patients. Paraplegia 13:247. 89. Rivas DA, ChancellorMB, Staas WE, Gomella LG (1995) Contact Nd:YAG laser ablation of the external sphincter in spinal cord injured men with detrusor sphincter dyssynergia. Urology, in press. 90. Schellhamer PT;, Hackler RH, Bunts RC (1973) External sphincterotomy: an evaluation of 150 patients with neurogenic bladder. J Urol 110:199-202. 91. Yalla SV, Fam BA, Gabilondo FB, JacobsS, DiBenedetto M, Rossier AB, Gittes RF (1977) Anteromedian external sphincterotomy: Technique, rationale and cornplications. J Urol 117:489-493.

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92. Lockhart JL, Vorstman B, WeinsteinD, Politano VA (1986)Sphincterotomy failure in neurogenic bladder disease. J UroZ 135:86-89. 93. Whitmore WF, Fam BA, Yalla SV (1978) Experience with anteromedian (12 O’clock) external urethral sphincterotomy in100 male subjects with neuropathic bladders. J UroE 50:99. 94. Chancellor MB, Rivas DA(1994) Current Management of Detrusor Sphincter Dyssynergia in Advances. In McGuire EJ, ed. UroZogy Mosby-Year Book, Chicago, IL. 95. Swash M, Snooks SJ, Chalmers DHK (1987) Parity as a factors in incontinence in multiple sclerosis. Arch NeuroZ44:504-508. 96. Mathers SE, Ingram DA, Swash M (1990) Electrophysiologyof motor pathways for sphincter control in multiple sclerosis. J Neuro Neurosurg Psych 53:955--960.

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Diagnosis and Treatment of Spinal Cord Injuries and M~eloneuropat~ies Steven W: Sukin, MD dnd Timothy B. Boone, MD, PHD CONTENTS INTRODUCTION SPINAL-CORD INJURIES MYELODYSPLASIA OTHERDISEASES OF THE SPINAL CORD LONG-TERM UROLOGIC MANAGEMENT FOLLOW-UP PREVENTION OF COMPLICATIONS REFERENCES

INTRODUCTION This chapter will cover the diagnosis and management of spinalcord injuries and myeloneuropathies. In order to understand the basis of management, we will focus initially on the historical background, the neurobiology, and the general patterns of voiding dysfunction in spinal-cord injury and myelodysplasia. The general evaluation of voiding dysfunction as it pertains to each particular lesion of the spinal cord will be discussed and we will review their respective management. Historically, the urologic complications of spinal-cord injury have been a primary source of morbidity and mortality. During World War I, the mortality after spinal-cord injury was approximately 80% owing to urinary tract infection and lack of antibiotics ( I ) . In the past, urologists

From: Current Clinical Urology: Voiding Dysfinction: Diagnosis and Treatment Edited by: R. A. Appell 0 Humana Press Inc., Totowa, NJ

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had advocated the theory of a “Balanced Bladder” (2). Patients were felt to be clinically stable if they were able to voidwithminimal residual urine. This theory was not based on objective data and did not take into account the intravesical pressure elevations during urine storage and elimination. Improvements in urological care involving antibiotics, management of nephrolithiasis, the use of intermittant catheterization, the use of an objective means of evaluating the “Balanced Bladder” through urodynamics, andclose life-long urologic follow-up have led to near-normal life expectancy for spinal-cord injury patients ( I ) . Currently, major causes of mortality after spinal-cord injury are no longer owing to renal failure, but owing to pulmonary andcardiovascular complications. Despite these advancements inurologic care, urological complications continue to be a source of patient morbidity. The normal pattern of micturition requires an intact neural axis for controlled and coordinated lower urinary tract function. The Two-Phase Concept of Micturition (3) is a functional method of understanding this process. Initially, normal voiding function requires bladder filling and urine storage with a bladder able to accommodate increasing volumes of urine at low pressures and a bladder outlet that remains closed. Bladder emptying requires a coordinated and sustained contraction of the bladder muscle with concomitant relaxation of the external urethral sphincter. This micturition reflex is organized in therostral brain stem. Parasympatheticand somatic components of the sacral spinal cord and sympathetic innervation from the thoracolumbar cord are highly integrated to regulate normal micturition (4). Voiding dysfunction occurs when there are abnormalities of filling, storage, and emptying (3). This may be a failure to store secondary to the bladder, the outlet, or both. Bladder filling canbe affected by hyperactivity from phasic involuntary contractions, low detrusor cornpliance, or both. Storage failure can occur secondaryto pain or hypersensitivity during filling. Outlet resistance may be decreased from any process that damages the innervation or structural elements of the smooth orstriated urethral sphincter. A failure to empty may result from decreased bladder contractility, increased outlet resistance, or both. Animal studies have been used to uncover the micturition reflex pathways in neurally intact animals andcomparenormal function to the dysfunction following spinal-cord injury. These studies have shown that the afferent limb of the uninjured micturition reflex, travelling via myelinated A-delta fibers, switches to “silent” C-fiber afferents following spinal-cord injury (Figs. 1 and 2) (5-7). These

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CMG - Pressure Flow Study

Fig. 1. Normal micturitionreflex pathways with A-delta afferents mediating sensory input to the Pontine Micturition Center.

Pontine Micturition Center

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f

SpinalTransection

Fig. 2. Following Spinal Cord Injury C-Unmyelinated fibers take over to mediate the afferent limb of the neurogenic bladder.

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findings also havebeen verified through electrophysiologic studies using capsaicin, a neurotoxin that disrupts C-fiber afferents (8). The rhythmic bladder contractions induced by bladder distention after spinal-cord injury are blocked by the intravesical instillation of capsaicin (5,9). After an injury to the spinal cord, the processes of edema, hemorrhage, and cord necrosis ensue. Wemmorrhagic necrosis primarily occurs in the gray matter of the cord and may extend both cephalad and caudad (10). The injury can be extensive or may be confined to several cord segments. Focal trauma induces rapid opening of the bloodspinal cord barrier (11) and the cord is exposed to a new environment including serum, platelets, neutrophils, monocytes, and macrophages with the subsequent release of cytokines. A vasogenic type of edema is present that includes transmitters from injured cells. Anoxia may occur after cord injury owing to decreased blood flow. A cascade of events develops by the accumulation of excitatory amino acids, of which glutamate is believed to be the primary onein the spinal cord (12), activation of various glutamine receptors, and increasing intracellular calcium (13).These processes lead to further cell injury, with neuronal damage and cell death. Regardless of the cause of a spinal-cord lesion, the general patterns of voiding dysfunction can be deciphered depending on the level of injury. An injury above the brainstem usually causes detrusor hyperreflexia. Injuries above the level of S2 most often cause detrusor hyperreflexia with detrusor external sphincter dyssynergia (DESD). Generally, complete lesions above this area, but below the area of the sympathetic outflow, result in detrusor hyperreflexia, smooth sphincter synergia, and striated sphincter dyssynergia. Lesions above the spinal cord level of T7 and T8 may result in smooth sphincter dyssynergia as well, Finally, lesions below the level of S2 most commonly cause detrusor areflexia with fixed external urethral sphincter tone. Many classification systems of voiding dysfunction havebeen used in the past. It is desirable to choose a system that is applicable for all types of voiding dysfunction and makes the treatment options fairly obvious by the category of dysfunction that is used. We feel that urinary bladder symptoms are best classified as fillinglstorage abnormalities, emptying abnormalities or combinations of the two (14). Using this functional classification, treatment canbe directed at the underlying physiologic abnormality that is responsible for the symptom.

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SPINAL-CORD INJURIES The major causes of spinal-cord injury during peacetime are motor vehicle accidents, diving accidents, and falls. Other causes include disc prolapse, acute myelitis, surgery of thoracic aortic aneurysms,and occasionally aortography (15,161.Over 12,000 new cases of traumatic, spinal-cord injury occur each year in the United States, with an incidence estimated at 32 new injuries per million annually and a prevalence of 906 cases per million (17).Eighty-five percent of all cases are in men. The majority of these injuries occur at or above the T-12 vertebral level. Approximately half of the injuries result in quadriplegia and the other half in paraplegia. Multiple-level injuries may occur, and even with a single-level injury, cord damage may not be confined to a single cord segment. Approximately 53.8% of injuries are incomplete and 46.2% are complete. After a spinal-cord injury occurs, spinal shock is seen, in which there is a period of decreased excitability of the spinal-cord segments at and below the level of the lesion. Both flaccidparalysis of the skeletal muscle mass and an absenceof visceral reflexes occur below the level of the lesion. This includes a suppression of autonomic and somatic activity. The bladder is areflexic and clinically develops urinary retention. Usually, reflex bladder activity returns within 2-12 wk, but may not return for as long as 6-12 mo. Most peripheral somatic reflexes of the sacral-cord segment, including the anal and bulbocavernosus, may never disappear, or if they do, may return within minutes orhours after the injury (18). Radiologically, the bladder has a smooth contour with no evidence of trabeculation. The bladder neck is usually closed and competent unless there has been prior surgery or in some cases of thoracolumbar injury where it remains open (19).By EMG, the maximum urethral closing pressure is lower than normal but is still maintained at the level of the external sphincter (20). A loss of voluntary control is, however, seen at the external sphincter. Overflow incontinence may develop, but because sphincter tone does continue, generally incontinence does not occur unless the bladder is grossly overdistended. The optimal initial management is intermittent catheterization. After a period of spinal shock, a recovery phase occurs in which there is a return of reflex activity. This stage of recovery usually lasts 6-12 wk in complete suprasacral spinal-cord lesions, but may last up to a year or two(21).Generally, there is a return of detrusor contractility, if the distal spinal cord is intact but is simply isolated from higher

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centers. Initially, the return of reflex activity is not strongly sustained and only produces low-pressure changes. The strength and duration of these involuntary contractions usually increases, producing involuntary voiding, usually with incomplete bladder emptying. This period is often manifested by involuntary voiding between catheterizations. Once there is no longer any sign of neurologic recovery, a stable phase is seen, in which the urodynamic pattern remains fairly stable over time. This stability in bladder function cannot be assumed, however. Inmany patients with detrusor areflexia, a loss of bladder compliance may develop over time with the development of high storage pressures. Both radiologic and urodynamicevaluations are essential in the care of patients with spinal-cord injury. Renal ultrasound has the advantage over intravenous pyelograms in following spinal-cord injury patients because it does not require a bowel prep, has reduced radiation exposure, and has no risk of anaphylaxis. Renal scintigraphy is useful in calculating the glomerular filtration rate, creatinine clearance, and differential renal function. The urodynamicevaluation is considered the best method of detecting and categorizing bladder dysfunction (22). Many sophisticated urodynamic modalities exist and the physician must decide which test is best based on availablity and experience. Urodynamics helps identify those patients at risk of developing urological sequelae and those patients that will require early intervention. One reason urodynamics is felt to be essential is that the type of voiding dysfunction a patient has after spinal-cord injury does not always correlate with the level of injury (22). Many patients suffer from multiple injuries, multiple levels of injury, or occasional occult brain injury. In 80% of patients, the clinical exam can give information on the type of neurogenic dysfunction, completeness of the injury, activity of the external sphincter, but urodynamics is required to accurately assess bladder pressures (23). The use of the ASIA (American Spinal Injury Association) Score and the SSEP (Somatosensory Evoked Potentials), which have beenhelpful in predicting overall neurologic recovery after spinal-cord injury, have shown to only correlate with the recovery of somatic nerve function (external sphincter) and not with the recovery of bladder function (24). The urodynamic findings of 489 consecutive patients with spinalcord lesions of varying causes have been retrospectively reviewed and have revealed three general patterns of voiding dysfunction depending on the level of injury (22). Detrusor hyperreflexia with synergistic external sphincter function is seen primarily after incomplete spinalcord injury; detrusor hyperreflexia with DESD is seen primarily after

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complete thoracic and cervical level lesions; and detrusor areflexia is seen after sacral and many lumbar injuries. Although there is a general correlation between the neurological level of injury and the expected vesicourethral function, this analysis verifies that the correlation is not absolute, and clinical neurological examination alone is not adequate to predict neurourological dysfunction. A urodynamic evaluation provides a more accurate diagnosis. Detrusor hyperreflexia may evolve into forceful, prolonged detrusor contractions from brief, low-level contractions as reflex activity returns (25).This is felt to bean exaggerated reflex response to bladder filling after suprasacral trauma from the collateral formation of new neural pathways, the loss of inhibitory impulse transmission, or the emergence of more primitive alternative pathways (26). Detrusor external sphincter dyssynergia is caused by a lesion that disrupts the coordination of signals between the pontine mesencephalic reticular formation center and the sacral reflex center of the spinal cord. Most patients with suprasacral spinal-cord injuries have evidence of DESD (22).With DESD, there is an inappropriate elevation in activity of the external urethral sphincter during an involuntary detrusor contraction (Fig. 3). This causes a functional obstruction with poor emptying and elevated detrusor pressures (27,28).Ten to twenty percent of men with. spinal-cord injury and DESD also demonstrate dysynergia of the bladder neck internal sphincter when the injury is above the level of T-6 (29). Patients with injuries to the sacral cord usually develop detrusor areflexia, with low pressures at volumes up to 5OOccs. This initial bladder compliance doesnot always remain unchanged. subset A of patients will develop low compliance and mayrepresent a complex response to neurologic decentralization (20,30). This increased tone has been shown in animal studies with lower motor neuron injuries, in which there is an adrenergic overgrowth in the bladder (31). The classic outlet finding after sacral spinal-cord injury is a competent but nonrelaxing smooth musclesphincter and a striated sphincter that retains some fixed tone but is not under voluntary control (18,19). There is little consensus onthe function of the bladder neck or smooth sphincter after a sacral injury, however. The goal of management of patients with spinal-cord injury is to avoid high-pressure voiding, maintain detrusor compliance, and prevent acute sepsis, autonomic dysreflexia, and the deterioration of renal function. Urologic care should always beginin the acute period after injury. Initial management usually involves the use of an indwelling catheter, but the method chosen has been shown to have no significant adverse

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1

r"urethrr;r

t

l

It.

EM

Fig. 3. Videourodynamic imageof Detrusor Hyperreflexia with Detrusor External Sphincter Dyssynergia (DESD).

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effect on eventual outcome (32). Clean intermittent catheterization (CIC) is most desirable once the patient is stable. CIC leaves the bladder without foreign material and provides regular complete emptying of the bladder (33). Irreversible surgery is usually not recommended in the first year after injury before the patient’s bladder function has stabilized. Once the patient recovers from spinal shock, a detailed evaluation of the lower urinary tract is carried out. Further discussion of the management of spinal-cord injury will occur later in this chapter.

MYELODYSPLrzSL4 Neural tube defects are the most commoncause of neurogenic bladder dysfunction in children. The incidence is approximately 1 in 1000 in the United States but varies by geography(34).Over the last decade, this incidence has declined (35). The development of the spinal cord and vertebrae begin approximately on the eighteenth day of gestation and the closure of the canal is completed byday 35. Spina bifida represents a spectrum of abnormalities in the development of the neural tube and spinal cord. Spina bifida occulta occurs when only a bony defect is seen. A meningocele is defined as a meningeal sac with intact neural elements. Myelomeningocele or spina bifida cystica contains neural elements within a skin covered intact sac, whereas the sac is open in spina bifida aperta. Myelomeningocele account for over 90% of all open dysraphic states (36).Most spinal defects occur at the level of the lumbar vertebrae, followed by sacral, thoracic, and cervical (35). The underlying etiology of myelodyplasiais thought to be multifactorial. Epidemiological studies have shownthat an environmental component is likely to be involved as the incidence of neural dysraphisms varies with geographyand different periods of time. Evidence for genetic sources are many with an increase in female preponderance, ethnic variability, and familial tendencies. Myelodysplasia is also associated with Mecklel’sSyndrome, trisomies 13 and 18, and cloacal exstrophy (37).In addition, there is a 2-5% chance that a second sibling will be born with the same condition when spina bifida is already present in a family member (38).A periconceptual folic acid deficiency has been implicated as a cause of spina bifida. One multicenter study reported a 72% reduction in the recurrence of newborn neural tube defects with women who received a 4 mg supplement of folic acid during the periconceptual period (39). Other studies have shown that

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the risk of occurrence of first-time neural tube defects decreased by 60% by the use of folic acid (40). The diagnosis of myelomeningocele is most often made at the time of delivery. A prenatal diagnosis can be made by ultrasound (41). Elevated alpha-fetoprotein (AFP)by amniocentesis may also make the diagnosis more suspect (42), although the use of AFP has been controversial since both false positives and false negative results have been reported (43).While the role of elective cesarean section in fetuses with myelodysplasia may reducethe risk of intrauterine trauma to the neural elements (44), this remains controversial (45). A full urological evaluation is required in all newborns with spinalcord dysraphisms. Initially, the neonatal assessment begins with a detailed physical examination. It is important to document neurologic status with attention to abdominal muscletone, sphincter tone, function of the sacral reflex arc, and lower extremity function. A urinalysis, urine culture, and serumcreatinine should be obtained. Documentation of the renal anatomy canprovide baseline information about the radiologic appearance of the upper and lower urinary tracts as well as the condition of the sacral spinal cord and the central nervoussystem (CNS). Theseinitial studies are important for many reasons. They help identify babies at risk of urinary tract deterioration, help the physician counsel parents about the child's future bladder and sexual function, and can be used to compare with later studies (46). Renal ultrasound should be done as soon as possible to document the state of the upper tracts and thickness of the bladder wall. The postvoid residual urine volume can be helpful in assessing the completeness of spontaneous voiding by the neonate. The ultrasound is also an important means of examining the entire spine to rule out other neural tube defects (43). Studies have shown that less than 10% of newborns with spina bifida have hydronephrosis. A voiding cystourethrogram (VCUG) is also mandatory after a negative urine culture has been documented. This examination should be done promptly if hydronephrosis is seen on ultrasound. Sixteen percent of newborns withmyelodysplasia have reflux while '23.5% have a bladder diverticulum. Urodynamics may bedelayed in the newborn until it is safe to transport the child to the urodynamic suite and place the baby in the supine position for the test. This evaluation is important as the level of the bony defect will not necessarily determine the functional cord level. The region of involvement may be affected by the degree of involvement of the spinal cord and nerve roots, CNS anomalies(hydrocephalus, Arnold Chiari malformation), and surgical trauma during sac

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of complianceandanopenbladderneck

throughout filling.

closure (47’).The typical patient with myelodysplasia showsan areflexic bladder with an open bladder neck (Fig. 4). The bladder generally fills until the resting fixed external sphincter pressure is reached, and then leaking ensues (detrusor leak-point pressure) (48).Urodynamic testing during the neonatal period may also have prognostic value in regard to the upper tracts (46).Patients with vesical filling pressure below 4.0

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mmHgdo not usually have vesicoureteral reflex, whereas 8 l% of patients with pressures greater than 40 mmHg havebeen noted to have ureteral dilation and 68% to have vesicoureteral reflux. Management of the neonate is based on the urologic evaluation including urodynamics. Diapers are acceptable and optimal if the neonate voids spontaneously. The Crede maneuver generally should be avoided, for reasons which will be discussed later in this chapter, but can be used initially if it is effective at emptying the bladder until the lower urinary tract can be evaluated. If the infant cannot empty his bladder by spontaneous voiding or Crede, then intermittant catheterization is started even before urodynamics is done. The neonate should be placed on antibiotics until the absence of refluxhas been documented by VCUC. The goal of management in children with neurogenic bladder dysfunction is to preserve renal function, prevent urinary tract infections, and allow socially acceptable continence. After puberty, many patients with myelodysplasia will note an improvement in their continence. These patients are less tolerant of any degree of incontinence, however (48). In the adult population, the management can be more complex because of prior surgery, loss of bladder compliance, and upper tract dysfunction.

OTHER DISEASES OF THE SPINAL CORD Any lesion of the cord can potentially cause voiding dysfunction. There are many rare and uncommon causes such as tabes dorsalis, pernicious anemia, transverse myelitis, central cord syndrome,and polio. Spinal-cord tumors, tuberculosis, and arteriovenous malformations involving the cord are morecommon sources of spinal-cord pathology.

LONG-TERM UROLOGIC MANAGEMENT In order to best manage a patient with voiding dysfunction caused by a spinal-cord lesion or injury, it is important to consider the patient' s age, sex, level of lesion, degree of ambulation, manual dexterity, and

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independence. On the basis of both the clinical and urodynamicevaluation, as mentionedpreviously, urinary bladder symptoms may be classified as fillinghtorage abnormalities, emptying abnormalities or a combination of these (14,19),and treatment can be directed at the underlying urodynamic abnormality. The goal of management is to preserve renal function, avoid infection, provide freedom fromcatheters, and maintain urinary continence. Urologic managementis directed towards achieving complete emptyingof the bladder with low pressures. If bladder storage pressures are suitably low or can be made suitably low by nonsurgical means, the problem can be treated primarily as an emptying failure, and intermittent catheterization can be used, when practical, as a safe and effective way of satisfying many of the goals of treatment. For patients with a lowermotorneuron lesion and an areflexic bladder, clean intermittent catheterization is the treatment of choice. Self-intermittent catheterization has been associated with few complications and provides periodic complete emptying of the bladder (50). Reports have shown that 87.5% of patients on CIC have stable upper tracts (Cass). These same reports have shown an associated decrease in vesicoureteral reflux in 75%, with 90% of patients maintaining sterile urine. Moreover, approx34-49% of patients remain dry on this regimen. Still, there are complications seen in male patients with greater than five years of intermittent catheterization (23), including vesicoureteral reflux, stone disease, pyelonephritis, and even loss of kidney function. The use of a chronic indwelling catheter is never desirable because of its complications including epididymitis, urethrocutaneous fistula, traumatic hypospadias, andsquamous cell carcinoma. Yet, chronic catheterization remains the mostcommonform of management in patients who are tetraplegic and bedridden. Manyfemale patients, unable to use an external collecting device, are managed with catheter drainage because they fail pharmacologic therapy and/or have limited hand function. McGuire followed 35 women managed with either an indwelling catheter or CICfor 2-12 yr following spinal-cord injury and found a significant reduction in the incidence of autonomic dysreflexia, febrile UTIs, pyelonephritic scarring by IVP, and bladder stones in patients managed with intermittent catheterization. This same study showed 92% of women with long-term indwelling catheters eventually had incontinence around the catheter and 54% had urethral erosion, whereas none on CIC had these complications (51).Catheterization or adult diapering with proper skin care in the individual unwilling or unable to catheterize is a better alternative to chronic catheterization.

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The Crede maneuver and “trigger voiding” (a reflex contraction initiated by manual stimulation over a sacral or lumbar dermatonie) continue to be popular methods of bladder management but are contraindicated in patients with high outlet resistance, decreased compliance, DESD, and severe vesicoureteral reflux. These methods of bladder emptying can cause vesicoureteral reflux and upper tract deterioration. External catheters are another alternative but contraindicated in patients with high detrusor leak-point pressures. Finally, a cystostomy tube is the simplest of all bladder diversions but carries many of the same risks as an indwelling urethral catheter (e.g., infection, stones, cancer). Pharmacologic therapy in the management of voiding dysfunction after spinal-cord injury is based on our knowledge of the innervation of the bladder and urethra as well as receptor localization for drug action in the lower urinary tract. Urodynamic studies define the condition as a failure to store or empty and pharinacologic therapy is designed to fit the overall bladder management. In the patient with a hyperreflexic bladder, a variety of antispasmodic and anticholinergic medications are available and effective. In patients with suprasacral injury causing hyperreflexia with DESD, the goal of pharmacotherapy is to control reflex bladder activity so that intermittent catheterization can be performed with a low pressure system. Alpha blockers may reduce outlet resistance and improve bladder emptying, although there is no evidence that this therapy is effective in helping with DESD. The effect of alpha blockers on bladder function in the spinal-cord patient has been investigated prospectively and has been shown to improve detrusor compliance by as much as 73% and improve episodes of dy sreflexia and incontinence (52). This therapy would therefore be optimal in patients that cannot tolerate anticholinergic agents or have persistently high bladder pressures. This suggests that in the spinal-cord-injured patient, alpha blockers may have an effect either on the receptors in the detrusor muscle or a central effect. Sundin et al. have shown that the alpha adrenergic receptors that are normally found in the bladder base become prominent in the detrusor body after decentralization (53). The use of cholinergic agonists such as bethanechol to facilitate bladder emptying in patients with areflexic bladders has not proven beneficial. While cholinergics have been shown to raise baseline bladder pressure and increase maximal detrusor pressure, they do not completely empty the bladder. Cholinergic agonists cause a simultaneous contraction of the bladder, bladder neck, and urethra, preventing coordinated micturition

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(54).Poor intestinal absorption of bethanechol is another reason that cholinergic agonists lack efficacy. Cholinergic agonists also havebeen shown to actually inhibit the release of acetylcholine from parasympathetic postganglionics via a presynaptic feedback mechanism(55-57). The potential use of capsaicin for the treatment of neurogenic detrusor hyperreflexia has been evaluated. A prospective, randomized study showed significant improvements in urinary continence, reduced voiding frequency, and general patient satisfaction (58).Urodynamic evaluation in patients who received capsaicin also had significant improvements in bladder capacity and maximum detrusor pressure vs those who received a placebo. Capsaicin is highly neurotoxic to unmyelinated C-fibers and has been used in the past for its analgesic properties. In this study, 100 mL of capsaicin in 30% ethanol was placed intravesically one time for 2-5 min, dependingon the patients’ tolerance of the medication. Side effects are common and almost systematic with suprapubic pain, urgency, flushing, hematuria, and autonomic dysreflexia, but usually resolve within 2 wk after installation. If conservative methods fail, surgical alternatives may be required. Patients are selected for surgical management on the basis of a careful neurourological evaluation, patient compliance, and hand function. A sphincterotomy is indicated in patients with DESD and elevated intravesical storage pressure that can be associated with deterioration of the upper urinary tracts (46).Sphincterotomy should lower the detrusor leak-point pressure to an acceptable level, thus treating the dysfunction primarily as one of emptying. The resultant storage failure can be handled withan external collecting device. For patients who are unable to self-cath, this procedure allows urinary drainage with low pressure, often significantly reducing postvoid residuals (59). In addition, there is evidence that 70-90% of patients show substantial improvement after sphincterotomy with a reduction in vesicoureteral reflux and upper tract deterioration (60). Use of this procedure has waned recently because of both the significant complications associated with this procedure and the long-term failure rates. Sphincterotomy, which involves the transurethral resection of the striated external urethral sphincter, is plagued with significant bleeding requiring blood transfusion in 5-23% (61-63). In addition, recurrent obstruction is reported in 12-26% (59,64) and erectile dysfunction in 2.8-64% (61,63,65,66).Less than 50% of patients, moreover, have beenreported to be successfully managed with a condom catheter after sphincterotomy, and eventually require a suprapubic tube (67).

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Sphincter prostheses and balloon dilation of the external sphincter are more recent options associated with reduced morbidity and acceptable patient satisfaction. The use of an artificial sphincter must be carefully planned to avoid infection and erosion in patients with loss of sensation. Balloon dilation of the sphincter works but may not be a durable treatment. Long-term studies evaluating urethral stents are underway. Initial results have revealed similar effectiveness with sphincterotomy but reduced morbidity. A prospective comparison of the UroLume endourethral Wallstent prosthesis (American Medical Systems, MN) vs sphincterotomy inpatients with DESD and voiding pressures greater than 60 mm H20 showed that sphincter prosthesis has similar efficacy but is easier technically, less morbid, andless expensive (68).Complications of sphincter prosthesis included migration of the prosthesis and bladder neck obstruction. Twenty-seven percent of patients in this study required a second prosthesis to bridge the entire external urethral sphincter. Bladder augmentation cystoplasty is designed to create a bladder with increased compliance andcapacity. It is primarily used in patients with a hyperreffexic, small-capacity, poorly compliant bladder, in which there is evidence of deteriorating renal function or incontinence between catheterization, which is refractory to medical therapy. This operation is ideal in patients who can perform intermittent catheterization but are incontinent or have upper tract deterioration. Renal insufficiency is a contraindication to augmentation enterocystoplasty. Urinary diversion is used only as a last resort but may be a patient’s only viable alternative once the problems associated with chronic catheterization develop. An array of diversions such as the ileal conduit, ileovesicostomy, or continent diversion are available to the patient based on the patient’s underlying renal function, motivation, compliance, and hand function. Supravesical diversion is indicated when there is progressive hydronephrosis andintractable upper urinary tract dilation, recurrent upper urinary tract infections, and considerable difficulty with the patient performing i n t e ~ i t t e ncatheterization. t With anydiversion, there is a high rate of long-term complications (69). The initial upper tract improvements seen in patients after ileal conduit diversion have been shownto give way to deterioration. Therefore, ileal loop diversion is a last resort treatment for neurogenic bladder dysfunction. Neurostimulation is a promising method currently under investigation using electrical stimulation to control micturition and urinary incontinence. This technique was initially introduced in the 1960s using implantable electrodes in the detrusor muscle (70). Both intradural and

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extradural techniques of sacral neurostimulation are available (71,72). Voiding dysfunction after suprasacral spinal-cord injury responds well to sacral-root stimulation but has not been effective in lesions at the level of the cauda equina and below. A majordifficulty in this treatment has been the inability to simultaneously relax the striated external sphincter and make the detrusor contract. Dorsal rhizotomy with both an extradural or intradural approach has become an important component of neurostimulation as it reduces detrusor hyperreflexia, improves bladder capacity, improves detrusor responses to ventral root stimulation and contraction, and diminishes the spasticity of the pelvic floor and external sphincter. A review of a multicenter experience using the Finetech-Brindley sacral anterior root stimulator showed that the technique of complete intradural posterior sacral rhizotomies, which was much more common than anextradural approach, and the implantation of a ~ine~ech- rind ley sacral anterior root stimulator improved continence, evacuation of urine, and bladder capacity (73). A reduction in vesicoureteral reflux, urinary tract infections, andautonomic dysreflexia was also noted. The stimulator can also assist in defecation and help men achieve penile erections, although only one-third of these patients actually use the stimulated erections for coitus. Long-term evaluation and comparison of sacral anterior root stimulation vs intermittent catheterization must be made in terms of safety, efficacy, and cost. Complications of these procedures can arise from potential infection of these implantedmedical devices or nerve electrodes, nerve destruction with rhizotomies, possible erectile dysfunction, and bladdersphincter dyssynergia (74).

FOLLOW-UP P"ENTION

OF COMPLICATIONS

Annual urologic follow-up is necessary in all patients with spinalcord injury or myeloneuropathies, regardless of the nature or ease of bladder management. In fact, approx 40% of all SCI patients would die of renal insufficiency if they were left completely untreated (7.5,76). The evaluation should rule out any chronic, symptomatic infection of the urinary tract or urolithiasis and include an upper urinary tract assessment with either an intravenous pyelogram or renal ultrasound. There is continuing debate on which of these radiologic evaluations is superior. Urinary-tract infections are the most common urologic complication in patients with spinal-cord injuries (77).All urinary infections in these

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patients are considered complicated becausean uncomplicated infection is defined ascommunity acquired without structural or neurologic abnormalities. IJTIs are responsible for many uroseptic episodes in the SCI population. Many risks exist including instrumentation, intermittent catheterization, stones, urethral strictures, benign prostatic hyperplasia, and detrusor external sphincter dyssynergia. Other causes include bladder overdistention, vesicoureteral reflux, large postvoid residuals, and high voiding pressures. The aim in management is to prevent, not to treat. This is best done by ensuring the well-being of the patient, providing adequate urinary drainage, and preserving healthy bacterial commenseral environment. Antibiotics should only beused during episodes of clinical infection, not asymptomaticbacteriuria. Asymptomatic bacteriuria does not usually need to be treated unless the patient has either a urease-producing organism, vesicoureteral reflux, or both. Approximately 23% of patients have vesicoureteral reflux after spinal-cord injury, as reported by Bors (77a). Causes include a Hutch para-ureteral diverticula, urinary infection, and highintravesicle storage pressure compromising the ureterovesical junction (78). Reflux can lead to reflux nephropathy with subsequent renal impairmentand chronic urolithiasis. Stone disease develops in 8-15% of patients with spinal-cord injury, often caused by urease-producing bacterial infections, forming primarily struvite stones. The highest incidence occurs in patients with indwelling catheters (79). Other causes include chronic infections, immobilization with hypercalcemia(80), increased age, and completeneurological lesions. Prompt recognition and treatment of stone disease is necessary to adequately eliminate infection from the urologic tract in these patients. Carcinoma of the bladder has an incidence of 2-10% in this population. Squamous-cell carcinomais the most commontype of malignancy. The primaryrisk is long-term use of an indwelling catheter and therefore should be avoided. Annual bladder surveillance in these patients has not influenced survival as most of these patients present with advanced disease. It is generally recommended that for patients with a 10-yr history of an indwelling catheter or greater, annual cystoscopy with bladder biopsy be performedalong with evaluation of the upper tracts. Autonomic dysreflexia is a potentially life-threatening complication in these patients. This disorder represents an autonomic response, which is primarily sympathetic, to specific visceral stimuli in patients with spinal-cord injury above the level of T6 (81).An incomplete compensatory parasympathetic outflow will occur above the level of injury. This

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phenomena is more common in patients with cervical injuries, and common triggers include bowel andbladder distention. Symptoms may involve piloerection, diaphoresis, pounding headache, flushing above the level of the injury, and may be associated with sudden and severe hypertension accompanied by reflex bradycardia. Although bradycardia is most common,tachycardia and arrythmias may be present. Hypertension may be of varying severity from causing a mild headache to a seizure or life-threatening cerebral hemorrhage. Therefore, it is necessary to monitor the blood pressure in these patients with any visceral stimulation. Immediate management whendysreflexia occurs is to discontinue the procedure. A life-threatening episode can be terminated by Procardia l0 mg sublingual (82), which has also been shown to be capable of preventing this syndrome when given orally 30 min prior to the procedure (82). The use of general or spinal anesthesia may be used in refractory cases. Prophylaxis against dysreflexia includes the elimination of visceral stimulation and chronic alpha-adrenergic blockade (83).In addition, a number of ablative procedures have beenused for intractable dysreflexia including sympathectomy, sacral neurectomy, rhizotomy, cordectomy, and dorsal-root ganglionectomy (81).

REFERENCES 1. Graham SD (1981) Present urological treatment of spinal cord injury patients. J Urol 126:l-4. 2. Bors E (1957) Neurogenic Bladder, Urol Sur 7:177-250. D (1988) Voidingfunction and dysfunction: a logical andpractical 3. Wein A, Barrett approach. Chicago: Year Book Medical Publishers. 4. Blaivias JG (1982) The neurophysiology of micturition: a clinical study of SS0 patients. J Urol 127:958-963. S. de Groat WC, Booth AM, Yoshiyarnd, M (1993) Neurophysiologyof micturition and its modification in animal models of human disease. In: Maggi CA, ed. The Autonomic Nervous System, vol. 3. London, Harwood Academic Publishers, 1993, pp. 227-290. 6. de Groat WC, Nadelhaft I, Milne RJ, BoothAM,Morgan C, Thor K (1981) Organization of the sacral parasympathetic reflex pathways to the urinary bladder and large intestine. JAuton New Syst 3:13S-160. 7. de Groat WC, Kawatani M, Hisarnitsu T, Cheng CL, Ma CP, Thor K, Steers W, Roppolo JR (1990) Mechanisms underlyingthe recovery of urinary bladderfunction following spinal cord injury. J Auton New Syst 30 (Suppl):S71”77. 8. Janig W, KoltzenburgM (1990) On the function of spinal primaryafferent fibres supplying colon and urinary bladder. J Auton New Syst 30 (Suppl):S89-96. 9. McMahon S, Morrison J (1982) Spinal neurones with long projections activated from the abdominal viscera of the cat. J Physiol (Lond) 322: 1-20. 10. Hughes J (1978) Puthology of the Spinal Cord. London: Saunders.

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11. Schall T, Bacon K (1994) Chemokines, leucocyte trafficking, and inflammation. Curr Opin Immunol6:865-873. 12. Fagg GE, Foster AC (1983) Amino acid neurotransmitters and their pathways in the mammalian central nervous system. Neuroscience 9:701-709. 13. Rothman S, Olney J (1987) Excitotoxicity and the NMP receptor. Trends Neurosc 10:299-302. 14. Wein AJ (1981) Classification of neurogenic voiding dysfunction. J UroZ 125:605609. 15. Bors E, Comm AE (1971) Disturbances of micturition: acute onset. Neurolog Urol University Park, Baltimore, MD. 1971. pp. 181-184. 16. Roaf R (1960) A study of the mechanics of spinal injuries. J Bone Joint Surg 42B:810-816. 17. DeVivo M,Rutt R, BlackK (1982) Trends in spinal cord injury demographics and treatment outcomes between1973 and 1986.Arch Phys Med Rehabil73:424-430. 18. Thomas D, O’FlynnK (1994) Urodynarnics: Principles,Practice, Application. In: MundyAR,StephensonTP,WeinAJ, Spinal Cord Injury. London: Churchill Livingstone, pp. 345. 19. Sullivan M, Yalla S (1992) Spinal cord injury and otherforms of myeloneuropathies. Problem Urol 6:643. 20. Fam B, Yalla SV (1988) Vesicourethral dysfunction in spinal cord injury and its management. Semin Neurol 8: 150-155. 21 * Wein A, Rovner E (1999) Adult voiding dysfunction secondary to neurologic disease or injury. In: Ball T, Jr., ed. AUA Update Series Vol. XVIII. AUA Office of Education, Houston, TX. pp. 42-48. 22. Kaplan SA, Chancellor MB, Blaivas JG (1991) Bladder and sphincter behavior in patients with spinal cord lesions. J Urol 146:113-1 17. 23. Wyndaele JJ (1992) Neurourology in spinal cord injured patients. Paraplegia 30:50-53. 24. Curt A, Rodic B, Schurch B, Dietz V (1997) Recovery of bladder function in patients with acute spinal cord injury: significance of ASIA scores and somatosensory evoked potentials. Spinal Cord 35:368-373. 25. Rudy D, Awad S, Downie J (1988) External sphincter dyssynergia: an abnormal continence reflux. J. Urol 140:105-1 10. 26. de Groat W, Karvatni M (1985) Neural control of the urinary bladder: Possible relationship between peptidergic inhibitory mechanisms and detrusor instability. Neurourol Urodyn 4:285-300. 27. Anderson RU (1983) Urodynamic patterns after acutespinal cord injury: association with bladder trabeculation in male patients. J Urol 129:777-779. 28. Ruutu M (1985) Cystometrographic patterns in predicting bladder function after spinal cord injury. Paraplegia 23:243-252. 29. Chancellor MB, Rivas DA, Linsenmeyer T, Abdill CA, Ackman CF, Appell RA, et al. (1994) Multicenter trial in North America of UroLume urinary sphincter prosthesis. J Urol 152:924-930. 30. McGuire E (1984) Clinical evaluation and treatment of neurogenic vesical dysfunction. In: Libertino J, ed., International Perspectives in Urology. Baltimore: Williams and Wilkins. 31. Sundin T, DahlstromA (1973) The sympathetic innervationof the urinary bladder and urethrain the normalstate and after parasympathetic denervation at the spinal root level. An experimental study in cats. Scand J Urol Nephrol 7:131-149.

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patients. 32. Lloyd L (1986)New trends in urologic management in spinal cord injured J Cent New Syst Trauma 3:3-12. 33. Guttman L, Frankel H (1966) The value of intermittent catheterisation in the early management of traumatic paraplegia and tetraplegia. Paraplegia 4:63-84. 34. Stein SC, Feldman JG, Friedlander M, Klein RJ (1982) Is myelomeningocele a disappearing disease? Pediatrics 6 9 5 11-514. 35. Laurence K (1989) A declining incidence of neural tube defects in UK. Z Kinderchir 44(Suppl 1):51. 36. Stark G (1977) Spina BiJida: Problems and Management. Oxford:Blackwell Scientific Publications. 37. Toriello H (1982) Periconceptual vitamin supplementation for the prevention of neural tube defects: a review. Spinal BiJda Therapy 459. 38. Scarff T, Fronczak S (1981) Myleomeningocele: a review and update. Rehab Lit 42:143-146. 39. MRC Vitamin Study Research Group (1991) Prevention of neural tube defects: results of the Medical Research Council Vitamin Study. Lancet 338:131-137. 40. Werler MM, Shapiro S, Mitchell AA (1993) Periconceptionalfolic acid exposure and risk of occurrent neural tube defects. JAMA 269: 1257-126 1. 41. Hobbins J, Grannum P, Berkowitz RL, et al. (1979) Ultrasound in the diagnosis of congenital anomalies. Am J Obstet Gynecol 134:331-345. 42. Brock DJH, Sutcliffe RC (1972) Alpha Fetoprotein in the antenatal diagnosis of anencephaly and spina bifida. Lancet 2:197-199. 43. Watson WJ, Chescheir NC, Katz VL, Seeds JW (1991) The role of ultrasound in evaluation of patients with elevated maternal serum alpha-fetoprotein: a review. Ohstet Gynecol 78:123-128. et al.(1984) Perinatal management of 44. ChervenakFA,DuncanC,MentLR, myelomeningocele. Obstet Gynecol 63:376-380. BK (1988) Open spina bifida: Does caesarian 45. Bensen JT, Dillard RG, Burton section improve prognosis. Obstet Gynecol 71 532-534. 46. McGuireE,Woodside J, Ta B, et al. (1981) Prognostic value of urodynamic testing in myelodysplastic patients. J Urol 126:205-209. 47. Kroovand RL, Bell W, Hart LJ, Benfield KY (1990) The effect of back closure on detmsor function in neonates with myelomeningocele. J U r d 144:423-425. 48. McGuire E, Denil J Adult myelodysplasia. In: AUA Update Series Vol. X. AUA Office of Education. Houston, TX. 1991. pp. 297. of bladderdysfunctioninmultiplesclerosis. 49. BlaivasJG(1980)Management Neurology 30:12-18. 50. Lapides J, Diokno A, Silber S, Lowe B (1972) Cleanintermittent self-catheterization in the treatment of urinary tract disease. J Urol 107:7458-7461. 51. McGuire E, Savastano J (1986) Comparative urological outcome in women with spinal cord injury. J Urol 135:730-731. J, McGuire 52. Swierzewski SJ, 3rd, Gormley EA, Belville WD, Sweetser PM, Wan EJ (1994) The effect of terazosin on bladder function in the spinal cord injured patient. J UroZ 151:951-954. 53. Sundin T, Dahlstrom A, Norlen L, Svedmyr N (19’77)The sympathetic innervation and adrenoreceptor function of the human lower urinary tract in thenorma1 state and after parasympathetic denervation. Invest Urol 14:322-328. 54. Sogbein SK, Downie JW,AwadSA (1984) Urethral response during bladder contraction inducedby subcutaneous bethanecholchloride: elicitation of a sympathetic reflex urethral constriction. J Urd 131:791-795.

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55. D’Agostino G, Kilbinger H, Chiari MC, Grana E (1986) Presynaptic inhibitory muscarinicreceptorsmodulating (3H) acetylcholine release in theraturinary bladder. J Pharm Exper Ther 239522-528. 56. Somogyi G, de Groat W (1990) Modulation of the release of (3H) norepinephrine from the base and body of the rat urinary bladder by endogenous adrenergic and cholinergic mechanisms. J Pharmacol Exp Ther 255:204-210. 57. Alberts P (l 995) Classification of the presynaptic muscarinic receptor subtype that refulates 3H-acetylcholine secretion in the guinia pig urinary bladder in vitro. J Pharmacol Exp Ther 274:458-468. 58. Seze M, Wiart L, Joseph P (1998) Capsaicin and neurogenic detrusor hyperreflexia: A double-blind placebo controlled study in 20 patients with spinal cord lesions. Neurourol Urodynamics 17513-523. spinal cordinjury 59. Perkash I (1976)Modifiedapproachtosphincterotomyin Paraplegia 13:247-260. patients: Indications, technique, and results in 32 patients. 60. Wein A, Raezer D, Benson G (1976) Managementof neurogenic bladder dysfunction in the adult. Urology 83432-434. 61. Carrion H, Braun B, Politano V (1979) External sphincterotomy at the12 o’clock position. J Urol 121:462. 62. Madersbacher H (1976) The twelve o’clock sphincterotomy: Technique, indications, results. Paraplegia 13:261-267. 63. KIiviat M (1975) Transurethral sphincterotomy:Relationship of site of incision to postoperative potency and delayed hemorrhage. J Urol 114:399-401. R (1973) Externalsphincterotomy:An evalua64. Schellhammer P, Hackler R, Bunts tion of 150 patients with neurogenic bladder. J Urol 110: 199-202. M, et al. (l 977) Anteromedian 65. Yalla S, Fam B,Gabilondo F, Jacobs J, DiBenedetto external sphincterotomy: technique, rationale, and complications. J Urol l 17:489493. 66. Thomas D (l 976) The effect of trans-urethral surgeryon penile erection in spinal injury patients. Paraplegia 13:286-289. 67. Vapnek JM, Couillard DR,Stone AR (1994) Is sphincterotomy thebest management of the spinal cord injured bladder? J Urol 151:961-964. 68. Rivas D, Chancellor M, Bagley, D (1994) Prospective comparison of external sphincter prosthesis placement and external sphincterotomy in men with spinal cord injury. J Endourol 8:89-93. 69. Moeller B (1977) Some observations on 31 spinal cord injury patients on whom the Bricker procedure was pedormed. Paraplegia 15:230. 70. Boyce WH, Lathem JE, Hunt LD (1964) Research related to the development of an artificial electrical stimulator for the paralyzed human bladder: a review. J Urol 91:41-51. 71. Brindley GS, Polkey CE, Rushton DN, Cardoza L (1986) Sacral anterior root stimulators for bladder control in paraplegia: The first 50 cases. J Neurol Neurosurg, Psychiat, 49: 1104-1114. 72. Tanagho EA, Schmidt RA, Orvis BR (1989) Neural stimulation for control of voiding dysfunction: a preliminary report in 22 patients with serious neuropathic voiding disorders. J Urol 142:340-345. 73. Kerrebroech P, KoldewijnE, Debruyne M (1993) Worldwide experience with the Finetech-Brindley Sacral Anterior Rootstimulator. Neurol Urodynamics 12:497503.

of incontinenceby electrical stimulation. 74. Merrill DC (1979) The treatmentdetrusor J Urol 122:515-5 17.

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75. Hackler RH (1977) A 25-year prospectivemortality study in the spinal cord injured patient: comparison with the long-term living paraplegic. J Urol 117:486-488. 76. Jonas U, Jones LW, Tanagho EA (1975) Recovery of bladder function after spinal cord transection. J Urol. 113:626-628. 77. Young J. Spinal cord injurystatistics:Experienceof regional spinal injurysystems, Good Samaritan Medical Center Phoenix, AZ. 1982 p. 152. 77a. Bors E (1957) Neurogenic bladder. Urologic Survey 7:177. 78. Duckett JW,Jr (1982) Ureterovesicaljunction and acquired vesicoureteral reflux. J Urol 127:249. 79. Hall MK, Hackler RH, ZampieriTA, Zampieri JB (1989) Renalcalculi in spinal cord-injured patient: association with reflux, bladder stones, and foley catheter drainage. Urology 34: 126-128. 80. Claus-Walker J, Campos R, Carter R, Vallbona C, Liscomb H (1972) Calcium excretion in quadraplegia. Arch Phys Med Rehabil 53:14-20. (1991) Autonomic dysreflexia and its urological implications: 81. Trop CS, Bennett CJ a review. J Urol 146:1461-1469. 82. Dykstra DD,Sidi AA, AndersonLC (1987) The effect of nifedipine on cystoscopyinducedautonomichyperreflexiain patients withhighspinalcord injuries. J Urol 138:1155-1157. IH, Stass WE Jr (1994) Prospective evaluation 83. Chancellor MB, Erhard MJ, Hirsch of terazosin for the treatment of autonomic dysreflexia.J UroZ 15 1:1 11-1 13.

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Diabetic Bladder Dysfunction

CONTENTS INTRODUCTION EPIDEMIOLOGY PRESENTATION DIAGNOSIS URODYNAMIC FINDINGS PATHOPHYSIOLOGY TREATMENT CONCLUSION REFERENCES

INTRODUCTION The prevalence of diabetes mellitus (DM) has reachedepidemic proportions among the population of the United States. The American Diabetes Association recently reported that the prevalence of diagnosed and undiagnosed DM in the United States is currently 6% and rising ( I ) . This increase is felt to be secondaryto a rising incidence of obesity as well as a change in the criteria for the diagnosis of DM (from a fasting blood glucose of 140 mgldL to 126 mgldL). Besides impaired blood glucose regulation, many direct and indirect sequelae of DM can occur. Lower urinary tract dysfunction is relatively common in this group of patients and the etiology of these symptoms is commonly attributed to DM. Owing to the high incidence of DM and its frequent involvement of the lower urinary tract, a complete understanding of

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its epidemiology, physiology, presentation, diagnosis, and treatment is essential for clinicians caring for these patients.

EPIDEMIOLOGY It is difficult to estimate exactly what percentage of diabetic patients suffer from bladder dysfunction. Though many patients are referred for evaluation of urinary symptoms, the total pool from which they are extracted is frequently hard to determine. In addition, many patients may have other co-existing problems which caneither mimic or mask the findings ofa diabetic neurogenic bladder. For example, women may have stress incontinence, prolapse, or pelvic floor dysfunction, whereas men may haveprostatic obstruction, urethral stricture disease, or a host of other obstructive processes, all of which can be confused with or coexist with a diabetic neurogenic bladder. In some series, as many as 52% of randomly evaluated diabetic patients werefound to have urologic symptoms (2). Evenamong “asymptomatic” patients, many have unrecognized symptoms. Uedaet al. (3) examined 53 “asymptomatic” diabetic patients and found that upon careful questioning 21 (40%) complained of voiding symptoms. They also noted no correlation of bladder dysfunction with type or duration of DM. In addition, the presence or absence of diabetic retinopathy did not correlate with the presence or absence of bladder dysfunction. Thus, a considerable number of patients with DM, even when asymptomatic, will be found to have bladder dysfunction upon careful evaluation.

PESENTATION Generally the onset of diabetic neurogenic bladder dysfunction is insidious and may not be recognized until it has reached an advanced stage. Early signs and symptoms may be overlooked by the patient, but impaired bladder sensation is usually the first manifestation of lower urinary tract involvement. Symptoms may begin as infrequent voiding, decreased stream, hesitancy in initiating the urinary flow, dribbling due to overflow incontinence, and the sensation of incomplete emptying. Upon questioning the primary symptom may be only the loss of desire to void with a resultant pattern of voiding by the clock

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or fromhabit only. This constellation of symptoms is classically referred to as “diabetic cystopathy” (4). It is becoming more evident, however, that a significant number of diabetic patients may present with symptoms of urgency andfrequency. A recent studyby Kaplan et al. (5) noted that the mostcommon symptoms in a group of diabetic patients referred for evaluation of urologic complaints were nocturia greater than two times (87%) and urinary frequency greater than every 2 h (78%). In contrast, the more classic diabetic cystopathy symptoms of hesitancy, decreased stream, and the sensation of incomplete bladder emptying were elicited in 62, 52, and 45% of the patients. Because the symptoms associated with the classic diabetic bladder are insidious in nature, perhaps those patients are not well-represented in studies such as Kaplan’s, which rely on patients referred for specific urologic symptoms. In any event, it is clear that patients with a diabetic bladder can present with any of a full spectrum of voiding complaints from urgency and frequency to difficulty emptying.

DIAGNOSIS When evaluating the diabetic patient for signs of bladder dysfunction, a complete history and physical exam as well as urine culture is essential. Many other conditions that may cause or aggravate vesico-urethral dysfunction must be considered since cerebrovascular or lumbar disc disease, as well as a host of other neurological disorders, can cause voiding symptoms that mimic those found in DM. Similarly, gross physical findings such as a cystocele or other forrns of pelvic prolapse in women or an enlarged prostate or indurated portion of the urethra (possible stricture) in men can contribute to significant voiding dysfunction. Testing of perineal sensation, sphincter tone, and the bulbocavernosus reflex can help identify a peripheral neuropathy consistent with DM. Urine culture may identify an infection that could be the source of the patient’s symptoms. In some patients, it may be difficult to separate the bladder dysfunction caused by diabetes from that of a coexisting disease. The diagnosis of diabetic neurogenic bladder and the exact type of dysfunction present is made mostreadily with urodynamic testing. This may include a simple cystometrogram, uroflow, simultaneous pressure/ flow studies, sphincter electromyography (EMG), and urethral pressure profilometry or evaluation of leak-point pressures. Obtaining a postvoid

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residual (PVR) may also help determine the efficiency of bladder emptying. The main differential diagnosis is stress incontinence (primarily in women) or outflow obstruction. The use of simultaneous pressure/ flow studies with determination of leak-point pressures or urethral pressures will help differentiate between these two entities and the diabetic neurogenic bladder, though in some cases with co-existing problems, the determination of the role played by each entity may be difficult. In addition, electrophysiologic testing may be useful for assessment of peripheral neuropathy.

URODYNMIC FINDINGS Classic urodynamic findings (6)include impaired bladder sensation, increased cystometric capacity, decreased bladder contractility, impaired uroflow, and an increased PVR. Cystometricexamination may show detrusor areflexia but detrusor instability is also frequently found (see Table l). Urethral closure pressure profiles or Valsalva leakpoint pressures are generally normal, but as noted previously, serve to exclude other forms of pathology.

Table 1 Urodpamic Features in Diabetes Mellitus

Cystometrogram Decreased bladder sensation Increased bladder capacity Bladder contractility Areflexic Hyperreflexic Uroflowmetry Normal or decreased Urethral pressure profile Normal Leak point pressure Absent (infinity) Sphincter EMG Normal or abnormal Electrophysiologically evoked response Normal or abnormal

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In Kaplan’s study (5),52% of the diabetic patients had urodynamically documented detrusor instability, 23% had impaired detrusor contractility, 24% had poor compliance, 1l % had indeterminate findings, and 24% had detrusor areflexia (5).Another study (7’) of elderly diabetic nursing home patients (mean age 80 yr; 19 women, 4 men) who presented with symptoms of urinary dysfunction showed that 61% had detrusor instability, 13% normal contractions, 17% voluntary contractions of low magnitude, and 9% no contractions at all. The authors concluded by emphasizing that one cannot assumethat elderly diabetic patients with urologic symptoms havepoorly contracting bladders (classic diabetic bladder), and that urodynamic studies can be helpful in determining the etiology andchoosing the appropriate therapy in these patients. In contrast, earlier reports (4) and the more recent study by Ueda et al. (3) have noted urodynamic changes more consistent with those described with classic diabetic cystopathy. Ueda etal. (3)noted detrusor instability in 25% of patients (study involved 28 women and 25 men), but noted that all of the patients (with detrusor instability) had a history of cerebrovascular disease. No patient without cerebrovascular disease had detrusor instability. In addition, they noted significant increases in bladder volume at first desire to void and maximalcapacity, decreases in detrusor contractility, and increases of PVR in their cohort of asymptomatic diabetic patients. Similarly, a study by Goldmanet al. (8)noted that diabetics who also had gastroparesis had delayed first Sensation, increased capacity, and increased PVR. Perhapsthe difference between these sets of findings is related to a selection bias regarding whether or not symptoms requiring evaluation were volunteered by the patients. In Kaplan’s study (5), patients had been referred because of voiding symptoms, whereas in Ueda’s study (3) the patients were unselected. It is clear though that there is no one set of urodynamic findings that applies to all cases of diabetic neurogenic bladder. Rather, it is imperative to test accurately for and diagnose the specific type of bladder dysfunction occurring in order to appropriately treat the patient.

PATHOPHYSIOLOGY The cause of the bladder dysfunction seen in DM is primarily the result of peripheral and autonomic neuropathy. The classic diabetic cystopathy has been attributed to diminished sensation leading to a chronically overstretched bladder, which results in myogenic failure

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and the inability to mount a satisfactory detrusor contraction. The findings of detrusor instability in a significant number of patients implies that the cortical or spinal regulatory tracts can be affected too. In diabetes, somatic and autonomic neuropathygenerally exist concurrently. This has been corroborated by studies demonstrating that the electrically stimulated bulbocavernosus reflex latency times are significantly prolonged (9).However, this is seen primarily in advanced peripheral pudendal neuropathy. More subtle changes in nerve function may be ascertained by detrusor and urethral electromyelography as described by Bradleyand colleagues (IO), where there can bean increased latency of the evoked response in the perineal musculature as well as anal and urethral sphincters. It should be remembered that when simultaneous dysfunction of bowel, bladder, and genitals occurs early, it may be owing to cauda equina infarction from the vascular complications of diabetes ( I I ). Currently, there are several theories regarding the pathophysiology of diabetic neuropathy. Symmetric peripheral neuropathy (polyneuropathy) may be the most commoncomplication of DM (12). The autonomic neuropathy associated with DM is "generally thought to occur later. Several forms of abnormalimpulseconduction patterns havebeen described, but in general, electrophysiologic studies show slowing of evoked responses (11). The impedanceof conduction has been demonstrated in demyelinated nervefibers, and when more severe conduction delay occurs this may result in not only temporal delay, but complete nerve blockade (13). Although fibers such as those in the autonomic nervous system may be affected first owing to their smaller diameter, shorter length, and smaller sudace-to-volume ratio, clinical manifestations generally appear later than peripheral symmetric polyneuropathy. Disturbance of the peripheral nerve metabolism is thought to play an important role in the neuropathy of diabetes as well. The metabolic derangement causes dysfunction of the Schwann cell with resultant segmental demyelination as well as axonal degeneration (14). It is hypothesized that increased tissue levels of sorbitol may account for the tissue destruction and peripheral neuropathy (15). Another postulated cause of peripheral nerve damage is the reduction of myo-inositol in peripheral nerves (15). Interplay may occur between the sorbitol and myo-inositol pathways, but it has not been confirmed(16).Finally, the increased glycation of peripheral nerve cytoskeleton proteins is felt to contribute to the pathogenesis of diabetic neuropathy (17'). Whatever the exact metabolic cause, recent studies have clearly demonstrated neural dysfunction involving the bladder. Steers et al.

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(18)demonstrated changesin both afferent and efferent pathways innervating the bladder in an animal model. Itoh et al. (19) demonstrated significant decreases of acetylcholinesterace staining and activity in detrusor muscle, suggesting the presence of an autonomic neuropathy. These and other findings indicate that the alterations in bladder function found in diabetic patients are the result of derangements in both the peripheral and autonomic nervous systems.

Treatment involves symptomatic relief, prevention of infection, maintenance of renal function, and achievement of continence while providing adequate bladder emptying (20). Often treatment decisions must be based on the results of urodynamic testing since effective therapy requires an understanding of the cause of the individual patient’s symptoms. Patients with detrusor instability are best managed with anticholinergic or smooth muscle relaxants to diminish the frequency and amplitude of involuntary contractions. Oxybutynin hydrochloride, imipramine, and dicyclomineare among the medications that are commonly used, although side effects may limit their application. The introduction of tolteradine and extended-release oxybutynin hydrochloride, which reportedly have fewerside effects, may increase the applicability of medical therapy. For those with impaired detrusor contractility or detrusor areflexia no cure is available, as yet. Timed voidings on a consistent and regular schedule is effective in those with diminished sensation but who still canempty their bladder. Significant detrusor decompensation will necessitate intermittent catheterization. Clean intermittent catheterization (CIC) is usually easily learned and accepted by most patients. By keeping the catheterized volumes under 400 mL (or less if poor compliance or elevated bladder pressures are noted on urodynamics studies the risk of renal damage is minimized. Occasionally, if recurrent urinary tract infections become a problem, antimicrobial prophylaxis is necessary. Metoclopromide, with its cholinergic effects, has been used to treat diabetic neurogenic bladder dysfunction, as improvement has been seen in patients with delayed gastric emptying (21). On the other hand, bethanechol chloride, a purely parasympathomimetic agent, is rarely effective (22). In short, the success of bladder rehabilitation in this subgroup of patients dependsupon the degree of detrusor decompensation.

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CONCLUSION Bladder dysfunction in those with DM is relatively common. Given the high incidence of DM in the general population, the clinician must be prepared to evaluate and treat these patients effectively. Though the classic diabetic cystopathy refers to the bladder with poor sensation and detrusor failure, many patients will have primarily detrusor instability. Thus, urodynamic testing is frequently crucial to determine the actual type of bladder dysfunction in the individual and to allow for the institution of appropriate therapy. Hopefully, future research will shed more light onto the exact pathophysiology of this disorder and allow for more effective bladder rehabilitation.

REFERENCES 1. American Diabetes Association (1998) Screening for type I1 diabetes. Diabetes Care 21520-22. 2. Ioanid CP, Noica N, Pop T (198 Incidence 1) and diagnostic aspectsof the bladder disorders in diabetics. Eur Urol 7:211-214. 3.Ueda T, Yoshimura N, Yoshida 0 (1997) Diabetic cystopathy: relationship to autonomic neuropathy detected by sympathetic skin response. J Urol 157:580584. 4. Frimoldt-Moller A (1980) Diabetic cystopathy: epidemiology and related disorders. Ann Intern Med 92:318-321. 5. Kaplan SA,Te AE, BlavisJG (1995) Urodynamic findings patients in with diabetic cystopathy. J Urol 152:342-344. 6. AppellRA,Whiteside HV (1991)Diabetesandotherperipheralneuropathies affecting lower urinary tract function. In: Gane RJ, Siroky MB, eds., Clinical Neurourology. Boston: Little, Brown, pp. 365-375. of bladder dysfunction in elderly 7. Starer P, Libow L (1990) Cystometric evaluation diabetic patients. Arch Int Med 150:810-813. 8. Goldman HB, Dmochowski RR (1997) Lower urinarytract dysfunction inpatients with gastroparesis. J Urol 157:1823-1825. 9. GoldsteinI,SirokyMB, mane RJ(1983)Impotence in diabetes mellitus. In: Krane RJ, Siroky MB, GoldsteinI, eds., Male Sexual Dysfinction, Boston: Little, Brown, pp. 77-86 10. Bradley WE, Timm GW, Rockswold GL, Scott FB (1975) Detrusor and urethral electromyelography.J Urol 114:891-894. 11. Bradley WE (1979) Neurologic disorders affecting the urinary bladder. In: Krane RJ, Siroky MB, eds., Clinical Neuro-Urology, Boston: Little, Brown, pp. 245-255. 12. Ellenberg M (1976) Diabetic neuropathy; clinical aspects. Metabolism 25:16271632. 13. Waxman SG (1980) Pathophysiology of nerve conduction; relation to diabetic neuropathy. Ann Intern Med 92:297-300.

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14. Spritz N, Singh H, Marinan B (1975) Decrease in myelin content of rabbit sciatic nerve with aging and diabetes. Diabetes 24:680-684. 15. Clements RS Jr (1979) Diabetic neuropathy: newconcepts of its etiology. Diabetes 28:604-611. 16. Finegold D, Lattirner SA, Nolle S, Bernstein M, Green DA, et al. (1983) Polyol pathway activity and myo-inositol metabolism. A suggested relationship in the pathogenesis of diabetic neuropathy. Diabetes 32:988-992. 17. RyleC,LeowCK,Donaghy M (1997) Nonenzymatic glycation of peripheral and central nervous system proteins in experimental diabetes mellitus. Muscle Nerve 20:577-584. 18. Steers WD, Mackway-Gerardi AM, Ciambotti J, deGroat WC (1994) Alterations in neural pathwaysto the urinary bladderof the rat in response to streptozotocininduced diabetes. J Auton New Syst 47:83-94. 19. Itoh H. Morikawa A, Maliino I (1994) Urinary bladder dysfunction in spontaneously diabetic Chinese hamsters. Diabet Res Clin Pract 22: 163-170. 20. Appell RA, BaumNH (1990) Neurogenic bladder in patients with diabetes mellitus. Practical Diabetology 9: 1-6. 21. Nestler JE, Stratton MA, Hakim CA (1983) Effect of metaclopromide on diabetic neurogenic bladder. Clin Pharmacol 283-85. 22. Mundy AR, Blaivis JG (1984) Nontraumatic neurological disorders. In: Mundy AR, Stephenson TP, and Wein AJ, eds., Urodynamic Principles, Practices and Application. Edinburgh: Churchill Livingstone, pp. 278-287.

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Lumbar Disc Disease Howard B. Goldman, MD and Rodney A. Appell, MD, FACS INTRODUCTION NEUROPATHOPHYSIOLOGY CLINICAL FEATURES EVALUATION TREATMENT CONCLUSION REFERENCES

INTRODUCTION A significant proportion of individuals withlumbar disc disease experience voiding dysfunction, Specifically, 27 (1)to 92% (2) of these patients are noted to have such dysfunction and in most cases detrusor areflexia is found. This chapter reviews the pertinent neuropathophysiology, clinical features, evaluation, and treatment for patients with voiding dysfunction resulting from lumbar disc disease.

NEIJROPATHOPWSIOLOGY A review of the relevant neuroanatomy is necessary before discussing the neuropathology resulting from lumbar disc disease. Innervation of the lower urinary tract is derived from both the autonomic andsomatic nervous systems. The parasympathetic pelvic nerves,

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Table l Innervation of the Lower Urinary Tract ~~

Spinal Cord Segment

Function

EHerent

Autonomic Parasympathetic (Pelvic nerve) S2-S4 Sympathetic (Hypogastric nerve) T11-L2 Somatic (Pudendal nerve)

s3-s4

Excitatory to bladder Inhibitory to bladder Excitatory to urethra Control over external sphincter

Aferent

Tension receptors in bladder wall initiation Micturition S2-S4 Nociceptors sensation Perineal S2-S3 Sensory

which emanate from the second through fourth sacral segments of the spinal cord, provide the principle excitatory input to the bladder. The somatic nerves originate from the third and fourth sacral segments and provide innervation to the external sphincter and other pelvic-floor musculature. Finally, the sympathetic pathways of the hypogastric nerves arise from the lower thoracic and upper lumbar segments and provide inhibitory input to the bladder body as well as excitatory input to the urethra and bladder base. Afferent activity may travel from the bladder to the spinal cord along both sets of autonomic nerves. However, those that convey information from tension receptors and nociceptors in the bladder wall and are the most important for initiating micturition travel via the parasympathetic nerves to the sacral segments of the cord. Sensory nerves from the vagina and clitoris travel in the somatic nerves to the sacral cord as well (see Table l) (3). In the adult, the sacral segments of the spinal cord are at the level of the first and second lumbar vertebral bodies. This distal end of the spinal cord is commonly called the conus medullaris. The spinal-cord segments are named for the vertebral body at which its nerve roots exit the spinal canal. Thus, though the first sacral segment of the spinal cord is located at Ll, its nerve roots run in the subarachnoid space posterior to the L2 to L5 vertebral bodies till reaching the first sacral

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vertebral body, at which point they exit the canal. Thus, all of the sacral nerves that originate at the L1 and L2levels run posterior to the lumbar vertebral bodies until reaching their appropriate site of exit from the spinal canal. This group of nerves running at the distal end of the spinal cord is more commonly referred to as the cauda equina. The mostfrequent sites of lumbar disc prolapse are the L4/5 andL51 S1 intervertebral spaces (4-6). Usually, prolapse is in a posteriolateral direction not affecting the majority of the cauda equina. However, in 1-15% of cases, central-disc prolapse occurs and compression of the cauda eyuina may result (4) (Fig. 1). In fact, in some instances a large posteriolateral disc prolapse may migrate medially and cause cauda equina compression as well (4). Thus, fusing this neuroanatomy with the known neural innervation of the lower urinary tract, one can see how prolapse anywhere along the lumbar spine could interfere with the parasympathetic (S2-S4) and somatic (S3-S4) innervation, whereas only prolapse at the upper lumbarspine, which is relatively rare, would affect the sympathetic (T11-L2) innervation. Along with interfering with parasympathetic and somatic innervation to the bladder and urethra, afferent stimuli from the bladder and perineal sensation, both served via sacral segments, would face interference as well. Thus, lumbar disc prolapse interferes with stimuli from the bladder needed to initiate micturition, excitatory input to the bladder required for detrusor contraction, and somatic innervation to the external sphincter and pelvic-floor musculature. The resultant urologic finding is one of detrusor areflexia frequently with an impaired sensation of filling. This urologic manifestation of compression of the sacral nerves is usually only one aspect of the cauda equina syndrome (compression of the lumbosacral nerves). Classically, saddle anesthesia, bilateral sciatica, lowerback pain-and in men, impotence-is noted (7). Though detrusor areflexia is the most commonfinding in these patients, detrusor hyperreflexia has been reported as well (8). It has been suggested that the mechanisms of injury in this group of patients is progressive disc herniation causing irritation and excitation of the sacral nerve roots. Besides direct compression, a prolapsing disc can affect the sacral nerves by interfering with blood flow to and from the cauda equina (9).Experimental investigations have shown changesin the intraneural venous blood flow with compression of these veins leading to congestion and ischemia of the nerve roots. Delmarter et al. (9) constricted the cauda equina to varying degrees in an animal model andevaluated changes in bladder function. Fifty percent constriction resulted in no

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Fig. 1. (A) MRI with sagital section showing prolapse of L5-S 1 disc into subarachnoid space.

significant cystometric changes, but did cause venous congestion of the nerve roots and ganglia. Seventy-five percent constriction caused detrusor areflexia, increased bladder capacity, and overflow incontinence, as well as arterial narrowing and venous congestion of the nerve roots and ganglia.

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Fig. 1. (B) Same patient, coronal view showing central disc prolapse with compression of sacral nerve roots.

Complete damage to the conus or sacral roots produces paralysis of the detrusor such that it is acontractile and must be emptied using external pressure (straining or Crede) or a catheter. Although detrusor contractility is absent, there may be poor compliance anda steady rise of detrusor pressure during the filling phase, which indicates that the injury to the cauda equina is incomplete. Fortunately, most of these lesions are partial and havea more profoundeffect on the autonomically innervated bladder than on the somatically innervated external sphincter. Therefore, if the conus medullaris is partially damaged evenwithout sacral-root damage, activity in the pelvic floor and external sphincter remains intact despite the loss of detrusor contractility. The efficiency with which the bladder empties in the absence of detrusor contractility depends on sufficient external force and the absence of any outflow

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obstruction. Even if detrusor function returns, it is usually inadequate to result in efficient emptying of the bladder and does not indicate detrusor-striated external sphincter dyssynergia, as itis a form of functional obstruction by the external sphincter because there is no detrusor contractility.

CLINICAL FMTIJRES Recent studies suggest that a minority of patients presenting with lumbar disc protrusion will have voiding dysfunction. Bartolin et al. ( 1 ) prospectively studied 114 patients (37 women, 77 men) who complained of low backpain and were found to have lumbardisc protrusion requiring surgical treatment. Of this group, 31 (27.2%) were found to have detrusor areflexia, whereas detrusor activity was normal in the remaining 83. Specifically, 3 of 8 with L3, 10 of 54 with L4, and 18 of 52 with L5 disc protrusion had detrusor areflexia. All of these 31 patients reported difficulty voiding requiring straining. Clearly, this is a select group as many patients do not require surgery and likely have less severe disc prolapse. Those with less severe prolapse probably have a lower rate of voiding dysfunction as well. In contrast to this report, Rosomoff et al. (2) reported rates of voiding dysfunction as high as 92%; however,his study had far less stringent diagnostic criteria for areflexia than that of Bartolin. As noted earlier, patients will frequently present with a constellation of symptoms representative of the cauda equina syndrome. O’Flynn et al. (4) reported on 30 patients with lumbar disc prolapse and urinary dysfunction. In 23 patients, a long history of lower back pain existed prior to the development of urinary symptoms. However, on occasion voiding dysfunction may be the only or first symptom of disc prolapse. Sylvester et al. (8)reported on twowomen who presented with painless urinary retention, but no other neurological findings were noted. In both cases, anMRI revealed lumbar central disc prolapse and, in retrospect, both patients noted the experience of minor lower backpain prior to presentation. A prolapsed intervertebral disc may produce a cauda equina syndrome with obstructive voiding symptoms ona permanent or intermittent basis. Therefore, the clinical presentation depends on the extent of injury to the autonomic parasympathetic nervous input to the lower urinary tract. Clinically, the patient describes pain in the lower back radiating in a girdle-like fashion along the lumbar dermatomeinvolved;

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physical examination may reveal reflex and sensory changes consistent with nerve-root compression (10). Voiding symptoms, when present, are obstructive in nature (11) and include compromised urinary flow rate, interrupted stream owing to abnormal straining to void, residual urine, and incontinence. The obstructive Symptoms are secondary to the degree of detrusor denervation. The incontinence, however, may be owing to lack of resistance at the level of the external sphincter owing to pelvic-floor denervation or overflow. Denervation is more commonly seen in patients with recurrent or repetitive intervertebral disc problems and spinal stenosis (11). The mostcharacteristic findings on physical examination are sensory loss in the perineum or perianal area (associated with the S2-4 dermatomes), sensory loss on the lateral foot (S 1-2 dematomes), orboth (12). A unilateral or mild sensory disturbance indicates a better prognosis, as prolonged sensory deficits imply that the bladder will not recover because its normal function requires an intact visceral reflex arc of the sacral roots (6,13). Thebulbocavernosus reflex (BCR) should be checked because reflects it pudendal (somatic) nerve function. Although this reflex is absent in all patients with complete lower motor neuron lesions of the sacral cord, care must be taken not to assume this is the case since 19% of healthy female subjects do not have a detectable reflex on physical examination alone (14).In one series, which included patients with injuries to the conus medullaris and cauda equina having various causes, the BCR reflex was absent or significantly diminished in 84% of the patients and perineal sensation and muscle-stretch reflexes were compromised in 77% of patients ( I S ) . These findings correlated well with a diagnosis of pelvic-floor denervation.

EVALUATION When other features of the cauda equina syndrome are present it is easy to suspect lumbar disc prolapse as the cause of voiding dysfunction. It is a more difficult diagnostic dilemma whenother signs, in particular pain, are absent. One’S suspicion should be aroused when faced with a woman who is straining to void or having difficulty emptying her bladder as outlet obstruction is unusual in females. A thorough history and physical examination with a focused neurological evaluation is mandatory. In the male, prostatic obstruction or urethral stricture disease may cause similar findings and should be excluded. Other disease states such as diabetes mellitus (DM), multiple sclerosis (MS), vitamin B12

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deficiency, or infectious neuropathies such as herpes simplex should be noted. Careful questioning concerning lower backpain, gait disturbances, or any other symptoms that were present when the voiding dysfunction began can be helpful. For example, the presence of flu symptoms andgait disturbance in the past may be related to an infectious neuropathy. Sensory examination of the perineal area and lateral foot (both associated with sacral segments) may give clues to a neurologic origin. The BCR and anal sphincter tone as well can suggest a lesion involving sacral segments or nerve roots. Assessment of the patients postvoid residual using either a straight catheter or an ultrasound bladder-scan device can also give information on the efficiency of bladder emptying. Further urodynamic testing is frequently required to document the voiding dysfunction. ~ r o d y n ~ i c a l ldetrusor y, motor dysfunction and weakened external sphincter activity are the primary findings even in urologically asymptomatic patients (11). A cystometrogram(CMG) with simultaneous pelvic-floor electromyography (EMG) is sufficient for urodynamicdiagnosis and the predominant finding is usually detrusor areflexia associated with sphincter neuropathy (5,10,11,15). However, simultaneous pressure flow studies are frequently needed if there is a question of outlet obstruction. As discussed previously, in cases in which the somatic innervation remains intact, the external sphincter may appear to be incapable of relaxing when the patient strains to void and actually constitutes an obstructive factor that may require pharmacologic manipulation orintermittent catheterization. Thus, confirmation that intravesical pressure elevation on the CMG is owing to abdominal straining and not a true detrusor contraction (indicating normal function or obstruction) can be obtained by using subtracted pressure measurements or by synchronous perineal floor and rectus abdominis EMG(16). Sacral-evoked potentials, specifically the bulbocavernosus reflex latency time, can be used to study the integrity of the sacral reflex arc further; in this set of patients the response is usually absent or prolonged(17). Table 2 summarizes the neurourologic features of patients with cauda equina syndrome (12). When lumbar disc disease is suspected, magnetic resonance imaging (MRI) of the lumbar spine should be performed. MRI defines the anatomical detail much more precisely than myelography (which was formerly the diagnostic test of choice). If MRI reveals lumbar disc prolapse, neurosurgical or orthopaedic consultation should be obtained.

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Table 2 Major Neurourologic Features of Lumbar Disc Disorders

SymptomsObstructivevoidingsymptomatology or perianal sensory loss Signs Perineal Absent or diminished bulbocavernosus reflex Tests CMG: detrusor areflexia EMG: neuropathic changes CMG, cystometrogram; EMG, electromyography.

Treatment consists of correcting the underlying cause of the problem, usually requiring laminectomy.However,insome instances laminectomy may not improve the voiding symptoms. Shapiro (7) reviewed the cases of 14 patients who presented with cauda equina syndrome secondary to lumbar disc herniation, of whom 13 had incontinence. When evaluating variables to predict resolution of incontinence, he noted that the time between onset of Symptoms and laminectomy was important. Seven of 7 patients operated on within 48 h regained continence, whereas only 2 of 6 operated on at lengths greater than 48 h from presentation regained continence. Other studies though, such as that by O’Flynn etal. (4)report a much poorer rate of detrusor recovery. They noted only 1 of 26 patients with prelaminectomy incontinence regained completely normal bladder function. This disparity between the reports of Shapiro (7) and O’Flynn et al. (4) may be owing to the use of different outcome measures-Shapiro used “continence” whereas O’Flynn used “completely normal bladder function.’’ Thus, though it is likely that many patients become continent and can void byabdominal straining, few may actually regain “normal” bladder function. The sequelae of laminectomy suchas spinal stenosis or arachnoiditis can affect bladder function as well. O’Flynn et al. (4)reported that four patients who had no urinary symptoms prior to surgery had voiding dysfunction postoperatively. The challenge for the clinician is to attain symptomatic relief for the patient by allowing adequate bladder emptying without incontinence while preserving upper urinary-tract function. Patients with lower motor neuron lesions do not develop reflex vesical activity, and storage function may or may not be normal. If bladder compliance is adequate, a trial of cholinergic stimulation with bethanechol chloride alone (50 mg

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up to four times daily) or in combination with metoclopramide (5-10 mg up to four times daily) may be given, but should not be continued if no significant response is attained by the time medication has been prescribed for a month (18). In most cases cholinergic therapy is unsatisfactory and clean intermittent catheterization (CIC) is required. Hypertonicity or decreased compliance with a concomitant fixedoutlet resistance can impair ureteral function and place the upper urinary tracts at risk. In these patients, a regimen of anticholinergic medications usually combined with self-catheterization should be utilized. When this is unsuccessful, bladder augmentation may be necessary to lower detrusor pressure and protect the upper urinary tracts. Again, emptying is handled by self-catheterization. When incontinence results from poor sphincter function, the options are similar to those of any patient with intrinsic sphincter dysfunction-an artificial urethral sphincter, collagen injections, or-in women-a pubovaginal sling. A sling is preferred whenever the patient may require self-catheterization postoperatively, as repeated catheterization may displace the collagen that is injected and render the patient incontinent again.

CONCLUSION Voiding dysfunction may present in conjunction with other neurologic symptoms or as an isolated event in patients with a prolapsed intervertebral disc. Damage to the parasympathetic, somatic, and sensory nervous innervation of the lower urinary tract is the usual mechanism of injury. In most cases detrusor areflexia results. A careful history andexaminationin conjunction with urodynamic testing andMRI imaging will establish the diagnosis. Although surgical intervention (laminectomy) may not always give complete bladder recovery, it can frequently allow for improvement. Variousbladder management techniques (of which CIC is the mainstay) will help achieve good bladder emptying and preservation of the upper urinary tracts.

REFERENCES 1. Bartolin Z, Gilja I, Bedalov G, Savic I (1998) Bladder function in patients with lumbar intervertebral disc protrusion. J Urol 159:969-971. the evaluation of 2. Rosomoff HL, Johnston JD,Gallo AE, et al. (1963) Cystometry in nerve compression in lumbar spine disorders. Surg Gynecol Obstet 117:263-270.

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3. deGroat WC (1 996) Neuroanatomy and neurophysiology: Innervation of the lower urinary tract. In:Raz S, ed. Female Urology, Philadelphia: WB Saunders,pp. 28-30. 4. O’Flynn KJ, Murphy R, Thomas DG (1992) Neurogenic bladder dysfunction in lumbar intervertebral disc prolapse. Br J Urol 69:38-40. 5. Andersen JT, Bradley WE (1976) Neurogenic bladder dysfunction in protruded lumbar disc and after laminectomy. Urology 8:94-96. lesions from disc prolapse. 6. Scott PJ (1965) Bladder paralysis in cauda equina JBone Joint Surg 47:224-227. 7. Shapiro S (1993) Cauda equina syndrome secondary to lumbar disc herniation. Neurosurgery 32:743-747. 8. Sylvester PA, McLoughlin J, Sibley GN, Dorman PJ, Kabala J, Ormerod IEC (1995) Neuropathic urinary retention in the absenceof neurological signs.Postgrad Med J 7 1:747-748 9. Delamarter RB, Bohlrnan HH, Bodner D, Biro C (1990) Urologic function after experimental cauda equina compression-cystornetrograrns versus corticalevoked potentials. Spine 15:864-870. 10. Bradley WE (1978) Neurologicdisorders affecting the urinary bladder. In:mane RJ,SirokyMB, eds., Clinical Neuro-Urology, 1st ed. Boston:Little,Brown, pp. 245-255. ( l 98 l) Assessment of vesico-urethral dysfunctionin lumbar 11. Appell RA, Levine RL spine disorders. In: Proceedings of the Eleventh Annual Meeting of the InternationaE Continence Society. Edited by T. Sundin, A Mattiasson, Sweden: Skogs Trelleborg, 186-7. 12. AppellRA(1993)Voidingdysfunctionandlumbardisc disorders. Problems Urol 7( 1):35-40. 13. Susset JG, Peters ND, Cohen SI, Ghoneim GM (1982) Early detection of neurogenic bladder dysfunction caused by protruded lumbar disc. UroEogy 20:461--463 14. Blaivas JG, Zayed AAH, LabibKB (1981) The bulbocavernosus reflex in urology: a prospective study of 299 patients. J Urol 126197-199. 15. Pavlakis AJ, Siroky MB, Goldstein I, Krane RJ (1983) Neurourologic findings in conus medullaris and cauda equina injury. Arch Neurol 40:570-573. a non-invasive 16. Koff SA,KassEJ(1982)Abdominalwallelectromyography: technique to improve pediatric urodynamic accuracy. J Urol 127:736-739 17. Krane RJ, SirokyMB (1 980) Studies in sacral evoked potentials. J Urol 124:872876. 18. Appell RA (1992)Clinical pharmacology in neurourology. Problems Urol 6622642.

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Treatment of Stress Urinary Incontinence

CONTENTS INTRODUCTION BEHAVIORAL INTERVENTIONS PHARMACOLOGICAL MANAGEMENT SURGICAL MANAGEMENT SUMMARY REFERENCES

INTRODUCTION Stress urinary incontinence (SUI) is defined as urinary leakage secondary to an increase in abdominal pressure (Valsalva maneuvers, which place “stress” on the bladder and bladder support mechanisms) and is classified for treatment purposes by urologist into anatomic hypermobility of the bladder neck and proximalurethra, intrinsic sphincteric deficiency, or a combination of both. Anatomic hypemobility-related SUI (accounting for 85% of SUI) develops most commonly with aging, hormonal changes, traumatic or prolonged vaginal delivery, and pelvic surgery. Some patients with a well-supported bladder neck andurethra will still have SUI dueto intrinsic sphinteric deficiency (15% of SUI). In these cases, intrinsic sphinteric deficiency may be owing to damage of the urethral closure mechanism after prior pelvic or anti-incontinence procedures, pelvic radiation, trauma, or neurogenic and medicaldisorders resulting in denervation injury. A combinationof anatomic hypermobility and intrinsic sphinteric deficiency often exist together, and

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Table 1 Outcomes of Treatment for Urinary Incontinence(') Treatment Surgical Pharmocolagic Behavioral

Improved (%) Cured (%)

54-95 12-16

77 44

78-92

contemporary theories suggest thatall cases of SUI have a component of intrinsic sphinteric deficiency,whether dynamically induced by the anatomic movement of a hypermobile bladder and urethra or inherently acquired by intrinsic dysfunction of the urethral closure mechanism, regardless of its anatomic position. The consolidationof the anatomic hypermobility and intrinsic sphincteric deficiency as etiologies of SUI provides a fundamental basis for expanding individual patient treatment options that incorporate various aspects of each management and treatment approach available for this condition. After the diagnosis and classification of SUI are established, the three major categories of intervention are broadly divided for discussion purposes into behavioral, pharmacologic, and surgical options. Successful intervention depends upon the understanding of treatment goals defined during the relationship established between the patient and physician. Ideally,the therapy should eliminate or improve symptoms, restore dysfunctional anatomy,and result inan improved qualityof life for the patient. In choosing from availablemanagement and treatment options, informed patients are those who have received informationon the expected outcomes, risk and benefits of each of these options for their particular problems(see Table 1). Management and treatment for all forms of urinary incontinence are traditionally staged with the least invasive forms of behavioral interventions offeredfirst, then the introduction of pharmacologic agents when indicated and tolerated, and finally, after optimization of the pelvic floor and bladder physiology, the use of reconstructive surgery that strives to restore a normal bladder state of continence and voiding function. The long-term efficacy and cost analyses of individual treatment options clearly favor the options of all forms of intervention over the benign neglect of this condition (2). The use of surgical interventions are clearly the most cost-effective approach in the long-term, yet the increased risk associatedwith these treatmentsand the limitednumber of specialist trained to perform these procedures have traditionally

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made nonsurgical options a priority. The concern of increased risk associated with these procedures are lessened with contemporaryreports defining better ways to perform traditional procedures using minimally invasive approaches (3-5), improvementsin anesthesia and overall reduction in their use (6,7'),and proper patient selection for procedures that continue to expand in number and indications (8). The reduction in risk associated with invasive procedures has shifted the focus of this risk management onto pharmaceutical interventions, which by necessity are used long-term and associated with significant side-effects ( l ) , especially in the setting of increased polypharmacy use in the elderly (9). The goal of treatment intervention offered by the physician to the patient with SUI seeking an improved quality of life is the integration of the three main treatment options defined in this review. When instituted properly and analyzed as a composite, all forms of outcome measures will reveal a rewarding endeavor established between the patient and physician.

BEHAVIORAL I N T E R ~ N T I O ~ S

Behavioral therapy may be easily initiated because it includes a range of behavioral modifications that are dependent on the type of voiding dysfunction diagnosed. For patients with incontinence, the understanding of normal voiding physiology, the awareness of the quantity of fluid intake, timing of fluid intake, and avoidanceof bladder stimulants can result in modest improvementof their urinary symptoms. Simple adjustment in the timing of medications such as the avoidance of diuretics before recumbency and emptyingthe bladder before reaching maximum functional capacity (timed 'voiding) are often overlooked changes a patient with SUI may be able to institute. Patients with congestive heart failure andlor fluid retention in the lower extremity will benefit from promoting a diuretic phase before periods of recumbency by elevation of the lower extremities when sitting, by initiating light walking programs for muscle pumping of congested veins in the leg, by using pressure gradient stockings, and by the judicious use of diuretics and an avoidance of high-salt diets. Changing access to the toilet (support bars and lighting), toilet substitutes (bedside commode), adjustment of garments for easier undressing, and providing mobility aids will prevent many episodes of mixed stress and urge incontinence

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in patients with congenitive dysfunction, mobility problems, and physical handicaps. Teaching methods to inhibit the urge sensation to void in order to gradually expand the voiding interval is a form of behavioral therapy often referred to as bladder retraining. Bladder retraining has its greatest benefit in patients with urge or mixed urge and stress incontinence. The excellent outcome results achieved with these methods should not be mistaken for the poor results associated with the treatment of pure stress incontinence or the stress component of mixed incontinence. These methods for treating urge incontinence rely on the sympatheticmediated negative feedback inhibition augmented by the somatic-mediated contraction of the external urinary sphincter on bladder contractions. By voluntary contraction of the external urinary sphincter, most patients are able to extinguish low-level bladder contractions (urgency). Retraining or improving a patient’s ability to increase her external urinary sphincter tone with a voluntary effort may aid in the treatment of urge and urge incontinence, lead to less urinary frequency, and improve functional bladder capacity. If the patient can predict the timing of a stress maneuver such as a cough, sneeze, or physical activity that will lead to incontinence, then bladder-retraining methods may help to augment the external urethral sphincteric resistance to leakage when employed prior to the occurrence of the stress maneuver. Other methods to inhibit the urge sensation include distraction techniques, and biofeedback using deep breathing and relaxation exercises. All these techniques of bladder retraining appear to work best in patients who have forms of urge or mixedincontinence but not stress incontinence. Furthermore these patients must be cognitively intact, properly motivated, and have the capacity to understand and follow instructions. This select group of patients has the highest rate of improvement scores owing to the treatment of urge incontinence and are some of the few patients who actually have a documented cure of their incontinence by behavioral intervention.

Biofeed&uck While biofeedbackmay aid in teaching patients behavioral interventions as previously mentioned for the treatment of urge incontinence, the merits of this therapy for treating stress incontinence are due to pelvic-floor muscle rehabilitation, training, and control. The goal of this form of behavioral therapy is to teach the patient to increase

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intraurethral pressure by contracting the periurethral muscles prior to activities that cause stress incontinence. Distinct from the concept of negative feedback inhibition on the bladder by external urethral sphincter contraction for treating urge incontinence, exercising the pelvicfloor muscles (the levator ani muscles) may result in decreasing urethral hypemobility and increasing urethral resistance for the prevention of SUI. Kegel exercises were originally proposed in 1941for strengthening the pelvic-floor musculature (lo),but since that time, these exercise have been improperly taught and improperly used by patients (11). Although many patients can be instructed on the identification of the proper muscle group for pelvic-floor muscle exercises in the office, the best results are achieved by repetitive training, use of biofeedback, and consultation or initiation of therapy by a physical therapist or a nurse with specialized training (12). Manometry and electromyography can be used to measure external and sphincter activity or vaginal muscle activity when teaching pelvic muscle contraction and relaxation. The most common error in pelvic muscle training involves the contraction of other muscle groups (abdominal, back, gluteal, or thigh muscles). Once the pelvic muscles are located and control obtained, the next goal of therapy isto increase the patient’s strength. Pelvic muscle rehabilitation alone can increase resting muscle tone, but active maximal contraction of the periurethral muscles through control and strengthening is needed to prevent incontinence through the urethra due totransient rises in abdominal pressures. Other forms of therapy for pelvic-floor muscle rehabilitation include intravaginal weighted cones for exercise, the use of electrical stimulation, and the introduction of electromagnetic energy. Vaginal cones introduced in 1985 for strengthening pelvic-floor muscles provide an inexpensive, effective, nonlabor intensive or time-consuming treatment for mild stress incontinence (13). Electrical stimulation involves the application of electrical current to the pelvic-floor muscle via rectal or vaginal electrodes. Although the side effects are minimal, the results appear to last only as long as the device is used, and may not show any added advantage over properly performed exercises except in those patients with a denervated pelvic-floor musculature (14,15).In addition to rehabilitation of the levator ani muscles, the rehabilitation of the obturator internus muscle may be of importance, as this muscle with its attendant fascia shares a common fascial insertion with the levator ani muscles called the arcus tendinous fascia. Whereas pelvic floor rehabilitation may appear to be useful for all patients, the etiology of

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SUI may result from a traumatic peripheral neuropathy ‘with resultant muscle atrophy and dysfunction typical of intrinsic sphincteric deficiency, rather than fascial breaks or lengthening associated with anatomic hypermobility. Therefore, standard rehabilitation techniques require at least partial innervation to the muscle groups of interest unless the nerves are bypassed by anelectrical stimulator or electromagnetic energy. Currently, there is no reproducible neurologic test that can determine which patients are likely to benefit from pelvic floor rehabilitation. The low risk of this noninvasive therapy, not the cost (office visits, labor intensity), has made pelvic-floor rehabilitation an acceptable first-line therapy for patients with mild SUI owing to anatomic hyperrnobility, not intrinsic sphinteric deficiency.

Containment Devicesand Support Prosthesis Conservative treatments such as urethral meatal occlusive devices, urethral inserts, plugs, and catheters, as well as vaginal pessaries (1618), tampons, and contraceptive devices (19)for bladder neck support provide successful management options for selected patients with stress incontinence. The success is dependent on multiple factors including patient selection, patient motivation, and training of the patient and instructor. Extensive patient education by a health care professional requires significant time and expensiveallocations that are resulting in the continued trend to develop nonsurgical alternatives that require minimal patient education with maximal acceptance. While use of these devices are not curative of the patient’ S underlying voiding dysfunction, they do provide management options for their symptoms that may serve as an adjuvant to other interventions listed below or may be the only choice of treatment available to the patient for a variety of medical and social reasons.

Estrogens The ability of sex hormones to induce physiological changes of the lower urinary tract during the menstrual cycle, pregnancy, and menopause is the rational for using these agents pharmacologically to

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maintain and augment urinary continence. In particular, estrogens are known to have a direct effect on lower urinary-tract organs and to modulate the autonomic nervous system activity of the bladder and urethra (20,21). Since the majority of women with stress incontinence are perimenopausal or postmenopausal, restoring the tissue integrity of the urethral, bladder neck, and vaginal epithelium with the use of estrogen therapy serves as a fundamental adjuvant to the other management options available for urinary incontinence. Clinical studies have revealed its subjective usefulness especially in conjunction with behavioral interventions and pharmacologic agents (22). By promoting upregulation of neurotransmitter receptor function, estrogen therapy may augment the effect of anticholinergics and alpha-adrenergic agonist (23). Therefore, it is recommended as baseline therapy for all forms of urinary incontinence and is usually initiated as a first-line intervention following the detection of estrogen deficiency on the pelvic examination performed on the initial physician visit. For patients with long-standing estrogen deficiency, symptoms of stress incontinence may not change with replacement therapy, but the restoration of tissue integrity through the increase in blood supply will aid in tissue manipulation associated with surgical interventions, urethral occlusive devices, or vaginal pessary use. Estrogens are used either systemically or topically. Side effects may include an increased risk for gynecological malignancies, fluid retention, depression, nausea, vomiting, elevated blood pressure, gallstones, and cardiovascular effects such as stroke and myocardialinfarction. However, in addition to the aforementioned benefits of improved voiding function, hormone replacementtherapy confers an overall benefit in mortality as compared to nontreated patients (24).Topical vaginal application through direct placement or vaginal implants are preferable because of the decreased systemic absorption and preferential local uptake (25). When mildatrophic changes of the vaginal epithelium are noted on pelvic examination despite systemic estrogen replacement, additional topical vaginal therapy may be useful in order to improve voiding function without incurring side effects from increasing the systemic administration. Yearly PAP smears and breast examinations should be performed when placing or following patients on estrogen therapy. In general, the use of estrogens is restricted in patients with. a history of deep venous thrombosis, embolization, and gynecologic malignancies.

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Adpba-Adrenergic Agents Because sympathetic-nerve stimulation of the alpha-adrenergic receptors located in the intrinsic sphincter or bladder neck region produces smooth muscle contractions, cases of mild stress incontinence have respondedto the use of oral alpha-adrenergic agents (26). In the case of stress incontinence, the most commonly used agents are ephedrine, pseudoephedine, and phenylpropanolamine; all are the active components of commonly used over-the-counter decongestants. The usual adult dosage of phenylpropanolamineis 25-100 mg in sustained-release form, given orally twice a day; that of pseudoephedrineis l 5-30 mg three times a day. Side effects are numerous andare associated with the drug’s lack of bladder neck selectivity. Typical manifestations of the nonspecific action of this medication include an increase in blood pressure, stomach cramping, and central nervous system (CNS) symptoms of excitation and drowsiness. These drugs must be usedwith caution in patients with hypertension, arrhythmias, angina, respiratory difficulties, hyperthyroidism, and diabetes. Imipramine, a tricyclic antidepressant, has adual action on the lower urinary tract by its effect on bladder contractions through its anticholinergic effects while increasing bladder neck resistance through its alpha-adrenergic agonist properties. Although only approved by the FDA for enuresis in children, the usual adult dosage is 10-25 mg once to three times daily. Side effects may include postural hypotension and cardiac conduction disturbances in the elderly. Reported outcomes measures for using a pharmacologic agent such as an alpha-adrenergic medication are clinically significant, both from an efficacy as well as a side-effect profile.

SURGICAL MANAGEMENT Introduction As stated earlier, SUI may be owing to anatomic hypermobility or intrinsic sphincteric deficiency of the urethral closure mechanism. Although no standardized methodology exist to clearly define these two forms of stress incontinence, most experts would agree that the available methods of urethral evaluation can determinethe contribution of these two factors in an individual patient. Thus, the classification of stress incontinence exists between the spectrum of anatomic displacement, which induces a transient incompetence of the urethral closure mechanism to a well-supported urethral that has intrinsic incompetence

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of its closure mechanism. Therefore, by definition, any women with evidence of SUI must have some component of intrinsic sphincteric deficiency, whether induced transiently by the dynamic hypermobility movement of the urethra during a stress maneuver or caused by a rise in intra-abdominal pressure that when transmitted through the stable bladder is greater than the closure pressure of the incompetent but supported urethra. Clinical experience with objective urodynamic evaluations (27’) support this classification of stress incontinence. The efficacy of any treatment option is based on how well the recommendation will address these two components of stress incontinence and is why surgical procedures produce the highest long-term efficacy rates of all available treatments. The surgical treatments outlined below have evolved in design over the years to better address the following: 1. Restoration of the urethra to its proper resting position and to stabilize this position during increases in intra-abdominal pressure; 2. Augmentation of intraurethralpressures for restoration of intrinsic urethral closure; or 3. A combination of both restoration of support and augmentation of urethral closure.

Implants Periurethral and transurethral injection of bulking agents at the level of the proximal urethra have been used extensively for years to increase the outflow resistance of the urethra for the treatment of SUI due to intrinsic sphincteric deficiency. Injectables are able to increase urethral closure function without significantly resulting in increases of urethral closure pressure, which would lead to a rise in voiding pressure. The effect is tocorrect the incompetent urethral closure mechanism without clinically disturbing voiding function. Although few are currently in use, many choices for injectable substances have been tried; they include sclerosing solutions (28), polytetrafluroethylene (PTFE) paste (29),glutaraldehyde cross-linked bovine collagen (GAX-collagen) (30), autologous fat (31), silicone particles (32), and many more. Currently, the only injectable materials acceptable for use in the United States are autologous material such as fat, and xenogenic collagen, Contingen TM (C.R. Bard Inc., Covington, CA). Autologous fat provides the advantages of easy accessibility, availability, affordability, and biocompatibility; however, the efficacy is abysmal owing to poor graft neovascularity and long-term viability (1O--ZO%)

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(33).The currently used GAX-collagenpreviously mentioned is a suspension of 35% highly purified bovine collagen in a phosphate buffer. The cross-linking and hydrolysis of the bovine collagen that is 95% type I and 1-5% type I1 collagen reduces its antigenicity and increases its resistance to collagenase degradation. Allergic reactions are still possible and skin testing is mandatory and may be positive in 4% of females (30). Adverse events occurring with this injectable are rare and self-limiting; they include transient retention (6%), urinary tract infection (6%),de novo urgency (12%), and hematuria (3%) as reported in the North American Contigen Study Group (34). Initial studies such as the North American Contigen Study Group suggested that the best candidates for successful Contigen injectable therapy were patients with good anatomicurethral support and intrinsic sphincteric deficiency. Additional studies whichhavefollowed the initial experiences with Contigen demonstrate equal efficacy in the treatment of patients with anatomic hypermobility and/or intrinsic sphincteric deficiency (35-37). These reports have demonstratedoverall success rates of 80% (40% cures, 40% improved) with the probability of remaining dry without additional collagen at 72% at 1 yr, 57% at 2 yr, and 45% at 3 yr. If deterioration in continence status occurs after achieving a successful outcome, repeat collagen injections will restore a successful condition. Based onthe aforementioned reports, all patients with SUI are potential candidates for Contigen injectable therapy as long as they do not have a known hypersensitivity to bovine collagen, an untreated urinary tract infection, or unmanaged detrusor instability, which may obviate the patient’s subjective awareness of achieving a successful treatment of stress incontinence. Techniquesand results of transurethral and periurethral injection have been reviewed in depth in several reports (38).For patients with intrinsic sphincteric deficiency, a larger amount of injectable material appears to be needed. For patients with transient induction of intrinsic sphincteric deficiency owing to anatomic hypermobility in which the posterior urethra moves away from the anterior urethra during rotational descent of the proximal urethra, technical consideration of placing the bulking agent between the 5:OO and 7:OO o’clock position is warranted in order to preserve a coapted urethral closure mechanism despite anatomic movement or location. While injectable therapy for stress incontinence has a learning curve and requires cystoscopic equipment, all patients may receive this therapy in the office or outpatient surgical setting under a local block and no postprocedure restrictions. The reliable, cost-effective and well-

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controlled method of administering this therapy places this surgical option at the forefront of all treatment algorithms for treating stress urinary incontinence in the absence of pelvic organ prolapse. While the safety and efficacy profile of Contigen injectable therapy is excellent, the ideal material is still being sought and should combine the ease of administration with minimal tissue reaction, no material migration, and persistence over time. Combined with estrogen replacement therapy and behavioral modification, injectable therapy will continue to find a high acceptance among patients and physicians.

Bhdder Neck Suspension Procedures RETROPUBIC APPROACHES BLADDER NECK SUSPENSIONS

FOR

In unoperated patients with stress incontinence predominantly owing to anatomic incontinence defined as hypermobility of the bladder neck and urethra with high abdominalleak-point or urethral pressure profiles, bladder neck suspensions procedures give adequate results in this highly selective group. The etiology and important implication that all stress incontinence is owing to various degrees of intrinsic sphincteric deficiency has only recently been considered since the original urodynamic description of this forrn of urethral dysfunction was introduced by McGuire in 1981 (39). At the time bladder neck suspensions were introduced in 1949 for correction. of stress incontinence, hypersuspensions, and overcorrection of anatomic changes of the bladder neck support were the prevailing theories. The first publication of an attempt to suspend the bladder neck describes an anterior urethropexy technique, Marshall-Marchetti-Krantz procedure, which has mostly fallen out of favor owing to the complications from sutures placed close or into the anterior urethra with subsequent high retropubic fixation to the symphysis pubis (40).Interestingly, the authors of this landmark paper suggested that stress incontinence was not entirely owing to lack of anatomic support since correction of the hypermobility failed to successfully treat stress incontinence in some patients. Modifications of retropubic bladder neck suspension procedures, which include stable suture fixation into Cooper’s ligament and lateral placement of the suspending sutures into the periurethral tissue at the level of the bladder neck, have popularized the use of the Burch bladder neck suspension (Fig. 1). With satisfactory long-term outcomes, the open abdominal Bur& procedure is considered one of the gold standards in the surgical treatment

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Fig. 1. Burch bladder neck suspension.

of anatomic stress incontinence when an abdominal approach is indicated. In twocontemporaryreviews of surgical procedures for the treatment of stress incontinence, retropubic bladder neck suspensions achieve an 83435% long-term objective success rate when used as a first-time procedure (41,42). The disadvantages of openabdominal approaches are well documented and the historical trend towards less invasive procedures popularized the development of transvaginal needle suspensions from 1959 to the 3990s.

TRANSVAGINAL APPROACHES LADDER NECKSUSPENSIONS Pereyra introduced the first description of a transvaginal approach to bladder neck suspensions that was later modified into its contemporary form by Raz and is now referred to as the Pereyra-Raz procedure (Fig. 2) (43). Despite the realization of poor long-term success of this procedure in recent reviews (43,44), several fundamental principles popularized through the use of this technique for surgical correction of stress incontinence warrant recognition. This transvaginal approach uses intraoperative endoscopy to insure procedural safety. Owing to the breakdown of the native supporting endopelvic fascia for entering the retropubic space, permanent suture to repair the iatrogenic paravaginal defect and to provide suspension of the bladder neck and urethra is required for long-term success (45). By 1973, Stamey introduced the concept of preserving the native endopelvic fascia support by using a ligature carrier, which is negotiated through the retropubic space under endoscopiccontrol (46).To prevent pull-through failures, pledget

.

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a

Fig. 2. Pereyra-Raz bladder neck suspension.

support was added to the sutures at the level of the endopelvic fascia and surgeons were advised to stabilize, not suspend, the urethra and bladder neck competency. When analyzed collectively, the long-term outcome success of 67% for these transvaginal procedures appears to be only slightly better than the 61% success rate for the use of the obsolete anterior colporrhaphy procedure (42). The real merits of transvaginal approaches for bladder neck suspensions is based on incorporating the knowledge gained from the clinical experience of performing these procedures into other retropubic and transvaginal approaches for the surgical correction of stress incontinence as demonstrated in the percutaneous bladder suspension procedure (Fig. 3) (2,4,46-50). These merits include the following: S. Retropubic dissection, which allowsfor scarification that supplements

the native support of the endopelvic fascia; 2. Use of permanent suture materialfor repair of an iatrogenic paravagi-

nal defect; 3. Stable suture fixation which allows

for unstressed scarification and potentially prevents suture pull-throughfailures from the vaginal wall and endopelvic fascia; and 4. Adjusting the tension of the supporting suturesto ensure stabilization, not suspension or overcorrection of the bladder neck and urethra.

LAPAROSCOPIC APPROACHES FOR BLADDER NECK SUSPENSIONS Interest in developing laparoscopic approaches to treat SUI has increased due toreduced patient morbidity and improved convalescence

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Symphysis pubis Arcus lev

~ r e t h r o p e ~complex vi~

Fig. 3. Percutaneous bladder neck suspension.

over traditional open, retropubic bladder neck suspensions (Fig. 3). While the early results of laparoscopic bladder neck suspensions are promising (51),the approach of this minimally invasive procedure has unfortunately led to changes in the method of a performing the Burch procedure to the point where few direct outcome comparisons can be made between the open vs laparoscopic approach (52). Changing the surgical access should not change the surgical method of performing a retropubic suspension; however, the fundamental techniques responsible for the success of the traditional open procedures have been abandoned in the rush to improve the operative time of this minimally invasive surgery using suture fixation and synthetic mesh devices (53,5#).

Sling Procedures Unlike bladder neck suspensions, sling procedures are specifically designed to address both anatomic hypermobility and intrinsic sphincteric deficiency components of SUI. Sling procedures have generally been reserved for the treatment of complex or previously failed cases of SUI, which has obviated their direct comparison to bladder neck suspensions in patients undergoing primarytreatment. Despite the historical use of sling procedures in complex cases of intrinsic sphinteric deficiency, the long-term success rate of 83% combined withthe report of general medical andsurgical complication rates equal to transvaginal or retropubic bladder neck suspension techniques suggest that the sling procedure should be considered as the primary surgical treatment of choice over bladder neck suspensions for stress incontinence (42). As

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Fig. 4. Modified pubovaginal sling.

outlined previously, incorporation of minimally invasive techniques of bladder neck suspensions has led to Contemporary modifications of sling procedures, which are now considered technically easier to perform than bladder neck suspensions. Although conceptually introduced in the early 1900s in various complex surgical forms, the contemporary reemergenceof sling procedures is credited to the introduction of the rectus fascia pubovaginal sling by McGuire and Lyton in 19'78 (55).Modifications of the original procedure include shorter sling length, less traumatic disruption of the native endopelvic fascia support, and securing the sutures to a nonmobile point of fixation (Fig. 4). In addition to autologous fascia, which has the advantages of durability and lower removal rate secondary to infection and erosion (42), allograft (56) and synthetic (57) materials are often considered as a substitute sling choice based onease of acquisition and surgeons preference for perf'oming quicker operative procedures. While a variety of other autologous tissues have been introduced, the use of the vaginal wall as a sling material by Raz (58)has undergone minor changesthat have resulted in its acceptance as a viable alternative for use in patients with acceptable tissue quality and vaginal capacity, especially those with concomitant poordetrusor function (59). The in situ vaginal wall sling (Fig. 5) with preservation of the urethropelvic complex (endopelvic fascia and vaginal wall attachments to the arcus tendineous) (60) provides durable results in patients with an abdominal leak point

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Fig. 5. In situ vaginal wall sling.

pressure greater than 50 cm of water (61). While many proponents of bladder neck suspensions such as the Burch procedure contend that these procedures do to some degree support the urethra on a sling of vaginal wall tissue owing to the location of the suppoting sutures, it is interesting to note in our recent report that patients undergoing an in situ vaginal wall sling with a Valsalva leak-point pressure less than 50 cm of water pressure (equivalent to a urethral closure pressure of 20 cm or less) have a failure rate similar to that of a Burch procedure (62). The similarity for risk of failure for these two nearly identical procedures that differ mainly in surgical approach, suggest that the elastic properties of the vaginal wall makes this sling material a poor choice in patients with overtly poor urethral incompetence who will need moresuburethral support than can beafforded by the vaginal wall tissue. Thus, in patients undergoing urodynamic evaluation for poor detrusor function with concomitant stress incontinence, the degree of intrinsic incompetence mustbe ascertained when a choice of using the vaginal wall as a sling material is being considered. Sling procedures have traditionally been performed from an abdominal-perineal approachandmore recently by laparoscopic methods (63,64).Two procedures incorporating a transvaginal approach are now under consideration. With the use of transvaginal bone anchors into the undersurface of the inferior pubic rami or areas of the pubic symphysis, fixation of the supporting sling sutures can beplaced from a transvaginal approach (65). Ulmsten has introduced a technique of synthetic sling

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placement via a transvaginal, retrograde, retropubic passage of the supporting sling to the level of the rectus fascia (5). Owing to the coefficient of friction between the sling material and all the intervening tissue, no effort is made to tie down the sling material to the rectus fascia in an attempt to reduce urethral obstruction from hypersuspension of the sling. Traditional sling procedures have a long history of producing successful long-term outcomes for patient with stress incontinence due to intrinsic sphincteric deficiency. With recent reports revealing that the general medical andsurgical complications (42),as well as the technical skills of these procedures are equal to those of bladder neck suspensions, the indications for slings have been extended to treat stress incontinence owing to anatomic hypermobility (66).Urodynamic evaluation of urethral competency, not detrusor dysfunction, may be obviated by choosing to use fascial and synthetic slings since these procedures can safely and successfully treat the entire spectrum of intrinsic sphincteric deficiency. Patients with stress incontinence and a urethral competence characterized or clinically judged as greater than 50 cm of water will do well with a vaginal wall sling procedure (61). Furthermore, based on comparative clinical outcome studies (59), the vaginal wall sling results in less mechanical obstruction of the urethra and should be considered as the sling of choice in patients with documented poor detrusor function and concomitant stress incontinence. There are currently no absolute indications for allograft or synthetic materials for sling formation. As such, concern over early failure rates of allograft fascia (67) and higher removal rates of synthetic materials (57) have tempered the enthusiasm for their use on a routine basis. With the introduction of techniques and technology that provide placement of slings entirely from a transvaginal approach that obviates counter incisions for harvesting autologous sling material, the need for obtaining material other than the vaginal wall will continue to drive the search for improvements in allograft, heterologous, and synthetic material. As improvements in behavioral, medical, and other surgical interventions for treating stress incontinence continue, surgical operations for stress incontinence will be reserved for patients with the concomitant need of additional abdominal or transvaginal surgery (tubal ligation, cholecystectomy, pelvic organ prolapse, and so on). Thus, the approach required for the additional concomitant surgery and knowledge of the degree of urethral competency will greatly influence the decision of the surgical technique chosen to treat the stress incontinence.

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Artificial Urinary Sphincter If the goal of surgical treatment is to establish a normal voiding pattern that allows the patient to remain dry between voiding, then the artificial urinary sphincter is oneof the best treatment options capable of achieving this result. The artificial urinary sphincter is intended to permit intermittent urethral compression for maintaining continence with voluntaryreduction of urethralresistanceduringvoiding,as opposed to other surgical procedures inwhich the compressive nature of static urethral resistance (i.e., injectable material, sling, suspension of periurethral tissue) to incontinence also results in voiding against a relative obstruction. However, not all females are candidates for the artificial urinary sphincter; indications for use include adequate manual dexterity, mental capacity, motivation to manipulate the device each time for voiding, normal detrusor function, and normal bladder compliance. Widespread use of the artificial urinary sphincter is limited by its technical difficulty in placement whether transvaginal or abdominal, and is usually reserved for patients with complex etiologies of SUI (68-70). With the infection rate for primary artificial urinary sphincter implants at 1 4 %and the nonmechanical failure rate at 13%, the overall 5-yr expected product survival is 72% (71).The dry continence rates of 67% limits the use of this device as a first line surgical treatment for SUI despite overall patient satisfactionnear rates 92%. When considered in the contextof implantation for complex cases of stress incontinence who have failed multiple prior procedures, the overall success and patient satisfaction rates are extremely impressive for these subset of patients with limited options for achieving continence.

SUMMARY

The overall emphasis on successful management of female urinary incontinence begins with the combination of a thorough evaluation, selection of individualized behavior modifications,and possibly pharmacologicsupplementation, Only forpatients who havefailedto achieve an acceptable continence statuswith nonsurgical management and who have maximized their potential for overall pelvic-floor rehabilitation and voiding function should reconstructive surgerythen be considered. A recent report (1)of a 10-yr expected costper elderly patient

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with chronic stress incontinence in 1994 dollars reveals that untreated incontinence is the most expensivehealth care choice ($86,726). Comparative costs are the lowest for surgical therapies and the highest for behavioral therapy (bladder neck suspensions, $25,388; pharmacologic therapy, $62,021;and behavioral therapy, $68,924). Through continued advances in prevention, patient evaluation, and optimization of the pelvic floor and bladder function, the current and future potential for increased long-term effectiveness of all management options for patients who seek an acceptable continence status to improve their quality of life will continue to have a favorable impact on the overall cost.

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32. Buckley JF, Scott R, Meddings R, Lingham V, Buck AC, Aitchison M, Deane RF, Kirk D, and Kyle KF (1992) Injectable siliconemicroparticles: a new treatment for female stress incontinence. J Urol 1473266A. of adipose 33. Bartynski J, Marion MS, Wang TD (1990) Histopathologic evaluation autografts in a rabbit ear model. Otolaryngol Head Neck Surg 102:314-321. collagen injection for urinary inconti34. McGuire EJ, Appell RA (1994) Transurethral nence. Urology 43:413-415. 35. Faerber GJ (1 996) Endoscopic collagen injection therapy in elderly women with type l stress urinary incontinence. J Urol 155(2):512-514. JC, Rackley RR (1997) Collagen injection therapy 36. Smith DN, Appell RA, Winters for female intrinsic sphincteric deficiency? J Urol 157:1275. 37. Herschorn S, Radomski SB (1997) Collagen injections for genuine stress urinary incontinence: patient selection and durability. Zntl Urogynec J 8: 18-24. 38. Winter JC, Appell RA (1996) Bioinjectables in the treatment of urinary incontinence. In: Smith AD, Badlani DH, Clayman RV, Jorda GH, Kavoussi LR, Lingeman JE, et al., eds., Smith’s Textbook of EndouroZogy. St. Louis: Quality Medical Publishing Inc. 1255-1265. 39. McGuire EJ, Woodside JR, Borden TA, Weiss RM (1981) Prognostic value of urodynamic testing in myelodysplastic patients. J Urol 126:205-209. 40. Marshall VF, Marchetti AA, Krantz KE (1949) The correction of stress incontinence by simple vesicourethral suspension. Surg Gynecol Obstet 88:509-518. 41. Jarvis GJ (1994) Surgery for genuine stress incontinence. Br J Obstet Gynaecol 101(2):371-374. 42. Leach GE, Dmochowski RR, Appell RA, et al. (1997) Female Stress Urinary Incontinence Clinical Guidelines Panel. Summary report on thesurgical management of Female Stress Urinary Incontinence. J Urol 158:875-880. 43. Pererya AJ (1959) A simplified surgical procedure for the correction of stress incontinence in women. West J Surg 67:223-226. 44. Trockman BA, Leach GE, Hamilton J, Sakamoto M, Santiago L, Zirnmern PE (1995) Modified Pereyra bladder necksuspension: 10-year mean followup using outcomes analysis in 125 patients. J U r d 154:1841-1847. 45. Korn A (1994) Does the use of permanent suture material affect outcome of the modified Pereyra procedure? Obstet Gyn 83(1):104-10’7. 46. Stamey TA (1973) Endoscopic suspensionof the vesical neckfor urinary incontinence. Surg Gynecol Obstet 136:547-549. 47. Gittes W, Laughlin KR (1987) No-incision pubovaginal suspension for stress incontinence. J Urol 138:568-570. 48. Benderev TV (1992) Anchor fixation and other modifications of endoscopic bladder neck suspension. Urology 40:409-418. 49. Nativ 0,Levine S, Madjar S, Tssaq E, Moskovitz B, BeyarM (1 997)Incisionaless per vaginal bone anchor cystourethropexy for the treatmentof female stress urinary incontinence. Experience with the first 50 patients. J Urol 158: 1742- 1744. 50. Leach GE (1988) Bone fixation technique for transvaginal needle suspensions. Urology 31:388-390. 51. Lobel RW, Davis GD (1997) Long results term of laparascopic Burch urethropexy. J Am Assoc Gynecol h p r o 4(3):341-345. 52. Polascik TJ, Moore RG, Rosenberg MT, Kavoussi LR (1995) Comparison of laparascopicand open retropubic urethropexy for treatment of stress urinary incontinence. Urology 45(4):647-652.

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53. ROSS (1996) J Two techniquesof laparascopic Burch repairfor stress incontinence: a prospective, randomized study. J Am Ass Gynecol Laparo 3(3):35-354. 54. Chau-Su 0,Presthus J, Beadle E (1993)Laparoscopicbladder neck re-suspension using hernia mesh and surgical staples. J hparoendoscop Surg 3(6):563-566. 55. McGuire EJ, LytonB (1978) Pubovaginalsling procedures for stress incontinence. J Urol 119232-85. 56. WrightJE, Iselin CE, C m LIS, Webster GD (1998)Pubovaginal sling using cadaveric allograft fascia for thetreatment of intrinsic sphincterdeficiency. J Urol 160:759-762. 57. Iglesia CB, Fenner DE,Brubaker L (1997) The use ofmesh ingynecologic surgery. Intl Urogynecol J 8:105-115. 58. Raz S, Siege1 AL, ShortJL, Snyder JA (1989) Vaginal wall sling. J Urol 141:43. 59. Kaplan SA, Santarosa RP, Re AE (1996) Comparison of fascial and vaginal wall slings in the management of intrinsic sphincteric deficiency. Urology 47:885. 60. Haas CA, Rackley RR, VasavadaSP, Winters JC, Appell RA (1997) Comparison of in situ vaginal wall sling procedures with and without preservation of the endopelvic fascia and use of bone anchor suture fixation. J Urol 175(4):1034A. of 61. Appell RA, Goldman HB, and Rackley RR (1998) Efficacy and predictors success for the in-situ anterior vaginal wall sling with bone anchoring. J Urol 159(5):161A. 62. Sand PK, Bowen LW, Ostergard DR, Nakanishi AM (1988) Hysterectomy and prior incontinence surgery as risk factors for failed retropubic cystourethropexy. J Reprod Med 33: 171-174. 63. Gilling PD, Fraundorfer MR, Sealey C,et al. (1994) Laparoscopicextraperitoneal approaches to female urinary incontinence: the colposuspension and pubovaginal sling. J Urol 151:334A. 64. Narepalem N, Kieder KJ, Winfeld HN, et al. (1995) Laparoscopic urethral sling for the treatment of intrinsic urethral weakness (type I11 stress urinary incontinence). Tech Urol 1(2):102-105. 65. Madjar S, Beyar M, Nativ 0 (1998) Pubic bone anchoring in the treatment of women with stress urinary incontinence: Newapplications to an old concept. Intl Urogynecol J 9:416-418. 66. Zaragoza MR (1996) Expanded indications for the pubovaginal sling: treatment of type 2 or 3 stress incontinence. J Urol 156:1620-1622. 67. Chaikin DC, Blavias JG (1998) Weakened cadaveric fascial sling: an unexpected cause of failure. J Urol 160:2151. 68. AppellRA(1988) Techniques and results in the implantation of theartificial sphincter in women with type I11 stress urinary incontinence. Neurourol Urodyn 7~613-619. 69. Long RL, Barrett DM (1996) Artificial sphincter: abdominal approach. In: Raz S, ed. Female Urology, 2nd ed., Philadelphia: WB Saunders Co., 419-427. 70. Wang Y, Hadley HR (1996) Artificialsphincter: transvaginal approach.In: Raz S, ed. Female Urology, 2nd ed. Philadelphia: WB Saunders Co., 428-434. 7 1. Elliot DS, Barrett DM (1998) The artificial urinary sphincter in the female: Indications for use, surgical approach, and results. Intl Urology J 9:409-415.

9

UrinaryRetention in Women Roger R. Dmochowski, MD, FACS CONTENTS INTRODUCTION PATHOPHYSIOLOGY EVALUATION ETIOLOGY TREATMENT REFERENCES

INTRODUCTION By definition, the woman afflicted with urinary retention is unable to completely emptyher bladder. However, itis difficult to characterize the condition of urinary retention on the basis of the magnitude of residual volume alone, andmore important to evaluate and render treatment for the presenting symptomatic complex and any associated urinary tract pathophysiology. Retention may besymptomatic or asymptomatic.Symptomscommonly associated with retention may include pure irritative (urgency, frequency), or obstructive (incomplete, bladder emptying, hesitancy) components, with or without abdominal or suprapubic discomfort, and urinary incontinence (either due to overflow incontinence or detrusor overactivity). Urinary tract sequellae associated with retention include: alterations in bladder storage characteristics such as compliance changes, which result in abnormal bladder filling pressures, detrusor overactivity, abnormalities in bladder sensation, and effects on renal function owing to abnormal vesical storage pressures and/or recurrent urinary tract infection.

From: Current Clinical Urology: Voiding Dysfinction: Diagnosis and Treatment Edited by: R. A. Appell 0 Humana Press Inc., Totowa, NJ

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Retention in women tends to be an overlooked diagnosis, insidious in onset, owing to the chronic time frame over which the condition evolves. In part, diagnostic delay results from the perceived lack of frequency of this condition in the general population. However, transient causes of urinary retention also can cause acute symptomatology, such as inability to void or spontaneous incontinence owing to overflow of urine. This chapter will provide an overview of the pathophysiology and etiologies of incontinence, with an emphasis placed on diagnostic evaluation to identify the aforementioned sequellae of retention and potential underlying etiologies. Therapeutic approaches pertinent to particular etiologies will also be discussed.

PATHOPHYSIOLOGY Normal bladder storage and emptying function depends on integration between detrusor and sphincter function. During filling, sphincteric closure provides continence. Bladder filling should occur at low pressures and these pressures should not substantially change (5 cm of water) during the storage cycle. No detrusor contractile activity should occur during this phase. At vesical capacity, detrusor contraction and sphincteric relaxation occur as essentially simultaneous events. Detrusor contraction should be of sufficient magnitude andadequately facilitated to empty the bladder. This intricate mechanism is dependent onintegrity of all the components of this process. Dysfunction of the urethral sphincter may result in obstruction, which is commonly associated with neurologic etiologies of retention. Detrusor dysfunction may arise from ultrastructural changes within the smooth muscle, bladder interstitium, or nerves intrinsic to bladder function. Although detrusor changes seen with aging (trebeculation, fibrosis, atrophy or hypertrophy, and decreased nerve receptor density) have long been recognized (1-3), recent work by Elbadawi andcolleagues has further elucidated the relationship between ultrastructural changes and concurrent symptoms (4-7).

EVALUATION As previously noted, knowledge of the time course of retention or urinary tract obstruction is necessary to determine the level and

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appropriateness of diagnostic work-up. Although urodynamicsare useful for assessing vesical compliance andpresence or absenceof detrusor instability, no urodynamic parameter has been identified as being singularly diagnostic for obstruction. Pressure/flow nomograms are standardized formales with outlet obstruction, but do not apply readily to females owing to variability in voiding dynamics in women. Voiding dysfunction in women is very poorly reported owing to the fact that women tend to underreport their voiding symptoms. Additionally, the diagnosis of obstruction and symptomaticcorrelation of symptoms have not been well delineated in patients. The most appropriate method with which to diagnose obstruction is to utilize a three-component analysis: history and physical findings (with cystoscopy considered as a component of physical examination), symptomatic appraisal (inclusive of subjective and objective methods), and urodynamicresults. Findings consistent with obstruction in any of the three categories should alert the diagnostician to the possibility of retention or obstruction in that particular patient. Thorough historical information provides the basis for accurate diagnosis and subsequent intervention. In addition to standard complete review of all prior surgical and medical interventions, some concept of the time focus of the patient’s symptoms should be delineated. Chronic onset of symptoms is more likely consistent with a degenerative process such as pelvic prolapse and/or the possibility of a neurogenic component. Retention or voiding obstructive symptoms that have an immediate time correlation to surgical intervention indicate iatrogenic cause as the main etiology of the obstruction. Retention occurring in the acute time frame may be indicative more of medication and/or surgical insult such as hemorrhoidectomy. Evaluation for retention in the acute time frame canoften be delayed until the presumed inciting etiology has been removedand/or modified. Initially, during this period, intervention should include clean intermittent catheterization (CIC). Persistent or continued retention prompts evaluation. It is best, if possible, to await ambulatory status and return to normal activities before pursuing neurourologic evaluation. If the patient is unable to continue intermittent catheterization or perform intermittent catheterization, chronic catheter drainage does remain an option. In addition to history and physical examination, vaginal examination remains a crucial component of the evaluation of the female with. chronic obstructive symptomatology. Definitive vaginal examination should include evaluation of not only the anterior vaginal wall to exclude

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cystocele formation, but also examination of the other components of vaginal vault support including the apeduterus and also the posterior wall to exclude rectocele. Therestingposition of theurethra and bladderneckshould be evaluated in the patientwho is status postsuspension, as hyperangulation of this area may be coexistentwith obstruction. The presence of significant periurethral fibrosis indicates potential iatrogenic cause for obstruc tion. Additionally the presence or absenceof incontinence at the time of the examination especially with stress maneuvers should be elucidated. Also during this time an assessment of the vaginal mucosa, specifically evaluating for atrophy, should be undertaken. Focused neurologic examination specifically evaluates the sensory and motor functionsof the sacral dermatomes. This should include not only assessment of perianal sensation but also the status of voluntary and resting anal sphincter tone and of the bulbocavernosusreflux. Longtrack evaluation of the lower extremities includes sensory,fine touch, pinprick, and reflex testing of the appropriate dermatomes. The urodynamic evaluationis a crucial componentof the evaluation of the female with chronic voiding dysfunctionand obstructive symptomatology. Given the reported lackof correlation between symptomatology, urodynamic testing does allow some baseline determination of underlying bladder function prior to intervention for obstructive symptomatology. However, it shouldbe kept in mind that urodynamic testing doesnot provide completely irrefutable data. Specifically, if the female patient is unable to void in the urodynamic lab, this finding may not be reflective of true retention. Therefore postvoid residual volume and simple noninvasiveuroflowometry should be used in conjunction with this analysis. Noninvasive uroflowometry does provide a simple screenwhen utilized with postvoid residualtesting. The identificationof high postvoid residual volume associated with a diminished flow may be indicative of outlet obstruction; however, the possibility of detrusor myogenic failure must also be considered (Fig. 1). ~ultichannelsubtracted pressure flow testing allows a more complete assessmentof bladder contractionwhen identified. Not only does multichannel study assess theability of the bladder to effectively store urine,italsoassessesforbladder filling pressuresassociated with compliancecharacteristics and thepresenceorabsence of detrusor instability. The assessment of total bladder capacity also is crucial in evaluating bladder storage capabilities. Electromyography (EMG) activity at rest may give some indication of possible denervation.

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Fig. 1. Screening uroflow may indicate possible obstructive phenomena. Curve at left is from stress-incontinent patient with no clinical signs or symptoms of obstruction. Curveat right is markedly prolonged andof low amplitude, possibly indicating obstruction, but also consistentwith poor detrusor contractility.

When pressure flow testing is performed, high-pressure, low-flow evaluation may indicate obstruction; "however, these criteria are not completely normalizedin females at this time. Electromyographic activity during voiding may be indicative of dyssynergic activity that may be linked to an underlying neurologic etiology for the obstructive symptomatology. Evaluation of abdominal pressure during the pressure flow evaluation is crucial to assess for the presence or absence of abdominal straining (8).Debate regarding criteria for outlet obstruction continues on the basis of pressure flow observations. Some investigators have attempted to validate diagnostic parameters of peak flow less than 15 cc/s, associated with peak voiding pressure of greater than or equal to 20 cm H20. However, other investigators feel that these criteria are too arbitrary in the absence of symptomatic assessment andcorrelation with parameters obtained from normal controls (9,lO). Massey and Abrams (ll )utilize four parameters including: significant residual volume, diminisheduroflow rate (less than 20 mL/s), peak detrusor voiding pressures of greater than 50 cm of water, and high urethral resistance indices. Other authors have utilized only flow rates and utilized cutoff values of 15 mL/s with voiding volumes of 200 d.., or more. Bass used 15 mL/s and100 ccs of voiding volume (1l a). Blaivas has utilized the previously mentioned criteria of peak pressures of 20 cm of water with peak flows of less than 12 (1lb). Authors with extensive experience in this field, however, have noted that the diagnosis of bladder outlet obstruction in women solely on the basis of pure urodynamics may be very difficult to define because no urodynamic parameter has been reported to be predictive of outcome after urethrolysis in patients felt to be obstructed after incontinence procedures. Specifically patients with low-pressure voiding may have outcomes similar to those patients with high-pressure voiding. In

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Chapter Retention 9 Urinary / Female

Fig. 2. Detrusorcurvesfromthreedifferentpatients.Allwerediagnosed

19 1

as

obstructed on the basis of symptoms, residual urine volume, and clinical examinationfindings. (A) Low-pressurevoidinginelderlywoman with high residual (B) Higher pressure contraction and periurethral fibrosis from needle suspension. accompanied by detrusorinstabilityduringfilling.Irritativesymptomswere marked, in this patient.(C) Pressures approximating 100 cm H20in woman with urethral obstruction from sling (complete and acute), note magnitude and quality of detrusor contraction.

women who void by perineal relaxation, even a small degree of outlet obstruction may cause significant voiding dysfunction. Therefore, standardized voiding pressures may not apply to this sub-group of women (12) (Fig. 2). Simultaneous pressure flow analysis coupled withradiographic (fluoroscopic) monitoring provides crucial data regarding simultaneous structural and functional activity within the lower urinary tract. Video urodynamics not only allows the assessment of exact point of obstruction, especially in the patient who is postsurgical, it also allows the determination of any functional element of obstruction in those patients who may have learned patterns of voiding dysfunction. This study does

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provide the gold standard to which all other testing modalities should be obtained (Fig. 3). In the absence of videourodynamics, sequential urodynamics supplemented by standing voiding cystourethrography (VCUG) will provide complimentary data. VCUG is performed in lateral, anterior-posterior,

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Fig. 3. Fluoroscopy and urethral obstruction. (A) Normal, patent, unobstructed urethra. Urethral lumen has no angulation. (B) Bladder diverticulum in woman with obstructive symptoms after sling. Volume of diverticulum was approximately 50 cc. (C) Oversuspended bladder neck with no mobility of funneling during voiding attempt. Patient had significant periurethral fibrosis on pelvic examination. (D) Prolapse and voiding dysfunction. Grade 2 cystocele, in patientwith persistent irritative complaints after suspension. (E) Prolapse and voiding dysfunction. Grade 3 cystocele. Patient had residual volumes of 150 cc. (F) Prolapse and voiding dysfunction. Grade4, central defect. Patient was unable tovoid except by manual relocation of vaginal contents. (G) Bladder neck angulation and torquing effect from suspension suture in close apposition to urethral wall ofatbladder level neck.

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Fig. 3. Continued

and slightly oblique positions with and without straining and allows assessment of functional integrity of the pelvic floor in relationship to urethral and bladder prolapse. VCUG is a very useful test in the patient who may have occult prolapse not recognized at the time of physical examination. This author believes that cystourethroscopy provides a crucial component of evaluation utilizing a 0 and 30" lens with a nonbeaked cystoscope. This modality provides for urethral mucosal evaluation andsome determination ofany obstructive phenomenacaused by periurethral lesions such asurethral diverticula. Also, hyper-angulation of the urethra can be identified with this approach. This is especially important in a post surgical patient who may have had sling rotation, distortion, or translocation. Additionally, cystourethroscopic evaluation is crucial to help identify any mucosal lesions within the urethra or bladder that may provide some component of obstruction or retention.

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Fig. 3. Continued

In summary, in the woman with obstructive symptoms, subjective and objective assessment of the patient’s presenting symptoms with voiding diary, symptom score, and assessment of symptomatic bother index combined with complex videourodynamic and endoscopic investigation will provide the most complete estimation of presence and

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Fig. 3. Continued

magnitude of definable urinary tract obstruction. Videourodynamics will localize the site of obstruction. Cystoscopy will identify the point of obstruction as well as to determine eo-existent lesions. No one study is felt (by this author) to be conclusive in terms of diagnostic potential.

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Fig. 3. Continued

ETIOLOGY Urinary retention in women can arise from numerous etiologies. As was previously mentioned, the time course of onset of retention should be determined (if possible, by symptomatic appraisal). Distinguishing

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recent initiation of symptoms may allow the examiner to determine a transient etiology such as: endocrine dysfunction, urinary tract infection, immobility, bowel dysfunction (including fecal impaction), or psychogenic cause. Any of these etiologies, alone or in combination, can produce acute loss of bladder contractile capabilities. Medication dose adjustments or addition of new medications to a therapeutic regimen is a particularly important cause of voiding dysfunction in patients with chronic neurologic conditions such as Parkinson’s disease, treatment of which is dependenton several classes of drugs with significant anticholinergic side effects (13). Chronic causes of urinary retention can be broadly classitied as anatomic/obstructive, neurogenic/functional, and physiologiclage related (see Table 1) (141.5).

SPECIFIC ETIOLOGIES Anutomic/Obstructive GYNECOLOGIC CAUSES OF BLADDER OUTLET OBSTRUCTION Gynecologic causes of voiding dysfunction arise from angulation or distortion of the proximal urethral and bladder neck causedby periurethral or perivesical gynecologic lesions. The most common gynecologic cause of outlet obstruction is that resulting from large cystocele formation. Cystocele formation results in acute kinking or angulation of the proximal urethra and bladder neck in relationship to the bladder base. The patient will often complain of positional voiding dysfunction (leaning forward, backward, or having to stand to completely evacuate). She may also report digital manipulation and/or manual reduction of the cystocele in order to void. These patients may also have co-existing recurrent urinary-tract infection and stress incontinence. In Gardy’s study, greater than 40% of women had a significant postvoid residual, however only 3% developed urinary retention owing to the large cystocele (54). These authors noted that cystoceles of high grades (Grades 111-IV) tend to have moresignificant postvoid residuals than do smaller grade cystoceles. Ureteral obstruction associated with prolapse of the anterior vaginal wall may result in oliguria, anuria, and hydronephrosis. Large enteroceles and/or rectoceles may also compress the proximal urethra and bladder neck when dislocated. Constipation and/or other

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Table l Etiologies of Chronic Urinary Retention Neurogenic/~unctional ~nato~ic/Obstructive

Gynecologic Prolapse Cystocele VaultlUterine prolapse Uterine Myoma Uterine retroversion Cervical carcinoma Endometrial carcinoma Urethral Carcinoma Congenital Ectopic ureterocele Female urethral valves Anterior vaginal wall cysts Inflammatory Urethral diverticulum Intrinsic stricture Skene’S duct Meatal stenosis Caruncle Bladder Neck Primary bladder neck dysfunction Iatrogenic Postsurgical Incontinence procedures Urethral instrumentation Inadequate urethral reconstruction

Upper motor neuron lesion Pseudodyssynergia Parkinsons’s disease Movement disorders Autonomic neuropathy True detrusor sphincter Dyssynergia Spinal-cord injury Demyelinating disease Lower motor neuron lesion Cauda equina injury Pelvic nerve injury Demyelinating disease Peripheral neuropathy Tabes dorsalis Diabetes mellitus Herpes zoster Spinal dysraphisrn Functional Dysfunctional voiding Psychogenic retention Hinman syndrome Physio~ogic/Age-Related

Detrusor hyperactivity impaired contractility syndrome (DHIC) Decreased tonus Age-related Prolonged obstruction

bowel dysfunction may exacerbate the voiding dysfunction. Impaired detrusor contractility may further complicate large prolapse (55). Treatment of vaginal prolapse is predominantly surgical by restoring normal vaginal access and depth as well as anterior vaginal wall support (56-63). Temporary therapy may be initiated with pessary support. In selected patients with severe intercurrent disease, this option may provide the best chronic management option.

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Less commoncauses of gynecologic obstruction include large uterine fibroids, especially those located in the anterior uterine segment or lower uterine segment (64-66). Benign or malignant uterine lesions as well as ovarian cysts or tumors mayalso lead to obstruction by compression or angulation of the proximal urethra and bladder neck (67). Vaginal, vulvar, and cervical lesions when large rnay also cause retention owing to impingement onthe bladder floor, trigone, or urethra. Uterine retroversion usually does not result in urinary voiding dysfunction unless associated with pregnancy (68,69).During the first trimester of pregnancy, retention has been reported because the lower uterine segment distorts, in a fulcrum-type fashion, the proximal urethra and bladder neck. This usually occurs in the first trimester before 16 wk (70,71).Therapy usually consists of manipulation of the uterus from the retroverted position. Usually, with enlargement of the uterus after the first trimester, retention resolves. Urethral lesions may also cause obstruction. This is most commonly seen with urethral diverticula although this author has noted the same finding with anterior vaginal wall cysts and Skene’s lesions. Additionally anterior urethral stricture disease, although uncommon in women may also result in obstruction (Fig. 4). Other rare causes of obstruction including urethral valves (72,73) and ectopic ureteroceles have been reported to cause urinary retention, especially in young girls. Urethral caruncles may also cause obstruction especially wheninflamed and enlarged. In elderly patients, complete urethral prolapse rnay also result in urinary retention. Urethral carcinoma, although rare in women, can obstruct the urethral lumen and result in urinary retention also (74). PrimaryBladderNeckObstruction. This entity initially was thought to be very common etiology for voiding dysfunction in women and has been termed Marion’S disease (44).It is defined as incomplete relaxation of the bladder neck in association with adequate magnitude and amplitude detrusor contraction. Several large series now have reported the very rare nature of this disease. Both Farrar and Massey have shown that in large groups of unscreened patients reporting for urodynamic evaluation, this is a very unlikely cause of obstructive symptomatology (45,46). However it can be well-delineated in some patients and should beexcluded with fluoroscopic evaluation. The underlying etiology may be representative of a learned voiding dysfunction, and/or a true organic disease as some authors have reported increased fibrosis and collagenous deposition within the bladder neck in these patients (47). Whether or not these histologic findings are cause or result of any component of bladder neck rigidity is unknown.

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Fig. 4. Two different casesof intrinsic, mucosal structure disease in women. (A) Demonstrates a pinpoint mid-urethral orifice in a woman who had undergone multiple dilatations. In (B) Definitive pelvic radiation had been administered for uterine malignancy. Both patients hadhigh residuals and predominantly obstructive complaints.

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Some authors have also attributed the abnormality to an increased number of sympathetic receptors in the bladder neck increasing sensitivity to normal neurogenic stimulation. Irritative symptoms (frequency, urgency, and nocturia) often predominate early, but may subsequently progress to a high postvoid residual and occasional retention in these patients. Urinary tract infections may also complicate this disease (48-52). Blaivas has defined the entity in urodynarnic terms as being associated with detrusor contraction of greater than 20 cm H20 associated with urinary flow rates of less than 12 mL/s and with evidence of a nonrelaxing bladder neck ( M ) . Other authors have identified patients with voiding pressures of greater than 60 cm of H20 with these same fluoroscopic components (52). The fluoroscopic evidence of primary bladder neck obstruction is the lack of funneling or poor opening of the proximal urethra and bladder neck in association with adequate amplitude and magnitude detrusor contraction. This results in poor or absent urinary flow. Therapy for this disease has rested on surgical ablation of the bladder neck using transurethral and/or open surgical technique. Transurethral technique has utilized two incisions vs a single midline incision in order to prevent sphincteric injury. In the largest series to date, 38 wornen with this disease were described mainly on the basis of symptomatology and cystoscopic evaluation. In this Scandinavian series, a 98% success rate at 1 m0 and a less successful 75% rate at greater than 4 yr follow-up was reported using transurethral incision (49). Other authors have described, making a 12-o’clock incision instead of low lateral incisions at the bladder neck as part of the transurethral treatment of this disease (53).Open correction of this entity has relied on WV plasty of the bladder neck. Other authors have described subjective improvement with alphaadrenergic blocking agents with well-reported urodynamic pre and post operative variables.

DIABETIC CYSTOPATHY Chronic manifestations of diabetes mellitus (DM) affect the lower urinary tract in both sexes. Often in diabetics, cystopathy is associated with demonstrable peripheral neuropathy in the patient who has insulindependent diabetes mellitus (IDDM).

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Diabetes is associated with segmental neuronal demyelination, axonal degeneration, and peripheral nervous system degeneration of the autonomicand somatic nervoussystemsin the affected population (16,17).It has been previously shown that reflex-evoked potentials in patients suffering from diabetes showed diminished conductionvelocities that may be subclinical even in the face of normal neurourologic examinations. This finding implies a chronic, progressive disease course with potentially insidious consequences for the patient, even if subtle physical examination signs are present. It is most often assumed that the diabetic presents with decreased bladder sensation resulting in urinary retention owing to chronic bladder overdistention and resultant poor bladder contractility. Often it is also presupposed that the patient has increased bladder capacity. Recent data would suggest that detrusor instability may be the most common manifestation of diabetic cystopathy and that impaired contractility or loss of bladder contraction may be less common except as a late manifestation of the disease in this patient population (18).The scenario of latent loss of sensation accompanied by increases in bladder capacity and highpostvoid residual volumes however remains the most profound manifestation of diabetes in the lower urinary tract (19-22). Therapy in this population depends at what stage the disease is identified. The goal is to improve bladder emptying and treat underlying bladder instability if identified on urodynamic evaluation. Because of the delay in reflex sensation activity (23,24), patients may do well with a timed voiding schedule with or without Crede or abdominal straining and/or double and triple voiding. With the presence of chronic over distention injury, catheter drainage may be necessary, with clean intermittent catheterization (CIC) providing the best management for this eventuation. Utilization of parasympathetic agonist agents has been recommended to facilitate emptying, but most recent data suggest that these agents are not useful (22,25). Resection or incision of the bladder neck has been reported to be useful in some patients but the possibility of causing iatrogenic sphincteric or mucosal injury and subsequent stricture disease must be considered (22).

PELVIC NERVE INJURY Extensive pelvic surgery is commonly the cause of injury to sympathetic and parasympathetic ganglia and roots in the true pelvis. In women, this is mostcommonly seen in colon surgery (abdominoperineal) resection as well aslow anterior resection. Also, radical

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hysterectomy (Wertheim hysterectomy) is responsible for significant disruption of pelvic afferent and efferent nervous function because of extensive lateral pelvic and uterine cervical dissection (26-30). The incidence of voiding dysfunction following these procedures is widely disparate and has been reported in up to 80% of patients. Injury may occur to all three branches of the nervous system (parasympathetic, sympathetic, and somatic-pudendaldistributions) and the resultant functional status may be representative of any combination of complete or incomplete injury of these three distributions (31). Recurrent pelvic malignancy may also affect all three branches of the nervous system within the pelvis. Often these patients present with an acontractile bladder; however, partial lesions may result in very poorly compliant andhighly unstable bladders that may havea component of poor emptyingas well (32-35). Bladder contractility may be retained in some of these patients unless total parasympathic denervation has occurred. Isolated sympathetic injury may result in sphincteric dysfunction and stress incontinence, which may be severe. Approximately 50% of patients with parasympathetic nerve denervation also experience sympathetic nerve injury. Radical dissection associated with the Wertheim procedure occurs distal to the level of the cervix and accounts for the combined dysfunctions noted in these patients. Patients often retain a sensation of fullness with poor contractility and in the early postoperative period may have a component of poor filling pressures. Urinary retention is usually short-lived, but may be chronic in up to 30-50% of patients (29,33).

NEUROGENIC DYSSYNERGIA Interruption of the descending tracks between the pontine mesencephalic reticular formation and the sacral cord results in disruption in communication between the detrusor and pudendal nucleus. This disruption results in a loss of coordination between bladder and sphincter. Subsequently, simultaneous bladder contraction and sphincteric activity occur resulting in high-pressure intravesical storage and emptying (75). Three patterns of dyssynergia have beendescribed, with TypeI being the most severe because of its presence throughout the voiding cycle. The most deleterious results of dyssynergia include upper-tract decompensation and bladder dysfunction, Spinal-cord injury is the most common cause of destrusor sphincter dyssynergia, but other neurologic diseases such as multiple sclerosis

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(MS), transverse myelitis associated with acquired immune deficiency (AIDS), andother demyelinating diseases are associated with this condition. Depending on the completeness of the neurologic injury, patients with a specific diagnosis may or may not demonstrate sphincteric dyssynergia. In a recent study of MS patients, only approximately 1/3 had detrusor sphincter dyssynergia presumably resulting from the incomplete nature of their disease (76).

LEARNED VOIDING DYSFUNCTION Non-organic Urinary Retention.Retention resulting from noovert organic basis is considered psychogenic until proven otherwise. This finding may be a phenomena that has contributing components both from central and peripheral nervous system stimulation. Retention has been reported in patients who are severely traumatized or otherwise recipients of psychologic stress. In a series evaluating a group of women presenting with acute retention, Barrett (36) found that the condition was usually temporary and responded to noninterventive managements and CIC. Urodynamics in these patients were normal aside from delayed appreciation of bladder-filling events. Several of those patients were noted to have large-capacity bladders. Despite the acute nature of the presentation, one-fifth of the patients reported by Barrett experienced detrusor myogenic decompensation and were dependent on chronic catheterization for bladder drainage. Dysfunctional Voiding. A less overt cause of urinary retention in women is that associated with dysfunctional voiding. The pathophysiologic event behind dysfunctional voiding is loss of coordination or incomplete coordination between detrusor and sphincteric activity during voiding in the absence of discrete neurologic lesion. This finding was first reported in children by Hinrnan (37).This presentation is now described as the Hinman syndrome andis also described as nonneurogenic neurogenic voiding dysfunction (38-40). The patients initially reported on by Hinman had dramatic changes in both upper and lower urinary tracts. This syndrome represents an end-stage variant of the dysfunctional voiding syndrome, whichactually manifests in less severe forms in a significant number of patients in general urologic practice (41,42).The patients with severe dysfunctional voiding habit will have associated encopresis and boweldysfunction as well as nocturnal voiding dysfunction and enuresis. They will also show dramatic upper-tract

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urinary-tract changessuch as hydronephrosis andeven renal functional compromise. Urodynamics may reveal incomplete bladder emptying and highpressure bladder storage. Fluoroscopic evaluation may show significant bladder trebeculation with vesicoureteral reflux and high voiding pressures (41). The patient’s voiding pattern will often be staccato or intermittent and associated with spontaneous sphincteric activity that occurs during the voiding event, indicating an attempt at volitional overriding of the voiding reflex arch (40). The electromyographic (EMG) burst activity results in decrease in urinary flow and marked increase in voiding pressure. Furthermore, there may be fluoroscopic evidence of urethral dilitation proximal to the sphincter owing to relative obstruction caused by pelvic-floor muscular contraction. This will be associated with interruption in the urinary flow pattern. McGuire (42) has postulated that the abnormality in these patients is detrusor overactivity (instability) resulting in volitional sphincteric activity to overcome suddenunanticipated detrusor activity. This represents an exaggeration of the normal reflex control (continence reflex) to prevent incontinence in patients who experience urgency-type symptomatology. However, once this becomes a chronic voiding habit, the habituation results in chronic voiding dysfunction. In light of this, McGuire has recommended anticholinergic medication as a primary modality to treat the hyperactive detrusor (42). Other components of pelvic-floor rehabilitation, including timed voiding and biofeedback have been reported to be useful in these patients. Some authors have used smooth andskeletal muscle-relaxing agents such as Baclofen and Diazepam (43), because these agents tend to be more successful with sphincteric dysfunction resulting from neurologic phenomenon. Strict behavior modification has also been reported to be useful in many of these patients by altering voiding habits and fluid intake.

OTHER CAUSES OF SPHINCTER DYSFUNCTION Other causes of sphincteric dysfunction arise from spasticity of the proximal urethra. Spasticity may result from irritation or urethritis as well as from periurethral inflammatory phlegmon suchas adnexal disease, vaginal infections, and abscesses of the glandular components in the periurethral area. Retention may result owing to high urethral closure pressures (77,78).

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External sphincter spasticity has also been clinically reported in patients who are status postanal and -rectal surgery. Pudendal nerve block has been reported as being salubrious in these patients by decreasing the tone of the surrounding pelvic-floor muscles (78). The etiology of this spasticity is thought to be owing to local factors such as pain resulting from infectious, inflammatory, or traumatic causes. Amelioration of the inflammatory or other insulting lesion with musclerelaxants and, when appropriate, antibiotics may be beneficial. Alpha-blockade has also been reported as being beneficial in these patients (77) (Fig. 5).

Physiologic/Age Related IMPAIRED DETRUSOR CONTRACTILITY Recently, aging related affects on the detrusor function had been reported to result in poor detrusor contraction and emptying. In their seminal work, Resnick and Yalla described detrusor hyperactivity associated with impaired contractility (DHIC) (4,5).These authors identified the syndrome in approximately 30% of elderly patients who demonstrated components of bladder overactivity (instability) associated with poor bladder emptying. This syndrome wasmanifested in the absence of overt outlet obstruction. During urodynamic evaluation, these patients demonstrated detrusor contractions of adequate magnitudebut of poor duration. The authors noted that approximately one-half of all of those studied whohad detrusor overactivity (instability) had functional impairment of the detrusor. Many of these patients demonstrated abdominal augmentation (straining) of voiding. Approximately onethird of the patients’ bladder volume was voided, the remainder being retained as residual volume, No patients were in retention as part of the entry criteria for this study. The authors felt that there could be a progressive nature to this disease and in fact several of the patients did progress over the study time frame (79). The exact etiology for this deterioration in detrusor function may result from collagenous ingrowth inthe detrusor, disrupting the smooth muscle syncytium. There may also be impairment in neuromuscular transmission that is related to the myopathic degeneration. These authors stressed the absolutely crucial nature of urodynamic evaluation to exclude outlet obstruction as a component of the presenting scenario (80).Also, it is necessary to exclude components suchas fecal dysfunction, constipation, andmedication effect as being causative to the dysfunction.

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Fig. 5. Fluoroscopy in two patients with sphincteric dysfunction. (A) T6 incomplete paraplegic with high pressure bladder filling and dyssynergia. Note significant trebeculation. (B) Small-capacity bladderwith early trebeculation in womanwith urgency/frequency syndrome and sphincteric overactivitywith voiding (Pseudodyssynergia).

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Fig. 6. Detrusor hyperactivity, impaired contractility ("DHIC). 80-year-old woman with mixed voiding complaints. Urodynamics demonstrates a poorly facilitated bladder contraction augmented by significant abdominal straining (arrow). Also note the low amplitude instability occurring earlier in the filling cycle.

Other patients manifest less overt detrusor hyperactivity and poor contractility and indeed may present only with impaired contractility that may lead to chronic detrusor decompensation and retention. Most common causes for this include medication affect, immobility, and fecal impaction. The underlying contribution of aging to this entire syndrome cannot be under estimated (Fig. 6).

TREATMENT Urinary outflow obstructionhetention after surgical procedures to correct incontinence can occur due to several technical factors. Suture tension and placement represent the most important variables. Oversuspension or hyper-suspension of the proximal urethra and bladder neck due to suture tension results in these structures being positioned

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high in the retropubic space. This high position produces a physiologic kinking effect at the urethra and bladder neck, effectively compressing the urethra during bladder contraction. Distal to mid-urethral or juxtaurethral placement of sutures under tension can also result in inefficient bladder emptying from angulation of that section of the urethra in relation to more proximal areas of the urethra and bladder neck. Zimmern et al. reported acute angulation of the urethra producing obstruction after Marshall Marchetti Kranz suspension, incorporating distal suture placement (81). This outcome has been commonly reported in the Marshall-Marchetti and some laparoscopic approaches. Because of this finding, Marshall actually modified his procedure to avoid suture placement in close proximity to the wall of the urethra. Obstruction may also result from periurethral fibrosis that may be caused by either extensive dissection and hemorrhage and/or extravasation of urine at the time of the procedure (82-88). Evenwell-performed procedures cancause increases in urethral resistance in the chronic time frame after suspension. This is manifested by increased voiding pressures (89).Patients with postoperative voiding dysfunction are most clearly delineated by the fact that they had normal emptying prior to the procedure, which postoperatively has been substantially altered. Voiding by abdominal straining or pelvic-floor relaxation when coupled with an outlet obstructive procedure may result in relative obstruction producing significant voiding dysfunction. Juma reported 20 of 77 patients with a noncontractile bladder preoperatively. Twelve of those women had significant postvoid residuals at greater than 90 d postoperatively. Overall patients with poorly contractile bladders accounted for approximately 90% of his patients with high postvoid residuals. When evaluating all patients the actual incidence of obstruction in this patient group was only 2.5% (90). Obstruction or retention resulting after sling procedures arises not only from excessive tension placed on the sling, but also from buckling or proximal migration of the sling, which produces a narrow bowstring effect under the bladder neck or urethra (Fig. 7). Additionally, sling displacement distally or uneven sling tension at the bladder neck producing a torque or rotational deformity at this location that will also result in disturbed voiding dynamics. The exact incidence of outlet obstruction after suspension procedures is probably underreported, given the variability in diagnostic criteria for obstruction (91-95). Due to the incomplete nature of complication reporting, the American Urologic Association’s Female Stress Incontinence Guidelines Panel,

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Fig. 7. Cystoscopic imagedin two women obstructed after sling. (A) Sling irnpression on ventrum of urethra at bladder neck. (B) Impression on urethra of sling that had translocated distally and caused obstruction owing to location at distal urethra. Cystoscope is just inside meatus. (C) Fluoroscopic imageof same patient. Note urethral narrowing distally,not related to sphincteric activity or to dysfunctional voiding.

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Fig. 9.7 Continued

by panel consensus, estimated the risk of obstruction after suspension procedures to be low. However, obstruction (as defined by need for catheter drainage greater than 4 wk after surgery) occurring after slingtype procedures was estimated to occur in 1 out of 20 operations (96). Explicit review of all collated data, indicated a tendency for slings and retropubic procedures to have moreassociated postoperative obstructive phenomena than transvaginal or anterior repair-type procedures. Urethrolysis is the fundamental therapy for retention causedby incontinence procedure. Results with urethrolysis vary; however, most authors report success rates (relief of obstruction and continence) in '70-80% of patients (see Table 2). Techniques to accomplish satisfactory urethrolysis include retropubic or transvaginal approaches. Semilunar, suprameatal dissection has been described as an isolated procedure, or has also been combined with more rigorous bladder neck urethrolysis performed from anintroital approach. The goal of all methods is complete lysis of adhesions and mobility of proximal urethra and bladder neck. This author performs urethrolysis from below when the inciting procedure was accomplishedby the same route. For patients who have

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had a laparoscopic suspension or open retropubic, the procedure is performed through a suprapubic approach. Slings may be incised in the midline as an initial stage, and this will often decrease resistance sufficiently so as to allow spontaneous voiding. Other authors use only one route preferentially. Adjunctive procedures include Martius labial interposition into the retropubic space to prevent re-fibrosis, and/or vaginal-wall interposition for the same purpose. Two current points of contention center on timing of urethrolysis and the need for re-suspension at the time of procedure. If the woman is not voiding by 4-6 wk postoperatively, most likely spontaneous voiding will not resume without intervention. Longer time delays result in more significant scarring, and add to the difficulty in performing the procedure. Early release of tension can often be performedby suture incision alone. Re-suspension has long been advocated as adjunctive at the time of urethrolysis to prevent recurrent stress incontinence. Several authors, including Goldman et al. (97) have recommended no attempt at re-suspension. Results data supports this approach, as the incidence of recurrent stress incontinence is no greater than after those procedures during which re-suspension is performed. In general, 70% of women will void satisfactorily and be continent after urethrolysis (98-101). The best solution for postoperative outlet obstruction is satisfactory intraoperative technique. Care in suture or sling placement, complete lack of tension (urethra supported in neutral position, i.e., parallel to floor), and sling fixation in planar configuration will minimize the possibility of retention. No fool-proof tension application exists, but laxity of suspending sutures is the most important preventative step that can be performed (l02,103).

Catheterization and Other Modzalities Treatment for these retentive and obstructive conditions hinges on adequate bladder drainage. The optimal form of bladder drainage at this time is clean intermittent catheterization (CIC). Chronic catheterization is to be decried andavoided if at all possible. CICwas first recommended by Goodman (I03b);however, Lapides (l04) popularized the utilization of this therapy in the lower urinary tract. It is a reasonable therapy for patients of all ages and with all conditions. It can also be utilized by caregivers and family members for those patients who lack manual dexterity and/or motivation to perform the procedure.

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Sterility is not crucial; however,adherence to frequency intervals is necessary to keep bladder volumes under 400-mL thresholds. A high risk of infection is associated with overdistension and this may be owing to ischemic injury as indicated by the work of Lapides and colleagues ( I 05-1 08). Pharmacologic manipulation with parasympathetic agonist agents has been utilized extensively in the past; however, meta-analysis of these agents has shown no significant effect on voiding or decrease in urinary residuals with administration of these medications through any route. These agents do have some effect on the lower urinary tract, but there is also simultaneous effect on other organ systems that may cause significant side effects. No controlled studies substantiate the utilization of these medications in patients with voiding dysfunction. However, there is some indication that these agents may be useful for patients with partial lower motor neuron lesions. Oral decomposition of these drugs indicates that the subcutaneous administration is probably the most adequate methodwith which to administer them. Administration by any route is associated with significant side effects, which tend to be lessened although not completely ameliorated by the subcutaneous administration route (109-1 15). A variety of valvular mechanisms are in clinical trails. These devices attempt to recreate intrinsic urethral function by providing an on demand control to activate voiding by decreasing internal valvular resistance. Current mechanisms employ pressure driven and magnetic controlled avenues. Clinical data is immature at this time. The newest intervention providing an option in the management of women with urinary retention is that of sacral neuromodulation. Previously demonstrated as efficacious in refractory urinary urgency and frequency syndromes, this modality has recently been reported as successful in women with urinary retention. Fifty-eight percent of women dependent on intermittent catheterization were able to void spontaneously and not require catheter drainage in one Dutch study (116). The pathophysiologic explanation for this is as yet unresolved; however, the concept of stochastic resonance has been proposed to explain the seemingly divergent salutary effect of neuromodulation on both urgency and frequency symptoms as well as urinary retention. Stochastic resonance refers to acoustic wave modulation, which occurs during harmonic activity (R. Schmidt, personal communication). Analogy betweenthis acoustic activity and neural signal transmission implies the possibility of nerve transmission manipulation in a similar fashion. Clinical data to support this thesis is not yet available.

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1. Susset JG, Servot-Viguier D,LamyF, et al. (1978) Collagenin155human bladders. Invest Urol 16:204-206. Structural changes in the agingsubmucosa:new 2. LevyBJ,WightTN(1990) morphologic criteria for the evaluation of the unstable human bladder. J Urol 144:1044-1055. 3. Gilpin SA, Gilpin CJ, Dixon JS, et al. (1986) The effect of age on the autonomic innervation of the urinary bladder. J Urol 150:168 1. 4. Elbadawi A, Yalla SV, Resnick NM (1993) Structural basis of geriatric voiding dysfunction. I. Methods of a prospective ultrastructural/urodynamic study and an overview of the findings. J Urol 150:1650-1656. 5. Elbadawi A, Yalla SV, Resnick NM (1993) Structural basis of geriatric voiding dysfunction. 11. Aging detrusor: normalversusimpaired contractility. J Urol 150:1657-1 667. 6. Elbadawi A, Yalla SV, Resnick NM (1993) Structural basis of geriatric voiding dysfunction. 111. Detrusor overactivity. J Urol 150:1668-1680. 7. Elbadawi A, Yalla SV, Resnick NM (1993) Structural basis of geriatric voiding dysfunction. IV. Bladder outlet obstruction. J Urol 150:1681-1695. 8. Barrett DM, Wein AJ (1995) Voiding dysfunction. Diagnosis, classification and management. In: Gillenwater JY, Grayhack JT, Howards SS, Duckett JW, eds., Adult and Pediatric Urology, 2nd ed., vol. 1, St. Louis: Mosby Year Book, p. 1001. 9. KraneRJ,Siroky MB (1991) Clinical Neuro-Urology, 2nd ed. Boston: Little Brown. KJ (1990). Voiding dysfunctionfollowing cystourethropexy: 10. Webster GI), Kreder its evaluation and management. J Urol 144:670-673. female. Br J U r d S 1. Massey J, Abrams PA (1988) Obstructedvoidinginthe 61:36-39. S 1A.Bass JS, Leach GE (1991) Bladder outlet obstruction in women.Prob U r d 5:141146. 11B. Chancellor MB, Blaivas JG (1992) Diagnostic evaluation. Problems in U r d ogy 6(4)~604-621. Distress 12. Lemack G, Z i m e r n P, Foster B ( l 999) Relationship between Urogenital Inventory-6 questionnaire and urodynamic findings. J U r d 161(4) 292(A):77. 13. Dmochowski RR(l 999) Female voiding dysfunction associated with Parkinson’s disease. Intl J Urogynecol (In press). complete urody14. Blaivas JG,Labib KB (1 978) Acute urinary retention in women: namic evaluation. Urology 4:383. 15. WeinAJ, Levin RM,Barrett DM (1995)Voiding function and dysfunction. Voiding function relevant to anatomy, physiology and pharmacology. In: Gillenwater JY, Grayhack JT, Howards SS, Duckett JW, eds., Adult and Pediatric Urology, 2nd ed., vol. l., St. Louis: Mosby Year Book, p. 933. 16. Ewing DJ, Clarke BF (1986) Diabetic autonomic neuropathy: present insights and future prospects. Diabetes Care 9:648-665. 17. Van Poppel H, Stessens R, Van Darnme B, et al. (1988) Diabetic cystopathy. Neuropathological examinationof urinary bladderbiopsies. Eur U r d 15:128- 131. JG (1995) Urodynamic findings in patients with 18. Kaplan SA, Te AE, Blaivas diabetic cystopathy. J Urol 153:342-344.

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disorders. 19. Frimodt-Moller C (1980) Diabeticcystopathy:epidemiology and related Ann Intern Med 92:318-321. diabetes 20. Ellenberg M (1980)Development of urinarybladderdysfunctionin mellitus. Ann Intern Med 92:321-322. 21. Bradley (1980) Diagnosis of urinary bladder dysfunction in diabetes mellitus. Ann Intern Med 92:323-326. 22. Frimodt-Moller C (1980) Treatment of diabetic cystopathy. Ann Intern Med 921327-328. sensation. Urology 23. Bradley WE, Timm GW, Scott FB(1975)CystometryV: 6:654. of diabetic visceral neuropathy. 24. Andersen ST, Bradley WE (1976) Early detection An electrophysiologic study of bladderandurethral innervation. Diabetes 25:1100-1105. 25. Mundy AR, Blaivas JG (1984) Nontraumatic neurological disorders. In: Mundy AR, Stephenson TP, Wein AJ, eds., Urodynamic Principles, Practices and Application. Edinburgh: Churchill Livingstone, p. 278. 26. Kirkergaad P, Hjortrup A, Sanders S (1981) Bladder dysfunctionafter low anterior resection for mid-rectal cancer. Am J Surg 141:266-268. 27. Forney JP (1980) The effect of radical hysterectomy on bladder function. Am J Obstet Gynecol 138:374-382. Moffatt LEF (1978) The incidence and consequencesof 28. Fowler JW, Brenner DN, damage to the parasympathetic nerve supplythe tobladder after abdominoperineal resection of the rectum for carcinoma. Br J Urol 50:95-98. radical abdominal hysterec29. Seski JC, Diokno AC(1977) Bladder dysfunction after tomy. Am J Obstet Gynecol 128:643-651. complicationsfollowing abdominoperineal 30. Eickenberg HC, et al. (1976) Urologic resection. J Urol 115:180. 31. Smith PH, Ballantyne B (1968) The neuroanatomical basis for denervation of the urinary bladder following major pelvic surgery. Br J Surg 55:929-933. 32. Marshall VF, Pollack RS, Miller C (l 946) Observations on urinary dysfunction after excision of the rectum. J UroE 55:40. 33. Woodside JR, Crawford ED (1980) Urodynamicfeatures in pelvic plexus injury. J Urol 124:657-658. following pelvic visceral 34. Yalla SV, AndrioleG (1984) Vesicourethral dysfunction ablative surgery. J Urol 132:503-509. 35. Pavlakis AJ (1991) Cauda equina and pelvic plexus injury. In: Krane RJ, Siroky MB, eds., Clinical Neuro-UroEogy, 2nd ed. Boston: Little, Brown, p. 333. 36. Barrett DM (l 978) Evaluationof psychogenic urinaryretention. J U r d 120:191192. from voiding 37. Hinman F, Raumann F W (1973) Vesicalandureteraldamage dysfunction in boys without neurologic or obstructive disease. J Urol 109:727732. 38. Allen TD (1977) The non-neurogenic neurogenic bladder. J Urol 117:232-238. 39. Allen TD, Bright I11 (1978) Urodynamic patterns in children with dysfunctional voiding problems. J Urol 119:247-249. (the Hinrnansyn40. Hinman F Jr(1986)Non-neurogenicneurogenicbladder drorne)-15 years later. J U r d 136:769-777. 41. Jorgensen TM, Djurhuus JC, Schroder HD (1982) Idiopathic detrusor sphincter dyssynergia in neurourologically normal patients with voiding abnormalities.Eur Urol 8: 107-1 10.

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42. McGuire EJ, Savastano JA (1984) Urodynarnic studies in enuresis and the nonneurogenic neurogenic bladder. J Urol 132:299-302. 43 Kaplan WE, Firlit CR, Schoenberg HW (1980) The female urethral syndrome. External sphincter spasticity as an etiology. J Urol 124:48-49. 44. Marion G (1933) Surgery of the neck of the bladder. Br J U r d 5:351. 45. Massey JA, Abrams PA (1988) Obstructed voiding in the female. Br J Urol 61~36-39. 46. Farrar DJ, Osborne JL,Stephenson TP, et al. (1976) A urodynamicview of bladderoutflowobstructioninthe female: Factorsinfluencingtheresults of treatment. Br J Urol 47:815. 47. Mayo ME (1982) Primary bladder neck obstruction. Surg Rounds 5:66. 48. Gronbaek K, Struckmann JR, Frimodt-Moiler C (1992) The treatment of female bladder neck dysfunction. Scand J Urol Nephrol 26: 113-1 18. 49. Norgaard JP, Swartz-Sorenson S, Djurhuus JC (1984) Functional bladder neck obstruction in women. Urology 39:207. Neurourol Urodyn 5:325. 50. Diokno AC (1986) Bladder neck obstruction in women. 51. Diokno AC, Hollander JB, Bennett CJ (1984) Bladder neck obstruction in women: a real entity. J Urol 132:294-298. 52. Axelrod SL, BlaivasJG(1987)Bladderneck obstruction inwomen. J Urol 137~497-499. 53. Delaere KPJ, Debruyne FMJ, Moonen WA (1983) Bladder neck incision in the female: a hazardous procedure? Br J Urol 55:283-286. 54. Gardy M, Kozminski M, DeLancyJ, et al. (1991) Stress incontinence and cystoceles. J Urol 145:1211-1216. 55. Nichols DH (1985)Vaginalprolapse affecting bladder function. Urol Clin N Am 12:325. of restoration of normal 56. Nichols DH, Milley PS, Randall CL (1970) Significance vaginal depth and axis. Obstet Gynecol 36:251-256. 57 Raz S, Nitti VW, Bregg KJ (1993) Transvaginal repair of enterocele. J U r d 149~724-730. 58. Raz S, Klutke CG, Golub J (1989) Four-corner bladder and urethral suspension for moderate cystocele. J Urol 142:712-715. 59. Raz S, Little NA, Juma S, et al. (1991) Repair of severe anterior vaginal wall prolapse (grade IV cystourethrocele).J Urol 146:988-992. 60. Nitti VW (1994) Transvaginal repair of enterocele, with variations. Conternp Urol 6(4):50. 61. Nichols DH (1982) Sacrospinous fixation for massive eversionof the vagina.Am J Obstet Gynecol 142:901-904. 62. Moschcowitz AV (1912) The pathogenesis, anatomy andcure of prolapse of the rectum. Surg Gynecol Obstet 14:7. 63. Raz S (1992) Vaginal prolapse. In: Raz S, ed., Atlas of Transvaginal Surgery. Philadelphia: WB Saunders, p. 103. 64. Ward JN, Lavengood RW Jr, Draper JW (1968) Pseudo Bladder neck syndrome in women. J UroE 99:64. 65. Carve11 JF, Stubbs SM (1977) Acute retention of urine in a woman due to an exoenteric leiomyoma. Br J Urol4950. 66. Kingsworth AN (1984) Urinary retention due to ovariancyst. Br J Urol56:439440. 67. Doran J, Roberts M (1978) Acute urinary retention in the female.Br J Urol47:793. I)

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68. Silva PD, Rerberich W (1986) Retroverted impacted gravid uterus with acute 69. 70. 71.

72. 73. 74. 75. 76.

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91. Bwch JC (1961) Urethrovaginal fixation to Cooper’s ligament for correction of stress incontinence, cystocele and prolapse. Am J Obstet Gynecoj 81281. 92. Shull BL, Baden WF (1989) A six-year experience with paravaginal defect repair for stress urinary incontinence. Am J Obstet Gynecol 160:1432-1439. 93. McGuire EJ, Letson W, Wang S (1989) Transvaginal urethrolysis after obstructive urethral suspension procedures. J U r d 142:1037. for urinary inconti94. Stamey TA (1980) Endoscopic suspensionof the vesical neck nence in females: Report on 203 consecutive patients. Ann Surg 192:465-471. 95. Spencer JR, O’Conor VJ Jr., Schaeffer AJ (1987) Comparison of endoscopic suspension of the vesical neck with suprapubic vesicourethropexy for treatment of stress urinary incontinence. J U r d 137:411-415. HR, Luber KM, et 96. Leach GE, DmochowskiRR, Appell RA, Blaivas JG, Hadley al. (1997) Female stress Urinary IncontinenceClinical Guidelines Panel summary report onsurgical management of female stress urinary incontinence.The American Urological Association. J Urol 158:875--880. of urethrolysis 97. GoldmanHB,RackleyRR,AppellRA(1999)Theefficacy without re-suspension for iatrogenic urethral obstruction. J UroE 161:196-199. 98. Can LK, Webster GD (199’7) Voiding dysfunction following incontinence surgery: diagnosis and treatment with retropubic or transvaginal urethrolysis. J Urol 157:821--823. 99. Foster HE, McGuire EJ(1993) Management of urethral obstructionwith transvaginal urethrolysis. J Urol 150:1448-145 l. 100. Dmochowski RR, Leach GE, Zimmern PE, Roskamp DA, Ganabathi K (1994) Urethrolysis to relieveoutlet obstruction after prior incontinence surgery. J Urol (part 2) 15 l :420A. 101. Wang AC (1996) Burch colposuspension vs Stamey bladder redo suspension. A comparison of complications with special emphasis on detrusor instability and voiding dysfunction. J Reprod Med 41529-533. 102. Rovner ES, Ginsberg DA,Raz S (199’7)A method for intraoperative adjustment of sling tension: prevention of outlet obstruction duringvaginalwall sling. Urology 50:273-276. 103. McLennon Mt, Bent AE (199’7) Sling incisionwithassociatedvaginalwall interposition for obstructed voiding secondary to suburethral sling procedure. Zntl Urogyn J 8:168. 103B. Guttman L (1954) Initial treatment of traumatic paraplegia. Proc R Soc Med 47: 1103-1105. 104. Lapides J,Costello RT, Zierdl DK, et al. (1968) Primarycauses and treatmentof recurrent urinary tractinfectioninwornen:preliminaryreport.J Urol100:552-555. AC, Silber SJ, et al. (l 972) Clean, intermittentself-catheteriza105. Lapides J, Diokno tion in the treatment of urinary tract disease. J Urol 107:458-461. 106. Lapides J, Diokno AC, Could FR, et al. (1976) Further observation on selfcatheterization. J Urol 116:169-1 71. 983) Fate of patients started on clean 107. Diokno AC,Sands LP, HollanderJB, et al. (I intermittent self-catheterization therapy l0 years ago. J U r d 129:l 120-1 122. 108. Bu&e A, Vollset SE (1993) Risk factors for bacteremia and clinical urinary tract infection in patients treatedwith clean intermittent catheterization. J Urol 14952’143l. 109. Barrett DM (1981)The effect of oral bethanechol chloride on voiding in female patients with excessive residual urine. A randomized double-blind study. J Urol 126:640-642.

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110. Wein AJ, Malloy TR, Shofer F, Raezer DM (1980) The effects of bethanechol chloride on urodynamic parameters in normal women and in women with significant residual urine volumes. J Urol 124:397-399. 111. Wein AJ, RaezerDM, Malloy TR (1980)Failure of the bethanecholsupersensitivity test to predict improved voiding after a subcutaneous bethanechol administration. J Urol 123:202-203. 112. Wein AJ, Hanno PM, Dixon DO, et al. (1978) The effect of oral bethanechol chloride on the cystometrogramof the normal male adult.J Urol 120:330-331. 113. Blaivas JG (1984) If you currently prescribe bethanechol chloride for urinary retention, please raise your hand. Neurourol Urodyn 3:209. 114. Awad SA, McGinnis RHJ, Downie JW (1984) The effectiveness of bethanechol chloride in lower motor neuronlesions: The importance of mode of administration. Neurourol Urodyn 3:173. 115. Downie JW (1984) Bethanechol chloride in urology-a discussion of issues. Neurourol Urodyn 321. 116. Koldewijn E, Meulman E, Bermelmans B, van Kerrebroek, Debruyne F (1999) Neuromodulation effective in voiding dysfunctiondespite high reoperationrate. J Urol 161(4), 984(A):255.

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Edward F, Ikeguchi, ALexis F. Te, James Cboi, and Steven A. KapLan INTRODUCTION PRESENTATION EVALUATION ETIOLOGIES AND TREATMENT REFERENCES

INTRODUCTION Bladder outlet obstruction in males may be a complex syndrome of either dynamic functional or fixed anatomic forces resulting in resistance to the flow of urine. Particularly in males, bladder outlet obstruction is a frequently encountered finding. From a diagnostic standpoint, the evaluation of bladder outlet obstruction relies heavily upon traditional methods. While the most common etiology of bladder outlet obstruction in males relates to prostatic obstruction, an accurate history and physical exam may alert the clinician that other causes may be at hand. Newer technologies have, however, proven to be particularly helpful to the clinician in ascertaining the correct diagnosis and etiology of bladder outlet obstruction prior to the institution of therapy. Urologists have also seen the treatment of bladder outlet obstruction change dramatically over the past decade. While transurethral prostate resection was the most commonly performed procedureby urologists of yesteryear, it now competes with multiple alternative surgical and medical From: Current Clinical Urology: Voiding Dysfinction: Diagnosis and Treatment Edited by: R. A. Appell 0 Humana Press Inc., Totowa, NJ 225

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therapies. Finally, in addressing bladder outlet obstruction in males, more attention has been given to functional voiding disorders commonly seen in younger malepopulations. Herein, an overview of the evaluation and treatment of bladder outlet obstruction in males will be presented, addressing the most commonly utilized therapies for the most commonly seen etiologies.

PRESENTATION The way a patient with bladder outlet obstruction presents depends upon the etiology and the chronicity of the problem. Unless symptoms are acute, few patients experience pain. Thus, what prompts a patient to seek medical attention is dependent on subjective symptoms, which are tolerated by individuals to varying degrees. While the majority of patients will admit to obstructive symptoms for some time prior to presentation, on occasion a patient will develop urinary retention, urinary sepsis, or incontinence as their first sign of bladder outlet obstruction.

EVALUATION Histoy Lower urinary tract symptoms (LUTS) may be divided into either obstructive or irritative symptoms. Patients with bladder outlet obstruction generally complain of obstructive symptoms.However,as the bladder reacts to the presence of outlet obstruction, the response may result in the onset of detrusor instability. Thus irritative voiding symptoms may also be present. The obstructive vs irritative voiding symptoms are listed below: Obstructive voiding symptoms: 1. 2. 3. 4.

Urinary hesitancy. Dribbling/weak urinary stream. Sensation of incomplete bladder emptying. Prolonged urination.

Irritative voiding symptoms:

1. Urinary frequency. 2. Nocturia.

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3. Urinary urgency. 4. Urge incontinence. In addition, the clinician should elicit a medical history pertinent to the various etiologies for bladder outlet obstruction. Thesemight include the presence of a split or narrowstream, the presence of concomitant medical/neurologic history, medication lists, and so forth. The urologist should make an assessment of the patient’s subjective complaints. This is best accomplished with the use of the American Urological Association (AUA) Symptom Index. The AUA index is based on a score ranging from 0 to 35, and classifies the patient’s symptoms as mild (0 to 7), moderate (8 to 19), or severe (20 to 35). Not only is the AUA symptom index helpful in determining the severity of symptoms, itmay be usedto monitor the progression of the disease. In addition, the AUA symptomindex may be the single most important parameter followed to determine the efficacy of treatment, since the patient’ S motivation in seeking medical attention usually relates to subjective complaints and quality of life.

The physical examination should be complete, though a focused urinary tract exam is the most pertinent in diagnosing bladder outlet obstruction. The abdominal examination should take note of suprapubic fullness or pain. The penis and scrotum should be inspected, as should the prostate via digital rectal examination to ascertain size, fluctuance or bogginess, and the presence of prostate cancer signs.

Lab Tests URINE Routine urine analysis and culture should be sent in order to rule out the presence of any infectious process. Frequently, in the face of true bladder outlet obstruction, urinary infection may be present on the basis of urinary stasis.

BLOOD Although there are no absolute guidelines for blood workin the case of bladder outlet obstruction, the clinician should bear several points in mind. Patients with bladder outlet obstruction may be subject to

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significant renal injury reflected in an elevated blood urea nitrogen and serum creatinine. Although we currently do not obtain these tests in all patients with LUTS, it should be considered, particularly for patients presenting with large postvoid residual volumes or patients presenting to an emergency department acutely with retention. In terns of analysis of serum prostate specific antigen (PSA), there currently is no established guideline for its testing. Although patients with bladder outlet obstruction are frequently in the agerange for prostate screening, routine PSA screening is still a point of controversy. Furthermore, bladder outlet obstruction and urinary retention may result in falsely elevated PSA levels, as can the diagnosis of benign prostatic hyperplasia (BPH).

Diagnostic Procedures URINARY FLOWRATE In general, urinary flow rates correlate poorly with patient symptoms. Nonetheless, urinary flow assessment is frequently used as an objective parameter to follow the progress of treatment. The measurement of urinary flow may also be used in conjunction with postvoid residual assessment in identifying patients with attenuated detrusor function. Patients with moderate to severe symptoms but without diminished peak urinary flow rates (>l5 mL/s) may benefit from more in-depth urodynamic testing, i.e., pressure/flow studies. Another aspect of urinary flow rate assessment is the interpretation of flow patterns. In general, a normal flow pattern should rise to a peak rate and return to baseline in the form of a sine-wave curve. Certain patterns may be indicative of abdominal straining. Although this is not pathognomonic for either bladder outlet obstruction or impaired detrusor contractility, it may be another finding that prompts more sophisticated urodynamic evaluation. Nonetheless, from a practical standpoint it is important to remember that urinary flow assessment is neither sensitive nor specific for bladder outlet obstruction. Significant bladder outlet obstruction may be present in the face of normal flow rates, and a poor urinary flow rate does not distinguish between bladder outlet obstruction and an impaired detrusor. OSTVOID RESIDUAL

As in the case of urinary flow rate, the postvoid residual has poor correlation with the degree of subjective complaints. The postvoid

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residual may, however, be helpful as a comparative parameter when assessments can be made before and after treatment. It may also serve as a helpful monitoring tool for patients with the diagnosis of bladder outlet obstruction being treated with medications. Nonetheless, as a single modality of assessment for the bladder outlet obstruction, postvoid residual measurement lacks both sensitivity and specificity. Patents with larger postvoid residual determinations should be considered for urodynamic evaluation. Recent data suggests that men with elevated residual urine at baseline may be at greater risk for urinary retention. We routinely obtain postvoid residual measurements as part of the initial evaluation of LUTS. CYSTOSCOPY

Cystoscopy in the male patient with symptoms of bladder outlet obstruction is an important part of its diagnosis. When the diagnosis of bladder outlet obstruction is clear, though the exact etiology is not absolutely certain (i.e., prostatic obstruction vs urethral stricture), the performance of a flexible cystoscopic examination underlocal anesthesia is an invaluable part of the work-up. Not only is there minimal morbidity to the patient, it may help further elucidate the patient’s underlying disease. Particularly in the case of prostatic obstruction, the clinician can determinecertain variables such as the presence or absence of obstruction at the level of the bladder neck, median lobe, lateral lobes, and measureprostatic urethral length. Ultimately, this information may be used by the urologist to cater therapy to each individual. RODYNAMICS

When the exact diagnosis or etiology of bladder outlet obstruction is not entirely clear, urodynamic evaluation coupled with cystoscopy may be an invaluable tool. In first making the diagnosis of bladder outlet obstruction, the patient requires a fully functional detrusor from the standpoint that a detrusor contraction should be able to be generated. If the patient is unable to generate a detrusor contraction greater than 15 cm H20during cystometry, the patient should be treated for impaired detrusor contractility or acontractile detrusor. In such situations, the concomitant presence of bladder outlet obstruction is unable to be ascertained. Provided the patient can generate an adequate detrusor contraction, the presence of bladder outlet obstruction is based on the combination

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of low urinary flow in the face of elevated detrusor pressure. Often this can be represented graphically with the use of the Abrams-Griffith nomogram. Furthermore, provided the patient is able to initiate a urinary stream during the study, the exact location of the obstruction may be determined with the simultaneous use of fluoroscopy. In general, conventional urodynamic parameters have not beenfound to correlate well with the AUA symptom score. At our institution, we have found that the two urodynamic parameters that most accurately correlate with worsening LUTSin males is the presence of involuntary detrusor contractions and the presence of prolonged detrusor contraction duration ( I ) . The degree to which urodynamic evaluation is utilized varies widely according to the medical center and the treating urologists’ practices. Nonetheless, urodynamic testing may in some cases be the only sure way to make an accurate diagnosis, short of the empiric institution of therapy.

ETIOLOGIES AND TREATMENT Prostatic Obstruction-Benign

Prostatic Hyperplmia

Although manydifferent prostatic conditions may result in symptoms of bladder outlet obstruction, the most commoncause is benign prostatic hyperplasia (BPH). Although BPH will be the focus of this section, the reader should bear in mind that other common conditions of the prostate resulting in bladder outlet obstruction are prostatic carcinoma and acute prostatitis. In most cases, the patient’s history and digital rectal examination will be suggestive of these diagnoses. BPH is a process by which there is an increased number of cells in both the epithelial and stromal compartments of the gland. BPH is highly prevalent in the aging population and has been reported in 90% of glands of menaged 85 in autopsy series. In the United States, approximately 250,000 transurethral prostate resections were performed in 1993 with a national expenditure in the billions of dollars. Even with the advent of better medical therapies, in 1996 approximately l 16,000 transurethral procedures were performed, comprising 94% of all prostate procedures performed for BPH (2). BPH also takes its toll upon the patient’s quality of life and sense of well being. It has been shown that over half of men between the

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ages of 40 and 79 without a prior diagnosis of BPH will curtail at least one activity of daily life owing to their urinary difficulties (3). The natural history of benign prostatic hyperplasia has been addressed in several studies. Most notably, in 1997, Jacobsen et al. reported their findings on the natural history of BPH in a cohort of over 2,000 randomly selected men aged 40-79 in Olmstead County, Minnesota. They found that in men with urinary symptoms andphysical findings consistent with BPH, the incidence of urinary retention was dramatically increased with age and symptoms. Theincidence of acute urinary retention among men in the general population in the studied age range was 7/1,000person-years of follow-up. This was in contrast to men in their 70s that had a 1 in 10 chanceof acute urinary retention within 5 years follow-up and even greater risk if they had urinary symptoms. Jacobsen al. et identified several risk factors for acute urinary retention as being age greater than 70 yr, AUA symptom index of 8 or greater, and a prostatic size determined by digital rectal examination of greater than 30 g in size (4).

MEDICAL THERAPY Medical therapy has revolutionized the way in which urologists approach the patient with bladder outlet obstruction owing to BPH. Once the diagnosis of BPH is made in a patient with LIJTS, they should be offered a trial of medical therapy. Only undercertain circumstances should a patient be considered better served with first-line surgical therapy. These situations would include the presence of bladder calculi, upper tract deterioration diagnosed by ultrasound, or acute urinary retention. The twomain theories behind the pathophysiology prostatic obstruction are based on the either the concept of a fixed obstruction caused by prostatic enlargement or the contraction of the prostatic urethra owing to a degree of sympathetic tone stimulating the alpha,-adrenoceptors of the prostatic smooth muscle(5).These theories may becorrelated with the currently available classes of medications available for the treatment of BPH. While the 5-alpha reductase inhibitors act upon the prostate by minimizing the hormonal stimulus to prostatic growth resulting in shrinkage, the alpha-blockers cause smooth muscle relaxation to ease the proposed tension around the urethra resulting in obstruction. Both forms of medical therapy will be discussed below. Alpha-blockade. Alpha-blockers represent the mainstay of medical therapy currently used for the treatment of bladder outlet obstruction

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owing to BPH. The rationale behind the mechanism of alpha-blocker therapy is the interaction of the smooth muscle (stromal) and glandular (epithelial) components of the prostate, resulting in a situation of dynamic obstruction from a sympathetic stimulation of smooth muscle receptors in the prostate. Alpha-blockers act on the alpha,-adrenoceptors that are found mainly in the prostatic stroma and capsule and the bladder neck (6). Given the mechanism of its action, alpha-blocker therapy manifests the expected adverse reactions on an individual basis. The most common adverse effects include weakness, asthenia, hypotension (particularly postural) and dizziness, and retrograde ejaculation. These complications are reversible with the discontinuation of therapy. In general, alpha-blocker therapy can be expected to result in an increase in peak urinary flow rate approximating 3.8 mL/s and 74% likelihood of improved subjective urinary symptoms. Many varieties of alpha-blockers have been shown to be both safe and effective. Elhilali et al. reported on this profile as seen with terazosin, as studied in 224 patients in a double-blind, placebo-controlled fashion. They found that compared to placebo, terazosin was safe and effective in improving both obstructive and irritative voiding symptoms as well as improved urinary flow rates (7).Terazosin was also found to have a beneficial anti-hypertensive effect onpatients with baseline hypertension while having minimal blood pressure alteration in normotensive patients (8). In a pooled analysis of three double-blind, placebo-controlled studies, the alpha-blocker doxazosin was assessed with regard to safety and efficacy. Doxazosin was found to have a statistically significant improvement in peak urinary flow rate, symptom severity, and bothersomeness when compared to placebo. Furthermore, doxazosin was found to have a greater impact when utilized for patients with more advanced symptoms when compared with patients with mild symptoms (9). Alpha-blockers as a class of BPW medical therapy have also been compared to the other major therapeutic class of drug, the 5-alpha reductase inhibitors, in a double-blind, placebo-controlled fashion. Safety and efficacy were compared in 1229 men with BPH randomized to groups consisting of placebo, terazosin, finasteride, and finasteride plus terazosin. At 1-yr follow-up, the changes in AUA symptom score and flow rate was statistically better in the terazosin and terazosin plus finasteride groups compared to the placebo and finasteride groups. ~inasteridewas found to be no efficacious than placebo (10).

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Selective vs Nonselective Alphal, Blockade. Recently another subclass of alpha-blockers has come into widespread clinical use. Pharmacologic analysis has revealed that there are two subtypes of the alpha,adenoceptor designated 1a and l b (1I ) . While the alpha,,-adrenoceptor is found in great quantities in the prostate, the alphalb-adrenoceptor is more responsible for the contraction of peri-arterial smooth muscle (12,13).It has thus been postulated that a medical therapeutic targeted to the alpha,,-receptor would be more specific to prostatic symptoms and result in fewer side effects. Tamsulosin is a selective alpha,,-adrenoceptor antagonist which, in doses ranging from 0.2-0.4 mg daily, has been found to have a beneficial effect on symptoms of BPH while minimizing complaints of dry mouth and dizziness (14). While it is difficult to exactly equate a dosage of tamsulosin to other nonselective alphal, blockers, one of the attractive features of the selective alphal, blockers is the fact that no titration is necessary, thus simplifying the patient’ S initial regimen. A comparison between tamsulosin at a dosage of 0.2 mg/d and terazosin at a tiltrated dosage of l-S mg/d has been conducted in a group of Korean patients followed with maximal urinary flow rate and International Prostate Symptom Score (IPSS) in a single-blind, nonplacebo controlled fashion. While both medications resulted in improved maximal flow rates and Symptoms, tamsulosin resulted in a statistically significant improvement in the occurrence of adverse events (15). While there are currently no specific guidelines regarding the usage of one form of alpha-blocker therapy over another, clinicians are encouraged to tailor therapy to each individual patient. eduetase Inhibitors. The S-alpha reductase inhibitors are a class of medications, which acts on the crucial conversion of testosterone to its most active form dihydro-testosterone. The major medication in the class has been finasteride. Finasteride has been found to induce prostatic tissue changes via a suppression of the prostatic epithelium. In human studies performed on men with BPH, finasteride has been found to result in an approx SO% decrease in serum prostate specific antigen levels as well as a 21% decrease in prostate volume (16). Furthermore, in clinical studies finasteride has been found to have beneficial effects on the signs and symptoms of BPH, as well as patients’ overall health-related quality of life. While the toxicity profile of finasteride is minimal, some studies have reported a slight reduction in sexual

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function (17). In general, finasteride therapy has an approximately 3% risk of erectile dysfunction 3% risk of dysfunctional ejaculation, and 3-5% chance of diminished libido. Although finasteride therapy has not been found to definitively result in retrograde ejaculation, a small percentage of patients may complain of their own subjective sense of abnormal ejaculation. Nonetheless, many of the positive reports of finasteride effects on signs and symptoms of BPH have not held-up in direct comparison studies with the alpha-blocker medications (10). However, in one of the largest clinical studies addressing finasteride, the long-term effects of finasteride therapy was addressed in a cohort of over 3000 men with moderate to severe symptoms relating to BPH. Over a 4-yr period in a randomized, double-blind, placebo-controlled fashion, finasteride was found to reduce the incidence of prostate surgery and acute urinary retention by approximately one-half, while improving urinary symptom score (18). Thus, in spite of conflicting reports, the 5-alpha reductase inhibitors may still have a significant role in the scheme of medical therapy for BPH. From this standpoint, a new concept in medicaltherapy of BPH may emergefrom a prophylactic standpoint, Asdemonstrated by Jacobsen etal., a subset of patients at greatest risk for the development of complications related to BPH may be able to be identified (4). In such case, clinicians should be alerted to those patients at higher risk of the ultimate development of BPH complications. The institution of prophylactic measures may prove to be beneficial to the patient and cost-effective for the economy in the long run.

SURGICAL THERAPY Transur~thralResection and TVP. The surgical therapy for BPH has a long and colorful history. While transurethral resection of the prostate (TURP) has remained the standard to which other therapies are compared, many newer techniques have found their own niche in the general scheme of surgical management of BPH. This is evidenced by the fact that the incidence of TURP in the United States reached its peak in 1987 and subsequently declined in use, most likely owing to improvements in medical therapy and the advent of several alternative surgical techniques (19). While the consensus remains that patients with LUTS should first be given a trial of medications, once medications have failed, the best remaining therapy appears to be surgical. In a multicenter randomized

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trial, the institution of TURP was compared to watchful waiting in over 550 men with moderate LUTS owing to BPH. Over an average follow-up period of 2.8 yr, immediate TURP was found to be superior to watchful waiting in regards to treatment failures and in eradicating moderate to severe LUTS (20). Conventional TURP is generally considered to be a well-tolerated procedure with a perioperative mortality rate of approximately 2%. The kinds of immediate postoperative complications vary widely and include: urinary tract infection, urinary retention, bleeding requiring blood transfusion, epididymitis, TURP syndrome, urinary incontinence, and sexual dysfunction. Regarding the risk of erectile dysfunction, although historical retrospective studies have reported risks ranging between 5-35%, more recent prospective studies have not found a greater risk of erectile dysfunction amongst men undergoing TURP when compared to men with BPH under watchful waiting protocols (20). Clearly, the most commonly reported form of sexual dysfunction after TURP is retrograde ejaculation, which may occur in as many as 75% of patients. The risks of retrograde ejaculation should be discussed with the patient prior to operation particularly in those men who are younger and sexually active. Long-term complication from TURP may include the occurrence of bladder neck contracture and urethral structure. Benefits of TURP on urinary parameters have generally been reported as an increase in peak urinary flow rate of about 9.8 mL/s and an 88% likelihood of an improvement in subjective symptoms. In addition to the standard techniques of transurethral resection, recent advancements in the area of transurethral electrovaporization of the prostate (TVP) have made this option increasingly popular. TVP utilizes conventional TURP equipment while using a combination of electrosurgical vaporization and coagulation energy delivered through a modified form of rolling TURP “loop” or “roller” in order to desiccate and vaporize obstructing prostatic tissue. The objective behind TVP is the minimize the risk of bleeding and TURP syndrome, thus allowing the clinician a longer operative interval during which resection may be carried out for larger sized prostates. The draw-backs of TVP have been sited as being the increased time required to complete the resection and the inability to obtain prostatic tissue for pathologic review. We have found that both of these difficulties may be overcome in any given patient with the use of a combination of conventional loop followed by electrovaporization. The safety and efficacy of TVP has been investigated. In a series of 93 consecutive patients with LUTS undergoing TVP, 96% of patients

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were able to undergo voiding trial within 24 h of operation and be discharged home.Bothpeak urinary flow rate and AUA symptom scores were found to improve in quantities comparable to TURP. The mean decrease in hematocrit was 1.4 mL/dL and TURP syndrome was not seen. No patients complained of erectile dysfunction although the incidence of retrograde ejaculation was 92%. An 8% incidence of irritative voiding symptoms was noted. TVP was concluded to be both safe and effective and minimized the postoperative hospital stay (21). TUP. Owing to the increasing body of evidence to suggest a significant role of the prostatic capsule in the pathophysiology of bladder outlet obstruction, the transurethral incision of the prostate (TUIP) has become popularized as a less extensive operation, which may offer symptomatic and objective relief. Rather than a full resection of the inner adenoma of the gland, either one or two incisions are made into the prostatic urethra between the limits of the bladder neck or trigone to the verumontanum. The incisions are generally made on either or both sides of the 6 o’clock position. While descriptions of the procedure have included use of any cutting device ranging from a cold knife to a laser, we currently utilize a resectoscope loaded withan electrovaporization roller. The extent of the incision should extend at least to the level of the prostatic capsule, with many reports advocating the usage of a through-capsule incision resulting in the visualization of extracapsular fat. While treatment outcomes are not superior to TURP, T U P is still reported to improve flow rates and symptom scores better than with medical therapy. The most notable aspect of T U P is the markedly lower incidence of retrograde ejaculation, which has varied between 0-37%. In a prospective trial comparing TURP, TUIP, and prostatic balloon dilation, in 60 men with LUTS, TUIP was found to be the method of choice for young patients with smaller prostatic adenoma and/or bladder neck obstruction (22). Minimally Invasive Surgical Therapies. As an effort to further lessen the invasive nature of TURP and TIJIP, several attempts have been made at developing technologies amenable to minimal (i.e. local) anesthesia. Although each treatment is less extensive; however, the minimally invasive nature often comes at the expense of efficacy. Given the risk of marginal efficacy for all of these therapies, patients should be well-informed of the risks. Clinicians should also try toappropriately select patients with mild to moderate symptoms, whichgenerally have a better chance at improvement than those with more severe problems.

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Furthermore, as in any algorithm for the treatment of BPH symptoms, patients should be offered a trial of medical therapy prior to attempts at surgical procedures. Inter~stitia~ Theories: ~ r a n s ~ r e t hNeedle r ~ l Ablation ( ~ ~ and~ A I~terstitiaZDiode Laser. Interstitial therapies of the prostate are attractive from the standpoint that there is no violation and resection of the prostatic urethral mucosa. It would seem intuitive that this would result in much less bleeding, urethral irritation, and intra-operative discomfort. Interstitial therapies are based upon the principal of delivering some form of destructive energy to the prostatic adenoma. Ultimately, the destroyed prostatic tissue is passively resorbed, resulting in a "defect" in the prostatic urethra. In general, these therapies work best for patients with smaller prostatic gland size and median lobe involvement. TUNA therapy utilizes radio-frequency energy delivered through a shielded needle device to ablate prostatic tissue. In a prospective study of patients with bladder outlet obstruction and LUTS, TUNA was performed under conditions of intra-urethral anesthesia in an outpatient setting. Patients starting with urinary symptoms measured by the international prostate symptom score (IPSS) at average 20.8 t- 4.5 improved to 6.2 t- 2.9 at l-yr follow-up. Likewise, urinary flow improved from an average baseline of 8.2 t- 3.4 mL/s to l 5.9 t- 2.1 at l-yr postoperatively (23). Interstitial laser coagulation of the prostate has also been studied recently. In a group of l12 men with LUTS secondary to BPH, interstitial laser therapy was undertaken. AUA symptoms score was found to decrease from a baseline average of 20.9-7.9 at 6-m0 follow-up. Peak urinary flow rate was also found to improve with therapy, from a baseline of 8.0 mL/s to 14.2 mL/s at 6 mo. Reported complications were minimal although a 2.7%of patients required re-treatment or underwent TURP (24). Prostatic ~ i c r o w a v eTherapy. Prostatic microwave therapy relies on hyperthermia produced by the emission of microwave energy from a specially engineered catheter. The energy is delivered to the lateral lobes of the prostate, while there is simultaneous cooling of the urethral mucosa. Intraprostatic temperatures attained by the currently available devices may reach 45"-75" C and patients generally undergo one or more hour-long sessions. Reports of treatment outcomes have been conflicting. In a metaanalysis of recent clinical studies, microwave therapy was found to result in significant sy~ptomaticimprovement as well as increased

)

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urinary flow rates of 35% above baseline (25). However, in another study comparing various microwave techniques to TURP in a randomized controlled fashion, microwave therapy did not result in any improvement in the objective parameters of bladder outlet obstruction as measured by urodynamics. Nonetheless, microwave therapies did result in an improvement in subjective symptoms with a mean AUA symptom score decrease from 18.4-5.2. Complications following prostatic microwave therapy have been found to be low but do include retrograde ejaculation in as many as 22% in some series (26). Urethral Stent. Urethral stents were first introduced in 1987 as an alternative means of treating urethral strictures. Its technology has since been applied to the treatment of bladder outlet obstruction secondary to BPH for patients who are at high surgical risk. From a technical standpoint, the most challenging aspect of obtaining a favorable outcome is in the proper initial positioning of the device. The device is a titanium mesh that is loaded into a delivery mechanism resembling a rigid cystoscopy apparatus. Under direct vision, the stent should be deployed from the bladder neck without extending beyond the verumontanum. The procedure is very fast to perform and can be performed under spinal or local anesthesia depending on the individual patient. Over a period of several weeks, the normal urethral epithelium will grow into the interstices of the stent and ultimately should result in an open urethra covered with epithelium. Complicationsfrom urethral stent placement include stent migration, stone formation, colonization, and persistent urinary infection and intractable detrusor instability. In an effort to study the long term efficacy and safety of urethral stent placement for the treatment of bladder outlet obstruction secondary to BPH, 144 patients underwent implantation and were followed for up to 24 mo. Amongst patients in urinary retention, at 24 mo, average AUA symptom score was 5.21 2 0.81 with an average peak urinary flow rate of 11.34 t- 1.12. Among patients treated for symptoms of bladder outlet obstruction, at 24 mo follow-up, AUA symptom score decreased from 15.89 J. 0.47 to 9.33 2 0.86 while peak urinary flow rate improved from 8.59 t- 0.41 mL/s to 11.43 2 1.12 mWs. Although the incidence of stent removal for migration was as high as 19%, the authors concluded that given proper placement, urethral stent placement was a safe and effective therapy for high-risk patients with prostatic obstruction (27). Primary BladderNeck Obstruction. Primary bladder neck obstruction is a condition usually seen in men of a slightly younger age group (20-50 yr) than those with BPH are. The exact pathophysiology of the

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disease is poorly understood, and patients are commonly treated for years with therapies geared towards other diagnoses such as chronic prostatitis. Typically, patients present with complaints of moderate to severe LUTS with diminished urinary flow rates and an overall clinical scenario consistent with bladder outlet obstruction. We currently employ video-urodynamicsin making the diagnosis, with which voiding cystourethrogram will reveal a “cut-off” demarcation of contrast at the bladder neck (28).

MEDICAL THERAPY Alpha-blockade. While previously primary bladder neck obstruction was thought to be a result of the deposition of fibrous tissue around the bladder neck, histologic analysis has found this to be untrue (29). Other theories of increased sympathetic nervous input to the bladder neck have also been proposed. This has lead to investigations mapping neuropeptides to the bladder neck, which have confined the presence of a possible neuropeptide-Y mediatedsympathetic dysfunction as the etiology of primary bladder outlet obstruction (30). Thus the rationale behind the usage of alpha-blocking agents as the treatment for primary bladder outlet obstruction extends from this theory. Nonetheless, alpha-blockers of all types have been found to be notoriously ineffective in treating this group of patients. While many patients presented with their options will choose an initial trial of medical therapy, most will ultimately come to operation. In a retrospective review of 36 men with primary bladder neck obstruction, Trockman et al. studied outcomes after treatment with alpha-blockers, TUIP, and watchful waiting. They found that of patients begun on alpha-blocker therapy, only 30% continued this treatment owing to a lack of efficacy (31). SURGICAL THERAPY Endoscopic Bladder Neck Incision and TUIP. As discussed previously, the mainstay of therapy for primary bladder neck obstruction is transurethral incision of the bladder neck, and in some cases TUIP. Formal TURPis usually not indicated since most patients with primary bladder neck obstruction will have small prostates on cystoscopic examination. Furthermore, since the majority of patients diagnosed with primary bladder neck obstruction are young, risks of retrograde ejaculation usually makemore aggressive surgical therapies unacceptable.

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Amongst men undergoing transurethral incision of the bladder neck, 'reported success rates have been excellent. In our own experience, of33 patients undergoing bladder neck incision, 30 had a marked improvement in symptoms and an average peak urinary Bow rate of 15.7 mL/s at 6 mo follow-up, with no patients developing retrograde ejaculation (32). ral Stricture Disease. Urethral stricture disease has plagued men for centuries, with descriptions of the problem dating back to the ancient civilizations of India, Egypt and Greece. To this day, urethral stricture disease remains a major etiology of bladder outlet obstruction. Common etiologies of urethral strictures include sexually transmitted diseases (STDs), trauma either incidental or iatrogenic, and least commonly carcinoma. Furthermore, as ever before, a single effective therapy remains elusive. Even amongst urologists, there is relatively little consensus. Part of the problem arises from that fact that few cases of urethral strictures are predictably categorized to correspond to prognosis. Although itis generally true that traumatic strictures are short while urethritis results in longer strictures, the behavior and disposition of a urethral stricture inany given patient rnay behave differently from one individual to the next. Owing to this unpredictability, the natural tendency of both clinician and patient is to favor less invasive techniques, which frequently prove to be suboptimal in efficacy. The diagnosis of urethral stricture disease is frequently suggested in the patient's history. Particularly in younger men, the history of pertinent risk factors and the onset of LUTS should prompt the clinician to be suspicious of an underlying stricture. Definitive diagnosis may be confirmed radiographically with antegrade and retrograde urethral contrast studies. In some cases, for patients presenting in urinary retention, an indwelling Foley catheter or suprapubic catheter rnay be required in order to temporize before definitive therapy may be instituted. ON, ENDOSCOPIC U~

T~ROTO~Y,

Endoscopic urethrotomy or urethral dilation is frequently the first line of therapy offered to patients when the diagnosis of urethral stricture is first made. Giventhe minimally invasive nature of the procedure, there are fewer operative risks. However, the problem with these therapies is their lack of long-term efficacy. Studies of long-term urethrotomy follow-up reveal a success rate of approx 70% for single short (4cm)

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strictures) and 18% for longer strictures. These percentages appear to be consistent regardless of the location or etiology of the stricture disease. Furthermore, witheach recurrence, the chance of stricture resolution with urethrotomyor dilation dwindles inan exponential fashion. Ultimately, the degree of urethral andspongiosa1 fibrosis extends to a point that re-incisions of failed urethrotomies are nearly useless. Clearly it behooves the clinician to move ahead with more aggressive open repair when an initial conservative attempt has failed. In addressing the issue of endoscopic urethrotomy versus urethral dilation, a recent prospective randomized trial was performed comparing the two. Among 210 men with proven urethral stricture disease, 106 underwent filiform dilation 104 underwent internal urethrotomy. For all patients, there was a 12-1310recurrence rate of 40% for strictures less than 2 cm and 80% for those greater than 4 cm. The authors found that both treatment modalities were equivalent in efficacy for the initial treatment of strictures and that both methods had a higher failure rate with increasing stricture length. They concluded that either dilation or urethrotomy could be used as first line therapy for strictures less than 2 cm, open urethroplasty for strictures greater than 4 cm, and a trial of dilation or urethroplasty for strictures measuring between 2 cmand 4 cm (33).

Urethral stent technology was initially developed for the therapy of urethral stricture disease and has since been extrapolated to the therapy of BPH (see above). In the treatment of urethral strictures, some studies have now revealed the efficacy of these devices. In general, urethral stents have been used for patients with short strictures located in the bulbar urethra. As in the case with its BPH indication, the procedure may be accomplishedwith minimal anesthesia and stress to the patient, and maybe ideal for patients who are poor surgical candidates. Deployment of the device is the most crucial factor and usually necessitates the performance of a urethral dilation or incision of the stricture. Once the delivery device is able to pass the stricture, the stent is disengaged such that the length of the stent overlaps the stricture. Although somestudies have reported success rates greater than 80971, most lack long-term follow-up. In 1995, Badlani et al. reported on the reports of a prospective multicenter study undertaken to evaluate the long-term efficacy of the Urolume stent used for patients with recurrent strictures of the bulbar urethra. Out of 175 patients enrolled, at I and

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2 yr follow-up, 139 and 8 1 patients were available for evaluation, respectively. The authors found that the re-treatment rate was 14.3% at l-yr postimplantation compared to 75.2% preimplantation, and concluded that the treatment of an excellent therapeutic option for recurrent bulbar urethral strictures (34).

3ehavioraZ Voiding Dysfinction (Pseudodyssynergia) Bladder outlet obstruction may also occur in the setting of an anatomically normal male patient owing to a dynamic obstruction caused by a lack of coordination between the detrusor and bladder neck smooth muscle (bladder neck dyssynergia) or striated muscle external sphincter (pseudodyssynergia). While psydodyssynergiagenerally implies a condition in a neurologically intact patient, similar conditions may be the result of a neurologic lesion (detrusor external sphincter dyssynergia, DESD) orin neurologically intact children (Binman’s bladder). Although the exact etiology of this condition is unknown, itis generally considered to be a learned behavior of failed pelvic relaxation. It has been postulated that the condition may arise as reaction to a negative response to micturition such as pain, and frequently is seen in younger male patients who have been treated for long periods for chronic prostatitis. Although not an absolute part of the syndrome, there is a preponderance of patients who are generally apprehensive and nervous young men who could be described as type A personalities. Typically, patients may complain of either obstructive or irritative symptoms withotherwise unremarkable prostatic examination andpostvoid residual determination. The definitive diagnosis of pseudodyssynergia requires the use of pressure-flow-EMG studies. The presence of increased striated sphincter activity corresponding with detrusor contraction in the absence of abdominal straining is consistent with the diagnosis. On voiding cystourethrography, there may be a demonstration of narrowing of the urethra at the level of the membranous urethra. As in any condition of bladder outlet obstruction, secondary bladder responses may be manifest in the form of detrusor hypertrophy, diminished capacity and compliance, and instability, or bladder decompensation with larger capacity and residual volumes. Therapy in these cases may frequently be started with a trial of alpha-blockers though this usually meets with minimal success. Preferred therapy for such patients include behavioral modification. and biofeedback, with symptomaticimprovement seen in over 80% of patients over a 6-m0 period (35).

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REFERENCES 1. Kaplan SA, Reis RB (1996) Significant correlation of the American Urological Association symptomscore and a novel urodynamic parameter:detrusor contrac-

tion duration. J Urol Nov; 156(5):1668-1672. Discharge Survey, 2. Graves EJ (1995) Detailed Diagnoses and Procedures, National 1993. National Center for Health Statistics. Vital Health Stat 13:122. 3. Garraway WM, Russell EBAW, Lee RJ, Collins GN, McKelvie GB, Hehir M, RogersACN,SimpsonRJ(1993) Impact of previouslyunrecognizedbenign prostatic hyperplasia on the daily activities of middle-aged and elderly men. Br J Gen Pract 43:318-321. T, Guess HA, Lieber 4. Jacobsen SJ, Jacobson DJ, Girman CJ, Roberts RO, Rhodes MM (1997) Natural historyof prostatism: risk factors for acute urinary retention. J Urol Aug 158(2):481-487. 5. Chapple CR (1995) a-Adrenergic blocking drugs in bladder outflowobstruction; what potential has al-adrenoceptor selectivity? Br J Urol 76 (Suppl 1):47-55. 6. Yamada S, Tanaka C, Kimura R, Kawabe K (1994) Alpha-l-adrenoceptors in human prostate: characterization and binding characteristics of alpha- 1-antagonists. Life Sci 54: 1845-1854. 7. Elhilali MM, Rarnsey EW, Barkin J, Casey RW, Boake RC, Beland G, Fradet Y, Trachtenberg J, Orovan WL, Schick E, Klotz LH (1996) A multicenter, randomized, double-blind, placebo-controlled study to evaluate the safety and efficacy of terazosininthetreatment of benignprostatic hyperplasia. Urology Mar 47(3):335-342. 8. Debruyne FM, Witjes WP, Fitzpatrick J, Kirby R, Kirk D, Prezioso D (1996) The international terazosin trial: a multicentre studyof the long-term efficacy and safety of terazosin in the treatment of benign prostatichyperplasia.The ITT Group. Eur Urol 30(3):369-376. 9. RoehrbornCG,Siege1 RL (1996) Safetyandefficacyofdoxazosininbenign prostatic hyperplasia: a pooled analysis of three double-blind, placebo-controlled studies. Urology Sep; 48(3):406-415. 10. Lepor H,Williford WO, BarryMJ, Brawer MK, Dixon CM, Gormley G, Haakenson C, Machi M, Narayan P, Padley RJ (1996) The efficacy of terazosin,finasteride, or both in benign prostatic hyperplasia. Veterans Affairs Cooperative Studies Benign Prostatic Hyperplasia Study Group.NEngE JMed Aug 22;335(8):533-539, Clarke DE, et al. (1995)InternationalUnion of Pharmacol11. Hieble JP, Bylund DB, ogy. X Recommendation for nomenclature of al-adrenoreceptor: Consensus Update. Pharmacol Rev 47:267-270. 12. Foglar R, ShibataK, Horie K, et al. (1995) Useof recombinant al-adrenoreceptors to characterize subtype selectivity of drugs for the treatment of prostatic hypertrophy. Eur J Pharmacol Mol Pharmaco1288:201-207. 13. Hatano A, Takahashi H, Tamalci M, et al. (1994) Pharmacological evidence of distinct al-adrenoreceptor subtypes mediating the contractionof human prostatic urethra and peripheral artery. Br J Pharmacol 113:723-728. 14. Chapple CR (1996) Selective al-adrenoreceptor antagonists in benign prostatic hyperplasia: rationale and clinical experience. Eur Urol 29: 129-144. 15. Lee E, Lee C (1997) Clinical comparison ofselective and non-selective alpha 1Aadrenoreceptor antagonists in benign prostatic hyperplasia: studies on tamdosin in a fixed dose and terazosin in increasing doses. Br J U r d Oct;80(4):606-611.

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16. Marks LS, Partin AW, Gormley GJ, Dorsey FJ, Shery ED, Garris JB, Subong EN, Stoner E, deKernion JB (1997) Prostate tissue composition and response to J Urol Gnasterideinrnenwithsymptomaticbenignprostatichyperplasia. Jun;157(6):2171-2178. 17. Ginnan CJ, Kolman C, Liss CL, Bolognese JA, Binkowitz BS, Stoner E (1996) Effects of finasteride on health-related quality of life in rnen with symptomatic benign prostatichyperplasia.FinasterideStudy Group. Prostate Aug; 29(2):83-90. 18. McConnell JD, Bruskewitz R, Walsh P, Andriole G, Lieber M, Holtgrewe HL, Albertsen P, Roehrborn CC, Nickel JC, Wang DZ, Taylor AM, Waldstreicher J (1998) The effect of finasteride on the risk of acute urinary retention and the need for surgical treatment among rnen with benign prostatic hyperplasia. Finasteride Long-Term Efficacyand Safety Study Group. N Engl J Med Feb 26;338(9):557563. JH, Wennberg JE (1994) Transurethral 19. Lu-Yao CL, Barry ML, Chang CH, Wasson resection of the prostate among Medicare beneficiariesin the United States: time trends andoutcomes. Prostate Patient Outcomes Research Team (PORT). Urology N0~;44(5):692-698. 20. Wasson JH, Reda DJ, Bruskewitz RC, Elinson J, Keller AM, Henderson WG (1995) A comparison of transurethral surgery with watchful waitingfor moderate symptoms of benign prostatic hyperplasia. The VeteransAffairsCooperative Study Group on Transurethral Resection of the Prostate. N EngE J Med Jan 12; 332(2):75-79. 21. Te AE, SantarosaR, Eaplan SA (I 997) Electrovaporizationof the prostate: electrosurgical modificationof standard transurethral resection in93 patients with benign hyperplasia. J EndouroE Feb; 1I( 1):7 1-75. 22. Saporta L, Aridogan IA, Erlich N, Yachia D (1996) Objective and subjective comparison of transurethral resection, transurethral incision and balloon dilatation of the prostate. A prospective study. Eur Urol 29(4):439-45. 23. Campo B, Bergamaschi F, CorradaP,Ordesi G (1997) Transurethral needle ablation (TUNA) of the prostate: a clinical and urodynarnic evaluation. Urology Jun;49(6):847-850, 24. Muschter R, de la Rosette JJ, Whitfield H, Pellerin JP, Madersbacher S, Gillatt D (1996) Initial human clinical experience with diode laser interstitial treatment of benign prostatic hyperplasia. Urology Aug;48(2):223-228. FM (1997) Current status of thermother25. de la Rosette JJ, D’Ancona FC, Debruyne apy of the prostate. J Urol Feb;157(2):430-438. 26. Ahrned M, Bell T, Lawrence WT, Ward JP, Watson GM (1997) Transurethral microwave thermotherapy (Prostatron version 2.5) compared with transurethral resection of theprostate for thetreatment of benignprostatichyperplasia: a randomized, controlled, parallel study. Br J Urol Feb 79(2): 181-185. RK, Morton WJ, Katz PG (1995) Long-term experienceutilizing 27. Kaplan SA, Chiou a new balloon expandableprostatic endoprosthesis:the Titan stent. North American Titan Stent Study Group. Urology Feb;45(2):234-240. J, Te AE, Miller SantarosaRP, D’ Alisera PM, Hendricks 28. Kaplan SA, Ikeguchi EF, MI (1996) Etiology of voiding dysfunction in men less than 50 years of age. Urology Jun;47(6):836-839. in young 29. Norlen LJ,Blaivas JG (1986) Unsuspected proximal urethral obstruction and middle-aged men. J Urol 135:972. 30. Crowe R, Noble J, Robson T, Soediono P, Milroy EJG and Burnstock G (1995) An increase of neuropeptide Y butnotnitric oxide synthase-immunoreactive

Chapter 10 / Male Bladder Obstruction Outlet nerves in the bladder neck from male patients with bladder neck

245 dyssynergia.

J U r d 154:1231.

31. Trockman BA, Gerspach J, Dmochowski R, Haab F, ZimmernPE,LeachGE (1996) Primarybladderneck obstruction: urodynamicfindingsandtreatment results in 36 men. J U r d Oct;l56(4): 1418-1420. 32. KaplanSA, Te AE,Jacobs BZ (1994)Urodynamic evidence of vesicalneck obstruction in menwithmisdiagnosedchronicnonbacterial prostatitis and the therapeutic role of endoscopic incision of the bladder neck. J UroE Dec;152(6 Pt 1):2063-2065. 33. Steenkamp JW,Heyns CF, de KockML(1997)Internalurethrotomyversus dilation as treatment for male urethral strictures: a prospective, randomized comparison. J Urol Jan 357(1):98-101. 34. Badlani GH, Press SM, DefalcoA,Oesterling JE, Smith AD (1995)Urolume endourethral prosthesis for the treatment of urethral stricture disease: long-term results of theNorthAmericanMulticenterUroLume Trial. Urology May 45(5):846-856. 35. Kaplan SA, Santarosa RP,D’AliseraPM,FayBJ,IkeguchiEF,Hendricks J, Klein L, Te AE (1997) Pseudodyssynergia (contraction of the external sphincter during voiding) misdiagnosed as chronic nonbacterial prostatitis and the role of biofeedback as a therapeutic option. J U r d Jun 157(6):2234-2237.

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1 l post-Prostatectomy Incontinence CONTENTS INTRODUCTION INCIDENCE OF INCONTINENCE AFTER PROSTATECTOMY ANATOMY OF THE PROSTATE GLAND AND URINARY SPHINCTER PROSTATECTOMY: TECHNICAL POINTS REGARDING PRESERVATION OF CONTINENCE ETIOLOGY OF INCONTINENCE FOLLOWING PROSTATECTOMY EVALUATION OF POSTPROSTATECTOMY INCONTINENCE TREATMENT OF POSTPROSTATECTOMY INCONTINENCE TREATMENT OF POSTPROSTATECTOMY INCONTINENCE: A COSTCOMPARISON SUMMARY REFERENCES

INTRODUCTION Adenocarcinoma of the prostate is the most frequently occurring cancer in men ( I ) . Recently, the AmericanUrologic Association released guidelines for the management of prostate cancer. These guidelines confirmed that radical prostatectomy is the optimal treatment for

From: Current Clinical Urology: Voiding Dysfunction: Diagnosis and Treatment Edited by: R. A. Appell 0 Humana Press Inc., Totowa, NJ

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localized prostate cancer in healthy men (2). Incontinence following prostatectomy is a condition with significant adverse effects on quality of life that all physicians caring for patients with prostate disorders will encounter. Complete knowledge of the etiology of incontinence following prostatectomy and the options of treatment will facilitate treatment of these often distressed patients.

INCIDENCE OF INCONTINENCE AFTER ~ R O S T A ~ E C T O ~ ~ The incidence of urinary incontinence is approximately l-3% in patients undergoing transurethral resection of the prostate or open prostatectomy for benign disease (3,4).The incidence of incontinence following radical prostatectomy has been reported to range from 2.5 (5) to 87% (6). This wide discrepancy is a result of several factors. The definition of incontinence varies widely among series, ranging from any degree of wetting or restricted to total incontinence. In addition, the method of data acquisition has a significant effect on reported rates of incontinence. Studies that involve patient questionnaires andlor direct patient input generally have higher rates of incontinence than data obtained by chart review or physician interview. In a sample of Medicare patients undergoing radical prostatectomy, 47% had leakage of urine daily, and 6% needed surgical intervention (7). Incontinence after prostatectomy has a significant negative impact on a patient’s quality of life. Herr discovered in a questionnaire-based study that in 26% of patients surveyed, incontinence seriously affected the overall quality of life, and that 53% of patients 5 years after surgery would not undergo surgery again (8). In a survey of quality of life issues in men treated for localized prostate cancer compared to a normal age-matchedcontrol, patients following radical prostatectomy scored significantly worse on a scale evaluating urinary function (9).Postoperative interval also may effect reported rates of continence, as urinary control progressively improves in the year following surgery (10).Almost all patients have some degree of incontinence immediately after catheter removal, but several series document a progressive reduction in incontinence rates up to one year after prostatectomy (11,12). Thus, it may take up to one year to determine the final continence status of a patient following prostatectomy.

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ANATOMY OF THE PROSTATE GLAND AND URINARY SPHINCTER The prostate gland is comprised of three glandular zones and one nonglandular region, the anterior fibromuscular stroma. The three glandular regions arise from different segments of the prostatic urethra (13).The transition zone constitutes about 5% of prostatic glandular tissue and is located on both sides of the prostatic urethra. It is in this zone that benign prostatic hyperplasia develops (14). The transition zone is separated from the central and peripheral zones of the prostate by the surgical capsule, which marks adequate depth of resection of adenomatous prostatic tissue when performing transurethral prostatectomy. The peripheral zone comprises about ’70% of the mass of the glandular prostate, and itis in this zone that most prostate cancers arise (15). It is located at the posterior and lateral aspects of the prostate gland with its ducts exiting from the base of the verumontanum to the prostatic apex. The central zone constitutes about 25% of the glandular tissue around the base of the prostate, and the ejaculatory ducts travel through the central zone to the verumontanum. The maleurethral sphincter consists of two anatomic zones responsible for continence (16) (Fig. l). The proximal ure~hralsphincter is centered at the bladder neck and includes smooth musculature of the bladder base, bladder neck, and prostatic urethra to the verumontanum. These smooth muscle fibers are arranged largely in a circular fashion at the bladder neck and proximal urethra, and this area has abundant alpha adrenergic innervation (17).The distal urethral sphincterextends from the verumontanum, across the apex of the prostate and into the perineal membrane. The distal urethral sphincter is comprised of three parts: smooth periurethral muscle along the prostatic and membranous urethra, the rhabdosphincter of specialized slow-twitch striated muscle fibers contributing to increased urethral tone, and extrinsic striated muscle, “the urogenital diaphragm,” containing fast-twitch striated fibers that are recruited under periods of increased intraabdominal pressure (18). The striated muscle fibers of the rhabdosphincter have a concentric, cylindrical design around the prostatomembranous urethra and are not contained within a “flat” urogenital diaphragm (19). Surrounding musculofascial and skeletal structures provide a framework critical for the male urethral sphincter to function properly (20). The pubourethral ligaments comprise a median suspensory mechanism for the urethra beneath the subpubic arch (21). Dorsal anchoring of

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“W”””

Fig. 1. Male urethral sphincter anatomy.

the rhabdosphincter is carried out by the connection of the sphincter to Denonvillier’s fascia by the midline dorsal raphe (22). It has been demonstrated that this raphe is continuous with a broad musculofascial plate providing a broad base of support, suspending andstabilizing the rhabdosphincter (20). These supporting structures facilitate urethral elevation and closure promoting continence. Variations of the shape of the prostatic apex have been shown to clinically important (23). Myers et al. noted that in “doughnut shape” prostates with large lateral lobes and prostatic hypertrophy anterior to the urethra, the urethra exits at the apex. In “croissant shape” prostates with little anterior hypertrophy and a prostatic notch, the urethra exits proximal to the apex of the prostate. The authors concluded that the variation in shape of the prostatic apex should be considered at radical prostatectomy so that dissection can spare urethral length and periurethral supporting structures (23).

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Prostatic surgery destroys the proximal urethral sphincter, and continence totally relies on the distal urethral sphincter (24). Therefore, a thorough understanding of the anatomy of the prostate and surrounding structures is essential to avoid destruction of the distal urethral sphincteric mechanism.

PROSTATECTOMY: TECHNICAL POINTS REGARDING PRESERVATION OF CONTINENCE A knowledge of male pelvic and sphincteric anatomy will facilitate surgeons to insure better outcomes and improved continence rates postoperatively. Perhaps the best treatment of incontinence following prostatectomy is to prevent it by preserving sphincteric anatomy and pelvic-floor supporting structures without compromising cancer control.

Transurethral Resection o f the Prostate and Open Prostatectomy In many cases, prostatic hypertrophy extends beyond the verumontanum (25,26) (Fig. 2). Thus, the verumontanum remainsa critical landmark when performing a transurethral prostatectomy. If the resection is carried past the veru, violation of the distal urethral sphincter will occur, resulting in postoperative incontinence. The distal limit of resection should be at the verumontanum, evenif a small rim of adenoma is left behind. This small amount of adenoma may provide some protection against stress urinary incontinence (27). Care should be taken to minimize bleeding to insure adequate visualization, and cautery should be employed judiciously in this area to avoid thermal muscle damage. Most frequently damage to the distal urethral sphincter occurs anteriorly between the 10 and 2 o’clock positions (16). When performing openprostatectomy for benign disease, great care must be taken to preserve the distal sphincteric mechanism. Most of these glands are quite large with adenomatous tissue extending beyond the veru. Meticulous technique should be employed when separating the urethra during enucleation. If one places the adenoma ontoo much upward traction, this may also pull upward a significant portion of the distal sphincter resulting in transection of the sphincter. One should avoid upward pulling of the distal adenoma during enucleation, and thin out the urethra as much as possible before transection. One may

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Fig. 2. Schematic illustratioii of benign prostate adenoma extending into distal urethral sphincter.

consider the enucleation of one lateral lobe at a time, or open the capsule and prostatic urethra to visualize the veru prior to enucleation of the distal adenoma.

Radical Retropubic Prostatectomy Radical retropubic prostatectomy has become the most predominately performed procedure to treat localized prostate cancer following observations by Walsh and colleagues that have allowed for a more anatomic dissection, resulting in decreased blood loss and preservation of erectile function in a significant number of patients (28). By preserving the cavernous nerves, O’Donnell and Finan reported that improved continence rates are achieved (29). However, Steiner et al. (30) in a larger series reported no difference in continence rates regardless of whether a nerve-sparing approach was used or not. They suggested

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“anatomic factors,” such as improved visualization and preservation of the urethra at the prostatic apex are responsible for improved continence. Bladder neckpreservation has been reported to promote continence by sparing circular fibers of the bladder neck and proximal urethra (31,32). Gomez et al. added that bladder neck preservation can be performed with no increased risk of isolated positive margin at the bladder neck (33). To date, there are no controlled urodynamic studies to verify that bladder neck preservation promotes continence. Licht et al. (34) noted that bladder neck preservation had no effect on continence postoperatively, and itappears that meticulous closure of the bladder neck around the catheter has no influence on postoperative continence (30).Bladder neck preservation doesappear to reduce the incidence of anastomotic strictures. At present, considerable interest lies in the preservation of urethral length and integrity as the major mechanism promoting urinary continence after radical prostatectomy. Urodynamic data has revealed that continent patients have significantly longer functional urethral length than incontinent patients (35). Myers (22) described the use of a vein retractor to elevate the prostatic apex in order to achieve the highest possible transection of the membranous urethra to preserve urethral length. Walsh et al. (36) described incorporating tissue of the dorsal venous complex inthe vesicourethral anastomosis, promoting an earlier return to continence. Klein (37) and Stamey (38)have described modified apical dissections incorporating the tissue posterior to the urethra into the vesicourethral anastornosis. Klein (39) describes a modification of technique allowing the urethra to remain attached to its posterior fascia (Fig. 3). He reported improved continence rates and an earlier return to continence. These modifications not only stress meticulous preservation of urethral length, but stabilize the urethra to the periurethral supporting structures which assist in maintaining continence.

Rudicul Perineul Prostutectomy The perineal approach to radical prostatectomy has been described as advantageous, because the urethra is better visualized facilitating the vesicourethral anastomosis (40). Harris and Thompson (41) noted that an “anatomic” approachto perineal prostatectomy achieved continence rates of 97.5% after 18 MO. Several important points were stressed

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Fig. 3. (A-E) Steps in apical dissection of urethra. (Note: Preservation of maximal urethral length by blunt mobilization of prostatic apex off urethra [A] division [D], and incorporationof Denonof Denonvillier’s fasciawith the urethra attached villier’sfasciaintoanastomoticsutures [E].) (Adapted with permissionfrom ref. 39.)

to achieve these excellent results: careful dissection of the striated urethral sphincter, transection of the urethra at the prostatic apex, and bladder neck preservation. Isolated positive margins at the bladder neck were encountered, and the authors stressed proper patient selection for bladder neck preservation.

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Table 1 Etiology of Postprostatectomy Incontinence Based on Urodynamic Findings

No. of ~-

patients

Khan 25.4 (42) 22.2 49.2 Goluboff 34 al. 5et (43) 61 Mayo and Chao 39 57 (44) 4 al. et Winters 27.7 70.8 (45)1.5 38.226.5 (46) 16.2 al. Fitispatrick et Yalla et al. (48) et

63 56 74 65 68 21

% Bladder dysfunction

38

% Sphincteric incompetence

62

% Combined

l0

ETIOLOGY OF INCONTINENCE FOLLOWING PROSTATECTOMY When considering the etiology of urinary incontinence, it is essential to identify that leakage may occur as a result of an abnormality of bladder and/or sphincteric function. Urodynamic studies provide information concerning the relative contributions of bladder andor sphincteric dysfunction in patients with incontinence after prostatectomy. The presence of isolated bladder dysfunction as the predominant cause of incontinence following prostatectomy has been identified in reports utilizing urodynarnic studies (42,43).These reports concluded that sphincteric weakness is not the major factor contributing to incontinence following prostatectomy. In contrast, sphincteric weakness alone has been implicated as the predominant cause of postprostatectomy incontinence (444.5) (see Table 1>.Several factors have been proposed to explain for this discrepancy (45). Many studies documenting a high incidence of bladder dysfunction alone contain a large percentage of patients following transurethral resection ofthe prostate (43,46,47). Bladder dysfunction has been found preoperatively in 45% of patients with symptomaticbladder outlet obstruction, and 38% of patients have persistent detrusor instability following prostatectomy (48). A high incidence of preoperative bladder dysfunction likely effected the results in manyseries identifying bladder dysfunction as the predominant cause of postprostatectomy incontinence. These findings were confirmed as Winters et al. noted a higher incidence of combined bladder and sphincter dysfunction in patients following TUN? compared to patients

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following radical prostatectomy in whom isolated sphincter dysfunction was the predominant cause (45).Detrusor instability owing to decreased compliance after prostatectomy has been documentedto improve within 1 year in a prospective evaluation in men (49). Thus, in groups of patients studied early after prostatectomy, the findings of bladder dysfunction may improve with time. This may explain the high incidence of bladder dysfunction in a recent review in which the mean time between prostatectomy and urodynamic study was only 19 mo (50). The principal importance of competent sphincteric function was identified by Hammerer and Huland, who noted statistically significant differences in maximal urethral closure pressure and functional urethral length between continent and incontinent patients without changes in bladder function (51). Valsalva leak-point pressures (VLPP) have not been identified to correlate with incontinence severity (45,52). Thus there appears to be no role utilizing the absolute value of VLPP in application of therapy for incontinence following prostatectomy. In summary, in patients following radical prostatectomy undergoing urodynamic studies 2 l year postoperatively, isolated sphincteric dysfunction is the most likely cause. A significant number of these patients will also have concomitant bladder dysfunction. In patients following TURP, a higher incidence of bladder dysfunction is present, and is likely to be the predominant cause if urodynamics are done less than 1 year postoperatively. It has been documented that symptoms do not accurately predict the diagnosis (49);therefore, urodynarnic studies are impo~ant-particularly if considering surgical treatment. Anastomotic strictures are a possible factor in the cause of incontinence following prostatectomy. Strictures may result inincomplete bladder emptying with resultant overflow incontinence or contribute to sphincteric weakness. Scarring of the anastomotic region may extend down into the urethral sphincteric mechanism and impair urethral closure. Dilatation andlor incision of urethral strictures are often followed by sphincteric weakness.

As with all clinical situations, the evaluation of postprostatectomy incontinence begins with a complete history and physical examination. The history should include detailed information about the urinary leakage. When did the leakage occur after surgery, and was any leakage

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present prior to surgery? The events occurring during leakage (activity, urgency or no sensation) as well as associated urinary symptoms (force of stream, complete emptying)are important factors. Day andnighttime pad usage should be documented to measure the severity of leakage. A pad-weight test may also more accurately quantify urine leakage. Any associated neurologic symptoms or history of previous incontinence therapy should be obtained. The physical examination should include focus on the neurologic status of the perineum and lower extremities. Rectal examination should be performedto rule out recurrence in cancer cases, and to assess the size of the prostate in patients following TURP. A urinalysis and residual urine should be obtained in all patients, and PSA testing should be considered in all patients with a history of prostate cancer to rule out recurrence. Cystourethroscopy should be performedto inspect for urethral strictures or bladder neck contractures. Gross inspection of the distal urethral sphincter may reveal abnormalities, but cystoscopic examination does not determine sphincter function. In cases of incontinence following TURP, distortion or absence of the verumontanum suggests sphincteric injury and the presence of residual adenoma can be confirmed. Bladder pathology (tumors, stones, or diverticuli) can bedetected. An important feature in performing cystoscopyis to assess the length of the urethra between the external sphincter and the bladder neck. If the urethrovesical anastomosis is at the level of the external sphincter without sufficient urethral length, a transurethral route for injection therapy may be difficult (53). Radiologic evaluation may consist of retrograde urethrography (RUG) or voiding cystourethrography (VCUG). Thesestudies are capable of identifying anatomic causes of incontinence (stricture or bladder neck contracture). The bladder neck is visualized during VCUG and should remain closed during filling. Straining films may detect leakage of urine across the bladder neck. The VCUGalso permits the identification of bladder trabeculation, diverticuli, vesicoureteral reflux, or residual urine. As with cystoscopy, these studies offer anatomic information alone and do not assess bladder or sphincteric function. Perhaps the greatest utility of VCUG is in combination with urodynamic studies, videourodynamics. Urodynamic evaluation is essential to determine the etiology of incontinence following prostatectomy, and should be performed in all patients for whom invasive therapy is considered or in patients who fail conservative treatment. The appropriate urodynamic investigation should allow determination of bladder and urethral function during filling as well as assess bladder contractility and the presence of

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obstruction during voiding. To delineate these functions, a multichannel pressure flow study is the most appropriate test. This study requires the presence of a rectal catheter to allow determination of true detrusor pressure, and the presence of simuultaneous uroflow to measure flow velocity during voiding. The use of electromyography of the pelvic floor in indicated in cases complicated by potential neurologic dysfunction. In routine cases it will add little to the diagnosis of postprostatectomy incontinence. Urethral pressure profilometry will provide infomation concerning urethral closing pressure and functional urethral length. There are no established normal values in male patients and the shape and magnitudeof the urethral pressure profile varies greatly with individual techniques (54).Videourodynamics provides the most complete evaluation, combining the anatomic detail of VCUG with the functional assessment of pressure-flow studies. During the filling phase of the pressure-flow study, information concerning detrusor compliance or instability as well as cystometric capacity is obtained. At 200, 250, and 300 mL volume, the patient is asked to strain. If urinary leakage occurs during straining in the absence of a rise in true detrusor pressure, sphincteric weakness is documented. As stated previously, the exact value of the VLPP is less important in males as is making the diagnosis of stress incontinence. The Jilling phase of the urodynamic study is critical, as one should determine the whether the bladder is stable with normal storage pressures and that the sphincter is competent during straining maneuvers. During the voiding phase, information regarding bladder contractility or the presence of bladder outlet obstruction is present. As in cases of outlet obstruction related to benign prostatic hyperplasia (BP€€),the voiding phase of the pressure flow study will distinguish between obstruction (high detrusor pressure, low urinary flow) and impaired contractility (low detrusor pressure, low urinary flow). The authors routinely perform pressure-flow studies followed by flexible cystoscopy inthe evaluation of incontinent patients following prostatectomy.

T ~ T M E N OF T POSTPROSTATECTOMY INCONTINENCE After performance of urodynamic testing to determine the exact etiology of postprostatectomy incontinence, appropriate treatment decisions can be made. Thefollowing treatment recommendations are based on these urodynamic findings.

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Sphincteric Incompetence CONSERVATIVE TREATMENT Pelvic-floor muscle exercises called Kegel exercises can speed the recovery of continence following prostatectomy; therefore, patients should be instructed and perform the exercises before prostatectomy (55). There are several studies which suggest the utility of electrical stimulation (56), behavior training (57),and biofeedback (58) in the management of incontinence after prostate surgery. Unfortunately, many of these studies contain only a small number of patients, and many patients still experience wetting requiring pad use even though considered “improved.” Theseconservative measures offer little promise in the correction of severe or total urinary incontinence.

PHARMACOLOGIC TREATMENT Alpha-adrenergic agents (ephedrine, pseudoephedrine, and phenylpropranolamine) may improveleakage by increasing outlet resistance. These drugs have a very limited effectiveness, and should be utilized mainly in mild cases in combination with timed voiding and behavioral therapy. Imipramine (10-25 mg tid) possesses anticholinergic activity and direct smooth muscle inhibition of the bladder. Imipramine also blocks reuptake of norepinephrine thus theoretically increasing outlet resistance. The efficacy of this drug is probably as a result of its effect on the bladder, but its use should be considered in cases of sphincteric incompetence (59).

INJECTION THERAPY The ideal material for periurethral injection is one that is easily injected, biocompatible, and causes little or no inflammatory reaction. There should be no migration of the injected material, and it should maintain its bulking effect for a long period of time. Polytetrafluoroethylene (Teflon) paste was oneof the first agents utilized in the treatment of male incontinence. Politano reported on ”70 males treated with Teflon injections, and found that 88% of patients post-TURP and 67% of patients following radical prostatectomy were cured or improved (60). However, other authors have not duplicated these results, and documented concerns of granuloma formation and particle migration have precluded the use of Teflon as an injectable agent (61).

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Table 2 Efficacy of Collagen in the Treatmentof Postprostatectomy Incontinence Mean

No. of Cases

Shortliffe et al. (63) McGuire and Appell (64)22 Aboseif et al. (65) Herschorn et al. (66) Cumrnings et al. (67) 4 Kageyama et al. (68) Griebling et al. (69) 2 Smith et al. (70) 2

Dry

Improvedl Social continence Failed

16 134

3

5 70

88 10

42 2

33 5

1

7 5

19 10 25 57

follow-up (mo)

7

42

8

13 3 8 4 15

20

35

9-23 > 12 10 5.7

10.4 NA 13.3

9.4

To date, the most commonly utilized injectable agent is collagen. Glutaraldehyde cross-linked bovine collagen (Contigen, CR Bard Co., Covington, GA) is both biocompatible and biodegradable. No inflammatory reaction or granuloma formation is elicited, and no cases of particle migration are identified (62). Shortliffe et al. were the first to utilize collagen for the treatment of urinary incontinence (63). In 16 male patients, 50% were either dry or improved. Results of initial studies utilizing transurethral injections of collagen in the treatment of postprostatectomy incontinence were encouraging. In a multi-center trial of 134 patients, 52% had significantly improved and 16% were dryat l-yr follow-up, and of 60 patients, 47%were significantly improved with 25% dry at 2-yr follow-up (64).Aboseif et al. reported on 88 patients with a 10-1110 follow-up. Forty-eight percent were dry and another 38% were improved (65). In this study it is important to note that patients required up to five injections, and some patients did not improve until after the fourth injection. Herschorn et al. reported less encouraging results with a 20% dry rate at 5.7 mo follow-up (66), and many reports that followed were not able to reproduce the earlier promising reports (67-70) (see Table 2). Smith et al. achieved social continence in only 38.7% of patients and documented poor results in patients with continuous supine leakage, those wearing penile clamps, patients with a bladder neck defect greater than l cm and patients following radiation therapy. The authors recommended these patients not undergo collagen-injection therapy (70). In an effort to improve the results of collagen implantation in men, Appell et al. (71) and

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Klutke etal. (72) introduced “antegrade” placement of collagen through a suprapubic tract. The rationale is to inject collagen into supple, wellvascularized tissue above the scar of the vesicourethral anastomosis to improve results. Utilizing this technique, Klutke et al. achieved dryness in 25% of patients and 45% were significantly improved (73).Vasavada and Appell (74)presented long-term follow-up in 29 men treated with the antegrade collagen injection technique. The initial (2 wk) dry rate was 76%. The dry rate decreased to 66% at 6 m0 and 24% at 1 yr. These authors concluded that early success is not predictive of a longterm outcome. From these data, it is apparent that collagen injection therapy is not the ideal treatment of incontinence following prostatectomy. Patients selected should be those with mild to moderate stress incontinence, and they should be counseled that multiple injections will be needed. It is important to stress that social continence is a more realistic goal than total dryness (70). ~ R T I ~ I C ~I ~RL I ~ SPHINCTER ~ R Y

To date, the AMS 800 artificial urinary sphincter (American Medical Systems, Minnetonka, MN) is the definitive procedure of choice in patients with moderateto severe sphincteric incompetence after prostatectomy. It is imperative that patients undergourodynamic studies preoperatively to insure that the bladder compliance is normal and that there are no involuntary bladder contractions. In males following prostatectomy, the sphincter cuff is placed around the proximal bulbous urethra via a midline perineal incision. The bulbospongiosus muscle is largely dissected off of the urethra (Fig. 4), and the measuring device is placed around the urethra to determine the appropriate cuff size (Fig. 5). Most frequently a 4.5-cm cuff is employed. Rarely are 4.0-cm cuffs utilized except in cases of tissue atrophy. Once the cuff is placed, the pressure reservoir is placed by incising the rectus fascia through a small suprapubic incision. The rectus muscle is then split bluntly, and the reservoir is placed in a subrectus pouch. Routinely a 61-70-cm reservoir is used. If the patient has poor-quality tissues or a history of radiation therapy, a 5 I-60-cm reservoir is used. The pump mechanismis placed in a dependent position in the scrotum throughthe suprapubic incision (Fig. 6). The sphincter is filled with isotonic contrast medium to allow radiologic identification of possible leaks. The mechanismis left deactivated for 6 wk. to prevent erosion. Long-term success rates and patient satisfaction are well-documented following i~plantationof artificial sphincters. Each patient should be

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Fig. 4. Perineal approach to bulbar urethra for placement

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of artificial urinary

sphincter.

counseled that some patients will experience “minor leakage” (social continence), and that there is a significant risk of reoperation. In a questionnaire-based study, Litwiller et al. revealed that 90% of patients reported satisfaction with the artificial sphincter and would have the procedure doneagain after a mean follow-up of 2 yr (7.5). An interesting finding was that the need for sphincter revision did not effect the rate of patient satisfaction adversely. Montague reviewedthe results of 156 men implanted with a mean follow-up of 41.6 mo (76).Total continence was achieved in75% of patients, and 15% were improved. Therevision rate in this series was 19.3%.Haabet al. (77) confirmed excellent patient satisfaction and results, as 54/68 men were socially continent with significant reduction in pad usage after 3.5 yr follow-up. These authors noted an overall revision rate of 25%. They cited a reduction in the revision rate from 44.4 to 12.4% after the introduction of sphincter modifications in 1987 (77). In perhaps the largest series, Elliot and Barrett (78) reviewed the revision rate of 313 men following artificial sphincter implantation with a mean follow-up of 68.8 rno. Forty-two percent of patients implanted before modifications in the artificial sphincter required revision surgery, but after sphincter modification,

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Fig. 5. The use of measuring “tape” to determine appropriate cuff size.The most common sizecuff implanted is 4.5 cm. A 4.0-cm cuff is employed in this particular case of tissue atrophy.

only 17% needed revision. It is very well-documented that following modifications in sphincter design, the revision rate is approx 20%. The most commoncauses of device failure are fluid leak or urethral tissue atrophy. Both problems create a decrease in closing pressure of the cuff. Alteration in pumping mechanicsmay signify device malfunction. When a patient experiences a leak in the device, the number of pumps may decrease, or the patient may not be able to pump the device at all. If contrast was placed in the balloon reservoir, a X-ray may confirm loss of fluid in the reservoir. It is important to remember that small leaks may be present with a normal appearing reservoir on Xray. The cuff is the most common site of a leak followed by the balloon (79).The site of the leak is determined at surgical exploration, and the device should be replaced. Occasionally the patient may describe an increasing number of pumps to empty the cuff. This may signify urethral tissue atrophy as increased fluid is allowed into the cuff. Atrophy should be suspected in any patient who has a normallyfunctioning device that starts leaking 2 6 mo after implantation. When this problem is confirmed, the simplest solution is to decrease the cuff size to a smaller

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Fig. 6. Schematic representationof artificial urinary sphincter implanted in a male. (Courtesy of American Medical Systems.)

size. Other options include proximal repositioning of a new cuff (80) or a double-cuff technique, which requires implanting a second cuff around the bulbar urethra (81). Cuff erosion is fortunately much less of a problem now that delayed activation is the rule (82). The most precise way to diagnose erosion is with urethroscopy. Patients may present urinary tract infection (UTI), perineal pain, irritative voiding symptoms, or pain and induration at the pump. These findings wmant consideration of possible erosion. Almost all cases of erosion should be managed by removal of the entire prosthesis. Occasionally, if identified early and associated with sterile urine, only the cuff may need to beremoved. The authors recommend this practice with great caution, as in our experience we have never been able to successfully salvage a sphincter in these circumstances. A repeat sphincter may be implanted after 4-6 mo. It is imperative that patients be instructed to carry medical identification cards andlor bracelets as one of the most common causes of erosion is instr~mentationof the urethra

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with the sphincter activated. Many patients assume that all hospital staff are aware of artificial sphincter function. In reality, we have all encountered patients who develop problems after instrumentation that probably could have been avoided. A difficult clinical problem is the management of simultaneous urethral strictures or bladder neck contractures and stress urinary incontinence. Mark et al. (83) reported 26 patients with stress incontinence and urethrovesical stricture no longer than 2.0 cm. They found synchronous incision of the stricture and insertion of an artificial urinary sphincter to be safe and provide excellent results. Haab et al. recommend incision of the stricture followed by 6 wk of patient self-catheterization. The sphincter is implanted 6 wk after stricture incision, and the patient may periodically continue self-catheterization after sphincter implantation (24). The implantation of an artificial sphincter following radiation therapy is controversial. With the use of a low-pressure (51-60 cm) balloon reservoir, acceptable success rates can be achieved with a higher revision rate (84,85). In these patients it is advisable to leave the sphincter deactivated for 12 wk after implantation.

MALE SUBURETHRAL SLING The use of pubovaginal slings in the management of female stress urinary incontinence (SUI) is well-established. The use of slings in male patients has been previously described (86).More recently, Schaeffer et al. (87) introduced a bulbourethral sling procedure utilizing Teflon bolsters achieving a 75% success rate-some patients required “retightening” procedures. In this series the revision rate was 27% with a 9% incidence of erosion or infection. These authors concluded that this procedure is effective in the management of postprostatectomy incontinence. At present we recommend this procedure only in experimental trials. More experience and follow-up with this procedure is needed, as the potential to create significant obstruction and/or irritative voiding symptoms exists.

Bludder Dysfinction CONSERVATIVE TREATMENT As in all clinical presentations of detrusor overactivity, the mainstay of therapy is timed voiding techniques, avoidance of dietary irritants and fluid restriction when appropriate.

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PHARMACOLOGIC THERAPY Anticholinergic therapy may be initiated with oxybutinin chloride (5 mg tid) or probantheline bromide (15 mg tid). Hyoscyamine may be given in as a sustained release tablet or in a sublingual immediate release preparation. For refractory cases of incontinence or in patients with a marked reduction in bladder capacity, imipramine (25 mg tid) may be added to either of these anticholinergic medications. Patients should be warned of anticholinergic side effects, which can be minimized by starting these medications at a low dose and increasing the dosage periodically. The addition of new anticholinergic formulations (tolterodine, ditropan XL) may minimize these side effects, which limit therapy in many patients.

SURGICAL THERAPY When aggressive therapy does not control incontinence, repeat urodynamic investigation should be undertaken to document persistent bladder dysfunction and to evaluate sphincter function. When aggressive anticholinergic therapy does not control bladder overactivity, bladder augmentation should be considered. The various procedures for bladder augmentation are discussed in detail in chapter 14.

Combined Bladder Dysfinction and SphinctericIncompetence The treatment of this patient group with postprostatectomy incontinence is most challenging. The basic approach to these patients involves initial behavioral and pharmacologicalattempts to control the detrusor dysfunction. Once the bladder storage function normalizes, the sphincteric incompetence can be corrected. This usually involves repeating the urodynamic study while the patient remains on anticholinergic therapy. This differentiates the cause of persistent wetting-either sphincteric incompetence alone or refractory bladder dysfunction. If isolated sphincteric incompetence is identified, the patient proceeds to correction of the sphincteric incompetence and remains onanticholinergic therapy. The treatment of the patient with refractory bladder dysfunction and sphincteric incompetence is controversial. Leach et al. (50) concluded that it is essential to control bladder dysfunction prior to insertion of an artificial sphincter, as this will minimize persistent leakage, damage to the upper tracts or possible worsening of bladder dysfunction. In

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this review of 215 patients, they did not encounter patients whose bladder dysfunction was refractory to medical therapy. The safety of simultaneous implantation of an artificial sphincter and enterocystoplasty (SS) indicates that this form of management may be applicable in this group of patients. These patients should be forewarnedabout the possible need for self-catheterization following surgery and the risk of infection. Perez and Webster (89) noted that there has never been a case report of upper tract deterioration in postprostatectorny men with a hyperactive detrusor following implantation of an artificial urinary sphincter. In patients with detrusor hyperactivity, acceptable rates of continence were achieved when compared to men with stable detrusor function after sphincter implantation (89). The authors concluded that men with postprostatectomy urinary incontinence should not be excluded fromconsideration from artificial urinary sphincter implantation based on the failure to meet ideal implantation characteristics. Only a controlled, prospective comparison of these patient groups will resolve this issue.

TREATMENT OF POSTPROSTATECTOMY INCONTINENCE: A COST COMPARISON Stothers et al. (90) reported on the results of 20 patients treated surgically for incontinence following prostatectomy. Ten patients underwent transurethral collagen injections and 10 patients underwent sphincter implantation. Only one collagen patient achieved complete dryness, and three collagen patients ultimately had a sphincter implanted. These authors concluded that an artificial sphincter is a more effective solution than collagen with a higher incidence of patient dryness and long-term success. Brown et al. (91) after reviewing the charges of hospital procedures and undergarments concluded that the cost of sphincter implantation compared favorably to the cost of collagen injections (general anesthesia) in patients requiring three injections. In patients with severe leakage (>9 undergarmentdd) the artificial sphincter is more cost-effective than continued pad usage.

SUMMARY Postprostatectomy incontinence can adversely effect one’S quality of life. Isolated sphincteric incompetence is the most commonetiology

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following radical prostatectomy and combined bladder dysfunction and sphincteric incompetence is the most common etiology following TURP. Urodynamicstudies are important in obtaining a precise diagnosis. Transurethral injection of collagen is moderately effective and can be utilized in cases of mild to moderate stress incontinence. The artificial urinary sphincter remains the most definitive treatment for sphincteric incompetence. In cases of combined bladder dysfunction and sphincteric incompetence, anticholinergic therapy should be given in an attempt to normalize bladder pressure prior to correction of sphincter deficiency. A thorough discussion of all the treatment options with patients is essential and allows the patient to actively participate in the treatment process.

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62. Remacle M, Marbaix E (1988) Collagen implants in the human larynx: pathologic dissemination of two cases. Arch Otolaryngol 245:203-209. 63. Shortliffe L, Freiha F, Kessler R, Stamey T, Constantinou C (1989) Treatment of urinary incontinence by the periurethral implantation of glutaraldehyde crosslinked collagen. J Urol 141:538-541. 64. Appell R, McGuire E, DeRidder P, Bennett A, Webster G, Badlaniet G, al. (1994) Summary of effectiveness in the prospective, open, multicenter investigation of Contigen implantfor incontinence due to intrinsic sphinctericdeficiency in males. J U r d , part 2, 151:217A (abstract 174). 65. Aboseif S, O’Connell H, Usui A, McGuire E (1996) Collagen injection for intrinsic sphincteric deficiency in men. J Urol 155:lO-13. 66. Herschorn S, Radomslci S, Steele D (1992) Early experience with intraurethral collagen injections for urinary incontinence. J Urol 148:1797-1 800. 67. C u m i n g s J, Boullier J, Parra R (1996) Transurethral collagen injections in the therapy of post-radical prostatectomy stressincontinence.J U r d 155:1011-1013. 68. Kageyama S, Kawabe K, Suzuki K, UshiyamaT, Suzuki T, Aso Y (1994) Collagen Implantation for post-prostatectomy incontinence: early experiencewith a transrectal ultrasonographically guided method. J Urol 152:1473-1475. 69. Griebling T, Kreder K, Williams R (1997) Transurethral collagen injection for treatment of postprostatectomy urinaryincontinencein men. Urology 49:907-912. 70. Smith D, Appell R, Rackley R, Winters J (1998) Collagen injection therapy in postprostatectomy incontinence. J Urol 160:364-367. 71. AppellR,Vasavada S, RackleyR,Winters J (1996)Percutaneous antegrade collagen injection therapy for urinary incontinence following radical prostatectomy. Urology 48:769-772. 72. Klutke C, NadlerR,Andriole G (1995)Antegradecollagen injection: New technique for postprostatectomystress incontinence (Surgeon’S Workshop) J Endourol 9:513-515. 73. Klutke C, Nadler R, Tiemann D, Andriole G (1996) Early results with antegrade collageninjection for post-radicalprostatectomystressurinaryincontinence. J Urol 156:1703-1706. 74. Vasavada S, Appell R, Rackley R, Winters J (1997) Long term follow-up in men treatedwith antegrade collagen for post-prostatectomy incontinence. J Urol 1573394A. 75. Litwiller S, Kim K, Fone P,White R, Stone A (1996) Post-prostatectomy incontinence and the artificial urinary sphincter: a long term study of patient satisfaction and criteria for success. J Urol 156:1975-1980. 76. Montague DK (1992) The artificial urinary sphincter (AS800): experience in 166 consecutive cases. J Urol 147:380-382. 77* Haab F, Trockman B, Zimern P, Leach G (1997) Quality of life and continence assessment of the artificial urinary sphincter in men with minimum 3.5 years follow-up. J U r d 158:435-439. D (1998)MayoClinic long-term analysis of the functional 78. ElliotD,Barrett durability of the AMS 800 artificial urinary sphincter: a review of 323 cases. J Urol 159:1206-1208. 79. Light JK (1990) Complications of surgery for male urinaryincontinenceincluding the artificial urinary sphincter. In: Marshall F, ed., Urologic Complications, 2nd ed. St. Louis, MO: Mosby Year Book, pp. 328-337. J, Stone A (1995)Proximal artificial sphincter cuff reposition80. Couillard D, Vapnek ing for urethral atrophy incontinence. Urology 45:653-656.

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82. Goldwasser B (1990) Avoiding the problemsof artificial urinary sphincter implantation. Probl Urol 4: 187-1 99. 83. Mark S, Perez L, Webster G (1994) Synchronous management of anastomotic contracture andstressurinaryincontinence following radical prostatectomy. J U r ~ 151:1202-1204. l 84. Martins F, Boyd S (1995) Artificial urinary sphincter in patientsfollowing major pelvic surgery andor radiotherapy: are theyless favorable candidates? J Urol 153~1188-1193. 85. "rang Y, Hadley R (1992) Experiences with the artificial urinary sphincter in the irradiated patient. J Urol 147:612-613. 86. Raz S, McGuireE,Erlich R (1988)Fascialslingtocorrectmaleneurogenic sphincter incompetence: the McGuire/Raz procedure approach. J U r d 139:528-531. 87. Schaeffer A, Clemens J, Ferrari M, Stamey T (1988) The male bulbourethral sling procedure for post-radical prostatectomy incontinence. J Urol 159:1510-1515. 88. GonzalezR,Nguyen D, Koleilat N,Sidi A (1989) Compatibility of enterocystoplasty and the artificial urinary sphincter. J Urol 144(2 pt 2): 502-504. 89. Perez L, Webster G (1992) Successful outcome of artificial urinary sphincters in men with post-prostatectomy incontinence despite adverse implantation features. J Urol 148:1166-1170. 90. Stothers L, Chopra A, Raz S (1995) A cost-effectiveness and utility analysis of the artificial urinary sphincter and collagen injections in the treatment of postprostatectomy incontinence. J Urol 1533278A. 91. Brown J, Elliot D, Barrett D (1998) Postprostatectomy urinary incontinence: A comparison of the cost of conservativeversussurgicalmanagement. Urology 51:715-720.

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12 Clinical Pharmacology Scott R.

SereLs and Rodney A. AppeLL

CONTENTS INTRODUCTION FAILURE TO EMPTY FAILURE TO STORE CONCLUSION REFERENCES

INTRODUCTION There are many types of voiding dysfunction that can betreated with pharmacologic therapy. These voiding problems are often described in one of two broadcategories. There are those problems related to storage (i.e., failure to store) and those related to emptying (i.e., failure to empty). Difficulty with storage can result from detrusor hyperactivity, stress urinary incontinence (SUI), or problems with permeability (i.e., interstitial cystitis). Failure to empty usually is caused by either a hypocontractile bladder or perhaps a bladder outlet obstruction such as that seen with benign prostatic hypertrophy (BPH) or the failure to relax the bladder neck and/or external sphincter. The treatments for the various types of voiding dysfunction are best understoodonce the neuroanatomy/anatomy is first delineated. The major anatomic areas that are involved in micturition are the detrusor, the smooth muscleof the posterior urethra, the prostate, and the striated muscle of the external sphincter. The neuroanatomyinvolves the pelvic, hypogastric, and pudendal nerves.

From: Current Clinical Urology: Voiding Dysfunction: Diagnosis and Treatment Edited by: R. A. Appell 0 Hurnana Press Inc., Totowa, NJ

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It is the afferent nerves from the S2-S4 levels that once Stimulated immediately act on the efferent nerves. This then leads to stimulation of the pelvic nerves resulting in relesae of acetylcholine (Ach). The Ach acts on the parasympathetic receptors on the detrusor muscle to cause a contraction. Furthermore, several other substances have been noted to be related after pelvic nerve stimulation. These substances include histamine, prostaglandin, and serotonin. These noncholinergic induced contractions are believed to beowing to the liberation of adenosine triphosphate. In addition, the afferents to the urethra that travel through the pelvic and pudendal nerves to the spinal cord can also result in Sympathetic outflow from the thoraco-lumbar region (i.e., epinephrine and norepinephrine). The adrenergic receptors of the urethra and bladder neck respond to norepinephrine released by the sympathetic nervous system, and this facilitates bladder storage and urinary continence. This is accomplished by relaxing the bladder body wherethe beta receptors are most prevalent as well as by contracting the bladder outlet via the alpha receptors. Beta receptors (i.e., beta-2) appear along with the acetylcholine (Ach) receptors in the bladder body and result in smooth muscle relaxation. On the other hand, the alpha receptors (i.e., alpha-l ) predominate in the bladder neck and proximal urethra where they cause contraction when stimulated. In addition, the striated muscle of the pelvic floor serves as the external sphincter and is innervated by the pudendal nerve which originates from the sacral cord and uses acetylcholine as its neurotransmitter. Figure 1 summarizes the neuroanatomy previously described. Micturition is a complex interaction of both the central and autonomic nervous system. During filling, the bladder suppresses reflex contractions by the help of the beta adrenergic system andthe cortico-regulatory tract. The voiding phase is initiated by relaxation of the external sphincter as well as the smooth muscle of the bladder outlet. This relaxation is then followed by a parasympathetic-induced contraction of the detrusor muscle. Rased onthe previous discussion, it is clear that voiding dysfunction can beaffected by manipulating the interaction of the neurotransmitters. Medications are available that can alter transport, synthesis, storage, release, binding to receptors, degradation, and/or reuptake of these neurotransmitters. However, mostagents that interact with the nervous system lack specificity for the lower urinary tract and therefore side effects are common.

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A

Ach

L

Hypogastric N. (sympathetic)

Ac

Ach

Fig. 1. Diagram showing the innervation to the bladder, bladder neck, and external sphincter

FAILURE TO EMPTY Medications to Fucilitute Bhdder Emptying Normal detrusor contractions can be inhibited by any alteration in the neuromuscular mechanism that is responsible for initiating and maintaining micturition. These canresult from spine injuries, neurologic diseases, or events such as pelvidperinealpain, psychogenic problems, and myogenic impairment that influence the nociceptor reflex mechanisms. Ach results in bladder contractions via the parasympathetic nervous system, but it cannot be used as a medication because it is rapidly broken downby acetylholinesterase. Bethanechol chloride (BC) is a cholinergic agent that is selective for the bladder and gastrointestinal tract without being affected by cholinesterase. Bethanecol has been used for many years to treat hypotonic detrusor activity ( I ) . It is used in the form of 5-10 mg subcutaneously if the patient is awake with no known outlet obstruction (2). For partial bladder emptying, oral bethanecol at a dose of25-100 mg four times daily may be used.

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Bethanecol has also been used to stimulate reflex bladder contractions in patients whohavehad suprasacral spinal-cord injuries (3). The contraindications include peptic ulcer disease, cardiac arrhythmias, bladder or bowel obstruction, bronchial asthma, and hyperthyroidism. In addition, acute circulatory arrest may be caused by intramuscular or intravenous injection. Other side effects include flushing, nausea, vomiting, diarrhea, bronchospasm, headache, salivation, sweating, and visual changes. Overall in several studies, BC has not been demonstrated to cause sustained physiologic bladder contractions in individuals with voiding dysfunction (4-7). Metoclopramide (Reglan) and cisapride are two drugs that may be useful in facilitating bladder emptying. Metaclopramide is a dopamine antagonist with cholinergic properties. On the other hand, cisapride is a synthetic benzamide that promotes release of ACH. Both of these drugs have been shown to be effective in the gastrointestinal tract. However, their efficacy in the lower urinary tract has yet to be proven conclusively (8). Prostaglandins (PG)havebeenused to facilitate emptying. It is thought that these substances contribute to the bladder tone and bladder contractile activity (9,lO). PGE2 and PGF2a, specifically, have been shown to cause bladder contractility. These medications, when administered intravesically, improved bladder emptying and reduced the frequency/duration of postoperative urinary retention (10-1 6). Nevertheless, the use of PG to facilitate bladder emptying has not been completely determined. The side effects include hypotension, hypertension, pyrexia, diarrhea, and vomiting. Alpha adrenergic blockers may facilitate transmission through the parasympathetic ganglia and inturn cause bladder contractility in addition to decreasing outlet resistance. There have been several studies that promoted the use of alpha blockade to prevent postoperative retention (17,18) or in the treatment of nonobstructive urinary retention (19). It is possible that the alpha adrenergic blockers may not just relax the bladder outlet, but rather facilitate the detrusor reflex by a direct or indirect effect on the Parasympathetic ganglia. This phenomenon was demonstrated by DeGroat through his studies on cats (20,21). Furthermore, opiod antagonists are thought to perhaps help stimulate reflex bladder activity, but the findings to support this hypothesis are not completelyconvincing (22-24). Their use is basedon the belief that opiods inhibit the micturition reflex, though the data is inconclusive.

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Medications to Decreuse Outlet Resistance As mentioned previously, the smooth muscle of the bladder base and proximalurethra contain predominately alpha-adrenergic receptors. Therefore, alpha-blockers primarily affect the smooth muscle of the bladder neck and proximal urethra as well as the striated sphincter tone. Phenoxybenzamine wasthe original alpha-adrenolytic agent used to treat voiding dysfunction. The side effects of this medication are orthostatic hypotension, reflex tachycardia, nasal congestion, diarrhea, meiosis, sedation, nausea, and vomiting. It has also been shown to have mutagenic activity, and in animals it induced peritoneal sarcomas and lung tumors (25). Terazosin (Hytrin), doxazosin (Cardura), and prazosin (Minipress) are selective alpha-blocking drugs. These drugs are selective for the alphal receptor. Prazosin differs because it has a short duration of action and therefore must be administered every 4-6 h. The other drugs can be given once daily (26,27). The use of these drugs has beenpromoted for the treatment of voiding dysfunction related to benign prostatic hypertrophy (BPH). In this scenario, they are believed to affect the alpha receptors in the prostatic stroma and capsule. Another agent, Alfuzosin, is a more selective alpha, antagonist with similar efficacy to prazosin (28). Tarnulosin is an alphal blocker that is selective for the alpha,, (majority of receptors on prostate stroma and likely bladder neck) and alphaldreceptor subtypes over the alphalb (29,301. This medication therefore causes less side effects (31-32). There are several other medications that have been tried to decrease bladder outlet resistance. Beta-adrenergic agonists have been shown to decrease urethral pressure but have not been proven to be clinically useful (33,341. Nitric oxide (NO) has been described as a possible relaxant of the smooth muscle of the bladder outlet (35). However, its role in the treatment of voiding dysfunction has yet to be completely elucidated. Furthermore, owing to its ubiquity, selectivity for the lower urinary tract seems difficult. Benzodiazepines (diazepam), dantrolene, and baclofen have been tried to treat voiding dysfunction owing to the striated sphincter. All of these dmgs are considered antispasmotics. Dantrolene worksdirectly on the skeletal muscle, and the other two medications affect the central nervous system through their interactions with inhibitory neurotransmitters. Benzodiazepines influence the neurotransmitter gamma-aminobutyric acid (GABA) at both the presynaptic and postsynaptic sites in the brain and spinal cord. The side effects are central nervous system

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(CNS) depression, which results in ataxia, lethargy, and drowsiness (36). These agents may be worthwhile in patients who cannot relax their pelvic floor, such as that seen in Hinman’s syndrome. However, it has not been proven to be effective in detrusor sphincter dysynergia that is seen with true neurologic disorders. Baclofen is thought to activate the GABA receptors which causes a decrease in the release of excitatory transmitters onto motor neurons by increasing potassium conductance or by inhibiting calcium influx. This in turn results in normalizing interneuron activity and decreasing motor neuronactivity, which reduces spasticity (37). It is primarily used to treat skeletal muscle spasticity in a variety of neurologic conditions. The usual dose is 5 mg twice daily (bid), which can be increased to three times daily (tid) until a maximum of 20 mg four times daily (qid). Side effects include drowsiness, insomnia, weakness, dizziness, rash, and purititis. Withdrawal suddenly of baclofen has provoked hallucinations, tachycardia, and anxiety and should as a result beperformed gradually. Administration of baclofen into the subarachnoid space by an infusion pump has resulted in decreased skeletal spasticity as well as decreased striated sphincter dysynergia and bladder hyperactivity (38-40). Dantrolene is believed to inhibit the release of calcium ions from the sarcoplasmic reticulum of the striated muscle fibers which inhibits muscle contraction. This inhibition, however, is not complete andcontraction is not totally abolished. It has nevertheless been reported to improve voiding dysfunction causedby detrusor-striated sphincter dysynergia (41).Hepatotoxicity, dizziness, diarrhea, and euphoria have all been reported side effects. Furthermore, the risk of hepatic injury is reported to be greater in women (42).

Medication to Treat Outlet Obstruction Cawed by Benign Prostatic Hypertrophy As part of the normal aging process, prostatic tissue continues to grow and can potentially cause a bladder outlet obstruction. Histologically, 50430% of the prostate volume is composed of stromal tissue, with the glandular tissue comprising the remaining 2040%. The alpha adrenergic blockers described previously act on the stromal tissue of the prostate. Finasteride (Proscar), a selective inhibitor of 5-alpha-reductase, decreases the conversion of testosterone to dihydrotestosterone. Therefore, it prevents the growth of the glandular component of the prostate. In several studies, Proscar has been shownto improve urinary symptoms

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Table 1 Mechanisms of Actions of Phytotherapeutic Agents _

_

_

_

_

Possible mechanisms of actions for phytotherapeutic agents

Salpha-reductase inhibition Anti-inflammatory effects Reduction in sex hormone-binding globulin Influences cholesterol metabolism Growth factor inhibition Improvement in detrusor function Anti-androgen effects Anti-estrogenic effects Arornatase inhibition

and reduce the volume of the prostate in men with benign prostatic hyperplasia and enlarged glands (43-46). In a more recent study by NIcConnell et al. Proscar was noted to reduce symptoms and prostate volume, increase the urinary flow rate, and reduce the probability of surgery for acute retention (47). The usual dose is 5 mg once daily. Another group of medications, known as phytotherapeutic agents because they are extracted from plants, is currently being investigated as a treatment for BPH. Theseextracts include: Saw palmetto, pygeurn africanum, beta-sitosterol, pollen extract, pumpkin seeds, and south african star grass. The exact mechanism of action is also uncertain. The proposed mechanisms are shown in Table l . There have been several studies performed looking at phytotherapy but at this point have not shown convincing evidencethat it is effective in relieving the symptoms of BPH (48,491. The studies thus far have been uncontrolled or of limited follow-up. Phytotherapy doesnot result in any serious side effects and does not seem to influence PSA values. Nevertheless, the exact role for this therapy has yet to be determined.

FAILURE TO STORE Medications to Decreuse Bhdder Contrdctility Acetycholine induces the postganglionic parasympathetic muscarinic receptor sites of the bladder smooth muscle. Therefore, anticholinergic agents have been used to depress bladder contractions. There are five genes that code for muscarinic receptors, represented by ml-m5 (SO).

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M1-M4 represent the protein products of these genes (51,52). M2 receptors are the most prevalent type of receptor in the bladder, whereas M3 receptors are believed to be most responsible for the contractile response (53,54). Propantheline bromide (Pro-Banthine) is an antimuscarinic drug that is used at an oral dose of 15-30 mg every 4-6 h. It is best absorbed if taken before meals. Atropine is also an agent that canbeused to decrease bladder contractility at a dose of 0.5 mg. Scopolamine is another belladonna alkaloid that is used in a “patch” form that delivers 0.5 mg daily. The results of this therapy have been mixed and its efficacy is uncertain (55-57). Furthermore, skin irritation has been a problem with the patch, Hyoscyamine (Cystospaz) and hyoscyamine sulfate (Levsin) are other belladonna alkaloids that can be used. All antimuscarinic agents can producethe following side effects: inhibition of salivary secretion, blockade of ciliary muscle of the lens to cholinergic stimulation (blurred vision for near objects), tachycardia, drowsiness, and inhibition of intestinal motility. These agents are contraindicated in narrow-angle glaucoma and should be used with great caution in those with bladder outlet obstruction. The side effects of the aforenoted medications tend to limit their use. Tolterodine is a new antimuscarinic agent that has been shown to be selective for bladder tissue over salivary tissue in both in vitro and in vivo cat studies (58,59). In fact, tolterodine has an eight times lower affinity for the parotid glandthan oxybutynin (60). These tissue selective effects seem to be as a result of differential affinities of tolterodine for the receptors of the bladder vs the salivary glands. The clinical studies thus farhaveshown a decrease in the number of micturitions, a decrease in the number of episodes of incontinence, and an increase in the voided volume (61-63). The usual dose is 2 mg bid. Musculotropic agents have been separated from pure anticholinergics because these agents have anesthetic properties in addition to their anticholinergic properties. Oxybutynin chloride (Ditropan) is the most commonly prescribed medication of this type. The recommended dose is 5 mg three to four times daily. The side effects appear to be doserelated. The summaryresults of six randomized controlled studies show a cure rate of 28-44% and a reduction in urge incontinence of 9-56%, with side effects occurring in 2-66% (64). Intravesical Ditropan has also been investigated andshown to be effective with less side effects (65-67).

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In addition, dicyclomine hydrochloride (Bentyl) has been shown to be effective for detrusor hyperreflexia (68,69).The usual dose is 10-20 mg three times a day. Flavoxate hydrochloride (Urispas) has been shown to have a direct inhibitory effect on smooth muscle but very minimal anticholinergic properties (70,71). It has been used successfully in treating detrusor hyperactivity (72,73),however, there are no studies from North America indicating any efficacy with this agent. The dosage is 100-200 mg three to four times daily. The intracellular release of calcium is paramount to the contractile response seen in all muscle, and bladder smooth muscleis no exception. Nifedipine, a calcium channelblocker, has been shownto inhibit bladder contractions (70,74).Palpitations, weakness, rash, nausea, constipation, dizziness, headache, facial flushing, hypotension, and abdominal discomfort are all potential side effects that may occur with calcium channel blockers. Potassium channel openers are a potentially useful therapy for detrusor overactivity. These medications relax smooth muscleby increasing potassium efflux which results in membrane hyperpolarization (70). However, there have been several clinical trials that have failed to demonstrate an improvement in detrusor hyperreflexia (75-77). Prostaglandin inhibitors have been usedto facilitate bladder storage. The proposed mechanism of action may be related to the modulation of the inflammatory response to local irritation or to a modification of the afferent sensory inervation (70,78). Unfortunately, clinical studies have failed to demonstrate a significant benefit (79,80).The side effects commonly seen are rash, constipation, nausea, vomiting, headaches, and indigestion. The bladder also contains beta adrenergic receptors, and thus their stimulation has been attempted to increase bladder relaxation. A beta agonist, terbutaline, has been notedto have somebenefit in the overactive bladder (81-83). These findings were not universal (W), and the exact role of beta agonists has yet to be determined. Tricyclic antidepressants (TCA), suchas imipramine hydrochloride, decrease bladder contractility and increase outlet resistance. These agents have essentially three major pharmacologicalactions: they block the reuptake of amine neurotransmitters (i.e., norepinephrine and serotonin), they act centrally as sedatives and possibly via antihistaminic properties, and they have both central and peripheral anticholinergic effects (85-88).

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Interestingly, the main anticholinergic effect of imipramine is systemic withonly a weak antimuscarinic effect (89,90),but it also causes a direct nonadrenergic and nonanticholinergic inhibitory effect (90-92). It has been noted that imipramine has an additive effect when used with antimuscarinic agents (93). The usual dose of imipramine is 25 mg four times a day with a reduced dose given to elderly patients. The dosage used to treat depression is much higher. This medication can also be used to treat nocturnal enuresis in children at a dose of 10-50 mg daily. The side effects are the same asthose seen with other systemic anticholinergics. One can see hypotension and CNS side effects such as weakness, Parkinsonian effects, fatigue, and tremors. Most importantly, TCAs can produce arrhythmias and should be used with caution in those with cardiac disease (86). There have also been several reports in children of severe side effects, such as vomiting, headaches, lethargy, abdominal distress, and irritability, following abrupt cessation, and therefore it should be discontinued gradually. Furthermore, its use is contraindicated in those taking monoamine oxidase inhibitors because serious CNS toxicity can be induced. Another potential mediator of smooth muscle relaxation is nitric oxide (NO) (94,95).NO is believed to be a nonadrenergic noncholinergic neurotransmitter but its exact role in treating bladder hyperactivity is still under investigation. Capsaicin is a new compound that is obtained from hot peppers and is highly selective for the sensory neurons in mammals (96,97). Thus, repeated administration of capsaicin, either systemically or topically, induces desensitization and inactivation of the sensory nerves by cresting reversible antinociceptive and anti-inflammatory action. The action of topical or local capsaicin is owing to the blockade of the C-fiber conduction and inactivation of the neuropeptides released from the peripheral nerve endings. By using systemic capsaicin, antinociception is produced by activating specific receptors on the afferent nerve terminals in the spinal cord, which results in blockade of spinal neurotransmission by the prolonged inactivation of sensory neurotransmitter release. Topical use prevents systemic side effects and acts primarily on the small diameter nociceptor receptors, which, in turn, prevents loss of sensation to touch andpressure as well as loss of motor function, which are owing to larger diameter nociceptor receptors. There have been several studies supporting the potential use of capsaicin for the hyperactive bladder (98-102). However, it is not commercially available. Local drug instillation has been associated with gross hematuria,

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severe pains upon instillation, and precipitation of autonomic dysreflexia in some.

Medications to Increme Outlet Resistance Alpha adrenergic agonists have been usedto increase bladder outlet resistance. Their use is based on studies that show an abundance of alpha-adrenergic receptors at the bladder neck and proximal urethra (103,104).Ephedrine is a treatment used for stress urinary incontinence (SUI).It enhances the release of norepinephrine from sympathetic neurons andstimulates directly the alpha and beta-adrenergic receptors (105). The usual dose is 25-50 mg QID and tachyphylaxis has been reported. Pseudophedrine, a steriosomer of ephedrine, can also be used at a dose of 30-60 mg QID.The use of these drugs for severe SUI is limited and may only beofbenefit for minimal wetting (106,107). Phenylpropanoamine (PPA)has the same pharmacologic properties as ephedrine and has been used for SUI at a dosage of 50 mg BID. The side effects of these medications include anxiety, headaches, tremor, weakness, palpitations, cardiac arrhythmias, hypertension, and respiratory difficulties. Thus, these medications should be used with caution in all patients with cardiac disease, hypertension, increased age, and/ or hyperthyroidism. Estrogen therapy for SUI has, as with other pharmacologic agents, been noted to have mixed results (108-118). It is hypothesized that estrogens may work by changing the autonomic innervation, the receptor content, the function of the smooth muscle, the estrogen binding sites, the supporting tissues, or the mucosal seal mechanism (119-123). There have beenothers that endorsed the use of estrogens in combination with alpha agonists ( I 11,112,116,124,125).Estrogens, however, can increase the risk of endometria1 cancer if they,are used unopposed in those with an intact uterus. Progestins exert a protective affect in these situations. There is also an association between breast cancer and estrogen replacement in those receiving such therapy for more than 15 years. The beneficial effects of estrogen include osteoporosis prevention and decreased cardiovascular disease. Estrogen therapy can beadministered orally, transdemally, subcutaneously implanted, and topically. Furthermore, the topical approach has been shown to have an added psychologic benefit (126).A new silicone ring impregnated with estradiol is being introduced for vaginal use. This new device offers a

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continuous delivery over a 90-d period and has shown to be very acceptable in certain women (126,127).

Medications f o r InJEammutory Conditions o f the Bladder Cuzlsing Storuge Failure Interstitial cystitis (IC) is a syndrome whosepathogenesis and etiology remain a mystery. Even the diagnosis of this entity is difficult and considered one of exclusion. There are four currently proposed etiologies for this syndrome: inflammation, vascular insufficiency, epithelial leak, and deficiency of proteoglycans (i.e., glycosaminoglycansGAG-). Dimethysulfoxide (DMSO), after being approved for use in 1977, has been shown to induce remission in 35-40% of the patients (128) and is a mainstay of treatment (129). However, no controlled clinical studies have been performed. DMSO is a derivative of lignin, which is a product of the wood-pulp industry. Its therapeutic properties include: anti-inflammatory properties, analgesic properties, collagen dissolution, muscle relaxation, and mast-cell histamine release. The usual dose is a 50% solution instilled for 5-10 min. This therapy can be used as a one time dose, repeated weekly for 6-8 wk, or continued weekly for 4-6 mo. Some even advocate using DMSO indefinitely. If the patient has pain with administration, she should receive 2% viscous lidocaine. A flare of symptoms has also been noted andusually disappears over 24 h and diminishes with subsequent treatments. DMSO is generally well-tolerated; however, reports of cataracts in animals have been noted with long-term use. Thus, it is recommendedthat patients receiving chronic therapy undergo slit-lamp evaluation at 3-6 mo intervals. Intravesical silver nitrate has been tried, but no good controlled studies have supported its implementation (130,131). This therapy should not be used after bladder biopsy because tissue damage may result if the silver nitrate is introduced outside the bladder. Heparin has been shownto have significant activity in approximately 50% of patients (133). It is believed to work by restoring the GAG layer of the urothelium. 10,000 units (U) of heparin is instilled daily for 3-4 mo and then reduced to 3-4 timedwk. If there is no effect after 3 mo, it can be increased to 20,000 U. It may take 2-4 mo to work and should be continued for at least 6 mo. Pentosanpolysulfate (Elmiron) is a sulfated polysaccharide, which is thought to augment the bladder surface defense mechanism or possibly detoxify urine agents that can irritate the bladder surface. In a controlled

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study, Elmiron improved the symptoms of 42% of the patients in the treatment group as compared to 20% in the placebo group(133).These findings were further corroborated in several other studies (134-136). The usual dose is 100 mgtid. Response to this medication is first seen after 6-10 wk, and patients generally do better after 6-12 mo. Other medications, including corticosteroids, have beentried but the data to support their use is sketchy. The assumptionis that if inflammation contributes to IC, steroids may help in the treatment. Thus, some physicians use an intravesical "cocktail," which includes heparin and steroids weekly for 6 wk. Antidepressant therapy have beenused in patients with chronic pain who lose sleep owing to depression. The usual medication is amitriptyline 25 mg at bed time. Fluxetine (Prozak) can be used at a dose of 20 mg and increasing to 40 mg as needed. Zoloft (sertraline) may also be used at a dose of 50-100 mg. Antihistamines have also been usedto inhibit mast-cell release (137140). Some patients benefit from this therapy although no controlled studies have been performed. The beneficial effects are thought to occur approximately 2-3 MO after treatment.

Medications to Treat Nocturnal Enuresis as a Cause o f Failure to Store A synthetic antidiuretic hormone peptide analog known as DDAVP ( l -deaminino-%" arginine vasopressin) is used to treat noctural enuresis in children and adults (141,142). The medication is administered by nasal spray at a dose of 10-40 pg at bedtime. Hyponatremia is a rare complication that must be watched for in all patients, especially the elderly. There is also an oral form available that may be useful in treating this entity.

CONCLUSION There area plethora of pharmacologic treatment options for voiding dysfunction. These medications can affect both the filling and storage phase of micturition. As a general principal, therapy should be started at a low dose and titrated upward as necessary. Thus, this will keep the side effects to a minimum while maximizing the therapeutic effects. Many advances in our understanding of neurophysiology and pharmacology are ongoing. There are many new drugs being developed as

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well as innovative new ways to administer them. It therefore is important that testing of these medications be conducted in properly developed and implemented trials so that the most useful information can be obtained. Effectively developed studies will, in turn, allow the advancement of pharmacologic treatment of voiding dysfunction and provide the best future care to our patients.

1. Lee L (1949) The clinial useof Urocholineindysfunctions of thebladder. J Urol 62:300. 2. Wein AJ (1986) Specific methods of pharmacologic treatment. In: Stanton SL, Tanagho EA, eds., Surgery of Female Incontinence New York, NY: SpringerVerlag, 229-250. 3. Parkash L (1975) Intermittent catheterization and bladder rehabilitation in spinal cord injury patients. J Urol 114:230. 4. Ban-ett DM, Wein AJ (1991) Voiding dysfunction: Diagnosis, classification and management. In: Gillenwater JY, Grayhack ST, Howards ST, Duckett JW, eds. Adult and Pediatric Urology, 2nd ed. St. Louis, MO: Mosby-Year Book, p. 1001. 5. Finkbeiner AK (1985) Is bethanechol chloride clinically effective in promoting bladder emptying? J Urol 134:443. 6. Wein AJ, Malloy T, Shofar FE (1980) The effects of bethanechol chloride on urodynamic parametersin normal women and in women with significantresidual urine volumes. J U r d 124397. 7. Wein AJ, Raezer DO, MalloyT (1980) Failure of the bethanecholsupersensitivity test to predict improved voiding after subcutaneous bethanechol administration. J Urol 123:202. 8. Wyndaele JJ, Van Kerrebroeck R (1995) The effects of 4 weeks treatment with cisapride on cystometric parameters inspinal cord injury patients. A double blind, placebo controlled study. Paraplegia 33:625. 9. WeinAJ,Levin M, Barrett DM(1991)Voiding function: relevantanatomy, physiology, and pharmacology. In: Duckett JW, Howards ST, Grayhack JT, Gillenwater JY, eds., Adult and Pediatric Urology, 2nd ed. St. Louis, MO: MosbyYear Book, p. 933. 10. Jaschevatsky OE, AnderTnanS, Shalit A (1985) Prostaglandin F2afor prevention of urinary retention after vaginal hysterectomy. Obstet Gynecol 66:244. 11. Bultitude M, Hills N, Shuttleworth K (1976) Clinical and experimental studies on the action of Prostaglandins and their synthesis inhibitors on detrusor muscle in vitro and in vivo. Br J Urol 48:631. 12. Despond A,Bultitude M, Hills N, et al. (1980) Clinical experiencewith intravesical prostaglandin E2: a prospective study of 36 patients. Br J Urol 53:357. 13. Vaidyanathan S, Rao M, Mapa M (1981) Study of instillation of 15(S)-15-methyl prostaglandin F2a inpatients with neurogenic bladderdysfunction.J Urol 126381. 14. Tammela TL, Kontturi M, Lukkarinen 0 (1987) Intravesical prostaglandin F2 for promoting bladder emptying after surgery for female stress incontinence. Br J Urol 60:43.

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for enhancing detrusor 15. Koonings P, Bergman A, Ballard CA (1990) Prostaglandins function after surgery for stress incontinence in women. J Reprod Med 35: l . 16. Stanton DL, Cardozo LD, Ken-Wilson R (1974) Treatment of delayed onset of spontaneous voiding after surgery for incontinence. Urology 13:494. 17. Tammela TL (1986) Prevention of prolonged voiding problemsafter unexpected postoperative urinary retention: comparison of phenoxybenzamine andcarbachol. J Urol 136:1254. 18. Goldman G , Levian A, Mazor A (1988) Alpha-adrenergic blockerfor posthernioplasty urinary retention. Arch Surg 123(1):35--36. in female patients. 19. Raz S, Smith RB (1976) External sphincter spasticity syndrome J Urol 115:443. 20. de Groat WC (1993) Anatomy and physiology of the lower urinary tract. Urol Clin N A m 20(3):383. 21. de Groat WC, Booth AM (l 984) Autonomic systems to the urinary bladder and Periph.eraZ Neuropathy. sexual organs. In: Dyck PJ, Thomas PJS, Lambert EH, eds. Philadelphia, PA: WB Saunders, p. 285. 22. Murray KHA, Fencley RC1 (1982) Endorphins: A role in urinary tract function? The effect of opioid blockade on thedetrusor and urethral sphincter mechanisms. Br J Urol 54:638. 23. Galeano C, Jubelin B, Biron L, et al. (1986) Effect of naloxone on detrusorsphincter dyssynergia in chronic spinal cat. NeurouroE Urodyn. 5:203. DJ, et al. (1987) Naloxone efficacy in bladder 24. Wheeler JS,Jr. Robinson CJ, Culkin rehabilitation of spinal cord injury patients. J U r d 137:1202. 25. Hoffman BB, Lefkowitz RJ (1990) Adrenergic receptor antagonists. In: Gilman, AG, RailTW, Nies AS,Taylor P, eds., Goodman and Gilrnan’sThe Phamacological Basis of Therupeutics. 8th ed. New York, NY: Pergamon Press, 221. 26. Physician’s Desk Reference. (1992) Montraler, NJ: Medical Economics Co. 27. Lepor H (1990) Role of long acting selective alpha-I blockers in the treatment of benign prostatic hyperplasia. Urol Clin N Am 17:651. 28. Buzelin JM,Herbert M, BiondinP ( 1993) Alpha-blocking treatment with afuzosin in symptomatic benign prostatic hyperplasia: comparative study with prazosin. The PRAZALF Group. Br J Urol 72(6):922. S, et al. (1995) Localizationof the alpha-IA-adrenore29. Lepor H, Tang R, Kobayashi ceptor in the human prostate. J Urol 154:2096. C, et al. (1997) The effects of tamulosin, 30. Noble AJ, Williams-Chess R, Couldwell a high affinity antagonist at functional aIA- and at D- adrenoreceptor subtypes. Br J Pharrn 120:23l . 31. Cbapple C, Wyndaele JJ, Nordling J, et al. (1996) Tamulosin, the first prostateselective alpha I adrenoreceptor antagonist. A meta-analysis of two randomized placebo-controlled, multicentrestudiesin patients with benign prostatic obstruction (symptomatic BPH). European Tamsulosin Study Group. Euro UroE 29(2):155. 32. Wilde M, McTavish D (1996) Tamsulosin. A review of its pharmacological properties and therapeutic potential in the management of symptomatic benign prostatic hyperplasia. Drugs 52(6):883. 33. Raz S, Caine M (1971) Adrenergic receptors in thefemale canine urethra. h e s t Urol 9:319. 34. Vaidyanathan S, RaoM,Bapna B (1980) Beta adrenergicactivityinhuman proximal urethra. J Urol 124:869. 35. Anderson IQ3 (1993) Pharmacology of lower urinary tract smooth muscles and penile erectile tissues. Pharmacol Rei1 45:253.

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36. Shader RI, Greenblatt DJ (1993) Use of benzodiazepines in anxiety disorders. N Engl J Med 328:1398. 37. Milanov IG (1991) Mechanisms of baclofen action on spasticity. Acta Neutral Scand 85:304. 38. Kurns JJM, DelhaasEM(1991) Intrathecal baclofen infusion in patients with spasticity and neurogenic bladder disease. World J Urol 9:99. R. Effect of intrathecalbaclofen on bladder and sphincter 39. Nannings J, Frost F, Penn function. J Urol 142:101. 40. Loubser PG, Narayan RK, Sadin KJ (1991) Continuous infusion of intrathecal baclofen: Long term effects on spasticity in spinal cord. Paraplegia 29:48. 41. Murdock M,Sax D, KraneR (1976) Use ofdantrolene sodium in external sphincter spasm. Urology 8: 133. 42. Ward AK, Chaffman MO, Sorkin EM (1986) A review of its p~~macodynamic and pharacokinetic properties and therapeutic use in malignant hyperthermia, the neurologic syndrome and an update of its use in musclespasticity. Drugs 32: 130. 43. Gomley GJ, Stoner E, Bruskewitz RC, et al. (1992) The effect of finasteride in men with benign prostatic hyperplasia. NEJM 327: l 3 85-91. 44. McConnell JD, Wilson JD, George F W , Geller J, Pappas F, Stoner E (1992) Finasteride, an inhibitor of Sa-reductase, suppresses prostatic dihydrotestosterone in men with benign prostatic hyperplasia. J Clin Endocrinol Metab 74:505-8. 45. Boyle P, Could AL, Roehrborn CG (1996) Prostate volume predicts outcome of treatment of benign prostatic hyperplasia with finasteride: meta-analysis of randomized clinical trials. Urology 48:398-405. 46. Andersen JT, NickelJC, Marshall VR, Schulman CC, BoyleP (1997) Finasteride significantly reduces acute urinary retention and need for surgery in patients with symptomatic benign prostatic hyperplasia. Urology 49:839-45. 47. McConnell JD, Bruskewitz R, Walsch P, et al. (1998) The effect of finasteride on the risk of acute urinary retention and the need for surgical treatment among men with benign prostatic hypertrophy. NEJM 338557-563. of benign prostatic hyperplasia: 48. Lowe FC,Ku JC (1996) Phytotherapy in treatment a critical review. Urology 48( 1):12-20. 49. Carraro JC,RaynaudJP,KochG, et al. (1996)Comparison of phytotherapy (Permixon) with finasteride in the treatment of benign prostate hyperplasia: a randomized international study of 1,098 patients. Prostate 29(4):231-40. SO. Bonner TI (1989) The molecular basis of muscarinic receptor diversity. Trends Neurosci 12:148. 51. Poli E, Monica B, Zappia L (1992) Antimuscarinic activity of telemyepine on isolated human urinary bladder: role no for M-l receptors. Gen PharmacoZ23:659. 52. Eglen RM, Watson N (1996) Selective muscarinic receptor agonists and antagonists. Plzarmacol Toxicol 78:59, 53. Nilvebrant L, Anderson ICE, GilibergPG,et al. (1997)Tolterodine-anew bladder-selective antimuscarinic agent. Eur J Pharm 327: 195. 54. Tobin G, Sjogren C (1995) In vivo and in vitro effects of muscarinic receptor antagonists on contractions and releaseof E3H] acetylcholine release in the rabbit urinary bladder. Eur J Pharm 28: 1. 55. WeinerLB,BaumNH, Suarez GM(1986)Newmethod for management of detrusor instability: transdermal scopolamine. Urology 28:208. 56. Cornelia JL, Bent AE, Ostergard DR, et al. (1990) Prospective study utilizing transdermal scopolamine in detrusor instability. Urology 35:96.

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77. Komersova K, Rogerson IW, Conway EL,et al. (1995) The effect of Levcromokalim (BRL 38227)on bladder function in patients with high spinal cord lesions. Br J Clin Pharm 39:207. 78. Downie JW, KarmazynM (1984) Mechanical trauma to bladder epithelium liberates prostanoids which modulate neurotransmission in rabbit detrusor muscle. J Pharmacol Exp Ther 230:445. 79. Cardozo LD, Stanton SL, Robinson H, et al.(1980) Evaluation of Aurbiprofen in detrusor instability. Br Med J 2:281. 80. Cardozo L, StantonSL (1979) An object comparisonof the effects of parenterally administered drugs in patients suffering from detrusor instability. J Urol 122:58. 81. Norien L, Sundin T, Waagstein F (1978) Beta-adrenoceptor stimulation of the human urinary bladder in vivo. Acta Pharmacol Toxicol 43:5. 82. Lindholm P, Lose G (1986) Terbutaline (Bricanyl) in the treatment of female urge incontinence. Urol Lnt 41:158. 83. Gruneberger A (1984) Treatment of motor urge incontinence with clenbuterol and flavoxate hydrochloride. Br J Obstet Gynecol 91:275. 84. Castieden CM, Morgan B (1980) The effect of beta adrenoceptor agonists on urinary incontinence in the elderly. Br J Clin Pharmacol l0:619. 85. Barrett DM, Wein AJ (1991) Voiding dysfunction: diagnosis, classification and management. In: Gillenwater, JY, Grayhack JT, Howards ST, Duckett W, eds., Adult and Pediatric Urology, 2nd ed. St. Louis, MO: Mosby-Year Book, p.1001. of psychiatric disorders.In: Gilman, 86. Baldesarini RJ (1990) Drugs and the treatment AG, Rail TW, Nies AS, Taylor P, eds., Goodman and Gilman 'S The Pharmacological Basis of Therapeutics, 8th ed. New York, NY: Pergamon Press, p. 383. 87. Hollister LE (1986) Current antidepressants.Ann Rev Pharmacol Toxicol 26:23. 88. Richelson E (1990) Antidepressants and brain neurochemistry. Mayo Clin Proc 65: 1227. 89. Levin RM,Staskin D, Wein AJ (1983)Analysis of the anticholinergic and musculotropic effects of desmethylirnipramine on the rabbit urinary bladder. Urol Res 11:259. 90. Levin RM, Wein AJ (1984) Comparative effects of five tricyclic compounds on the rabbit urinary bladder. Neurourol Urodyn 3:127. 91. Benson GS, Sarshik SA, Raczer DM, et al. (1977) Bladder muscle contractility: Comparative effects and mechanisms of action of atropine, propantheline, flavoxate and irniprarmine. Urology 9:31. 92. Olubadewo J (1980) The effect of imipramine on ratdetrusor muscle contractility. Arch Int Pharmacodyn Ther 145:84. 93. Raezer DM, Benson GS, Wein AJ (1977) The functional approach to the management of the pediatric neuropathic bladder: a clinical study. J Urol l I7:649. 94. James MJ, Birmingham AT, Hill SJ (1993) Partial medication by nitric oxide of the relaxation ofhuman isolated detrusor strips in responseto electrical field stimulation. Br J Clin Pharmarcol 35:366. 95* Andersson W3 (1993) Pharmacology of lower urinary tract smooth muscles and penile erectile tissues. Pharmacol Rev 45:253. 96. Maggi CA (1992) Therapeutic potential of capsaicin-like molecules-Studies in animals and humans. Life Sci 5 l :1777. 97. Dray A (1993)Mechanism of action of capsaicin-like molecules on sensory neurons. Life Sci 5l : 1759. 98. Maggi CA (1991) Capsaicin and primary afferent neurons: from basic science to human therapy? J Auton New Syst 33:1-14.

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99. Maggi CA, Barbanti G, Santicioli P, et al. (1989) Cystornetric evidence that capsaicin-sensitivenerves modulate the afferent branch of micturition reflex in humans. J Urol 142:150. S, et al. (1996) Intravesical capsaicin for treatment 100. Fowler CJ, Beck RO, Gerrard of detrusor hyperreflexia. J Spinal Cord Med 19:190. 101. Das A, Chancellor M, WatdnabeT, et al. (1996) Intravesical capsaicin in neurologic impaired patients with detrusor hyperreflexia. J Spinal Cord Med 19:190. 102. Chandiramani VA, Peterson T, Duthie CS, et al. (1996) Urodynamic changes during therapeutic intravesical instillations of capsaicin. Br J U r d 77(6):792. 103. Nilvebrant L, Sundquist S, Giliberg PG (1996) Tolterodine is not subtype (mlm5) selective but exhibits functional bladder selectivity in vivo. Neurol Urodyn 15:310. 104. Wein AJ, Van ArsdalenW, Levin RM (1991) Pharmacologic therapy. In: Krane RJ, Siroky MB, eds. Clinical-Neuro-Urology Boston: Little Brown, p. 523. agonists. In: Gilman l 05. Hoffman BB, Lefkowtiz RJ (1990) Andrenergic receptor AG, Rail TW, Nies AS, Taylor P, eds., Goodman and Gilman’s The Pharmacological Basis oj’l’herapeutics, 8th ed., New York, NY: Pergamon Press, p. 221. 106. Diokno A, Taub M (1975) Ephedrine intreatment of urinaryincontinence. Urology 5:624. 107. O’brink A, Bunne G (1978) The effect of alpha adrenergic stimulationi n stress incontinence. U r d Intl 12:205. 108. Salmon UJ, Walter RI, Geist SH (1941) The use of estrogens in the treatment of dysuria and incontinence in postmenopausal women. Am J Obstet Gynecol 42:845. 109. Rud T (1980) The effects of estrogens and gestagens on the urethral pressure profile of urinary continent and stress incontinent women.Acta Obstet Gynecol Scand 59:265. 110. Raz S, ZieglerM,Caine M (1973)The role of female hormonesinstress incontinence. Proc 16th Congr Society International d’urologic, vol. I, Paris, p. 397. 111. Schreiter F, Fuchs P, Stockamp K (1976) Estrogenic sensitivity of a-receptors in the urethra musculature. Urol Intl 3 1:13. 112. Beisland HO, FossbergE, Moer A, et al. (1984) Urethralsphinctericinsufficiency in postmenopausal females: treatmentwithphenylpropanolamineandestriol separately and in combination. Urol Intl 39:211. 113. Bhatia NN, Bergman A, Karrain MM (1989) Effects of estrogen on urethral function in women with urinary incontinence. Am J Obstet Gynecol 160:176. 114. Karram MM, YekoTR, Sauer MV, et al. (1989) Urodynamic changes following hormonal replacement therapy in women with premature ovarian failure. Obstet Gyneco174:208. 115. Walker S, Wolf H, Barleto H, et al. (I 978) Urinary incontinence in post menopausal women treated with estrogens. Urol Intl 33:135. 116. Hilton P, Stanton SL (1983) The use of intravaginal estrogen cream in genuine stress incontinence. Br J Obstet Gyneco190:940. 117. Samsioe G, Jansson L, Mellstrom D, et al. (1985) Occurrence, nature and treatmentof urinary incontinence in a 70-year-old fernale population. Mut~ritas. 7:335.

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119. Bump RC, Friedman CL (1986) Intraluminal urethral pressure measurements in the female baboon: Effects of hormonal manipulation. J Urol 136:508. 120. Batra SC, Losif CS (1983) Female urethra: a target for estrogen action. J Urol 129:418. 121. Batra S, Byellin L, Sjogren C (l 986) Increases in blood flow of thefemale rabbit urethra following low dose estrogens. J Urol 136:1360. 122. Rud T (1980) Urethral pressure profile in continent women from childhood to old age. Acta Obstet Gynecol Scand 59:331. 123. Versi E, Cardozo L, Buncat L, et al. (1 988) Correlation of urethral physiology and skin collagen in post menopausal women. Br J Urol Gynecol95:147. 124. Kinn AC, Lindskog M (1988) Estrogens and phenylpropanolamine in combination for stress urinary incontinencein postmenopausal women. Urology 32:273. 125. Walter S, Kjaergaard B, Lose G, et al. (1990) Stress urinary incontinence in postmenopausal women treated withoral estrogen (estriol) and an alpha-adrenoceptor stimulating agent (phenylpropanolamine):a randomized double-blind placebo-controlled study. Intl Urogynecol J 1:74. 126. Ayton RA, Darling GM,MurkiesAL,et al. (1996) A comparative study of safety and efficacyof continuous low dose estradiol released froma vaginal ring compared with conjugated equine estrogen vaginal cream in the treatment of postmenopausal urogenital atrophy. Br J Obstet Gynecol 103:351. 127. Johnston A (1996) Estrogens: pharmacokinetics and pharmacodynamics with special reference to vaginal administration and the new estradiol formulationEstring. Acta Obstet Gynecol Scan 165:16. 128. Parsons CL and Parsons KJ (1996) Interstitial cystitits. In: Raz S, eds., Female Urology Philadelphia, PA: WB Saunders, pp. 167-182. 129. Sant GR (1987) Intravesical 50% dimethyl sulfoxide (RIMSO-50) in treatment of interstitial cystitis. Urology 29:17-26. 130. Dodson AI (1926) Hunner’s ulcer of the bladder: a report of 10 cases. Virginia Med Monthly 53:305. 131. Pool TL (1967) Interstitial cystitis: clinical considerations and treatment. CEin Obstet Gynecol 10:185. 132. Parsons CL, Housley T, Schmidt JD, Lebow D (1994) Treatment of interstitial cystitis with intravesical heparin. Br J Urol 73504-7. 133. Parsons CL, MulhollandSG (1987) Successfultherapy of interstitial cystitis with pentosanpolysulfate. J Urol 138513-516. 134. Mulholland SG, Hanno P, Parsons CL, Sant GR, Staskin DR (1990) Pentosan polysulfate sodium for therapy of interstitia1 cystitis: a double-blind placebocontrolled clinical study. Urology 35(6):552-58. 135. Parsons CL, BensonG,Childs SJ, Hanno P, Sant GR, Webster G (1993) A quantitatively controlled method to prospectively study interstitial cystitis and which demonstrates the efficacy of pentosan polysulfate. J Urol 150:845-48. 136. Hanno PM (1997) Analysis of long-term Elmiron therapyfor interstitial Cystitis. Urology 49(5A S~ppl):93-99. 137. Larsen S, et al. (1982) Mast cells in interstitial cystitis. Br J Urol 54:283. 138. Smith B, Dehner LP (1972) Chronic ulcerating interstitial cystitis. A study of 28 cases. Arch Pathol 93:76. 139. Bohne AW, Hodson JNI, Rebuck JW, Reinhard RE (1962) An abnormal leukocyte response in interstitial cystitis. J U r d 88:387.

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140. S i m o n s JL (1961) Interstitial cystitis: an explanation for the beneficial effect of an antihistamine. J UroE 85:149. 14 l. Norgaard JP, Rillig S, Djurhuus JC (1989) Nocturnal enuresis: an approach to treatment based on pathogenesis. J Pediatr 114:705. 142. Rew DA, FundleJSH (1989) Assessmentof the safetyof regular DDAVP therapy on primary nocturnal enuresis. Br J UroE 63:352.

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Treatment of Detrusor Instability pvith Electrical Stimulation Steven K Siegel MD CONTENTS NORMAL URINE STORAGE AND EVACUATION DISRUPTED MICTURITION BALANCE MECHANISM OF ACTION OF ELECTRICAL STIMULATION ELECTRICAL STIMULATION AS A TREATMENT MODALITY CONCLUSIONS REFERENCES

There are an estimated 13 million Americans who suffer from incontinence. Urge incontinence is conservatively estimated to account for 40% of all urinary incontinence patients ( I ) . Of this population, twothirds suffer from chronic or established incontinence. Yet patients diagnosed with urinary incontinence owing to detrusor instability have had limited treatment options. Nonsurgical interventions, including diet modification, behavioral techniques (pelvic muscle exercises, biofeedback, timed voiding), drug therapies, and containmentdevices are commonly used to treat the condition. If these therapies are unsuccessful or unsatisfactory to the patient, surgical interventions such as bladder denervation procedures, augmentation cystoplasty, or urinary diversion may be considered. These alternatives have their own set of risks and consequences, making them unattractive to the majority of patients. According to the 1996 National Association for Continence (NAFC) survey of 2,000 incontinent persons in the US, although more treatments

From: Current Clinical Urology: Voiding Dysfunction: Diagnosis and Treatment Edited by: R. A. Appell 0 Hurnana Press Inc., Totowa, NJ

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are available to urge incontinent patients, 63% of these patients reported they were "not satisfied" with their treatment outcomes. The lack of effective treatments for urge incontinence is particularly disturbing given the debilitating nature of this condition. Incontinent patients commonly experience loss of self-esteem, shame, depressive symptoms, embarrassment, anger, and a significant loss of quality of life ( I ) . Urge incontinence is especially difficult given the severity and unpredictable nature of leaking episodes. Consequently, patients restrict or avoid social interactions, and have difficulties meeting daily responsibilities. Over the past 30 years, advances have been made in the treatment of urinary incontinence via electrical stimulation of neural pathways that control bladder function. New therapies have emerged offering treatment that is reversible and does not preclude other complimentary alternatives for management. Theyinclude use of transvaginal/transanal Stimulation, needle stimulation, and sacral nerve stimulation (SNS) devices. Electrical stimulation therapies involving these devices may differ in their mechanism of action, patient compliance andacceptability, efficacy, and suitability for a given underlying condition. The various forms of electrical stimulation have been used for symptoms of stress, urge and mixedincontinence, urgency-frequency syndromes, urinary retention, and painful bladder disorders. Regardless of clinical diagnosis, the goal of therapy is to alter lower urinary tract function by stimulation of pudendal or sacral nerves and modulatepelvic visceral and striated muscle behavior.

NORMAL URINE STORAGE AND EVACUATION Normal micturition relies on urine storage and release as reciprocal functions in which there is precise coordination between the detrusor, striated muscles of the pelvic floor (levator anihphincter), and the external urinary sphincter. Storage of urine during bladder filling requires the bladder to be compliantin order to distend without increased pressure, and stable, so that the detrusor does not contract causing sudden increased pressure and possible incontinence. Coordination of these muscles systems is controlled by nervous system components located in the brain, spinal cord, bladder, and urethra via reflex mechanisms. Tension (afferent) receptors in the bladder wall respond to distention, transmitting signals through the A-delta fibers when transvesical pressure approaches 5-10 cm H20 (2,3). As the bladder fills, the detrusor remains relaxed and the pelvic floor tightens (guarding

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reflex). With continued filling, the afferent signals to the sacral cord and brain stem become stronger, and the guarding reflex increases accordingly. Upon initiation of voluntary voiding, the pelvic floor relaxes and the detrusor contracts (4).A positive feedback loop between bladder afferent and pelvic efferent neurons allows for efficient bladder emptying with minimal residual. This action is facilitated by supraspinal input through the pontine micturition center.

DISRUPTED MICTURITION BALANCE Conscious control allows voiding to occur at convenient times. Inhibitory reflexes (autonomic and somatic) coordinated by the pons are needed to keepthe sacral micturition reflex in balance. If these reflexes are overly inhibited, the balance is tipped towards urgency and urge incontinence. If they are overly facilitated, the balance is shifted towards urinary retention. Viewed in this way, detrusor instability and urge incontinence simply represent the flip side of urinary retention. Both syndromes represent a central nervous system (CNS) dysfunction, which secondarily affects pelvic visceral function. It also follows that symptoms of bowel dysfunction (irritable bowel or chronic constipation) are likely to beowing to the same imbalance of reflexes. It becomes clear that any therapy directed at the end organ (i.e., anticholinergics, denervation procedures, augmentation) or any therapy that does not positively affect both bladder and bowel function (i.e., anticholinergics) is unlikely to be completely successful.

MECHANISM OF ACTION OF ELECTRICAL STIMULATION The way in which electrical stimulation improves voiding dysfunction is unknown, but most experts agree that the therapies work by producing a modulatory effect on sacral nerve reflexes (5-40).Stimulation restores a balance between sacral reflexes that are either overly inhibited or facilitated. Depending on where the stimulation is delivered, the mechanism and potential benefit may be different. For example, transvaginal or transanal devices first stimulate skin receptors and myelinated A-delta fibers, causing the striated muscles of the pelvic floor to contract, and secondarily turning off inappropriate detrusor contractions by augmenting the guarding reflex. These actions may

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be duplicated by conscious efforts and practiced behaviors (Kegel exercises), but they must be incorporated into everyday behavior in order to have long term success. If effective over the long term, there is an implication that the abnormal reflex activity can be modified by consistent corrective behavior, or that the dysfunctions in the nervous system can be altered permanently. Sacral nerve stimulation may work in a similar fashion, but also affects the nervous system throughdirect stimulation of unmyelinated C-fiber sacral nerve afferents, which have a much higher threshold of stimulation than the myelinated A-delta fibers. It is certain that these nerves playan important role in abnormal bladder activity and in syndromes with pelvic pain (10).Because SNS devices are implanted, they can continue to modulate abnormal reflex activity even if the patient is incapable of conscious behavioral change, or if the changes in the CNS are otherwise permanent.

ELECTRICAL STIMULATION AS A TREATMENT MODALITY Devices for electrical stimulation therapy are the result of observations that spontaneous or artificially evoked bladder hyperactivity can be inhibited by electrical stimulation of the pelvic floor and sacral nerves (5-7). Animal experiments and electrophysiologic studies in humans have confirmedthat spinal inhibitory systems capable of interrupting a detrusor contraction can be activated by electrical stimulation (11,12). The afferent anorectal branches of the pelvic nerve, afferent nonmuscular somatic (sensory) fibers in the pudendal nerve, and muscle afferents from the limbs have all been foundsensitive to low-frequency stimulation (6,8,13-19). Various devices are currently on the market utilizing these nerve paths. There are two maintypes of electrical stimulation in use, long-term, or chronic, and acute maximal functional electrical stimulation. Chronic stimulation is delivered below the sensory threshold usually for more than 6 h a dayover a number of months, or-with the newer implantable devices-for years. Maximal functional Stimulation is used for short periods of time (15-30 min) at varying intervals from daily to weekly, for lengths of time ranging for 10-20 wk. In both types of stimulation electrical current is pulsed at frequencies based on clinical diagnosis. In detrusor instability, the goal of therapy is to increase inhibitory impulses to the bladder using afferent nerve pathways (see Fig. 1).

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Fig. 1. Position points and nerve pathways for electrical stimulation devices.

Electrical stimulation also has an effect on the striated pelvic muscles responsible for inhibition of bladder contraction. Control of voiding mediated by electrical stimulation does not appear to be the result of a placebo effect, though this has notreceived extensive study. The nature of the treatment intervention generally precludes double-blind studies. There is evidence to suggest, however, that a significant placebo effect is not present. A study of vaginal stimulation included a period of active electrical stimulation followed by a period of mechanical stimulation of a vaginal electrode without connection to a pulse generator. There was noeffect on incontinence in the absence of electrical stimulation (2). Clinical trials of the InterStimB device have also included a therapy evaluation period when electrical stimulation was turned off. Regardless of the clinical incontinence diagnosis, incontinence levels returned to the baseline values measured prior to

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Fig. 2. Electrode placement at the S3 nerve root. The sacral foramina are probed with an insulated needle using bony landmarks as a guide. There is little risk of direct nerve impingement with correct orientation of the needle.

implantation of electrodes. The results suggest that a placebo effect is not apparent; electrical stimulation is necessary for inducing incontinence control in treated patients (20).

Trunsvuginul and Trunsunal Electrical Stimuhtion Devices Noninvasive electrical stimulation of the pelvic floor using an externally applied electrical source offers potential for retraining the basic physiologic responses of intact muscle tissue for patients with stress, urge, or mixed incontinence. Electrical stimulation induces a Kegeltype movement of the pelvic floor muscles andtherefore may be useful

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in patients who are unable to coi-rectly perform these exercises using verbal, written, or other visual cues. Devices of this type have been used transvaginally in females and transanally in males. The therapy involves vaginal or rectal probes connected to an external power source (see Table 1). Stiinulation causes the pelvic-floor muscles to contact involuntarily. The frequency of stimulation is modified depending on the type of incontinence. A frequency of 50Hz may be used in treatment of stress incontinence; lower frequencies, below 25Hz, are used for the treatment of urge incontinence (21). Typical treatment regimens involve use of the devices for 15-30 min twice per day, every other day. This regimen allows the muscles to recover from the refractory period induced by maximal functional stimulation. Studies have demonstrated improved continence in 54-7796 of patients at follow-up periods from 6 wk to 2 yr (22-26), although there has been some conflicting evidence (27-29). Differences in stimulation protocols make direct comparisons of the literature difficult (30).When pelvic-floor stimulation is combined with other therapies or pelvic floor muscle exercises are continued after treatment, curehmprovements rates have increased (31).This form of treatment is desirable because it may be effective for urge, stress, and mixed incontinence. Another obvious advantage of this type of therapy is its ease of use and relatively low cost. Patients can be taught easily, the cost is considerably less than a yearly prescription of tolterodine, and the therapy is completely reversible. Very few side effects were noted in clinical trials (22.25). Compliance with stimulation regimens is an important issue. A study of daily or every-other-day stiinulation for a treatment period of 20 wk found that either regimen was effective in treating stress, urge, and mixed incontinence (22,25). Compliance was found to be significantly higher for the every-other-day protocol (up to 93% during the 20-wk evaluation period). The studies also demonstrated that a period of up to 12 wk was needed to determine if a patient would benefit from the stimulation. Compliance over longer periods of use has not been assessed. To maintain improvement, long-term attention must be paid to pelvic floor behavior, making the issue of compliance critical to the ultimate success of this therapy (22).

Needle Stimulation Devices Needle stimulation for the treatment of urinaiy incontinence is an adaptation of transcutaneous electrical nerve stimulation (TENS). A stainless steel needle is inserted approx 5 cni cephalad from the medial

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malleolus just posterior to the margin of the tibia and then advanced to the medial edgeof the fibula. Maximal functional electrical stimulation is applied using the posterior tibial nerve to inhibit the sacral micturition center. Stimulation via this route has been proposed as the optimal choice for patients with neurological lesions, in whom complete pelvic floor rehabilitation is not a clinical goal (32).Results from one study of 90 patients using needle electrical stimulation has been reported (33). Patients with various voiding disturbances were treated once weekly for 20-30 min per session for 10 consecutive wk. Successful outcomes (at least 50% improvement in symptoms documented by voiding diaries) were reported for 81% of treated patients. The length of the trial period to assess efficacy of treatment is not known at this time. As with transvaginalltransanal stimulation, compliance is an issue of critical concern. In the case of the reported form of needle stimulation, patients must receive treatment during an outpatient office visit one to two times per week. To be desirable, it must be shown that a sustained benefit can beobtained without ongoing office-based treatment.

Sacral Nerve Stimulation Sacral nerve stimulation (SNS) therapy acts on the neural reflexes of the bladder at the level of the S3sacral nerves. The therapy is based on conclusions from animal experimentation and electrophysiologic studies that electrical stimulation of sacral nerves can modulate neural reflexes that influence bladder, sphincter, and pelvic-floor behavior (8,14,15,18,34)(see Fig. 2). The effects of SNS depend on the electrical stimulation of afferent axons in the spinal roots, which in turn modulate voiding and continence reflex pathways in the CNS (10). Electrical stimulation of the S3nerve ramus is optimal because itcontains the sensory fibers from the genitals and perineum, afferent and efferent fibers from the anterior part of the levator ani and urethral sphincter, and autonomicfibers from the detrusor (15,35).Neuromodulation at this level involves unmyelinated fibers so that very low frequencies, around 10-25Hz, can be utilized. An SNS device consists of a lead implanted adjacent to a targeted sacral nerve, a pulse generator ( P G ) implanted in the lower abdomen or upper buttocks, and an extension that connects the lead to the IPG. Electrical pulses from the IPG are transmitted through the extension

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and lead to the targeted sacral nerve via electrodes located at the distal end of the lead.

TESTSTIMULATION The first stage in the implantation of the device is test stimulation using a temporary electrode. ‘Unlike other electrical stimulation modalities, SNS provides the opportunity to test potential candidates, and to select the patients most suitable for long-term therapy (Fig. 3). During acute stimulation, a temporary electrode is used to determine the functional integrity of the sacral nerves. A successful response to subchronic test stimulation indicates that the patient’s symptoms are owing to CNS dysfunction, and are treatable with neuromodulation. Studies have reported constant reproducibility of the results of the subchronic test Stimulation compared to those of the surgical neuroprosthetic implant (36).

TEMPORARY ELECTRODE IMPLANTATION Patients are placed in the prone position with pillows under the chest and abdomen to flatten the back and draped in a sterile manner. Bony landmarks are used to define the level of the sacral foramina on either side. The S3 is located at the level of the greater sciatic notch, one fingerbreath lateral to the midline spinous process. After infiltration of the skin and subcutaneoustissue with 1% lidocaine, the posterior surface of the bony sacrum is probed with an insulated needle. Each plane of resistance, including the subcutaneoustissue, fascia, and posterior sacral surface is flooded with local anesthetic. The probing needle is oriented to follow the natural course of the sacral ramus throughthe bone table. When the foramen is localized, the spinal needle will drop off the posterior surface of the sacrum into the sacral foramen. Once the electrically insulated needle has been positioned for acute Stimulation, a graduated current amplitude is applied to the nerve to determine responses consistent with an S3pattern. Because S3is primarily responsible for levator function and has less contribution to the motor function of the lower extremity, stimulation at this level is preferable. The S3 responses are deepening of the buttocks groove (“bellows” response) and plantar flexion of the great toe only. When these responses have been discerned, a test stimulation lead is threaded through the needle lumen, and the needle is withdrawn, leaving the

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Fig. 3. Surgical Implantationof the SNS device. The lead is maintained by securing

to the posterior sacral periosteum. The proximal portion of the electrode is routed toward the flank or upper buttock using an extension. The pulse generator is implanted in an abdominal pouch.

lead in place. The portion of the test stimulation lead above the skin is secured using a breathable membrane dressing and position of the electrode confirmed by antero-posterior and lateral sacral radiograph. If the positioning of the temporary lead is appropriate and S3 responses are obtained, a subchronic test is performed. The proximal end of the lead is connected to an external stimulator and a test period of 3-7 d follows. Patient responses to stimulation sensations aid in determining the electrical stimulus patterns that meet their individual needs and changes in incontinent symptoms are quantified in the voiding diary. Patients are contraindicated for implant if, during the test period, SNS is not found satisfactory in alleviating target symptoms, if the patient is unable to operate the device, or the treatment is not acceptable to the patient. The test stimulation lead is removed, and the patient is free to explore other treatment options. Patients who experience a 50% reduction of symptoms in at least one key symptom variable such as number of incontinence episodes, pads, or severity scores are considered candidates for long-term therapy.

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SURGICAL IMPLANTATION The second stage, surgical implantation, is performed under general anesthesia. The patient receives prophylactic intravenous antibiotics, and is then placed in a prone position supported by a laminectomy frame. During surgery, the feet will remainexposed so that nerve responses may be assessed. A 6-12-cm midline incision is made over the spinous process to the level of the underlying lumbodorsal fascia, which is then cleaned and incised longitudinally. The underlying paraspinous muscle is split in the direction of its fibers, and with blunt dissection the posterior surface of the sacrum is exposed. An insulated needle is inserted into the foramen in the direction of the course of the nerve, and proper S3responses are again identified as in the test stimulation. If necessary the position of the needle may be changed to obtain appropriate responses and, when determined, removed to allow insertion of a surgically implanted lead into the needle puncture site to a depth limited by a fixation cuff. The distal end of the lead contains four electrical contact points, which are tested intraoperatively to confirm the response obtained during prior test stimulation procedures. Theperineumand foot are observed carefully for typical motor responses, and if necessary, the electrode may be removed and reinserted to improve the response. Ideally, the response at the perineum should be greater than that at the great toe. When satisfactory responses are obtained, the position of the lead is maintained by securing a preattached fixation cuff to the posterior sacral periosteum. The proximal portion of the electrode is routed toward the flank or upper buttock. A subcutaneous pouch for the IPG is created in the upper buttock, lateral to the edge of the sacrum, and below the posteror-superior iliac crest. The pouch is created in a position such that belts or clothing will not put pressure on the area. The IPG and the electrode are connected by an extension lead tunneled in the subcutaneous tissue between the midline and upper buttock incisions.

CLINICAL EFFICACY A randomized, multicenter, clinical trial conducted in the US, Canada, and Europe evaluated the safety and efficacy of SNS therapy in three different patient populations: urge incontinence (155 patients), urgency-frequency (220 patients) and urinary retention (177 patients). Study inclusion criteria required that patients be refractory to conservative forms of medical treatment. After a successful test stimulation

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procedure, qualified patients were randomizedinto one of two treatment groups: a stimulation group (treatment) and a delay group (control). The delay group served as the control arm of the study, and continued to use conservative treatments to manage their symptoms for a period of 6 mo. Control patients were then allowed to cross over to the treatment a m of the study upon conclusion of the delay period. Voiding diasies were used to collect efficacy outcomei n f o ~ a t i o non accepted measures for each of the three patient populations. Health-related quality of life was also examined. Efficacy was evaluated by comparing outcomes of the treatment and control groups at 6 mo. Urge Incontine~ce.Of the 155 patients diagnosed withurge incontinence who underwent test stimulation, 98 qualified for implantation; 58 patients were implanted and had data at 6 mo. Results of group sequential data analysis demonstrated that, compared to the control group, patients in the treatment group demonstratedclinically and statistically significant reductions in the frequency of urge incontinent episodes, the severity of leaking episodes, and the use of absorbent pads/ diapers. At 6 mo, 74% of the treatment group patients reduced the frequency of incontinent episode by greater than 50%; 47% of these patients were completely dry. Of the treatment group patients who experienced heavy leaking at baseline, 77% had eliminated these types of leaks at 6 mo postimplant. The results were sustained at 12-1310 and 18-1110 postimplant. Analysis of SF-36 results indicated statistically significant improvements inthe domains of Physical Functioning, Vitality and General Health (20). U r ~ e n c y ~ r e q u e n Of ~ y .the 220 patients with urgency-frequency, 80 patients qualified for surgical implantation following a successful test stimulation procedure; 47wererandomizedinto the treatment group and 33 into the control group. At 6 mo postimplant, statistically significant reductions were documented in the treatment group with respect to the three primary diary variables: number voids/day, the volumehoid, and the degree of urgency ranking. 88% of the treatment group patients documented clinical success on these measures compared with 32% of patients in the control group. Patients in the treatment group demonstrateda significant reduction in pelviclbladder discomfort at 6 m0and also documented clinically and statistically significant changes in the ability to store urine, the ability to empty urine, and a decrease in incontinent episodes per day; control group patients documented no statistically-significant changes in these parameters. Sustained clinical benefit wasdocumented at 12and at 18 m0 post-implant.

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Six months postimplant treatment group patients demonstrated significant improvements in 7 of the 10 health-related quality of life domains measured by the SF36 (Physical Functioning, Role Physical, Bodily Pain, General Health, Vitality, Social Functioning, and Mental Health). Implant patients also had more favorable perceptions of their general health status over time as compared to control patients (20). Retention. Of the 177 patients presenting with urinary retention, 68 patients qualified for surgical implantation following a successful test stimulation procedure; 37 were randomized into the treatment group and 3 1 into the control group. Treated patients documented significant reductions in catheter volumes at 6-mo postimplant; 69% of the treated patients completely eliminated catheterization, with an additional 14% demonstrating 50% reduction in catheter volumes. Successful results were therefore achieved by 83% of the treated patients. Patients in the control group remained clinically unchanged with only 9% demonstrating a clinically-meaningful change in retention symptoms. There were also significant improvements in the ability to empty urine (decreased number of catheterizations per day, decreased total catheter volume per day, decreased maximum catheter volume); the ability to void urine (increased number of voids per day, increased total volume voided per day, increased average volume voided per void, increased maximum voided volume, improved urine stream forcej; and increased patient comfort among implanted patients. Evidence of improved bladder function was further demonstrated by the statistically significant reduction in urinary tract infections for the treatment group at 12 mo postimplant. Sustained clinical benefit was documented at 12 mo and at 18 mo postimplant. At the 6-mo follow-up analysis implant patients demonstrated significant improvements in Bodily Pain, as measured by the SF36 and had more favorable perceptions of their general health transition compared to control patients (20). The efficacy of SNS in the treatment of voiding dysfunction has been demonstrated and reported in earlier literature (13,34).Published results of clinical trials using the InterStimB device suggest that SNS in a safe and effective treatment alternative for a variety of urinary incontinence problems (8,15,18,36,37).The FDA approved the use of the Inters timB Continence Control System for the indication of refractory urge incontinence in 1997. The Food and Drug Administration (FDA) is currently reviewing data for expanded indications of urgencyfrequency and urinary retention. The device has been available for these indications in Canada, Europe, and Australia since 1994.

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Adverse events related to the therapy, the device, or implant procedure have been comprehensively recorded in the multicenter trial and include: pain at the lead implant site (21%) or at the IPG site (17%), which may require surgical revision but are resolvable. The probability of surgical revision. computed from survival analysis of clinical trial data, was 29% within the first 6 mo, and 12% in the second 6 nio, suggesting that the potential for surgical revision declines over time. It is likely that further refinements in technique, such as positioning of the IPG in the upper buttocks instead of the lower abdomen, and monitoring of sacral evoked response potentials during lead placement, will reduce the need for surgical revision in the future. Other adverse events associated with use include infectionhkin irritation (7%), technical problems (7%), and transient increases in electrical sensation (6%). Changes in bowel function (5%), nuinbness (1.3%), and suspected nerve injury tnay result during chronic treatment (<0.5%) (20). SNS therapy has not been associated with deterioration of bladder function with continued use (20). The potential for adverse events using SNS is significant, but must be considered against the nature of the underlying complaint. Patients who suffer the debility of chronic, intractable voiding dysfunction are otherwise likely to experience ongoing symptoms, drug side effects, andlor the acute and chronic risks of inore major surgical interventions, such as augmentation cystoplasy. Patients who undergo a test stimulation are able to make an informed decision about the potential benefit of surgical iniplanation. Once implanted, there is a high likelihood of significant and prolonged relief of the underlying voiding complaint. Even if an adverse event occurs, almost all are resolvable to the point where the benefit of the therapy is reestablished. If not, SNS is completely reversible. Upon cessation of therapy or removal of the implanted devices, the patients are free to use alternate therapies or proceed to surgical intervention if necessary.

CONCLUSIONS The goal of any treatment for incontinence is restoration of normal bladder function, prevention of secondary health consequences, and improvement in the quality of life of individual patients. The various electrical stimulation techniques, in development since the 1960s and available for clinical use today, offer alternatives to more conservative

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therapies and surgery. While itis reasonable to attempt other conservative treatments first, when these options fail or are otherwise not indicated, electrical stimulation should be considered before offering surgical treatment. Therapies involving electrical stimulation are based on the concept that urge incontinence owing to detrusor instability is not m end organ problem, but that the condition represents a CNS dysfunction. The problem, in turn, may be manifest as symptoms of urge incontinence, urgency-frequency syndromes,urinary retention, or bowel dysfunction (38). Stimulation therapies are able to modulate abnormal reflexes between the bladder, pelvic floor, and external sphincter. Unlike other electrical stimulation techniques with more limited applications, SNS holds great promise for a large number of patients who suffer a spectrum of lower urinary tract dysfunction. Implantation of an SNS device in properly selected patients is likely to provide significant and sustained relief from debilitating eurologic symptoms, is totally reversible, and doesnot preclude the use of other standard treatments.

REFERENCES 1. Fantl JA, Newman DK, Colling J, et al. (1996) Urinary Incontinence in Adults: Acute and Chronic Management, Clinical Practice Guideline No. 2 1996 Update. Rockville, Maryland: U.S. Department of HealthandHuman Services, Public Health Service, Agency for Health Care Policy andResearch, AHCPR Publication No. 96-0682, March. 2. Fall M (1985) Electricalpelvic floor stimulation for the control of detrusor instability. Neurourol Urodyn 4:329-335. 3. Fall M, Lindstrom S (1991) Electrical stimulation: a physiologic approach to the treatment of urinary incontinence. U r d Clin NA 18(2):393-407. 4. Wein AJ, Bmet DM (1988) Voiding Function and Dysfinction: A hgical and Practical Approach. Chicago: Yearbook Medical Publishers, Inc. 5. Schmidt RA, Senn E, Tanagho EA (1990) Functional evaluation of sacral nerve root integrity: report of a technique. Urology 3.5(5):388-392. 6. Schmidt RA (1988) Applications of neurostimulation. Neurourol Urodyn 7:585. 7. Tanagho EA, Schmidt RA (1988) Electrical stimulation in the management of the neurogenic bladder. J U r d 140:1331. 8. Thon W, Baskin L, Jonas U,et al. (1991) Neuromodulationof voiding dysfunction and pelvic pain. World J U r d 9:138-141. 9. Mersdorf A, Schmidt RA, Tanagho EA (1993) Topographic-anatomical basis of sacral neurostimulation: neuroanatomical variations. J Urol 149:345-349. 10. ChancellorMB,deGroat WC (Submitted for publication)Hypothesesonhow sacral nervestimulationworks for thetreatment of detrusor overactivityand urinary retention.

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11. Blok BFM, van Maarseveen JTPW, Holstege G (1998) Electrical stimulation of the sacral dorsal graycommissureevokes relaxation of the external urethral sphincter in the cat. Neurosci Letters 249:68-70. 12. Schultz-LampelD, Jiang C, Lindstrom S, Thuroff JW (1998)Experimentalresults on mechanismsof action of electricalneuromodulation inchronic urinary retention. World J Urol 16:301-304. 13. Vapnek JM,SchmidtRA (1991) Restoration of voiding inchronic urinary retention using the neuroprosthesis. World J Urol 9:142-144. of voiding dysfunction with an implantable neuro14. Siegel SW (1992) Management prosthesis. Urol Clin N Am 19(3):163-170. 15. Diijkema H, Weil EHJ, Mijs P, Janknegt RA (1993) Neuromodulation of sacral nerves for incontinence and voiding dysfunctions. Eur Urol 24:72-7’7. 16. Hassouna M (1994) Neural stimulation for chronic voiding dysfunction. J Urol 153:2078-2080. 17. Koldewijn EL, et al. (1994) Predictors of success with neuromodulation inlower urinary tract dysfunction: results of trial stimulation in 100 patients. J Urol 15212071-2075. 18. Bosch J, Groen J (1995) Sacral (S3) Segmentalnerve stimulationas a treatment for urge incontinence in patients with detrusor instability: results of chronic electrical stimulation using an implantable neural prosthesis. J Urol 154:504-507. 19. Bosch J, Groen J (1996) Treatment of refractory urge urinary incontinence with sacral spinal nerve stimulationin multiple sclerosis patients. Lancet 348:717-719. 20. Medtronic data on file; MDT-103. 21. Empi (1994) The ~ndamentalsof pelvic ftoor stimulation: innovative treatments for urinary incontinence. St. Paul, MN: Empi, Inc. 22. Siegel SW, Richardson DA, Miller ILL, Karram MM, et al. (1997) Pelvic floor electrical stimulation for the treatment of urge and mixed urinaryincontinence in women. Urology 50(6):934-940. 23. BentAE,Sand PK, OstegardDR,Brubaker L (1993) Transvaginal electrical stimulation in the treatment of genuine stress incontinenceand detrusor instability. IntE Urogynecol J 4:9-13. 24. Sand PK, Richardson DA, Staskin DR,al.et(1995) Pelvic floorelectrical stimulation inthetreatment of genuine stress incontinence: a multicenter,placebocontrolled trial. Am J Obstet Gynecol 183:72-79. ILL, Siegel SW, et al. (1996) Pelvic floor electrical stimula25. Richardson DA, Miller tion: a comparison of daily and every-other-daytherapy for genuine stress incontinence. Urology 48( 1):llO-118. (1996) of transvaginal 26. Elgamasy AN, Lewis V, Hassouna ME, Ghoniern GM Effect stimulation in the treatment of detrusor instability. Urol Nurs 16(4):127-130. 27. Brubaker L, Benson JT, Bent A, et al. (1997) Transvaginal electrical stimulation for female urinary incontinence. Am J Obstet Gynecol 177:536-540. 28. Luber KM, Wolde-Tsadik G (1997) Efficacy of functional electrical stirnuIation in treatinggenuine stress incontinence: a randomized clinical trial. Neurourol Urodyn 16543-55 1. E (1998) Evaluationof the subjective 29. Kulseng-Hanssen S, Kristoffersen M, Larsen and objective effect of maximal electrical stimulation in patients complaining of urge incontinence. Acta Obstet Gynecol Scand 168(Suppl):12-15. incontinence. 30. Bo K (1998) Effect of electrical stimulation onstress and urge urinary Clinical outcome andpractical recommendations based on randomized controlled trials. Acta Obstet Gynecol Scand 168 (Suppl):3-11.

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31. Davila GW, Bernier F (1995) Multimodality pelvic physiotherapy treatment of urinary incontinence in adult women. Intl Urogynecol J 6:187-194. 32. McGuire EJ, Shi-Chun Z, Horwinski ER, et al. (1983) Treatment of motor and sensory detrusor instability by electrical stimulation. J Urol 129:78-79. stimulation for pelvicfloor dysfunction. 33. Stoller ML (1998)Afferentnerve J Endourol 12(1):S108 (Abstract F2-6). 34. Elabbady AA, HassounaMM, Elhilali MM (1994) Neural stirnulationfor chronic voiding dysfunctions. J Urol 152:2076-2080. 35. Appell RA (1998) Electrical stimulation for the treatmentof urinary incontinence. Urology 51 (2A Suppl):24-26. 36. Shaker HS, Hassouna M (1998) Sacral nerve root neuromodulation: an effective treatment for refractory urge incontinence. J Urol 159:1516-15 19. 37. Shaker HS, Hassouna M (1998) Sacral root neuromodulation in idiopathic nonobstructive chronic urinary retention. J UroZ 159:1476-1478. 38. Stadelmaier MKE, HohenfellnerM, Gall FP (1995) Electrical stimulation of sacral spinal nerves for treatment of faecal incontinence. Lancet 346(8983):1124-1.127.

l 4Treatment of Detrusor Instability With Augmentation Cystoplasty

Joseph M. Khoury CONTENTS CLASSIFICATION OF CYSTOPLASTY INDICATIONS FOR AUGMENTATION CYSTOPLASTY CONTRAINDICATIONS TO AUGMENTATION CYSTOPLASTY SURGICAL CHOICES IN ACHIEVING THE COALS OF BLADDER RECONSTRUCTION COMPLICATIONS REFERENCES

Augmentation cystoplasty can provide significant relief of refractory storage symptoms such as frequency, urgency, and urge incontinence in those patients who havefailed conservative measures suchas pharmacotherapy, behavioral techniques, and minimally invasive procedures such as neurornodulation. The conceptof augmenting bladder capacity is not a new one. Von Mikulicz in 1899 was the first to use ileum to restore normal bladder capacity in humans (1). Other investigators at the turn of the century used different segments of bowel; however, enthusiasm waned until the early 1950s, when pioneers such as Kuss (21, Couvelaire (3),and Gil-Vernet (4) restored the impetus to pursue bladder reconstruction. The primaryindication for augmentation enterocystoplasty at that time was tuberculous cystitis, which caused a stmcturally contracted bladder. Unfortunately, the postoperative mortality and morbidity was exceedingly high and other supravesical diversions such as the ileal conduit urostomy became the technique of choice in

From: Current Clinical Urology: Voiding Dysfinction: Diagnosis and Treatment Edited by: R. A. Appell 0 Humana Press Inc., Totowa, NJ

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the urologic community. The long-term sequelae of the Bricker loop became manifest after several years and included recurrent urinary infections, dissatisfaction with a wet urostomy, and the psychosocial stigma associated with an external collection device (5,6). In the 1960s a new surge of enthusiasm developedin reconstructive urology. Fluoroscopic multichannel urodynamics providedthe scientific foundation for establishing the urophysiologic mechanismsthrough which the detrusor and outlet function in a coordinated manner. Likewise, Lapides’ hallmark contribution in 19’72 of clean intermittent selfcatheterization (clean intermittent catheterization; CIC) revolutionized the management of voiding dysfunction, particularly in patients with neuropathic bladder (7,8).In addition, the discovery of pharmacological agents to treat abnormal bladder storage and emptying characteristics established a new avenue for managing urinary incontinence in conjunction with intermittent self-catheterization (9). In spite of all the new technology anddrugs to manage urinary incontinence, there are patients who remainrefractory to such therapy and in whom surgery is necessary to correct their underlying disorder. Augmentation enterocystoplasty is a safe operation for this purpose.

CLASSIFICATION OF CYSTOPLASTY Augmentation cystoplasty is a procedure used to increase bladder capacity by incorporating a segment of intestine or stomach into an unresected bladder. Augmentation cystoplasty is used commonly to manage intractable symptoms resulting from detrusor instability hyperflexia or impaired detrusor compliance. Substitution cystopZasty is an operation whereby a significant amount of bladder wall is resected prior to incorporating an intestinal segment with the bladder remnant. This procedure is used commonly in hypersensitive bladder states such asinterstitial cystitis. The bladder is usually resected to its trigonal remnant and an isolated intestinal segment is then substituted for the resected bladder. Replacement or orthotopic cystoplasty is reserved for those cases in which a total cystectomy is necessary as in patients undergoing radical Cystectomy for bladder cancer. The urethra and distal sphincter mechanism are left intact so that the intestinal reservoir can be anastomosed to it. Autoaugmentation is a relatively new surgical procedure in which the detrusor muscle is dissected off from the bladder usually on its

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anterior, lateral, and superior surfaces creating a large mucosal bulge or wide-mouth diverticulum. It obviates the potential complications of incorporating bowel segments into the urinary system and, therefore, is an alternative procedure in those patients who maybe a candidate for augmentation enterocystoplasty. This procedure has also been termed detrusor myomectomy.

INDICATIONS FOR AUGMENTATION CYSTOPLASTY The major indications to perform enterocystoplasty have changed considerably since the early 1950s. Antituberculous drugs have significantly decreased the end-stage manifestations of tuberculous cystitis, and, therefore, bladder reconstruction is rarely needed. In contemporary times, cystoplasty is now performedfor detrusor hyperactivity resulting from suchentities as poor bladder wall compliance, refractory detrusor instability or hyperreflexia, and a structurally reduced bladder capacity owing to inflammatory disease. Regardless of the etiology, these bladders are contracted and bladder capacity reduced, resulting in the symptoms of frequency, urgency, and urge incontinence. As notedearlier, the majority of patients with bladder overactivity and/or impaired detrusor compliancerespond to anticholinergic agents; however, end-stage inflammatory bladders, particularly with thick-walled fibrosis do not, and surgical intervention is often necessary. In addition to the bladder other variables that may need to be addressed include the upper tracts and the bladder outlet. The presurgical evaluation will determine those variables that will need to be addressed and determine the magnitude of the urinary reconstruction.

PREOPEMTIVE EVALUATION The preoperative surgical evaluation should include a thorough history and physical examination to determine the underlying etiology of the bladder dysfunction, as well as laboratory, radiographic, endoscopic, and urodynmic studies. It is largely upon these results that the surgeon will decide whether the patient requires augmentation or substitution cystoplasty and whatappropriate management of the ureters and outlet should be.

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LABORATORY STUDIES The preoperative laboratory evaluation is necessary to assess renal function and acid-base status. Serum creatinine, a blood urea nitrogen (BUN), and 24" creatinine clearance are helpful measures to assess renal status, particularly in those individuals who may have renal insufficiency or chronic renal failure. Urinalysis and culture should be performed to identify urinary infection, which should be eradicated prior to reconstruction. Urinary cytology may be helpful in those patients with sensory urgency in order to exclude carcinoma in situ.

RADIOLOGIC STUDIES The entire urinary tract needs to be imaged prior to reconstruction. Upper tract evaluation will initially begin with intravenous urogram to assess the upper tracts, particularly if ureteral reconstruction is necessary. Voiding cystographywill identify bladder abnormalities that may influence a decision regarding bladder substitution rather than simple augmentation andwill identify the presence and severity of vesicoureteric reflux. A cystogram may help to characterize the competence of the sphincter mechanisms and lower urinary tract patency.

URODYNAMIC EVALUATION Urodynamic studies should evaluate bladder and outlet function during filling, storage, and voiding. This is best accomplished by using multichannel fluorourodynamics, whichcombine electronic urodynamic data collection and simultaneous cystourothrography. Filling cystometrogram will assess compliance, stability, storage, sensation, and capacity. Storage after filling will further define stability and competence of the outlet. Pressure flow studies will document voiding dysfunction and the Valsalva leak-point pressure can be used to evaluate the bladder outlet for intrinsic sphincter deficiency (10). Other urodynamic tools such as the urethral pressure profile, electromyography, and fluoroscopy may further enhance information regarding the continence mechanisms.

CYSTOURETHROSCOPY Endoscopic evaluation should precede all urinary tract reconstructive procedures to identify any structural bladder or urethral problems that

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may alter the choice of the proposed reconstructive procedure. Significant outlet findings, urethral stricture disease, ortrauma may help predict continence or catheterization difficulties, particularly in those individuals who have had prior outlet procedures performed. Finally, cystourethroscopy will identify any concomitant bladder pathology such as tumors, stones, or diverticuli that need to be identified prior to the reconstruction.

CONTRAINDICATIONS TO AUGMENTATION CYSTOPLASTY There are relatively few contraindications to cystoplasty. Compromised renal function in the past was initially considered an absolute contraindication to bladder reconstruction as it could exacerbate metabolic problems owing to the absorptive surface of the bowel within the urinary tract. However, if the etiology of the underlying renal impairment is owing to hostile detrusor function, then augmentation cystoplasty may stabilize or improve renal function. It is of utmost importance to counsel the family that renal deterioration may continue even after bladder reconstruction and result in the need for renal transplantation. A well-motivated and compliant patient is imperative as bladder reconstruction surgery can be fraught with relatively severe postoperative problems should timely follow-up and review not be kept. From the outset the patient and family should be well aware that intermittent self-catheterization might berequired on a routine basis and that deviation from this routine could precipitate severe injury to the urinary tract or metabolic problems such as uremia.

SURGICAL CHOICES IN ACHIEVING THE GOALS OF BLADDER IXECONSTRUCTION The goals of bladder reconstruction are to create a low-pressure, capacious reservoir that is continent and guards the upper tract from the damaging effects of reflux, infection, and highintravesicle pressure. Therefore, the surgeon not only needs to consider reconstruction of the bladder reservoir but also whether ancillary procedures are necessary to correct reflux and outlet incompetence. These three variables will be addressed individually.

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MANAGEMENT OF THE BLADDER Management of the bladder remnant should address the extent of bladder resection, choice of bowel segment, and reconfiguration of the bowel segment.

Extent o f Bhdder Resection and Preparation The extent of bladder resection, if at all, is determined by the pathology of the underlying disease for whichcystoplasty is being performed. Patients with an overactive detrusor owing to neurologic or non-neurologic disease may benefit from simple augmentation without bladder resection. In this situation the bladder is incised, either sagittally or longitudinally, and a segment of detubularized bowel is incorporated into the valved bladder. Partial or supratrigonal cystectomy is recommended when the bladder is structurally diseased or symptomatic as in interstitial cystitis, or in those cases in which the bladder diverticulae are present or when the bladder is extremely thick-walled. When performing augmentation cystoplasty without bladder resection, the main objective is to achieve as long an anastomosis as possible with the intestinal segment, avoiding an hourglass configuration with the bowel patch acting as a diverticulum. This goal may be best accomplished by incising the bladder in the sagittal plane, which simplifies the procedure by avoiding dissection of the lateral pelvic walls and bladder incision close to the intramural ureters. This incision is begun approximately 2 cm cephaladto the bladder neck anteriorly and extends posteriorly 2 cm above to the interureteric ridge. This defect is then augmented using either a single segment of open bowel or commonly a cup patch (11).

Choice of Bowel Segment Almost all segments of the gastrointestinal tract, including stomach, have been usedfor bladder augmentation. Each bowel segmenthas its own advantages and disadvantages, anditsown strong proponents (12-14). Several factors influence the type of bowel employedin reconstruction. These include availability, anatomic considerations, impact on nutrition, bowel andrenal function, the need to preserve the ileocecal valve, particularly in patients with myelodysplasia, and finally, the

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surgeon’s preference. It is my preference to use ileum for simple augmentation; however, in somecases, particularly in patients with myelodysplasia, sigmoid colon lends itself to bladder reconstruction because of its redundancy and proximity to the bladder.

Bowel S e p e n t Reconfiguration The ultimate outcome incystoplasty reconstruction is a large-capacity, low-pressure system with normal compliance. This is best accomplished by remodeling a tubular section of intestine into a sphere, thereby not only increasing capacity but also disrupting the normal propagation of peristaltic contractions so as to keep cystoplasty activity to a minimum (13,1543). The volume within a sphere is determined by its radius (V = 4/3R3); therefore, the surgical technique chosen should increase the overall radius of the system. In any event, cystoplasty size should achieve a total bladder volume of 500 cc to ensure a normal functional capacity of the reconstructed bladder.

MANAGEMENT OF THE URETERS AND UPPER TRACTS Generally speaking, if reflux is present at the time of cystoplasty, then ureteral reimplantation is usually necessary. There are some reports indicating that vesicoureteral reflux is based solely on hostile detrusor factors and if a low-pressure reservoir is created through bladder reconstruction, the reflux will then resolve (19). Likewise, this has been the author’s experience for those patients withlower grades of reflux; however, those patients with either unilateral or bilateral Grade IV or V reflux may be better served with ureteral reimplantation. A high number of myelodysplastic patients undergoing cystoplasty will require simultaneous reimplantation (20). It is less common in the adult spinal cord-injured patient with neurogenic bladder dysfunction, and relatively uncommon in non-neurogenic patients with detrusor instability. Factors such as length of available ureter, peristaltic activity of the ureter, and nature of the bladder remnant will guide the most appropriate surgical technique. When the bladder remnant is not heavily trabeculated or fibrotic, the Cohen cross-trigonal reimplant may correct low-grade reflux (21). The ileal intesusception nipple technique is optimal for reimplantation of large, dilated poorly peristaltic ureters for the ileal intesusception has very low resistance and is unlikely to cause ureteral

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obstruction (22). Direct reimplantation into the augmenting bowelsegment has been favorable in those circumstances where the bladder remnant is either too small or pathologyprecludes standard reimplantation. Examples of these include the split cuff nipple as described by Turner-Warwick (23), the Goodwin (24) and Carney-LeDuc(25) reimplantations. All of these are appropriate techniques to implant the ureter into bowel.

MANAGEMENT OF THE BLADDER OUTLET Many treatment options are available to manage the incompetent outlet and these are determined by the type andmagnitude of the incontinence, dexterity of the patient and ambulatorystatus. Mild bladder neck incompetence can be treated pharmacologically by using drugs such as alpha agonists to increase outlet resistance (26). Formore debilitating types of incontinence, a number of surgical procedures are available and include injection of periurethral bulking agents such as collagen or polytetrafluoroethylene (2 7), bladder neck reconstruction (28-30), sling cystourethropexy, or placement of an artificial urinary sphincter (31).

COMPLICATIONS Metaliolic and Electrodyte Disorders Hyperchloremic metabolic acidosis is a potential problem whenever bowel is interposed within the urinary tract as a conduit or reservoir. The total surface area exposed to urine and the patients renal function are the two most important predisposing factors that will potentiate systemic acidosis. Nurse andMundy reported on 48patients who underwent assessment of acid-base and electrolyte balance following incorporation of different intestinal segments into the urinary tract (32). All patients had abnormal blood gases with most demonstrating metabolic acidosis with respiratory compensation. One-third of their patients had hyperchloremia. In a follow-up study of 28 patients, Mundy and Nurse investigated the consequences of metabolic acidosis with respect to calcium balance and skeletal mineralization (33). All of their patients had normal serum and 24 h calciumlevels. Of the 28 patients, l 2 were women betweenthe ages of 45 and 50 and all had normal dual-photon absorptiometry bone scans, demonstrating no bone demineralization.

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Of the 16 children in their series, 10 underwent ileocystoplasty and 6 underwent colocystoplasty. All children with ileocystoplasties continued to grow within the same percentile as before their cystoplasty; however, 50% of the children with colocystoplasty demonstrated an approximately 20% diminution in their postcystoplasty growth rate. Although there were nodramatic changes in calcium balance or skeletal ~ i n ~ r a ~ i z a t ithe o n authors , concluded that follow-up may be too short and that these changes may take several years to develop with chronic metabolic acidosis.

Voiding DzficuZties It is not unusual for patients to experience voiding difficulty or incomplete bladder emptying after bladder reconstructive procedures particularly in those undergoing an outlet procedure. Preoperatively these patients should understand that clean intermittent self-catheterization may be necessary to allow for completebladder emptying. Neurologically intact patients undergoing clam augmentation cystoplasty usually void efficiently following bladder reconstructive surgery. Those neurologically impaired patients, though, rarely void normally after cystoplasty and will require CIC.For those patients who do need to perform clean intermittent self-catheterization a large catheter (16 French) should be used in order to evacuate mucous plugs that may obstruct the outlet, particularly in those children and young adults with myelodysplasia.

Incontinence When urinary incontinence occurs following bladder reconstructive surgery urodynamic evaluation is necessary to identify whether the cystoplasty or the outlet is responsible. Should cystoplasty function be hyperactive initial therapy with anticholinergic agents may be helpful; if this fails, further augmentation using a patch of ileum can besuccessful. If the outlet is incompetent, then one of the previously discussed techniques may be needed for its correction.

Urinary Infection Bacteriuria following augmentation cystoplasty is commonand should be anticipated in those patients on CIC.Pyelonephritis, however,

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is uncommon, andif it does occur then imaging studies may be necessary to rule out ureteral reflux, urinary obstruction, or urinary calculi.

Neoplasms of the bladder and/or bowel segment are relatively rare following bladder reconstructive surgery. Only 14 cases of neoplasms have been reported in patients undergoing cystoplasty, and over half of these operations were performed ontuberculous contracted bladders (34).The latency period from time of bladder reconstruction to diagnosis of tumor ranged from 3 to 24 years. The tumor histology was adenocarcinoma in 7 patients, transitional cell carcinoma in 5, small cell in l and sarcoma in 1. These and other anecdotal cases further emphasize the need for chronic surveillance in patients undergoing such procedures, particularly those in whom gross hematuria may occur. Filmer and Spencer recommend yearly cytologies and cystoscopywith biopsy beginning 10 years after enterocystoplasty (35).

Spontuneozts Peforution Spontaneous perforation following cystoplasty is not an uncommon occurrence and is being reported more frequently in the literature. It is important to consider this diagnosis following cystoplasty in those patients who may have signs and symptoms of an acute abdomen as it is a potentially lethal complication of enterocystoplasty. The incidence is reported to be between 3-6.1% (36,37). The diagnosis should be prompted by a very high index of suspicion, and many times the diagnosis may be confirmed by retrograde cystogram or radionucleide cystography.

Pregnancy A . e r B h d d e rReconstruction Pregnancy following enterocystoplasty is becoming more common as women who undergo bladder reconstruction for congenital problems enter their childbearing years. These women during their pregnancy could potentially have significant morbidity including febrile urinary infections, premature labor, urinary tract obstruction, and compromised renal function. Renal function should be monitored vigilantly in these women with monthlyserum creatinines and, when indicated, renal ultrasonography. Hill and Gamer (38) recommend that those women

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who have undergone bladder reconstruction with the continence mechanism unaltered, be allowed to deliver vaginally. However, those who have had a bladder neck reconstruction, fascial sling, cystourethropexy, or artificial urinary sphincter, should undergo Cesareansection to avoid disruption of the underlying continence mechanism.

REFERENCES 1. Von Mikulicz J (1899j Zur Operation der angeborenen Blasenspalte. Zentralbe Chir 20:64 1-643. 2. Kuss R, Bitker M, Camey M, et al. (1970) Indications and early and late results of intestinocystoplasty:a review of 185 cases. J UroE 103:53. 3. CouvelaireR(1950) La “petite vessie”destuberculeuxgeniourinaires: essai de classificationpacelore et variantesioutedes cysto-intestine-plasties. J U r d (Paris) 56:38 1. 4. Gil-Vernet JM (1965) The ileocolic segment in urologic surgery. J UroE 94:418. 5. Pitts WR, Muecke EC (1979) A 20-year experience with ileal conduits: the fate of the kidneys. J Urol 122:154. in children: computer 6. Schwarz GR, Jeffs RD (1975) Ilea1 conduit urinary diversion analysis of followup from 2 to 16 years. J Urol 114:285. to myelodysplasia. 7. DioknoAC, Kass E, Lapides J (19’76) Anewapproach J Urol 116:771-772. 8. Lapides J, Diokno AC, Silber SJ, et al. Clean intermittent self-catheterizationin the treatment of urinary tract disease. J Urol 107:458. chloride combined with 9. Mulcahy JJ, James HE, McRoberts JW (1977) Oxybutynin intermittent clean catheterization inthe treatment of myelomeningocele patients. J Urol 118:95. j Stress leak point pressure: EJ, Bloom DA, and Ritchey ML (1993 10. Wan J, McGuire a diagnostic tool for incontinent children. J Urol 150:700. 11. Bramble FJ (1982) The treatment of adult enuresis and urge incontinence by enterocystoplasty.Br J Urol 54:693. Gastrocystoplasty: analternative 12. AdamsMC, Mitchell ME,RinkRC(1988) solution in the severely compromised patient. J Urol 140:1152-1158. 13. Sidi AA, Reinberg Y, Gonzalez R (1986) Influence of intestinal segment and configuration onthe outcome of augmentationenterocystoplasty.J Urol 136:12011204. 14. Kuss R (1959) Colocystoplasty rather than ileocystoplasty. J Urol 82:587. 15. Cheng C, Whitfield HN (1990) Cystoplasty: tubularization or detubularization? Br J U r d 66:30-34. 16. Hinman F (1988) Selectionof intestinal segments for bladder substitution:physical and physiological characteristics. J Urol 139:5 19. 17. Koff S (1988) Guidelines to determine the size and shape of intestinal segments used for reconstruction. J Urol 140:1150-15 1. 18. Goldwasser BZ, Barrett DM, Webster GD, et al. (1987) Cystometric properties of ileum and right colon in patients following bladder augmentation, substitution and replacement. J UroE 138 (part 2): 1007-1008.

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19. Nasrallah PF, Aliabadi HA (1991) Bladder augmentation in patients with neurogenic bladder and vesicoureteral reflux. J Urol 146563. 20. Gittes RE; (1977) Bladder augmentation procedures.In: Libertino JA, Zinman L, eds., Reconstructive Urologic Surgery: Pediatric and Adult, Baltimore: Williams & Wilkins, pp. 216-226. 21. CohenSJ(1975)Ureterozystoneostomie: eine neueantireflux Tecnik. Aktuel Urol 6:1. 22. King LR (1987) Protection of the upper tracts in undiversion. In: King LK, Stone AR, Webster GD, eds.Bladder Reconstruction and Continent Urinary Diversion, Chicago: Year Book Medical Publishers, pp. 127-153. 23. Kirby RS, Turner-WarwickR (1987) Substitutioncystoplasty.In: King LK,Stone AR, Webster CD, eds. Bladder Reconstruction and Continent Urinary Diversion. Chicago: Year Book Medical Publishers, pp. 61. 24. Goodwin WE,Harris AP, KaufmannJJ, Beal JM (1953) Open transcolonic ureterointestinal anastomosis: a new approach. Surg Gynecol Obstet 97:295-300. 25. LeDuc A, Camey M,Teillac P (1987) An original antireflux ureteroilealimplantation technique: long term followup. J U r d 137:1156. 26. Wein AJ (1987) Lower urinary tractfunction and pharmacologic managementof lower urinary tract dysfunction. Urol Clin N Am 14:273. 27. Lewis RI, Lockhart JL, Politano VA (1984) Periurethral polytetrafluoroethylene injections in incontinent female subjects with neurogenic urinary incontinence. J Urol 131:459. 28. YoungHH(1922)Anoperation for the cure of incontinence associated with epispadias. J Urol 7: l . 29. Dees JE (1949) Congenital epispadias with incontinence. J Urol 62:513. 30. Leadbetter GW (1964) Surgical correction of total urinary incontinence. J Urol 91:261. DM (1989)Augmentation 31. StrawbridgeLR,KramerSA,CastilloOA,Barrett cystoplasty and the artificial genitourinary sphincter. J UroE 142:297-301. AR (1989)Metaboliccomplications of cystoplasty. Br J 32. NurseDE,Mundy Urol 63:165-170. and mineralization 33. Mundy AR, Nurse DE (1992) Calcium balance growth skeletal in patients with cystoplasties. Br J Urol 69:257-259. 34. Golomb J, KlutkeCG, Lewin KJ,et al. (1989) Bladder neoplasms associated with augmentation cystoplasty:report of 2 cases andliterature review. J Urol 142:377380. 35. Filmer RB,Spencer JR (1990) Malignancies in bladder augmentations and intestinal conduits. J Urol 143:671-678. 36. Hensle TW, Burbige KA (1990) Complications of urinary tract reconstruction. In: Marshall FF, ed., Urologic Complications, 2nd ed. St. Louis: CV Mosby Year Book. of theaugmentedurinary 37. BravermanRW,LeboweitzRL(1991)Perforation bladder in nine children and adolescents: importance of cystography. Am J Roentgenol 1575. of pregnancyafteraugmentation 38. HillDE,KramerSA(1990)Management cystoplasty. J Urol 144 (part 2): 457-459.

INDEX 5-alpha reductase inhibitors, 233-234 ALPP, 45-46 American Spinal Injury Association Abdominal examination, 3 1 (ASIA) Score, 120 Abdominal leak-point pressure (ALPP), American Urologic Association Symp45-46 tom Index, 29-30 Abdominal stoma, 100 Anatomic etiology Abdominal straining female urinary retention, 198-202 voiding, 2l0 Anterior vaginal wall Abrams-Griffiths Nomogram, 47f prolapse, 198 Absent volitional control of the external Anticholinergics, 73, 101, 158, 266, sphincter (AVCS), 68, 69t 28 1-282 Acetylcholine (Ach), 276, 281-282 Antidepressants, 287 Acontractile bladder Antihistamines, 287 female urinary retention, 204 Antimuscarinic agents, 284 Acquired immune deficiency syndrome Anuria (AIDS) female urinary retention, 198 female urinary retention, 205 Areflexic bladder Activities of daily living (ADL) LMN MS, 99 CIC, 127 Acute urinary retention myelodysplasia, 125, 125f CVA, 67 Artificial urinary sphincter, 26 1-265, ADL 262f-264f MS, 99 erosion, 264 Age related etiology failure, 263-264 female urinary retention, 207-209 SUI, 180 AIDS ASIA Score, 120 female urinary retention, 205 Assistive devices, 99 Alcohol injection Atropine, 282 MS, 103-1 04 Augmentation cystoplasty, 3 16 Alfuzosin, 279 bladder management, 320-32 l Alpha adrenergic blockers,168-1 69, bladder resection, 320 23 l-233,239,242,259,278,285 bowel segment reconfiguration, l32 SCI, 128 bowel segment selection, 320-32 1 bladder outlet, 322 selective vs nonselective, 233

A

327

328

complications, 322-325 electrolyte disorders, 322-323 incontinence, 323 metabolic disorders, 322-323 neoplasms, 324 pregnancy, 324-325 spontaneous perforation, 324 urinary infection, 323-324 voiding difficulties, 323 contraindications, 3 19 detrusor instability, 315-325 indications, 3 17 MS, 105-1 09 preoperative evaluation, 317-3 19 cystourethroscopy, 318-3 19 laboratory studies,3 18 radiologic studies, 3 18 urodynamic evaluation, 3 18 surgery, 3 19 ureters, 321-322 Autoaugmentation, 3 16-3 17 Autologous fat, 170-17 1 Autonomic dysreflexia SCI, 132-1 33 Autonomous neurogenic bladder, 17 AVCS, 68,69t Axonal degeneration female urinary retention, 203

B Baclofen, 279-280 Bacteriuria, 323-324 Balanced Bladder, l 16 Balloon dilation external sphincter SCI, 130 BCR, 88 lumbar disc disease, 155 Bedside cystometrics,49-5 l Behavioral modification MS, 99-100 poststroke, 78 Behavioral therapy SUI, 165-166

Index

Behavioral voiding dysfunction, 242 Benign prostatic hyperplasia (BPH) bladder outlet obstruction, 230-242 pharmacological therapy, 23 1-234, 280-28 1 surgery, 234-238 incontinence, 73 natural history, 23 l Bentyl, 283 Benzodiazepines, 279-280 Beta adrenergic agonists, 279 Beta-sitosterol, 28 1 Bethanechol chloride, 128, 145, 157-158, 277-278 Biofeedback SUI, 166-1 68 Bladder endoscopy, 52-53 hyperactive filling, 5 innervation, 277f Bladder augmentation cystoplasty, 320-32l SCI, 130 lumbar disc disease, 158 Bladder autoaugmentation MS, 105 Bladder cancer SCI, 132 Bladder chimney, 106 Bladder dysfunction post-prostatectomy, 265-267 conservative treatment, 265 pharmacologic therapy, 266 with sphincteric incompetence, 266-267 surgery, 266-267 Bladder emptying abnormalities, 5-1 0 facilitation, 9t failure treatment, 10 Bladder filling abnormalities, 5-1 0 facilitation, 8t

Index

329

MS, 104 requirements, 4 Bladder leak-point pressure (BLPP), 46 Blood tests, 33,227-228,3 18 BLPP, 46 Bladder neck Bors-Comarr classification endoscopic incision, 239-240 voiding dysfunction, 11-1 3, l 1t female urinary retention, 188 Bowel dysfunction, 30 Bladder neck obstruction female urinary retention, 198 female urinary retention, 200 Bowel neoplasms, 324 primary BPH. See Benign prostatic hyperplasia male, 238-242 Bladder neck suspension (BPH) Bradley classification Burch voiding dysfunction, 14-1 5 SUI, 173-174,174f Bulbocavernosus reflex (BCR), 88 percutaneous, 175, 176f lumbar disc disease, 155 Pereyra-Raz, 174, 175f Burch bladder neck suspension SUI, 173-1 76 SUI, 173-1 74,174f Bladder neoplasms, 324 Bladder outlet augmentation cystoplasty, 322 c endoscopy female, 53-54 Capsaicin, 129, 284285 male, 54 Cardura, 74,232,279 Bladder outlet obstruction Catheterization, 2 14-2 15 diagnosis, 44--45,46f Cauda equina syndrome, 154-155 female urinary retention,189-1 9 1 Cerebral shock, 67 gynecologic causes, 198-200 Cerebrovascular accidents (CVA), 6344 male, 225-242 bladder dysfunction behavioral voiding dysknction, 242 early presentation, 67 BPH. See Benign prostatic late presentation, 67 hyperplasia hemispheric dominance, 70 cystoscopy, 229 patient history, 71-72 lab tests, 227-228 urinary incontinence, 64-65 patient history, 226-227 alternative therapy, 78-79 physical, 227 female, 77-78 postvoid residual, 228-229 incidence, 66 presentation, 226 male, 77 primary bladder neck obstruction, pathophysiology, 66-67 23 8-242 urinary retention urinary flow rate, 228 female, 76-77, 76f urodynamics, 229-230 male, 74-76 Bladder retraining urodynamic studies, 68-70, 68t-70t urological evaluation, 7 l SUI, 166 Bladder storage, 186 Cervical lesions Bladder suspension urinary retention, 200 female urinary retention,209-2 l0 Cholinergic agonists Bladder transection SCI, 128-1 29

330

Chronic continence incidence, 297 Chronic indwelling catheter LMN and areflexic bladder, 127 Chronic urinary retention etiology, 199t CIC. See Clean intermittent catheterization (CIC) Cisparide, 278 Clean intermittent catheterization (CIC), 74,76, 187,2 14,323 DM, 145 LMN and areflexic bladder, 127 lumbar disc disease, 158 poststroke, 79 CMG, 38"43,40f, 42f Cohen cross-trigonal reimplant, 32 1 Collagen, 26O-26 1,260t injection, 77 lumbar disc disease, 158 Collagenous ingrowth detrusor, 207 Colon surgery female urinary retention, 203-204 Compliance, 4 1 Condom catheter poststroke, 79 SCI, 129 Conticath, 74-75,75f Contigen, 172-1 73 Continent urinary diversion MS, 105-1 09 Continuous leakage, 29 Corticoregulatory tract, 16 Corticosteroids, 287 Crede maneuver, 126, 128 CT scans, 56 CVA, see Cerebrovascular accidents (CV4 Cystocele formation female urinary retention, 198 Cystocystoplasty MS, 104 Cystolysis MS, 104

Index

Cystometrics bedside, 49-5 l Cystometrogram (CMC), 38"43,40f, 42f Cystometry elderly, 72 Cystoplasty augmentation MS, 105-1 09 classification, 316-3 17 Cystoscopic image sling obstruction, 2 1 1 f cystoscopy female urinary retention, 196 Cystospaz, 266,282 Cystourethroscopy, 51-55, 194,318-3 19 I)

Dantrolene, 279-280 DDAVP ( 1-deaminino-8-D arginine vasopressin), 100,287 Decreased outlet resistance, 5-45 Denervation MS treatment, 102 Depression, 99 DESD. See Detrusor external sphincter dyssynergia (DESD) Detrusor collagenous ingrowth, 207 Detrusor areflexia DM,145 MS, 96f, 108-109 SCI, 121 Detrusor contractility impaired, 207-209 lumbar disc disease, 153-154 Detrusor contraction, 186 Detrusor curves female urinary retention,19Of-19 1 f Detrusor dysfunction, 186 Detrusor external sphincter dyssynergia (DESD), 85 MS, 92f-93f, 95f detrusor hyperreflexia, 107, 108

331

Index

SCI, 8, 121 stents, 108 Detrusor function, 186 Detrusor hyperactivity with impaired contraction (DHIC), 77,207,209f Detrusor hyperreflexia, 12-14, 18,41 CVA, 67,68 DESD MS, 107-108,108 SCI, 120-121, 122f MS, 91f-95f treatment, 101-1 02 neurogenic capsaicin, 129 SCI, 120-1 l2 urethral obstruction MS, 106-107, 108 Detrusor instability, 4 1 augmentation cystoplasty, 3 15-325 DM treatment, 145 electrical stimulation, 297-3 12 Detrusor myectomy MS, 105 Detrusor myotomy MS, 104 Detrusor sphincter dyssynergia (DSD) CVA, 69 spinal-cord injury, 204-205 DHIC, 77,207,209f Diabetes mellitus (DM), 139-146 diagnosis, 140-141 epidemiology, 139 female urinary retention, 202-203 pathophysiology, 143-145 presentation, 139-140 prevalence, 139 treatment, 145 urodynamic findings, 142-143, 142f Diabetic cystopathy, 14I,143-144 female urinary retention, 202-203 Diabetic neurogenic bladder diagnosis, 141-142 Diazepam, 279 Dicyclomine, 145

Dicyclomine hydrochloride, 283 Dimethysulfoxide (DMSO), 286 Distal urethral sphincter, 249 Ditropan, 101, 145,266,282 Diuresis renography, 56 DM, See Diabetes mellitus (DM) DMSO, 286 Doxazosin, 74,232,279 DSD CVA, 69 spinal-cord injury, 204-205 Dysfunctional voiding female urinary retention, 205-206 Dyspareunia, 30 Dysuria, 28

E Elderly urodynamic studies technical difficulties, '72 Electrical stimulation, 167 action mechanism, 299-300 acute maximal functional, 300 chronic, 300 detrusor instability,297-3 12 electrode placement, 302f needle stimulation devices, 304-305 nerve pathways, 301f overview, 303t position points, 30 1 f SNS, 305-3 1l transanal devices, 302-304 transvaginal devices, 302-304 Electrolyte disorders augmentation cystoplasty, 322-323 Electromyography (EMG), 46-48 CVA, 69 elderly, 72 female urinary retention,188-1 89,206 Elmiron, 286-287 EMG. See Electromyography (EMG) Emptying function, 186.See aZso Voiding Endocrine dysfunction

332

female urinary retention, 198 Endoscopic urethrotomy, 240-24 1 Endoscopy bladder, 52-53 extraurethral incontinence, 54-55 female bladder outlet,53-54 male bladder outlet, 54 Enteroceles female urinary retention,198-1 99 Ephedrine, 170,259,285 Estrogen, 168-1 69,285-286 External sphincter innervation, 277f spasticity, 207 Extraurethral incontinence endoscopy, 54-55

Index

Fluid restriction poststroke, 78 Fluoroscopy elderly, 72 pressure flow testing, 19 1-1 92 sphincter dysfunction, 208f urethral obstruction, 192f-197f Fluxetine, 287 Foley catheter poststroke, 79 Frequency, 28 SNS, 309-3 10 Functional etiology female urinary retention, 202-207 Functional system classification voiding dysfunction,5t4t, 2 1-23, 26-27

F Failure to empty pharmacological therapy, 277-28 1 bladder emptying facilitation, 277278 BPH outlet obstruction, 23 1-234, 280-28 l decrease outlet resistance, 279-280 Failure to store phamacological therapy, 281-287 decrease bladder contractility, 28 1-285 increase outlet resistance, 285-286 inflammatory bladder conditions, 286-287 nocturnal enuresis, 287 Fecal impaction female urinary retention, 198 Female bladder outlet endoscopy, 53-54 Female urethra endoscopy, 54 Finasteride, 232,233-234,280-281 Finetech-Brindley sacral anterior root stimulator, 13 1 Flavoxate hydrochloride, 283

G Gait, 88 Genitals male examination, 32 Glutaraldehyde cross-linked (GAX) bovine collagen, 172,260 Gynecologic causes bladder outlet obstruction, 198-200

H Hald Bradley classification voiding dysfunction, 13-14, 13t Hemiplegia urodynamic studies, 70t Heparin, 286 Hinrnan’s syndrome, 205-206,280 Holium laser, 75 Hydronephrosis female urinary retention, 198 Hyoscyamine, 266,282 Hyoscyamine sulfate, 282 Hyperactive bladder filling, 5 Hyperchloremic metabolic acidosis, 322

333

Index

Hysterectomy female urinary retention, 204 Hytrin, 279

I

IS, 5,286 IVU, 55-56

K

Kegel exercises, 167,259 IDDM female urinary retention, 202-203 L 1 Ilia1 intesusception nipple technique, 32 Imipramine, 145,259,283-284 Laminectomy, 157 Irnrnobility Lapides classification female urinary retention, 198 voiding dysfunction, 15-1 7, 16t Impaired detrusor contractility, 207-209 Laser sphincterotomy Implants MS, 108 SUI, 170-1 73 Leak-point pressure, 45-46 Indigo laser prostatectomy, 75 Learned voiding dysfunction, 205-206 Indwelling Foley catheter Lesions poststroke, 79 lower motor neuron (LMN),1-12 In-Flow device, 76, 76f urinary retention, 200 Ingelmann-Sundberg procedure vaginal MS, 102-1 03 urinary retention, 200 Injection therapy, 259-26 1 Levsin, 282 Insterstitial diode laser, 237 Linear PURR nomogram, 48f Insulin-dependent diabetic mellitus LMN (IDDM) areflexic bladder female urinary retention, 202-203 CIC, 127 Intermittent catheterization lesion, 1-1 2 myelodysplasia, 126 Low bladder compliance Internittent flow pattern, 36, 37f MS Intermittent self catheterization, 108-109 male, 97f International Continence Lower motor neuron (LMN) Society Classification areflexic bladder voiding dysfunction, 19-2 l , 19t CIC, 127 International Prostate Symptom Score, lesion, 1-12 29-30 Lower urinary tract InterStim Continence Control System,10 3 central innervation, 65-66 InterStirn device, 301 innervation, 149-1 54, 150t Interstitial cystitis (IS), 5, 286 Lower urinary tract symptoms (LUTS), 25 Intervertebral disc male bladder outlet obstruction, 226 prolapsed, 154-1 55 Lumbar disc disease, 149-1 58 Involuntary detrusor contractions clinical features, 154-1 55 classification, 4 1 evaluation, 155-1 56 Irritative voiding neurologic features, 157t symptoms, 28 neuropathophysiology, 149-1 54, 15Ot male bladder outlet obstruction, treatment, 157-1 58 226-227

334

104 transection, bladderurodynamics, 156 Lumbardiscprolapse,15 1-1 52,152f-153f LUTS, 25 male bladder outlet obstruction, 226

M Male bladder outlet endoscopy, 54 Male genitals examination, 32 Male suburethral sling, 265 Marion’s disease female urinary retention, 200 Meningocele, 123 Metabolic disorders augmentation cystoplasty, 322-323 Metoclopramide, 145, 158,278 Microwave therapy prostatic, 237-238 Micturition, 1 16,276,298-299 CVA, 67 disrupted, 298-299 neurophysiology, 85-90 reflex pathways, 1 16-1 18, 1 17f two-phase concept, l 16 Micturition cycle,4,4647 Micturition diary urinary incontinence, 87 Micturition reflex, 85 Minipress, 279 Motor paralytic bladder, 16 MRI, 56 MS. See Multiple sclerosis (MS) MS 800 artificial urinary sphincter, 261 Mucosal structure disease female, 20 l f Multichannel subtracted pressure flow testing female urinary retention, 188 Multiple sclerosis (MS),83-1 09 ADL, 99 alcohol injection, 103-104 augmentation cystoplasty, 105-109 behavior modification,99-1 00

Index

c o m o n urodynamicpatterns,90, 9 f-97f l concurrent stress incontinence, 109 continent urinary diversion,105-1 09 cystolysis, 104 denervation treatment, 102 detrusor areflexia, 108-1 09 detrusor hyperreflexia DESD, 107-1 08 DESD and urethral obstruction, 108 treatment, 101-1 02 urethral obstruction, 106-1 07 detrusor myectomy, 105 detrusor myotomy, 104 diagnostic evaluation, 86 etiology, 84 female urinary retention, 205 incidence, 83 laser sphincterotomy, I08 physical examination, 88-89 sphincter stent, 108 subtrigonal phenol injection,103-1 04 transvaginal denervation, 102-1 03 upper urinary tract evaluation, 89 urinary tract symptoms, 86 urodynamic evaluation, 89-90 urologic history, 86-88 videourodynamics, 90, 9 l f-97f Myelodysplasia, 123-1 26 etiology, 123-124 ureteral reimplantation, 32 1 Myelomeningocele child urodynamic study, 50f diagnosis, 124-1 25 Myo-inositol peripheral nerves, 144

N Nd:YAG laser MS, 108 Needle electrical stimulation devices, 304-305

335

Index

Neoplasms augmentation cystoplasty, 324 Neural tube defects children incidence, 123 Neurogenic bladder diabetic diagnosis, 141-142 ureteral reimplantation, 321 Neurogenic detrusor hyperreflexia capsaicin, 129 Neurogenic dyssynergia female urinary retention, 204-205 Neurogenic etiology female urinary retention, 202-207 Neurologic evaluation, 32-33 female urinary retention, 188 Neurostimulation SCI, 130-1 3l Nifedipine, 283 Nitric oxide (NO),279,284 Nocturia, 28 selective elderly, 72 Noninvasive uroflowmetry female urinary retention, 188 Non-organic urinary retention fernale urinary retention, 205-206 North American Contigen Study Group, 172

Orthotopic cystoplasty, 3 16 Overworked bladder, 41 Oxybutynin chloride, 101, 145,266,282

P

Pad test post-prostatectomy incontinence, 257 urinary incontinence, 8’7 Parasympathetic agonist agents pharmacologic manipulation female urinary retention, 2 15 Parkinson’s disease female urinary retention, 198 Pelvic floor muscle exercises, 99-1 00, 167, 259 Pelvic floor relaxation voiding, 2IO Pelvic nerve injury female urinary retention, 203-204 Pelvic pain, 30 Pelvis examination, 32 Pentosanpolysulfate, 286-287 Percutaneous bladder neck suspension, 175, 176f Pereyra-Raz bladder neck suspension, 174, 175f Peripheral nerves myo-inositol, 144 Peripheral nervous system degeneration 0 female urinary retention, 203 Pessaries Obstruction diagnosis vaginal, 168 method, 187 PG, 278 Obstructive etiology Pharmacologic manipulation female urinary retention, 198-202 parasympathetic agonist agents Obstructive voiding female urinary retention, 2 15 symptoms, 28 Phenoxybenzamine, 279 male bladder outlet obstruction, 226 Phenylpropanolamine (PPA), 170, Oliguria 259,285 female urinary retention, 198 Physiologic etiology Open prostatectomy, 251-252 female urinary retention, 207-209 Phytotherapeutics, 281,281t Opioid antagonists, 278

336

PMC, 65-66 Pollen extract, 281 Polyneuropathy DM, 144 Polytetrafluoroethylene (Teflon) paste, 259-260 Pontine micturition center (PMC), 65-66 Post-prostatectomy incontinence, 247-268 etiology, 255-256,255t evaluation, 256-258 cystourethroscopy, 257 pad-weight test, 257 patient history, 256-257 physical examination, 257 RUG, 257 urinalysis, 257 urodynamic, 257-258 VCUG, 257-258 VLPP, 258 incidence, 248 open prostatectomy, 251-252 radical perineal prostatectomy, 253-254 radical retropubic prostatectomy, 252-253,254f treatment, 258-267 bladder dysfunction, 265-266 bladder dysfunction/sphincteric incompetence, 266-267 cost comparison, 267 sphincteric incompetence, 259-26 l TUR, 251-252 Postvoid residual (PVR), 34,228-229 elderly, 72 Potassium channel openers, 283 PPA, 170,259,285 Prazosin, 279 Pregnancy augmentation cystoplasty, 324-325 Pressure flow testing female urinary retention, 189 radiographic monitoring, 191-1 92 Primary bladder neck obstruction female urinary retention, 200

Index

Pro-Banthine, 266, 282 Procardia, 133 Prolapsed intervertebral disc, 154-1 55 Prompted voiding schedule poststroke, 78 Propantheline, 266,282 Propantheline bromide, 282 Proscar, 232-234,280-28 l Prostaglandin inhibitors, 283 Prostaglandin (PG), 278 Prostate adenoma, 252f Prostate gland anatomy, 249-25 1 examination, 88 Prostatic microwave therapy, 23 7-23 8 Prostatic stents, 74 Proteoglycans, 286 Proximal urethra spasticity, 206-207 Proximal urethral sphincter, 249 Prozak, 287 Pseudodyssnergia, 242 Pseudoephedrine, 170,259,285 Psychogenic cause female urinary retention, 198 Pubovaginal sling, 78, 177f lumbar disc disease, 158 Pumpkin seeds, 281 PURR nomogram, 48f PVR, 34,228-229 elderly, 72 Pyelonephritis, 323-324 Pygeum africanum, 28 l

R Radical hysterectomy female urinary retention, 203-204 Radical perineal prostatectomy, 253-254 Radical retropubic prostatectomy, 252-253,254f Radiographic monitoring pressure flow testing, 19 1-1 92 Rectoceles female urinary retention,198-1 99

Index

Reflex neurogenic bladder, 17 Regian, 145, 158,278 Renography, 56 diuresis, 56 Replacement cystoplasty, 3 16 Retention SNS, 310-311

S Sacral dermatomes, 88 Sacral nerve stimulation(SNS), 299-300, 305-3 1l adverse effects, 3 1 1 clinical efficacy, 308-3 1l retention, 310-3 1 1 urge incontinence, 309 urgency/frequency, 309-3 10 surgical implantation, 308 temporary electrode implantation, 306307 test stimulation, 306, 307f Sacral neuromodulation female urinary retention, 2 15 Saw palmetto, 28 l SCI. See Spinal cord injury(SCI) Segmental neuronal demyelination female urinary retention, 203 Selective nocturia elderly, 72 Self catheterization lumbar disc disease, 158 Self intermittent catheterization. LMN and areflexic bladder, 127 Sensation, 40 Sensory neurogenic bladder, 15-1 6 Sertraline, 287 Sexual dysfirnction, 30, 64 Silver nitrate, 286 Sling pubovaginal, 177f suburethral male, 265 vaginal wall, 178f, 179 Sling displacement

337

female urinary retention, 2 10-2 12 Sling obstruction cystoscopic image, 21If Sling procedures female urinary retention, 2 10-2 12 SUI, 176-1 80, 177f-178f Smooth muscle relaxants, 145 Smooth sphincter, 4 Smooth sphincter dyssynergia, 19 SNS. See Sacral nerve stimulation(SNS) Somatosensory Evoked Potentials (SSEP), 120 South african star grass, 281 Spasticity external sphincter, 207 proximal urethra, 206-207 Sphincter activity urodynamic testing, 47 artificial urinary, 26 1-265,262f-264f erosion, 264 failure, 263-264 SUI, 180 balloon dilation SCI, 130 distal urethral, 249 dysfunction female urinary retention, 206-207 fluoroscopy, 208f dyssynergia, 19 external innervation, 277f spasticity, 207 function, 186 prostheses SCI, 130 proximal urethral, 249 smooth, 4 stent MS, 108 striated, 19 urethral dysfunction, 186 male, 249,250f urinary

338

Index

anatomy, 249-25 l SCI, 132 artificial, 180 SSEP, 120 Sphincteric incompetence Stents post-prostatectomy urethral, 241-242 artificial urinary sphincter, 26 1-265, BPH, 238 262f-264f Storage with bladder dysfunction, 266-267 symptoms, 28 conservative treatment, 259 Stranguria, 25 injection therapy, 259-26 l, 260t Stress incontinence, 29 male suburethral sling, 265 female pharmacologic treatment, 259 urodynamic study, 49f Sphincteric relaxation, 186 management, 168 Sphincterotomy MS, 109 SCI, 129 Stress urinary incontinence (SUI),16318l Spina bifida aperta, l23 behavioral interventions, 165-1 68 Spina bifida cystica, 123 behavioral therapy, 165-1 66 Spina bifida occulta, 123 biofeedback, 166-1 68 Spinal cord dysraphisms containment devices, 168 neonatal support prosthesis, 168 management, 124126 bladder neck suspension,173-1 76 renal ultrasound, 124 laparoscopic, 175-1 76 urodynamics, 124-1 26 retropubic, 173-1 74, 174f urological evaluation, 124-1 25 transvaginal, 174-1 75, 175f-176f VCUG,124 pharmacological management, Spinal cord injury (SCI), l 19-123, 168-1 70 121, 123 alpha-adrenergic agents, 170 cause, l 19 estrogen, 168-1 69,286-287 complication surgery, 170-180 prevention, 131-1 33 artificial urinary sphincter, 180 detrusor sphincter dyssynergia, bladder neck suspension,173-1 76 204205 implants, 170-1 73 long-term urologic management, 126sling procedures, 176-180, 13 1 177f-178f mortality, l 15-1 16 treatment outcome, 163-1 65, 164t pharmacologic therapy, 128 Striated sphincter dyssynergia, 19 recovery phase, l 19-120 Stroke. See Cerebrovascular accidents spinal shock, 1 19 Substitution cystoplasty, 3 16 surgery, 129 Subtrigonal phenol injection ureteral reimplantation, 32 1 MS, 103-104 urodynamic evaluation, 120-1 2 1 SUI. See Stress urinary incontinence(SUI) Spinal shock, l 19 Suprapubic catheter Split cuff nipple, 322 poststroke, 79 Spontaneous perforation Surgery augmentation cystoplasty, 324 prio Squamous cell carcinoma urinary tract function, 3l

339

Index

Surgical capsule, 249 Suture placement female urinary retention,209-2 l0 Suture tension female urinary retention,209-2 10 Symmetric peripheral neuropathy DM, 144

TUNA, 75,237 TUR, 236236,25 1-252 TVP, 235-236 Two-Phase Concept of Micturition, l 16

U

Ultrasonography, 56 Unconscious incontinence, 29 Uninhibited neurogenic bladder, 16 Tamsulosin, 233 Upper motor neuron (UMN) lesion,1-12 Ureteral obstruction TCA, 10 1,283-284 female urinary retention, 198 Teflon injections, 259-260 Ureteral reimplantation TENS, 306305 Terazosin, 74,232,279 augmentation cystoplasty, 321 Timed voiding Ureters DM, 145 augmentation cystoplasty, 32 1-322 schedule Urethra poststroke, 78 female SUI,165-166 endoscopy, 54 Tolterodine, 77, 101, 266, 282 Urethral dilation, 240-24 l Transanal electrical stimulation devices, Urethral obstruction 302-3 04 detrusor hyperreflexia Transcutaneous electrical nerve stimulaMS, 106-107,108 tion (TENS), 306305 fluoroscopy, 192f-197f Transurethral electrovaporization of Urethral sphincter prostate (TVP), 235-236 dysfunction, 186 Transurethral incision of prostate male, 249,250f (TUIP), 236,239-240 Urethral stent, 241-242 Transurethral microwave thermotherapy, BPH, 238 75 Urethral stricture disease, 240 Transurethral needle ablation(TUNA), 75, Urethra position 237 urinary retention, 188 Transurethral resection (TUR),236236, Urethra suspension 25 1-252 female urinary retention,209-2 l0 Transvaginal denervation Urethrolysis MS, 102-1 03 clinical experience, 213t Transvaginal electrical stimulation defemale urinary retention, 12-2 2 14 vices, 302-304 Urge incontinence, 29 Transverse myelitis incidence, 297 female urinary retention, 205 SNS, 309 Tricyclic antidepressants (TCA), 10 l, 283therapy, 166 284 Urgency, 28, 166 Trigger voiding, 128 SNS, 309-3 10 TUIP, 236,239-240 Urinalysis, 33, 227, 318

T

340

Urinary diversion continent MS, 105-1 09 SCI, 130 Urinary incontinence, 28-29 augmentation cystoplasty, 323 child urodynamic study, 50f micturition diary and pad test, 8'7 Urinary infection augmentation cystoplasty, 323-324 Urinary retention female, 185-2 15 etiology, 197-209 evaluation, 186-1 98 pathophysiology, 186 treatment, 209-2 15 Urinary sphincter anatomy, 249-25 1 artificial SUI, 180 Urinary tract lower function, 3-5 innervation, 149-1 54, 150t Urinary tract imaging, 55-57 lower, 57 upper, 55-56 Urinary tract infection female urinary retention, 198,202 SCI, 131-1 32 Urinary tract symptoms multiple sclerosis (MS), 84-85, 86 Urine evacuation, 298-299 Urine storage, 298-299 abnormalities, 5-1 0 facilitation, 8t failure, 2 1 requirements, 4 Urispas, 283 Urodynamic classification voiding dysfunction, 18-19, 18t female urinary retention, 206 simplification, 75

Index

Uroflowmetry, 35-37,35f female urinary retention, 188 Urogenital diaphragm, 249 Urolume, 75, 108 Urosurge, 77,78f

v Vagina examination, 31-32, 88-89 urinary retention, 187-1 88 Vaginal cones, 16'7 Vaginal lesions urinary retention, 200 Vaginal pessaries, 168 Vaginal prolapse treatment,199-200 Vaginal stimulation, 30 1 Vaginal wall prolapse, 198 sling, 178f, 179 Valsalva leak-point pressure,45-46 Valvular mechanisms female urinary retention, 2 15 VCUG, 57 female urinary retention,192-1 94 Vesical capacity, 186 Vesicoureteral reflux SCI, 132 Videourodynamics, 48"49,52f, 196 Voiding abdominal straining, 2 10 pelvic floor relaxation, l0 2 symptoms, 28 Voiding and intake diary, 34 Voiding cystourethrography (VCUG), 57 female urinary retention,192-1 94 Voiding difficulties augmentation cystoplasty, 323 Voiding dysfunction,25-57 classification, 1&23,26-27 Bors-Comarr, l 1-1 3, l l t Bradley, 14-1 5 functional system,5 t 4 , 2 1-23, 26-27

341

Index

Hald Bradley, 13-14, 13t International Continence Society Classification, 19-2 1, 19t Lapides,15-17,16t urodynamic, 18-19, 18t endoscopy, 5 1-55 bladder evaluation, 52-53 extraurethral incontinence, 54-55 female bladder outlet,53-54 male bladder outlet, 54 functional classification, 5t expanded, 6t laboratory testing, 33 learned, 205-206 patient history, 27-3 1 physical examination, 31-33 testing, 33-38 pad test, 37-38 postvoid residual, 34 uroflowmetry, 35-37,35f voiding and intake diary, 34 urinary tract imaging,55-57 lower, 57 upper, 55-56

urodynamics, 38-5 1 bedside cystometrics,49-5 1 CMG, 38-43,40f, 42f electromyography, 46-48 leak-point pressure,45-46 videourodynamics, 48-49,52f voiding pressureflow study, 43-45, 45f, 51f Voiding function, 186 Voiding pressureflow study, 43-45,45f, 51f Voiding reflux inhibition, 10 Vulvar lesions urinary retention, 200

W Wertheim hysterectomy female urinary retention, 204

z Zoloft, 287