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VOIDING DYSFUNCTION

URRENT CLINICAL UROLOGV 

Eric A. Klein, SERIES EDITOR 

Voiding Dysfunction: Diagnosis arzd Treatment, edited by Rodney A. 

Appell, 2000 

~ana~e~ent of Prostate Cancer, edited by Eric A. Klein, 2000

VOIDING 

DYSFUNCTION 

DUGNOSIS 

Edited by 

RODNEY A. APPELL, 

Chehnd Clinic Foundntion, 

Chehd OH 

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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. WJ 146 

V889 20001 

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6 16.6'24~2 1 

DNLM/DLC 00-027599 

for Library of Congress CIP

PREFACE 

The purpose of Voiding Dysfunction: Diagnosis and Treatment is 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 occur during 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 of the 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 problems are 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 by the extent to which people will go to try 

therapies (many unproven) at tremendous expense to make small improvements 

in the quality of their respective lives. 

Fortunately, knowledge of lower urinary 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: Diagnosis and Treatment for their timely response to my 

request to put down on paper, in an explicable manner, the current states of the 

art and science of voiding dysfunction. First, there is a presentation on the 

current background information necessary, to understand the physiology of the 

normal lower urinary tract and how to 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 and their adverse effects 

on voiding fbnction. This section includes discussions of specific diseases 

V

vi 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 modali- 

ties 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. 

References 

Rodney A. Appell, MD 

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 Pathophysiology and Classification 

of Voiding Dysfunction ..................................................... 3 

Alan J. Wein and Eric S. Rovner 

2 Voiding Dysfunction: Diagnostic Evaluation ....................... 25 

Victor W. ~ittj and ~ichael Ficazzola 

Part II, Neurogenic Vesico-Urethral Dysfunction 

3 Cerebrovascular Accidents ................................................ 63 

Serge Peter ~arinkovjc and Gopal H. Badlani 

4 Multiple Sclerosis ............................................................... 83 

Jerry G. Blaivas 

5 Diagnosis and Treatment of Spinal Cord injuries 

and Myeloneuropathie ................................................. 1 15 

Steven W. Sukin and Timothy B. Boone 

6 Diabetic Bladder Dysfunction ............................................ 139 

Howard B. Goldman and Rodney A. Appell 

7 Lumbar Disc Disease ....................................................... 149 

Howard B. Goldman and Rodney A. Appell 

Part 111. Female Voiding Dysfunction 

8 Treatment of Stress Urinary Incontinence ........................ 163 

Raymond Rackley 

9 Urinary Retention in Women ............................................ 185 

Roger R. Dmochowski 

Part N . Male Voiding Dysfunction 

10 Bladder Outlet Obstruction in Males ................................. 225 

Edward F. Ikeguchi, Alexis E. Te, James Choi, 

and Steven A. Kaplan 

Vii

... 

v111 Contents 

11 Post-Prostatectomy Incontinence ..................................... 247 

Harriette M. Scarper0 and J. Christian Winters 

Part V. Treatment Modalities 

12 Clinical Pharmacology ..................................................... 275 

Scott R. Serels and Rodney A, Appell 

13 Treatment of Detrusor Instability 

with Electrical Stimulation ............................................ 297 

Steven W. Siege1 

14 Treatment of Detrusor instability 

with Augmentation Cystoplasty ........................................ 31 5 

Joseph M. Khoury 

Index.. ................................................................................... ,326

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 Hyde Park, NY 

JERRY G. BLAwAs, 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 

JAMES CHOI, MD * Department of Urology, Columbia University Medical 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 University Medical 

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 


STEVEN A. KAPLAN, MD Department of Urology, Columbia University 


hsEPn M. KHOURY, MD, SCD 9 Division of urology, University ofNorth Carolina 

Medical Center, Chapel Hill, NC 

SERGE PETER MARINKOVIC, 

Medical Center, New Hyde Park, NY 

VICTOR W. NITTI, 


RAYMOND RACKLEY, MD 0 Section of Voiding Dysfunction, Department 

of Urology, Cleveland Clinic Foundation, Cleveland, OH 

ERIC S. ROVNER, MD Division of Urology, Hospital of the University 

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 

MD 0 Department of Urology, Long Island Jewish 

MD * Department of Urology, New York University Medical 

ix

X Contributol 

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

Nomvalk, CT 

STEVEN W. SIEGEL, MD Metropolitan Neurologic Specialists, St. Paul, MN 

STEVEN W. SUKIN, MD Scott Department of Urology, Baylor College 

of Medicine, Houston, TX 

ALEXIS E. ?"E, MD * Department of Urology, Columbia University Medical 


ALAN J. WEIN, PHD 0 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

I INTRODUCTION

This Page Intentionally Left Blank

l Pathophysiology and Classification 

of Voiding Dysfunction 

Alan J. Wein, MD, 

and Eric S. Rovner? MD 

CONTENTS 

NORMAL LOWER URINARY TRACT FUNCTION 

ABNORMALITIES OF FILLING/STORAGE 

AND EMPTYING: OVERVIEW 

CLASSIFICATION OF VOIDING DYSFUNCTION 

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 to make the 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 

3

4 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 second is that, 

whatever the details involved, one can 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 closed at 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 an anatomic 

sphincter, and one that is not under voluntary control (this includes 

the smooth musculature of the bladder neck and proximal urethra). 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 in the 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 more of 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 and emptying abnormalities. Within 

this scheme, however, these become readily understandable, and their 

detection and treatment can be logically 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 and Classification 5 

Table 1 

The Functional Classification of Voiding Dyshnction 

Failure to store 

Because of the bladder 

Because of the outlet 

Failure to empty 



during filling/storage or emptying (see Table 3). One can easily classify 

all known treatments for voiding dysfunction under the broad categories 

of whether they facilitate fillinghtorage or emptying and whether they 

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 S FILLING/STORGE 

AND EMPTYING: OVERVIEW 

The pathophysiology of 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 be expressed as phasic involuntary contractions, as low compliance, 

or as a combination. Involuntary contractions are most commonly seen 

in association with neurologic disease or following neurologic injury; 

however, they may also be associated with aging, inflammation or 

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


Table 2 

The kpanded Functional Classification 



Detrusor hyperactivity 

Involuntary contractions 

Suprasacral neurologic disease 

Bladder outlet obstruction 

Idiopathic 

Decreased compliance 

Neurologic disease 

Fibrosis 

Idiopathic 

Detrusor hypersensitivity 

Inflammatory 

Infectious 

Neurologic 

Psychologic 

Idiopathic 


Stress incontinence 

Nonfunctional bladder necldproximal urethra 


Because of the 

Neurologic 

Myogenic 

Psychogenic 

Idiopathic 

Because of the 

Anatomic 

bladder 

outlet 

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.


Table 3 

Urodynamics Simplified" 

Bladder 

FILLING/STORAGE Pvesb Pde,"(FCMGd) UPPf 

PHASE DLPPe 

FLUOROh 

EMPTYING 

PHASE 

Pve; (VC?V~G)~ Pde/ 

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,,,) and detrusor (Pdet) pressures during a filling cystometrogram 

(FCMG). 

dFilling cystometrogram. 

eDetrusor leak point pressure. 

fUrethral pressure profilometry. 

g Valsalva leak point pressure. 

h Fluoroscopy of outlet during fillinglstorage. 

"jTotal bladder and detrusor pressures during a voiding cystometrogram (VCMG). 

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 mechani- 

cally increasing bladder capacity; or, toward increasing outlet resis- 

tance, 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


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 


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 and Classification. 9 

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 


Parasympathomimetic agents 

Prostaglandins 

Blockers of inhibition 


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 


Transurethral resection or incision of the bladder neck 

Y-V plasty of the bladder neck 


Beta-adrenergic agonists 

At the level of the striated sphincter 

Biofeedback and psychotherapy 


Skeletal muscle relaxants 

Benzodiazepines 

Baclofen 

Dantrolene 

Surgical sphincterotomy, botulinum A toxin 

Urethral overdilation 

Urethral stent 

Pudendal nerve interruption 


Circumventing the problem 


Continuous catheterization 

Urinary diversion


may result from temporary or permanent alteration in one or more of 

the neuromuscular mechanisms necessary 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 muscle function, 

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. 


The purpose 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 be categorized in a number 

of descriptive systems. None are perfect.


Sensory neuron lesion 

Incomplete, balanced 

Complete, unbalanced 

Motor neuron lesion 

Balanced 

Imbalanced 

Sensory-motor neuron lesion. 

Upper motor neuron lesion 

Complete, balanced 



Incomplete, unbalanced 

Lower motor neuron lesion 

Complete, balanced 



Incomplete, unbalanced 

Mixed lesion 

Table 6 

The Bors-Comarr Classification 

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


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 in a similar analogy 

to the somatic nervous system to 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 neuron bladder 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 from these 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 LMN lesion is assumed to exist, implying detrusor 

areflexia. Exceptions occur and are 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 13 

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 measures the patient may use 

to increase intravesical pressure during attempted voiding are not suffi- 

cient 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 urodynamic variability exhib- 

ited 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 secondary to a number of factors such as chronic overdistention, 

infection, and reinnervation or reorganization of neural pathways fol- 

lowing 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


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 neuropathy is 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 based upon a conceptualization 

of central nervous system control 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 15 

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 neurons to the 

periurethrla striated musculature which synapse on pudendal motor 

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 loop 3, pudendal nerve afferents produce excitatory 

postsynaptic potentials in those motor neurons through loop 4B. 

These provide for contraction of the periurethral striated muscle during 

bladder filling and urine storage. The related sensory impulses arise 

from muscle spindles 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 recog- 

nizable 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

16 Wein Rovner 

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, one sees normal sensation with an involuntary 

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


initiate a bladder contraction voluntarily, but is often unable to do so 

during cystometry because sufficient urine storage cannot occur before 

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 neurogenic bladder 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 and is 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 or sensory 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 denervationlcentralization with secondary neuromorphologic 

and neuropharmacologic 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 and striated 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, and mixed 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.

18 Wein Rovner 

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 commonly associated 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 characteristi- 

cally associated with detrusor hyperreflexia and striated sphincter dys- 

synergia. Detrusor areflexia may be secondary 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 hyper- 

reflexia or normoreflexia exists. Thus, a typical Tl0 level paraplegic 

exhibits detrusor hyperreflexia, smooth-sphincter synergia, and striated- 

sphincter 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


Table 10 

The International Continence Society Classification“ 

Storage Phase Voiding Phase 

Bladder Function 

Detrusor activity 

Normal or stable 

Overactive 

Unstable 

Hyperreflexic 

Bladder sensation 

Normal 

Increased or hypersensitive 

Reduced or hyposensitive 

Absent 

Bladder capacity 

Normal 

High 

Low 

Compliance 

Normal 

High 

LOW 

Urethral Function 

Normal 

Incompetent 

“Adapted with permission from ref. 11. 

Bladder Function 

Detrusor activity 

Normal 

Underactive 

Acontractile 

Urethral Function 

Normal 

Obstructive 

Overactive 

Mechanical 

are many voiding dysfunctions that do not fit neatly into a urodynarnic 

classification system that is agreed upon by all “experts.” As sophisti- 

cated urodynarnic technology and understanding improve, this type of 

classification system may supplant some others in general use. 

International Continence Society Classz;ficdtion 

(see Table IO 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).


Normal bladder function during fillingktorage implies no significant 

rises in detrusor pressure (stability). Overactive detrusor function indi- 

cates 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. Normal urethral 

function during filling/storage indicates a positive urethral closure pres- 

sure (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 secondary to genuine stress incontinence, intrinsic sphinc- 

ter 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 be suppressed 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 (nonrelax- 

ation) with attempted micturition. Contraction may be owing to 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 inconti- 

nence would most likely be classified during storage as overactive


hyperreflexic detrusor, normal sensation, low capacity, normal compliance, 

and normal urethral closure function. During voiding, the dysfunction 

would be classified as normal detrusor activity and normal urethral 

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 et al. (13), and is an excellent alternative 

when a particular dysfunction does not readily lend itself to a generally 

agreed upon classification elsewhere, This simple-minded scheme 

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 use of 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 be recognized to properly utilize this system of classification. The


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 combi- 

nation 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 hyper- 

reflexia) can be circumvented (in a male) with an external collecting 

device. Alternatively, the deficit can be converted primarily to an empty- 

ing 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 insuffi- 

ciency” 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 underly- 

ing concepts can be used repeatedly to simplify many areas in neurourol- 

ogy. 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


of storage or emptying. Additionally, although the functional classifica- 

tion 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 thor- 

ough 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. 

1. 

2. 

3. 

4. 

5. 

6. 

7. 

8. 

REFERENCES 

Wein AJ. Barrett DM (1988) Voiding Firriction and Dysfimctioii: A Logical and 

Prnctical Approach. Chicago: Year Book Medical Publishers, Tnc. 

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. 

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. 

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. 

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. 

Bors E. Cornarr AE (197 1) Neurological Urology. Baltimore: University Park 

Press. 

Hald T, Bradley WE (1982) The Urirtai? Bladder: Neurology and Dynamics, 

Baltimore: Williams and Wilkins. 

Lapides J (1 970) Neur~muscular, vesical and ureteral dysfunction. In: Campbell 

MF and Harrison JH, eds., Urology. Philadelphia: WB Saunders Co, pp. 1343- 

1379.


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 Nertro- 

Urology. 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. lid 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 


HISTORY 

PHYSICAL EXAMINATION 

LABORATORY TESTING 

SIMPLE TESTS 

FOR EVALUATING VOIDING DYSFUNCTION 

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 diffi- 

culty 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 


Edited by: R. A. Appell 0 Hurnana Press Inc., Totowa, NJ

26 Nitti and Ficazzola 

or pelvic pain may exist. The second way in which voiding dysfunction 

presents is in the form of urinary tract decompensation such as 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. There are also patients who have diseases 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 and degree of bother of symptoms, the 

presence of urinary tract decompensation, and coexisting 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. Before discussing 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. 


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 clas- 

sification system proposed and popularized 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:

Chapter 2 I Diagnostic Evaluation 27 

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. 

These two concepts can be combined so that one can imagine 

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 

an underactive-or hypocontractile-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 Diokno et 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. Each symptom should be characterized as to its onset,


frequency, duration, severity, and bother; and exacerbating or relieving 

factors. It is important to note whether the onset of the symptom 

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 present with 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 types of voiding dysfunction. Urgency 

is defined as an intense desire to void 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 reflect excessive 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 micturition and implies bladder, urethral, 

or prostatic inflammation. Obstructive voiding symptoms include 

decreased force of urinary stream, straining to void, 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 consistent with the functional classification 

presented above and may be more useful when evaluating patients 

initially by history. 

One of the most distressing of all urinary symptoms is incontinence. 

When evaluating the symptom of 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

Chapter 2 / Diagnostic Evaluation 29 

loss of urine, however, this can be further characterized according to 

the information relayed by the patient: 

1. 

2. 

3. 

4. 

Urge incontinence: The symptom is incontinence is associated with a 

sudden uncontrollable desire to void. This condition is usually due to 

involuntary detrusor contractions. 

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 condi 

tion may be caused by sphincter abnormalities or bladder overactivity 

provoked by physical activity. 

Unconscious incontinence: The symptom of incontinence is uncon- 

scious and occurs without patient awareness of urges or stress or 

increases in abdominal pressure. This condition may be caused by 

bladder overactivity, sphincter abnormalities, overflow, or extraurethr 

causes such as a fistula or ectopic ureter. 

Continuous leakage: The symptom is a complaint of continuous loss 

of urine. This may be caused by sphincter abnormalities or extraure- 

thral 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 and when 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 symptoms are acute, or subacute, history may reveal 

an obvious cause of transient voiding dysfunction as amedication or acute 

nonurologic illness. This is demonstrated by the 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. Two such 

example are the American Urologic Association Symptom Index (International 

Prostate Symptom Score), originally designed to assess men 

with LUTS secondary to benign prostatic hyperplasia (6), and the I- 

QOL, 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 on an individual 

patient' S quality of life that drives evaluation and treatment decisions. 

Symptom scores and quality of life assessments are very useful in


monitoring response to treatment for an individual or in clinical 

trials. 

After a thorough assessment of 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 symptoms that 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 and voiding 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. Examples of 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 hormone status (pre-, 

peri-, or postmenopausal) and the onset of symptoms with changes in 

status should be noted. Estrogen deficiency may cause or contribute


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 (urologi- 

cal, 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 is important; however, certain aspects of 

the exam need to be emphasized. A focused physical examination 

should be performed to: 

1. 

2. 

3. 

4. 

5. 

6. 

Assess the bladder for masses and fullness; 

Assess the external genitalia; 

Assess the pelvic floor, including anal sphincter tone, and thoroughly 

examine for support defects, prolapse, and other pelvic conditions 

in women; 

Assess the prostate in men; 

Demonstrate incontinence in patients with that symptom; 

Detect neurologic abnor~alities that 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 performed to 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


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, bulbocav- 

ernosus 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 regard- 

ing voiding dysfunction. Symptoms related to voiding dysfunction may


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 with a 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 medical illness such as diabetes, which can be discovered as a result 

of an abnormal urine analysis. When abnormalities are found on urine 

analysis, further testing may be warranted such as urine 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 on patient 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


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 extremely useful 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 an indication 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 determined noninvasively by ultrasonography. Portable 

bladder scanners based on ultrasound technology are now available to 

determine bladder volume.


'I 

I J 

i time to maximum tiow 

I 

Flow time 

maximum 

time I 

I 

I 

Fig. 1. Normal flow curve and pattern 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 int~~ittent pattern. 

4. Maximum flow rate (Qmax): The highest flow rate achieved during the 

voiding episode (i.e. the highest point on the curve).


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 Qave in 

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 Qmax 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 dysfunc- 

tion. 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


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

125 ml& Flow Rate : 

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

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

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

Results of UROFL 

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

Voiding Time T100 65 S 

Flow Time TQ 42 S 

Time to max Flow TQnax 17 S 

Max Flow Rate Qmax 5.5 ml/s 

Ruerage Flow Rate Qave 2.8 ml/s 

Vo i ded Vo 1 ume Vcomp 118 m1 

Fig. 2. Abnormal flow pattern, showing interrupted stream and low Qmax 

(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, Qtnm and 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 median of 20.3 mL/s (40-44 yr) to 11.5 

mL/s (75-79 yr), and voided volume decreased 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 used to quantify urine loss based on the measurement 

of weight gain of absorbent pads over a period of time. Several


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 commonly used 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 used to 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 how 

when and why a urodynamic investigation should be performed. There 

are situations in which the information gained from history and physical 

exam, and simple 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 more comprehensive and 

precise way. For example, sometimes a 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 from the 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 a study. 

2. Design the study to answer these questions. 

3. Customize the study as necessary.


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 and the 

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 moni- 

toring of bladder pressure during filling (cystometrogram), monitoring 

of bladder pressure and simultaneous urinary flow rate during voiding 

(voiding pressure Bow study), and monitoring of pelvic Boor and exter- 

nal sphincter activity (electromyography). Usually abdominal pressure 

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 com- 

bined 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 cooper- 

ation 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) or gas (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).


Filling/storage phase 

Volume 

Fig. 3. Idealized normal adult cystometrogram. Phases I, 11, and I11 occur during 

filling and phase IV during voiding. Phase I 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 properties of the bladder reach 

their limit phase, IT1 is entered where pressures begin to increase just prior to 

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 there- 

fore 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, under certain 

circumstances, a bladder may contract involuntarily. Involuntary con- 

tractions 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, 

or in many cases is “idiopathic.” Activity may be spontaneous or 

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 feel Comfortable classifying any involuntary 

rise in detrusor pressure that is accompanied by an urge as detrusor 

instability. 

2. Detrusor hyperreflexia: involuntary contractions associated with a 

known neurologic lesion. Typically, these are upper motor neuron 

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 

as smooth muscle is replaced by collagen. It can 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 shown to have a deleterious effect on the kidneys.


pressure 

cm water 

Involuntary contractions 

PHASIC INSTABILITY 

Detrusor instability 

or 

Destrusor hyperreflexia 

Volume 

ml 

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 and that distinction would be determined by the absence or 

presence of a neurological lesion. 

McGuire and associates have shown 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) is probably less important than the absolute 

bladder pressure during filling (Fig. 5). 

When bladder pressure is monitored through a 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 abdominal pressure 

(Pabd) is subtracted from Pves to give the detrusor pressure (Pdet). 

Abdominal pressure can be recorded via a small balloon catheter that


Fig. 5. Impaired compliance. This CMG shows a gradual loss of compliance 

between 40 and 280 m1 with filling pressures of 17 cm H20 at 280 mL. Between 

280 m1 and 330 mL there is a rapid rise in pressure to 41 cm H20 which continues 

to rise to 51 crnH20 until filling is stopped at 400 mL. The storage pressures 

occurring from 300 m1 on clearly present potential danger to the kidneys, Adapted 

with permission from ref. 26. 

is place~d in 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 FLOW STUDY 

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 measure- 

ment 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,


a 

B 

. . 

- loo 

- 100 

- rm 0 

-100 0 

0 

WeS 

cm HZO 

-5 

.. . 

cm H20 

P-bd 

ern H20 

Wet 

em H20 

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.


I l l I I I I I i l l 1 1 I I I I I I I I I I 

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

"W 

. , . : , . . , . : . * , . . : * . * * . : , . . . . . flow 

. . . . . . . . . . . . . . . . . . . . . . . . . ' . * E. 

. . . . . . . . . . . . . . . . . . . . . . . . . . *t 

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 loa0 UDS-120 

425min 

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 

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

. . . . . . . . . . . . . . . . . . . . . . . . . . ’1% . flaw 

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . - 0 

. . . . . . . . . . . . . . . . . . . . . . . . . . . - 8- 

. . . . 

Fig. 8. Classic bladder outlet obstruction seen as high pressure-low flow voiding. 

Pves, intravesical pressure; Pabd, abdominal pressure; Pdet, detrusor pressure. 

Adapted with permission from ref. 29a. 

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 leak 

point pressures are suggestive of intrinsic urethral dysfunction. 

2. Bladder leak-point pressure (BLPP). This pressure, also known as 

detrusor leak-point pressure, is the amount of detrusor pressure require 

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, 

usually in cases of impaired compliance (Fig. 12). The higher the 

BLPP, the more resistance is provided by the sphincter and the more 

likely is upper tract damage. BLPP that is 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


200 

Pdet 

Unobstructed 

0 t I 

0 Flow 25 

Fig. 9. The Abrams-Griffiths Nomogram. Maximum flow rate and the conesponding 

detrusor pressure at maximum flow are plotted against each other, with detrusor 

pressure in cm H20 on the y-axis and uroflow rate in mL/s on the x-axis. Data 

from 117 males (>55 years) evaluated for possible prostatic obstruction were used 

to create zones on their graph representing obstructed, unobstructed and equivoc 

micturition. The location of 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 inconti- 

nence. 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 (detrusor- 

external sphincter-dyssynergia). Either can result in significant voiding


20 30 40 50 

pre 17/18 TURP 19/20 post 

Grade: IllN -> OIN 

Type: corn pro3 I v e 

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 I11 to VI, increasing severity of obstruc- 

tion. 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 radio- 

graphic 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


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

UDS-l20 

J I I I I I I I ~ I I I I I I I I I 1 I I I I ~ I I I I I I I ~ ~ 

*;til ' 1Iw 

l 

~ 1 I 

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

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

*)it ' ' '190 

.............................. M 

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

I 

0 

an H20 

Fig. 11. Urodynarnic study of a 60-year-old female with stress incontinence. The 

multiple spikes in Pves and Pabd represent coughing and straining. The point 

where leakage was demonstrated, marked by the vertical line, was at a Pves (and 

Pabd) of 11 1 cm HzO. This is the abdominal leak point pressure (ALPP) which 

is usually measured on the Pabd curve. 

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, can be performed without any special urodynamic equipment. 

The urodynamic information 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 undue discomfort 

for a particular patient. Simple CMG can be done with a 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


j : I 

1: 

l I l t l l l l l l I I I I l I l I I l l l l l l l Y l l l l l l l l t 

. 45 ' 

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

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

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

BL 

t 

* 

* ' 

I 

I " 

I 

' * " " ' 

* I 

" ' " " ' ' 

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

.................... ...'.!...'..... 

. f 

. I 

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

l * . p"'. 

UDS-120 

PIbd 

Fig. 12, Urodynamic study of a child with myelomeningocele and incontinence. 

The patient bas poorly a compliant bladder with Pdet rising during filling. 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. The catheter 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, or abdominal 

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


Fig. 13. Normal electromyography of the pelvic floor during a pressure flow study. 

Note the voluntary increase in ENIG activity during the involuntary detrusor 

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 be raised 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 and voiding dysfunction in order to assess 

the bladder, the urethra, and prostate and look for extraurethral causes 

of incontinence.

52 Nitti 

Ficazzola 

Fig. 14. Videourodynamic evaluation of 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 forth flow) is as well 

as fluoroscopic image during voiding. There is a sustained detrusor contraction 

of >40 cm H20 with no opening of the bladder neck and flow. no Without imaging, 

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 sug- 

gest 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 an unstable bladder unless 

microscopic hematuria is present (40,41). This would support the rou- 

tine 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


Fig. 15. Bedside or eyeball urodymanics. A urethral catheter is placed in the 

bladder and raised vertically. A syringe (without its plunger) is connected to the 

end of the catheter and the bladder filled. is Adapted with permission from ref. 26. 

intravesical pathology. However, cystourethroscopy is extremely help- 

ful 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 dysfunc- 

tion is managed by a chronic indwelling catheter or bladder augmen- 

tation or substitution. 

Evaluation of the Fmale Bhdder Outlet 

Endoscopic evaluation of the female bladder outlet in cases of stress 

incontinence has been advocated by several authors (433). However, 

others have found it to be inferior to other tests such as urodynamics 

(44-46). Most experts would now agree 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 extremely helpful; 

for example, in cases of urethral trauma or foreshortening, previous


anti-incontinence surgery, suspected intraurethral pathology (e.g., ure- 

thral 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 of 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 impaired detrusor 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 on BPH made the following recommendation: 

“Diagnostic endoscopy of the lower urinary tract is an optional test 

in the standard patient with symptoms of 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 an 

invaluable 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


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 scan- 

ning, are an important part of the evaluation. Specifically, when detri- 

mental 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 work- 

up 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 be 

a 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 evalua- 

tion. 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 intra- 

venous urography (IVIJ), ultrasonography, computerized tomography 

(CT scan), magnetic resonance imaging (MRI), and isotope scanning. 

The usefulness of each individual test often depends on local exper- 

tise. 

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


anomalies, fistula, stones, and tumors 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). Confirmation of 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 it is 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 be used 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 in response 

to treatment. 

CT scanning can also provide much useful information about the 

anatomy of the upper urinary tract. Information can be independent of 

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 

advantage over 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).


Lower Urinary Truct Imuging 

When anatomical factors are considered as a possible cause of void- 

ing dysfunction, lower urinary tract imaging can be useful. A plain 

radiograph of the abdomen and pelvis (KUB) can determine the pres- 

ence 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 be useful 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 urody- 

namic studies is important. We prefer videourodynamics in such cases 

(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. 

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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. 

52. Hvistendahl JJ, Pedersen TS, Schmidt F, Hansen W, Djurhuus JC, Frokier J (1987) 

The vesico-renal reflex mechanism modulates urine output during elevated bladd 

pressure. Scand J Urol Nephrol 186(31 suppl.): 24. 

53. O’Reilly PH (1992) Diuresis renography. Recent advances and recommended 

protocols. Br J Urol 69: 113.

GO Nitri and Ficazzola 

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 in women. 

J UPUZ 161: 1535-1540.

11 NEUROGENIC VESICO-URETH 

DYSFUNCTION


3 Cerebrovascular Accidents 

serge Peter Mdrinkovic, MD 

md Gopd H. Badhi, MD 

CONTENTS 

INTRODUCTION 

CENTRAL INNERVATION 

OF THE LOWER URINARY TRACT 

AND THE PONTINE MICTURITION 

CENTER (PMC) 

INCONTINENCE 

INCIDENCE OF URINARY 

PATHOPHYSIOLOGY OF INCONTINENCE 

EARLY PRESENTATION 

LATE PRESENTATION 

URODYNAMICS STUDIES 

HEMISPHERIC DOMINANCE 

AND VOIDING DYSFUNCTION 

UROLOGICAL EVALUATION 

HISTORY 

TECHNICAL DIFFICULTIES 

INTERPRETATION OF THE STUDY 

SPECIFIC SITUATIONS 

MEDICAL AND SURGICAL 

URINARY RETENTION IN WOMEN 

URINARY INCONTINENCE IN MEN 

AND WOMEN 

ALTERNATIVE THERAPIES 

SUMMARY 

REFERENCES 

MANAGEMENT 

From: Current Clinical Urology: Voiding Dysfinction: Diagnosis and Treatment 

Edited by: R. A. Appell 0 Hurnana Press Inc., Totowa, NJ 

63

64 Marinkovic 

INTRODUCTION 

Cerebrovascular accidents (CVA) or stroke are a common and serious 

neurologic event in the elderly. The residual effects can be permanent 

or temporary and vary in their morbidity. These impairments may 

include the loss of memory, vision, speech, motor function, and control 

of micturition. A CVA is defined as the acute onset of a focal neurologic 

deficit caused by an occlusive event (i.e., cerebral emboli or atherosclerotic 

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 predominantly occurs 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 medical conditions can effect the genitourinary 

system (e.g., Diabetes mellitus, vascular dysfunction, coronary 

artery disease). Furthermore, changes secondary to 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.

Chapter 3 / Cerebrovascular Accidents 65 

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 regis- 

tered 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 on the 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. 

The PMC 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 

between the reticulospinal tracts and the sacral intermediolateral 

cells carrying the preganglionic parasympathetic neurons that 

innervate the bladder detrusor muscle, Electrical stimulation of the

66 Marinkovic 

Badlani 

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 an increase 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 1 mo, 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 demonstrated that by 2 mo 55% were 

continent and at 6 mo this increased to 80%. However, the 2 and 3 yr 

follow-up data demonstrate an incidence 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 concomitant diagnosis of dementia and benign prostatic hyperplasia 

(BPH) in males and urethral incontinence in females may also contribute


to urinary incontinence. However, it must be emphasized that inconti- 

nence 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 symptoms of 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. The mean 

time from CVA to urodynamic evaluation was 19 m0 (range 1 1 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.

68 Marinkovic and Badlani 

Table 1 

Patient Urodynamic Findings on CMG and EMG 

Group CMG EMG 

Normal Normal 

Hyperre flexic Normal 

H y perreflexc AVCS 

Hyperreflexic DSD 

Areflexic 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 hyper- 

reflexia 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 simultane- 

ous 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) exhib- 

ited an areflexic bladder, whereas only 10% (n = 4) of the ischemic 

CVA’s demonstrated detrusor areflexia (see Table 3). Will the type of


Table 2 

Site of CVA Correlated with Urodynamic Findings 

Site of lesion Group I Group 2 Group 3 Group 4 Group 5 

Frontalparietal 0 0 6 0 2 

Occipital 1 0 0 0 0 

Temporal 1 0 0 0 0 

Multifocal 0 0 2 0 

Internal capsule 2 0 12 0 4 

Basal ganglia 2 2 3 0 4 

Combined 0 0 1 3 0 

Thalamus 2 0 0 0 2 

Pons 0 0 2 0 3 

Cerebellum 0 0 0 0 6 

Totals 8 2 24 5 21 


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 preced- 

ing detrusor contractions with resultant urinary incontinence (15). Inter- 

estingly, 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 involun- 

tary detrusor contraction, may be more commonly observed in the 

recovery phase and 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 Group I Group 2 Group 3 Group 4 Group 5 

Hemorrhagic (n = 20) 1 0 1 1 17 

Ischemic (n = 40) 7 2 23 4 4 

Totals (n = 60) 8 2 24 5 21 

Used with permission from ref. 33.

70 Marinkovic 

No of patients 

Average age 

Capacity 

No hyperreflexia 

No areflexia 

No normal 

Table 4 

Urodynamic Results with Right Hemiplegia 


13 males 

77 yr 

288 mL 

6 

2 

5 

HEMISPHERIC DOMINANCE 

AND VOIDING DYSFUNCTJON 

11 females 

84 yr 

317 mL 

6 

3 

2 

Hemispheric dominance 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 et al. (14) postulated 

that patients after nondominant CVAs were less likely to have urinary 

incontinence. If so, what effects would a dominant hemispheric stroke 

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 CVA to 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 no signifi- 

cant difference in bladder dysfunction with dominant and nondominant 

hemispheric WAS. 

Table 5 

Urodynamic Results with Lek Hemiplegia 

No of patients 14 males 6 females 

Average age 78 yr 86 yr 

Capacity 210 mL 416 mL 

No hyperreflexia 6 2 

No areflexia 0 4 

No normal 8 0 

Used with permission from ref. 12.


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 urodynarnic study (What is incidental due to aging? 

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 func- 

tioning, 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

72 Marinkovic 

Badlani 

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 such as 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. More importantly, nocturia can be owing simply to 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 hematuria follows. If hematura is present 

appropriate assessment with cytology, intravenous pyelogram and 

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 them void 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.

Chapter 3 I Cerebrovascular Accidents 73 

INTERP~TATION OF 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 and 25-35% in men. Other age-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 overacti- 

vity 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 urody- 

namic 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 void- 

ing 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 anticholin- 

ergics and postprostatectomy. These patients will be significantly incon- 

tinent. 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


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 hyper- 

reflexia 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, detru- 

sor 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 hyper- 

reflexia 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 

avail able. 

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


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 be utilized. 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 performing a 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 age greater 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.

76 Marinkovic 

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. Although CIC 

offers excellent long-range management of urinary retention, its use 

in CVA is restricted by the inability of the patient to perform this 

procedure owing to 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 for a 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


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 in males and detrusor hyperactivity with 

impaired contraction (DHIC) in males and females 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 DHIC patients 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 und 

endoscopic guidance similar to collagen therapy; and

78 Marinkovic 

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

incontinence 

Badlani 

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 or morbidity as com- 

pared 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 both determined 

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


severely handicapped (aphasia, dementia, or immobility) incontinent 

patients had normal functioning bladders. Interesting, even these debilitated 

patients benefited from prompted voiding schedules and fluid 

restriction. This method of patient management is very labor intensive 

and works best in a home environment with 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 reduce morbidity through an accurate diagnosis and implementation 

of noninvasive or minimally invasive therapies. 

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dysfunction and brain injury after cerebrovascular accident. J Urol 126:86-88. 

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in Southeast England. Stroke 25:352-357. 

16. Wade DT, Hewer RL (1978) Outlook after an acute stroke: Urinary incontinence 

and loss of consciousness compared in 532 patients. Quart J Med 56:601- 

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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. 

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28. Khan 2, Starer P, Yang WC, et al. (1990) Analysis of voiding disorders in patients 

with cerebrovascular accidents. Urology 35:265-270. 

29. Motola JA, Mascarenas B, Badlani GH (1988) Cerebrovascular accidents: urodynamic 

and neuroanatomical findings. J Urol 139:512A. 

30. Tsuchida S, Noto H, Yamaguchi 0, et al. (1983) Urodynamic studies on hemiplegic 

patients after cerebrovascular accident. Urology 2 1 :3 15-3 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 

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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 possibilities of 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 

enlargements with micturitional vesicourethral static pressure profiles. J Urol 

125~685-689. 

41. Lightner DJ, Barrett DM, Schmidt R, et al. (1998) Conticath: a simple new 

catheter designed for continence and volitional voiding past the obstructed urethra. 

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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.


45. Gillenwater JY, Conn RL, Chrysant SG, et al. (1995) Doxazosin for the treatment 

of benign prostatic hyperplasia in-patients with mild to moderate essential hypertension: 

A double blind, placebo controlled dose response multicenter study. 

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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, Oesterling J (1998) Transurethral needle ablation of the prostate: A 

minimally invasive treatment for symptomatic benign prostatic hyperplasia. 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. Issa MM, Townsend M, Jimine VK, Miller LE, Anastasia K (1998) A new 

technique of intraprostatic fiber placement to minimize thermal injury to prostatic 

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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 oxybutynin in-patients 

with an overactive bladder. Br J Urol 81(6):801-810. 

54. Stanton S, Monga AK (1997) Incontinence in elderly women: 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, Webster G (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 


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 CONTINENT URINARY 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, 



83

84 Blaivas 

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 (64, 

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 and either the duration of illness or age of 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, Samellas et 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). With development of sophisticated urodynamic 

testing, modern therapeutic interventions and more careful 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 with severe incontinence 

who were managed with indwelling catheters or men who had 

DESD. Women who developed DESD 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

Chapter 4 I Multiple Sclerosis 85 

hypertrophy are probably as common in 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 and urethra 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 and when 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. Although these 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.

86 Blaivas 

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 and consisted 

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 over the 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 markedly different 

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, and for 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

Chapter 4 / Multiple Sclerosis 87 

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 how often 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. A number of pad tests have been 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,

88 Blaivas 

simply asking the patient whether or not the diary and pad test were 

representative of a “good” or “bad” day will usually suffice for clini- 

cal 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 may be 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 or don’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


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 Urinu y 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). Renal ultrasound is recommended 

for screening because this is the easiest, least expensive and devoid of 

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 and to 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 video/pressure/~ow~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 the uroflow normal, i.e., is there a likelihood of either urethral 

obstruction or impaired detrusor contractility? 

5. Is urinary incontinence a complaint? If so, the nature of the incontinence

90 Blaivas 

and the severity should be determined from a 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? 


Synchronous measurement and display of urodynamic parameters 

with radiographic visualization of the lower urinary tract videourody- 

namics 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 urody- 

namics and to conventional cystography and voiding cystourethrogra- 

phy . 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 appreci- 

ate their interrelationships and identify artifacts with ease. 

Common Urodynamic Patterns in MS 

Detrusor hyperreflexia is seen in over 50% of patients with MS 

(9,II, 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 pat- 

terns: 

1. Detrusor hyperreflexia without bladder outlet obstruction (Fig. l). 

2. Detrusor hyperreflexia and detrusor-external sphincter dyssynergia 

(Figs. 2 and 3). 

3. Detrusor hyperreflexia with vesical necldprostatic urethral obstruction 

(Fig. 4). 

4. Detrusor hyperreflexia and detrusor-external sphincter dyssynergia 

with vesical necldprostatic urethral obstruction (Fig. 5). 

5. Detrusor areflexia and normal bladder compliance (Fig. 6). 

6. Low bladder compliance.


Fig. 1. Detrusor hyperreflexia in a 54 year old woman with exacerbating & 

remitting multiple sclerosis. (A) Urodynamic tracing. At a bladder volume of 165 

m1 there was an 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

92 Blaivas 

r 

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

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

, , 1 1 1 , 4 . , 1 , . 

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

.......... I IUW 

........... 

........... i f 0 

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 Jerp G. Blaivns, MD, with permission


I . . I , . . . t . l . . l . ~ . l . " . . . . . . , . . . * . . * 

* . . * . . l * . . . . . 4 . 

Fig. 3. Detrusor hyperreflexia and detrusor-external sphincter dyssynergia a in 53 

year old paraplegic man. (A) Urodynamic tracing. At a bladder volume of 165 ml 

there was an 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. The of point obstruction is the external 

urethral sphincter, marked by the arrow. Courtesy of Jerry G. BEaivas, MD, 

with permission

94 Blaivas 

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 

(arrow) which reached a maximum of 88 cm H20and Qmax = 6 ml/S. Throughout 

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 

obtained at Qmax shows a diffusely narrowed prostatic urethra. Courtesy of Jerry 

G. Blaivas, MD, with permission


Fig. 5. Detrusor hyperreflexia and detrusor-external sphincter dyssynergia with vesical ne 

prostatic urethral obstruction in a 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 reached a maximum of 187 cm H20 with no flow at all. Throughout the det 

contraction, there was increased EMG activity. At pdetmax, was there no contrast was visualized 

in the urethra, indicating both vesical neck obstruction and DESD. The fall in detrusor 

pressure in the middle of the detrusor contraction occurred as the external sphincter relaxed a 

bit and the urethra opened a bit, but the uroflow was too low to be measured by the flowm 

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. 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

96 Blaivas 

Fig. 6. Detrusor areflexia and normal bladder compliance in a 61 year old women 

with occult spina bifida. (A) Urodynarnic tracing. The bladder was filled to capacity 

(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


Fig. '7. (DS j Low bladder compliance and vesicoureteral reflux a 48 in yearold neurologically 

normal man. (A) Urodynamic tracing. The bladder was filled to capacity (850 mlj 

at which point he felt uncomfortably full. Pdetmax during filling 50 was cm H20 and there 

was a steep rise in detrusor pressure. When asked to void, he had a detrusor contraction to 

75 cm H20, without any flow all at and no contrast 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 the urethra. Courtesy ofJerry 

G. Bluivus, MD, with permission

98 Blaivas 

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 by a 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 an indwelling 

vesical catheter (which predisposes her to urinary infection). 

The unpredictable course of MS makes it difficult to know what to 

expect or how to 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. 

2. 

3. 

Identifying and treating remediable causes of MS exacerbations (see 

above), 

Techniques to maximize the patient’s independence and activities of 

daily living, 

Behavior modification to treat and deal with symptoms,


4. Biofeedback and pelvic floor exercises, and 

5. Absorbent pads and incontinence appliances. 

Remediuble Cuwes of MS Exucerbutions 

There are a number of remediable factors that can precipitate an 

exacerbation of MS; these should be sought and 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 of Dui4 Living 

For patients with disabilities, there are many environmental and 

behavioral interventions that can increase their independence and functionality. 

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 circum- 

stances. Simple behavioral techniques, such as diary keeping, adjust- 

ment 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 awareness about bladder and sphincter 

events. Contraction of the pelvic floor muscles and urinary sphincter

100 Blaivas 

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 enure- 

sis 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 complica- 

tions 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


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 anticholin- 

ergic 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 oxybu- 

tynin, 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 antide- 

pressants 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 contrac- 

tions. However, the warning time (from the onset of the urge to void 

until the iiicontinent episode) remains unchanged (52). Thus, the useful- 

ness of these medications may be enhanced by a behavior modification

102 Blaivas 

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 success- 

ful, 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 baclo- 

fen 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 DENERVATI ON 

(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


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 and to 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 wall is 

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 must taken 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 20 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

104 Blaivas 

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 augmentation cystoplasty 

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 Ashken in 1967 (68). The procedure is 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 and others have used this 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.


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 an extraperitoneal approach and a 

plane developed between the detrusor and underlying mucosa. Detrusor 

muscle fibers on the anterior surface and dome 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 more clinical 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 and psychosocial 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 improved self-image and sexual experiences (81). 

The purpose of 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

106 Blaivas 

operative procedure is necessary. However, when sphincteric incontinence 

is present a concomitant pubovaginal sling 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 anastomosed to 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 would predispose 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

Chapter 4 / Multiple Sclerosis 10’7 

hyperreflexia (owing to multiple sclerosis) from detrusor instability 

(owing to prostatic obstruction). Logic dictates that detrusor overacti- 

vity 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 conse- 

quence 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 and contingency plans for managing 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 used for 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-

108 Blaivas 

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 been recently 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. 

Demor 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 both the 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


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 an indwelling 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 unre- 

lated 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 con- 

tinue in that pattern for long periods of time; these patients are best 

managed conservatively for as long as possible.

110 Blaivas 

1. 

2. 

3. 

4. 

5. 

6. 

7. 

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5 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 

OTHER DISEASES OF THE SPINAL CORD 

LONG-TERM UROLOGIC MANAGEMENT 

FOLLOW-UP PREVENTION OF COMPLICATIONS 

REFERENCES 

INTRODUCTION 

This chapter will cover the diagnosis and management of spinal- 

cord 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 void- 

ing 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 



115

116 Sukin and Boone 

had advocated the theory of a “Balanced Bladder” (2). Patients were 

felt to be clinically stable if they were able to void with minimal 

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, and close 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 and cardiovascular 

complications. Despite these advancements in urologic 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 the rostral brain stem. 

Parasympathetic and 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 can be affected by 

hyperactivity from phasic involuntary contractions, low detrusor cornpliance, 

or both. Storage failure can occur secondary to pain or hypersensitivity 

during filling. Outlet resistance may be decreased from any 

process that damages the innervation or structural elements of the 

smooth or striated 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 and compare normal 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

Chapter 5 / Spinal Cord Injuries 117 

CMG - Pressure Flow Study 

Fig. 1. Normal micturition reflex pathways with A-delta afferents mediating sen- 

sory input to the Pontine Micturition Center. 

11.11 

f Spinal Transection 

Pontine 

Micturition 

Center 

Fig. 2. Following Spinal Cord Injury C-Unmyelinated 

fibers take over to mediate 

the afferent limb of the neurogenic bladder.


findings also have been 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 one in 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 have been 

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 can be directed 

at the underlying physiologic abnormality that is responsible for 

the symptom.


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 flaccid paralysis of the skeletal 

muscle mass and an absence of 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 or hours 

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


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. In many 

patients with detrusor areflexia, a loss of bladder compliance may 

develop over time with the development of high storage pressures. 

Both radiologic and urodynamic evaluations 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 urodynamic evaluation 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 been helpful 

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

Chapter 5 I Spinal Cord Injuries 121 

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 be an 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 does not always remain unchanged. subset A 

of patients will develop low compliance and may represent 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 muscle sphincter and a striated sphincter that retains 

some fixed tone but is not under voluntary control (18,19). There is 

little consensus on the 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 begin in 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


r"urethrr;r 

EM 

1 

t l It. 

Fig. 3. Videourodynamic image of Detrusor Hyperreflexia with Detrusor External 

Sphincter Dyssynergia (DESD).


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 common cause 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 by day 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 myelodyplasia is thought to be multifactorial. 

Epidemiological studies have shown that an environmental component 

is likely to be involved as the incidence of neural dysraphisms 

varies with geography and 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’s Syndrome, 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


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 reduce the 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 muscle tone, sphincter tone, function 

of the sacral reflex arc, and lower extremity function. A urinalysis, 

urine culture, and serum creatinine should be obtained. Documentation 

of the renal anatomy can provide 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 nervous system 

(CNS). These initial 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 with myelodysplasia 

have reflux while '23.5% have a bladder diverticulum. 

Urodynamics may be delayed 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


Fig. 4. Areflexic bladder with loss of compliance and an open bladder neck 

throughout filling. 

closure (47’). The typical patient with myelodysplasia shows 

an 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


mmHg do not usually have vesicoureteral reflex, whereas 8 l% of 

patients with pressures greater than 40 mmHg have been 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 neo- 

nate 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 catheteriza- 

tion is started even before urodynamics is done. The neonate should 

be placed on antibiotics until the absence of reflux has been documented 

by VCUC. 

The goal of management in children with neurogenic bladder dys- 

function 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 malforma- 

tions involving the cord are more common 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


independence. On the basis of both the clinical and urodynamic evaluation, 

as mentioned previously, 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 from catheters, and maintain 

urinary continence. Urologic management is directed towards achieving 

complete emptying of 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 lower motor neuron 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, approx 34-49% 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, and squamous cell carcinoma. Yet, chronic 

catheterization remains the most common form of management in 

patients who are tetraplegic and bedridden. Many female 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 CIC for 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.


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 contrain- 

dicated 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 per- 

formed 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 anticholiner- 

gic 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 blad- 

der 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


(54). Poor intestinal absorption of bethanechol is another reason that cholinergic 

agonists lack efficacy. Cholinergic agonists also have been 

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, depending on 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 with an 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 been reported to be successfully managed 

with a condom catheter after sphincterotomy, and eventually 

require a suprapubic tube (67).


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 in patients with DESD and voiding pressures greater 

than 60 mm H20 showed that sphincter prosthesis has similar efficacy 

but is easier technically, less morbid, and less 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 and capacity. 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 and intractable upper urinary tract dilation, 

recurrent upper urinary tract infections, and considerable difficulty with 

the patient performing inte~ittent catheterization. With any diversion, 

there is a high rate of long-term complications (69). The initial upper 

tract improvements seen in patients after ileal conduit diversion have 

been shown to 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


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 major difficulty 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 an extradural 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, and autonomic 

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 implanted medical 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 spinal- 

cord 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


patients are considered complicated because an uncomplicated infection 

is defined as community 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 be used during 

episodes of clinical infection, not asymptomatic bacteriuria. 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 high intravesicle storage 

pressure compromising the ureterovesical junction (78). Reflux can 

lead to reflux nephropathy with subsequent renal impairment and 

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 complete neurological 

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 carcinoma is the most common type of malignancy. 

The primary risk 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 performed along 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


phenomena is more common in patients with cervical injuries, and 

common triggers include bowel and bladder 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 when dysreflexia 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 been used for 

intractable dysreflexia including sympathectomy, sacral neurectomy, 

rhizotomy, cordectomy, and dorsal-root ganglionectomy (81). 

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45. Bensen JT, Dillard RG, Burton BK (1988) Open spina bifida: Does caesarian 

section improve prognosis. Obstet Gynecol 71 532-534. 

46. McGuire E, 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 Urd 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. 

49. Blaivas JG (1980) Management of bladder dysfunction in multiple sclerosis. 

Neurology 30: 12-18. 

50. Lapides J, Diokno A, Silber S, Lowe B (1972) Clean intermittent 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 

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52. Swierzewski SJ, 3rd, Gormley EA, Belville WD, Sweetser PM, Wan J, McGuire 

EJ (1 994) 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 the norma1 state 

and after parasympathetic denervation. Invest Urol 14:322-328. 

54. Sogbein SK, Downie JW, Awad SA (1984) Urethral response during bladder 

contraction induced by subcutaneous bethanechol chloride: elicitation of a sympathetic 

reflex urethral constriction. J Urd 13 1 :791-795.

136 Sukin Boone 

55. D’ Agostino G, Kilbinger H, Chiari MC, Grana E (1 986) Presynaptic inhibitory 

muscarinic receptors modulating (3H) acetylcholine release in the rat urinary 

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 

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57. Alberts P (l 995) Classification of the presynaptic muscarinic receptor subtype 

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J Pharmacol Exp Ther 274:458-468. 

58. Seze M, Wiart L, Joseph P (1998) Capsaicin and neurogenic detrusor hyperreflexia: 

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Neurourol Urodynamics 17513-523. 

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patients: Indications, technique, and results in 32 patients. Paraplegia 13:247-260. 

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in the adult. Urology 83432-434. 

61. Carrion H, Braun B, Politano V (1979) External sphincterotomy at the 12 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. 

64. Schellhammer P, Hackler R, Bunts R (1973) External sphincterotomy: An evaluation 

of 150 patients with neurogenic bladder. J Urol 110: 199-202. 

65. Yalla S, Fam B, Gabilondo F, Jacobs J, DiBenedetto M, et al. (l 977) Anteromedian 

external sphincterotomy: technique, rationale, and complications. J Urol l 17:489- 

493. 

66. Thomas D (l 976) The effect of trans-urethral surgery on penile erection in spinal 

injury patients. Paraplegia 13:286-289. 

67. Vapnek JM, Couillard DR, Stone AR (1994) Is sphincterotomy the best 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 

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of an artificial electrical stimulator for the paralyzed human bladder: a review. 

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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, 

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J Urol 122:5 15-5 17.

Chapter 5 / Spinal Cord Injuries I37 

75. Hackler RH (1977) A 25-year prospective mortality study in the spinal cord injured 

patient: comparison with the long-term living paraplegic. J Urol 117:486-488. 

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Good Samaritan Medical Center Phoenix, AZ. 1982 p. 152. 

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78. Duckett JW, Jr (1982) Ureterovesical junction and acquired vesicoureteral reflux. 

J Urol 127:249. 

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cord-injured patient: association with reflux, bladder stones, and foley catheter 

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excretion in quadraplegia. Arch Phys Med Rehabil 53:14-20. 

81. Trop CS, Bennett CJ (1991) Autonomic dysreflexia and its urological implications: 

a review. J Urol 146:1461-1469. 

82. Dykstra DD, Sidi AA, Anderson LC (1987) The effect of nifedipine on cystoscopyinduced 

autonomic hyperreflexia in patients with high spinal cord injuries. 

J Urol 138:1155-1157. 

83. Chancellor MB, Erhard MJ, Hirsch IH, Stass WE Jr (1994) Prospective evaluation 

of terazosin for the treatment of autonomic dysreflexia. J UroZ 15 1 : 1 1 1-1 13.


6 Diabetic Bladder Dysfunction 

CONTENTS 

INTRODUCTION 

EPIDEMIOLOGY 

PRESENTATION 

DIAGNOSIS 

URODYNAMIC FINDINGS 

PATHOPHYSIOLOGY 

TREATMENT 

CONCLUSION 

REFERENCES 

INTRODUCTION 

The prevalence of diabetes mellitus (DM) has reached epidemic 

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 secondary to 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 



139

140 Goldman Appell 

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 can either mimic or mask 

the findings of a diabetic neurogenic bladder. For example, women 

may have stress incontinence, prolapse, or pelvic floor dysfunction, 

whereas men may have prostatic 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 were found to have urologic symptoms (2). Even among 

“asymptomatic” patients, many have unrecognized symptoms. Ueda et 

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

Chapter 6 / Diabetic Bladder Dysfunction 141 

or from habit 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 and frequency. 

A recent study by Kaplan et al. (5) noted that the most common 

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 most readily 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

142 Goldman and Appell 

residual (PVR) may also help determine the efficiency of bladder empty- 

ing. 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. Cystometric examination 

may show detrusor areflexia but detrusor instability is also frequently 

found (see Table l). Urethral closure pressure profiles or Valsalva leak- 

point 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


In Kaplan’s study (5), 52% of the diabetic patients had urodynamically 

documented detrusor instability, 23% had impaired detrusor contractility, 

24% had poor compliance, 1 l% 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 assume that elderly diabetic 

patients with urologic symptoms have poorly contracting bladders (classic 

diabetic bladder), and that urodynamic studies can be helpful in 

determining the etiology and choosing 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 et al. (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 maximal capacity, decreases 

in detrusor contractility, and increases of PVR in their cohort of asymptomatic 

diabetic patients. Similarly, a study by Goldman et al. (8) noted 

that diabetics who also had gastroparesis had delayed first Sensation, 

increased capacity, and increased PVR. Perhaps the 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. 


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


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 neuropathy generally 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 Bradley and colleagues (IO), where there can be an 

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 common complication of DM (12). The autonomic 

neuropathy associated with DM is "generally thought to occur later. 

Several forms of abnormal impulse conduction patterns have been 

described, but in general, electrophysiologic studies show slowing of 

evoked responses (11). The impedance of conduction has been demonstrated 

in demyelinated nerve fibers, 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.


(18) demonstrated changes in 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 dicyclomine are 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 fewer side 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 

can empty 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 depends upon the degree of detrusor 

decompensation.


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 aspects of 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 157:580- 

584. 

4. Frimoldt-Moller A (1980) Diabetic cystopathy: epidemiology and related disorders. 

Ann Intern Med 92:318-321. 

5. Kaplan SA, Te AE, Blavis JG (1995) Urodynamic findings patients in with diabetic 

cystopathy. J Urol 152:342-344. 

6. Appell RA, Whiteside HV (1991) Diabetes and other peripheral neuropathies 

affecting lower urinary tract function. In: Gane RJ, Siroky MB, eds., Clinical 

Neurourology. Boston: Little, Brown, pp. 365-375. 

7. Starer P, Libow L (1990) Cystometric evaluation of bladder dysfunction in elderly 

diabetic patients. Arch Int Med 150:810-813. 

8. Goldman HB, Dmochowski RR (1997) Lower urinary tract dysfunction in patients 

with gastroparesis. J Urol 157: 1823-1825. 

9. Goldstein I, Siroky MB, mane RJ (1983) Impotence in diabetes mellitus. In: 

Krane RJ, Siroky MB, Goldstein I, 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 25:1627- 

1632. 

13. Waxman SG (1980) Pathophysiology of nerve conduction; relation to diabetic 

neuropathy. Ann Intern Med 92:297-300.

Chapter G / Diabetic Bladder Dysfunction 147 

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: new concepts 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. Ryle C, Leow CK, 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 pathways to the urinary bladder of 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, Baum NH (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.


7 

/ 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 with lumbar 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 neuropathophysi- 

ology, 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 

and somatic nervous systems. The parasympathetic pelvic nerves, 



149

150 Goldrnan Appell 

EHerent 

Autonomic 

Parasympathetic 

(Pelvic nerve) 

Sympathetic 

(Hypogastric nerve) 

Somatic 

(Pudendal nerve) 

Table l 

Innervation of the Lower Urinary Tract 

Spinal Cord Segment Function 

S2-S4 

T11-L2 

s3-s4 

Excitatory to bladder 

Inhibitory to bladder 

Excitatory to urethra 

Control over 

external sphincter 

Aferent 

Tension receptors in bladder wall 

Nociceptors S2-S4 Micturition ini 

Sensory S2-S3 Perineal sensa 

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 

~~

Chapter 7 / Lumbar Disc Disease 151 

vertebral body, at which point they exit the canal. Thus, all of the 

sacral nerves that originate at the L1 and L2 levels 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 most frequent sites of lumbar disc prolapse are the L4/5 and L51 

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 lumbar spine, 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, lower back pain-and in men, impotence-is noted (7). 

Though detrusor areflexia is the most common finding 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 changes in 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 and evaluated 

changes in bladder function. Fifty percent constriction resulted in no

152 Goldman and Appell 

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

noid 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 inconti- 

nence, as well as arterial narrowing and venous congestion of the nerve 

roots and ganglia.


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 and a 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 have a more profound effect on the autonomically 

innervated bladder than on the somatically innervated external sphincter. 

Therefore, if the conus medullaris is partially damaged even without 

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

154 Goldrnan Appell 

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 it is a form of func- 

tional obstruction by the external sphincter because there is no detru- 

sor 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 back pain and were found to have lumbar disc 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 two women who presented with painless 

urinary retention, but no other neurological findings were noted. In 

both cases, an MRI revealed lumbar central disc prolapse and, in 

retrospect, both patients noted the experience of minor lower back pain 

prior to presentation. 

A prolapsed intervertebral disc may produce a cauda equina syndrome 

with obstructive voiding symptoms on a 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 dermatome involved;


physical examination may reveal reflex and sensory changes consistent 

with nerve-root compression (1 0). 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 most characteristic 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), or both (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). The bulbocavernosus 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 (IS). 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 when other 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

156 Goldman ADD^ 

deficiency, or infectious neuropathies such as herpes simplex should 

be noted. Careful questioning concerning lower back pain, gait disturbances, 

or any other symptoms that were present when the voiding 

dysfunction began can be helpful. For example, the presence of flu 

symptoms and gait 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. ~rodyn~ically, detrusor 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 urodynamic diagnosis 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 or intermittent 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 (1 7). 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.

Chapter 7 I Lumbar Disc Disease I57 

Table 2 

Major Neurourologic Features of Lumbar Disc Disorders 

Symptoms Obstructive voiding symptomatology 

Signs Perineal or perianal sensory loss 

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, in some 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 et al. (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 

by abdominal straining, few may actually regain “normal” bladder 

function. The sequelae of laminectomy such as 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


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 (1 8). In most cases cholinergic therapy is unsatis- 

factory and clean intermittent catheterization (CIC) is required. 

Hypertonicity or decreased compliance with a concomitant fixed- 

outlet 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, colla- 

gen 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 neuro- 

logic symptoms or as an isolated event in patients with a prolapsed 

intervertebral disc. Damage to the parasympathetic, somatic, and sen- 

sory nervous innervation of the lower urinary tract is the usual mecha- 

nism of injury. In most cases detrusor areflexia results. A careful history 

and examination in conjunction with urodynamic testing and MRI 

imaging will establish the diagnosis. Although surgical intervention 

(laminectomy) may not always give complete bladder recovery, it can 

frequently allow for improvement. Various bladder management tech- 

niques (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. 

2. Rosomoff HL, Johnston JD, Gallo AE, et al. (1963) Cystometry in the evaluation of 

nerve compression in lumbar spine disorders. Surg Gynecol Obstet 117:263-270.


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. 

6. Scott PJ (1965) Bladder paralysis in cauda equina lesions from disc prolapse. 

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 

(1 995) Neuropathic urinary retention in the absence of 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) Neurologic disorders affecting the urinary bladder. In: mane 

RJ, Siroky MB, eds., Clinical Neuro-Urology, 1st ed. Boston: Little, Brown, 

pp. 245-255. 

11. Appell RA, Levine RL (l 98 l) Assessment of vesico-urethral dysfunction in lumbar 

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. Appell RA (1993) Voiding dysfunction and lumbar disc 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, Labib KB (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. 

16. Koff SA, Kass EJ (1982) Abdominal wall electromyography: a non-invasive 

technique to improve pediatric urodynamic accuracy. J Urol 127:736-739 

17. Krane RJ, Siroky MB (1 980) Studies in sacral evoked potentials. J Urol 124:872- 

876. 

18. Appell RA (1992) Clinical pharmacology in neurourology. Problems Urol 6622- 

642.


I I I FEMALE VOIDING DYSFUNCTION


8 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 sec- 

ondary 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 hypermobil- 

ity of the bladder neck and proximal urethra, intrinsic sphincteric defi- 

ciency, 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 and urethra 

will still have SUI due to 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 medical disor- 

ders resulting in denervation injury. A combination of anatomic hyper- 

mobility and intrinsic sphinteric deficiency often exist together, and 



163

164 RacMey 

Table 1 

Outcomes of Treatment for Urinary Incontinence(') 

Improved (%) 54-95 

Cured (%) 12-16 

Treatment 

Behavioral Pharmocolagic 

77 - 

44 78-92 

contemporary theories suggest that all 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 consolidation of the anatomic 

hypermobility and intrinsic sphincteric deficiency as etiologies of SUI 

provides a fundamental basis for expanding individual patient treatm 

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 in an improved quality of life 

for the patient. In choosing from available management and treatment 

options, informed patients are those who have received information on 

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 offered first, 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 associated with these treatments and the limited number 

of specialist trained to perform these procedures have traditionally

Chapter 8 I Stress Urinary Incontinence 165 

made nonsurgical options a priority. The concern of increased risk 

associated with these procedures are lessened with contemporary reports 

defining better ways to perform traditional procedures using minimally 

invasive approaches (3-5), improvements in 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 INTER~NTIO~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 avoidance of bladder 

stimulants can result in modest improvement of their urinary symptoms. 

Simple adjustment in the timing of medications such as the avoidance of 

diuretics before recumbency and emptying the 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

166 Racklev 

in patients with congenitive dysfunction, mobility problems, and physi- 

cal 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 sympathetic- 

mediated negative feedback inhibition augmented by the somatic-medi- 

ated contraction of the external urinary sphincter on bladder contrac- 

tions. 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 biofeed- 

back using deep breathing and relaxation exercises. All these techniques 

of bladder retraining appear to work best in patients who have forms 

of urge or mixed incontinence 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 biofeedback may aid in teaching patients behavioral interven- 

tions 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


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 194 1 for 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 is to 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 to transient 

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

168 Rackley 

SUI may result from a traumatic peripheral neuropathy ‘with resultant 

muscle atrophy and dysfunction typical of intrinsic sphincteric defi- 

ciency, rather than fascial breaks or lengthening associated with ana- 

tomic hypermobility. Therefore, standard rehabilitation techniques 

require at least partial innervation to the muscle groups of interest 

unless the nerves are bypassed by an electrical stimulator or electromag- 

netic 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 Devices and Support Prosthesis 

Conservative treatments such as urethral meatal occlusive devices, 

urethral inserts, plugs, and catheters, as well as vaginal pessaries (16- 

18), 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 expensive allocations 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


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 myocardial infarction. 

However, in addition to the aforementioned benefits of improved 

voiding function, hormone replacement therapy 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 mild atrophic 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.

170 RacMey 

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 responded to 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 phenylpropanolamine is 25-100 mg in sustained-release form, 

given orally twice a day; that of pseudoephedrine is l 5-30 mg three times 

a day. Side effects are numerous and are 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 used with 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 determine the 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

Chapter 8 / Stress Urinary Incontinence 171 

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’) sup- 

port this classification of stress incontinence. The efficacy of any treat- 

ment 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 intraurethral pressures 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 to correct the incompetent urethral closure mechanism without 

clinically disturbing voiding function. 

Although few are currently in use, many choices for injectable sub- 

stances have been tried; they include sclerosing solutions (28), polyte- 

trafluroethylene (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, availabil- 

ity, affordability, and biocompatibility; however, the efficacy is abysmal 

owing to poor graft neovascularity and long-term viability (1O--ZO%)

172 Racklet. 

(33). The currently used GAX-collagen previously 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 anatomic urethral support and intrinsic 

sphincteric deficiency. Additional studies which have followed 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 demonstrated overall 

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 on the 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. Techniques and 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-


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 excel- 

lent, the ideal material is still being sought and should combine the 

ease of administration with minimal tissue reaction, no material migra- 

tion, 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 

FOR BLADDER NECK SUSPENSIONS 

In unoperated patients with stress incontinence predominantly owing 

to anatomic incontinence defined as hypermobility of the bladder neck 

and urethra with high abdominal leak-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

174 Racklev 

Fig. 1. Burch bladder neck suspension. 

of anatomic stress incontinence when an abdominal approach is indicated. 

In two contemporary reviews 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 open abdominal 

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 NECK SUSPENSIONS 

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 endoscopic control (46). To prevent pull-through failures, pledget


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 trans- 

vaginal approaches for bladder neck suspensions is based on incorporat- 

ing 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. 

2. 

3. 

4. 

Retropubic dissection, which allows for scarification that supplements 

the native support of the endopelvic fascia; 

Use of permanent suture material for repair of an iatrogenic paravaginal 

defect; 

Stable suture fixation which allows for unstressed scarification and 

potentially prevents suture pull-through failures from the vaginal wall 

and endopelvic fascia; and 

Adjusting the tension of the supporting sutures to 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 to reduced patient morbidity and improved convalescence

176 Rackley 

Arcus 

lev 

Symphysis pubis 

~rethrope~vi~ complex 

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 sphinc- 

teric 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 primary treatment. Despite the his- 

torical use of sling procedures in complex cases of intrinsic sphinteric 

deficiency, the long-term success rate of 83% combined with the report 

of general medical and surgical 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


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 reemergence of 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 on ease 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 changes that 

have resulted in its acceptance as a viable alternative for use in patients 

with acceptable tissue quality and vaginal capacity, especially those 

with concomitant poor detrusor 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

178 RacMey 

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 more suburethral support than can be afforded by the vaginal wall 

tissue. Thus, in patients undergoing urodynamic evaluation for poor 

detrusor function with concomitant stress incontinence, the degree of 

intrinsic incompetence must be 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 

approach and more 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 be placed from a transvaginal 

approach (65). Ulmsten has introduced a technique of synthetic sling


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 and surgical 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.

180 Raclcley 

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 one of the best treatment options capable 

of achieving this result. The artificial urinary sphincter is intended to 

permit intermittent urethral compression for maintaining continence 

with voluntary reduction of urethral resistance during voiding, as 

opposed to other surgical procedures in which 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 14% 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 satisfaction near rates 92%. When considered 

in the context of 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 pharmacologic 

supplementation, Only for patients who have failed to 

achieve an acceptable continence status with nonsurgical management 

and who have maximized their potential for overall pelvic-floor reha 

tation and voiding function should reconstructive surgery then be considered. 

A recent report (1) of a 10-yr expected cost per elderly patient


with chronic stress incontinence in 1994 dollars reveals that untreated 

incontinence is the most expensive health care choice ($86,726). Com- 

parative 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 over- 

all cost. 

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60. Haas CA, Rackley RR, Vasavada SP, 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. 

61. Appell RA, Goldman HB, and Rackley RR (1998) Efficacy and predictors of 

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) Laparoscopic extraperitoneal 

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: New applications 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. 

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ed. Female Urology, 2nd ed. Philadelphia: WB Saunders Co., 428-434. 

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for use, surgical approach, and results. Intl Urology J 9:409-415.

9 Urinary Retention in Women 

Roger R. Dmochowski, MD, FACS 

CONTENTS 

INTRODUCTION 


EVALUATION 

ETIOLOGY 

TREATMENT 

REFERENCES 

INTRODUCTION 

By definition, the woman afflicted with urinary retention is unable 

to completely empty her bladder. However, it is difficult to characterize 

the condition of urinary retention on the basis of the magnitude of 

residual volume alone, and more important to evaluate and render 

treatment for the presenting symptomatic complex and any associated 

urinary tract pathophysiology. Retention may be symptomatic or 

asymptomatic. Symptoms commonly 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. 


Edited by: R. A. Appell 0 Humana Press Inc., Totowa, NJ

186 Drnochowski 

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 evalu- 

ation to identify the aforementioned sequellae of retention and potential 

underlying etiologies. Therapeutic approaches pertinent to particular 

etiologies will also be discussed. 


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 and adequately facilitated 

to empty the bladder. 

This intricate mechanism is dependent on integrity 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 and colleagues 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

Chapter 9 / Female Urinary Retention 187 

appropriateness of diagnostic work-up. Although urodynamics are useful 

for assessing vesical compliance and presence or absence of detrusor 

instability, no urodynamic parameter has been identified as being singularly 

diagnostic for obstruction. Pressure/flow nomograms are standardized 

for males 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 symptomatic correlation 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 urodynamic results. 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 can often be delayed 

until the presumed inciting etiology has been removed and/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

188 Dmochowski 

cystocele formation, but also examination of the other components of 

vaginal vault support including the apeduterus and also the posterior 

wall to exclude rectocele. 

The resting position of the urethra and bladder neck should be 

evaluated in the patient who is status postsuspension, as hyperangulation 

of this area may be coexistent with obstruction. The presence of significant 

periurethral fibrosis indicates potential iatrogenic cause for obs 

tion. Additionally the presence or absence of 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 functions of 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 bulbocavernosus reflux. Longtrack 

evaluation of the lower extremities includes sensory, fine touch, 

pinprick, and reflex testing of the appropriate dermatomes. 

The urodynamic evaluation is a crucial component of the evaluation 

of the female with chronic voiding dysfunction and obstructive symptomatology. 

Given the reported lack of correlation between symptomatology, 

urodynamic testing does allow some baseline determination 

of underlying bladder function prior to intervention for obstructive 

symptomatology. However, it should be kept in mind that urodynamic 

testing does not 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 noninvasive uroflowometry should be used in conjunction 

with this analysis. 

Noninvasive uroflowometry does provide a simple screen when utilized 

with postvoid residual testing. The identification of 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). 

~ultichannel subtracted pressure flow testing allows a more complete 

assessment of bladder contraction when identified. Not only does 

multichannel study assess the ability of the bladder to effectively store 

urine, it also assesses for bladder filling pressures associated with 

compliance characteristics and the presence or absence 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.


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. Curve at right is markedly prolonged and of low amplitude, possibly 

indicating obstruction, but also consistent with poor detrusor contractility. 

When pressure flow testing is performed, high-pressure, low-flow 

evaluation may indicate obstruction; "however, these criteria are not 

completely normalized in 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 and correlation 

with parameters obtained from normal controls (9,lO). Massey and 

Abrams (l l) utilize four parameters including: significant residual volume, 

diminished uroflow 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 and 100 ccs of voiding volume (1 l a). Blaivas has utilized 

the previously mentioned criteria of peak pressures of 20 cm of water 

with peak flows of less than 12 (1 lb). 

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 9 / Female Urinary Retention 19 1 

Fig. 2. Detrusor curves from three different patients. All were diagnosed as 

obstructed on the basis of symptoms, residual urine volume, and clinical examination 

findings. (A) Low-pressure voiding in elderly woman with high residual 

and periurethral fibrosis from needle suspension. (B) Higher pressure contraction 

accompanied by detrusor instability during filling. Irritative symptoms were 

marked, in this patient. (C) Pressures approximating 100 cm H20 in 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, stan- 

dardized voiding pressures may not apply to this sub-group of women 

(12) (Fig. 2). 

Simultaneous pressure flow analysis coupled with radiographic (flu- 

oroscopic) 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 obstruc- 

tion, 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


provide the gold standard to which all other testing modalities should 

be obtained (Fig. 3). 

In the absence of videourodynamics, sequential urodynamics supple- 

mented by standing voiding cystourethrography (VCUG) will provide 

complimentary data. VCUG is performed in lateral, anterior-posterior,

Chapter 9 I Female Urinary Retention 193 

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 examinati 

(D) Prolapse and voiding dysfunction. Grade 2 cystocele, in patient with 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. Grade 4, central defect. Patient was unable to void except by manual 

relocation of vaginal contents. (G) Bladder neck angulation and torquing effect 

from suspension suture in close apposition to urethral wall of at bladder level neck.


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 physi- 

cal 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 

and some determination of any obstructive phenomena caused by 

periurethral lesions such as urethral 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.

Chapter 9 / Fernale Urinary Retention 195 


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 inves- 

tigation will provide the most complete estimation of presence and



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.



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

198 Dmochovvski 

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 dependent on 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 caused by periure- 

thral or perivesical gynecologic lesions. The most common gynecologic 

cause of outlet obstruction is that resulting from large cystocele forma- 

tion. 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 (lean- 

ing 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 more significant 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


Table l 

Etiologies of Chronic Urinary Retention 

~nato~ic/Obstructive Neurogenic/~ 

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 

S kene’ 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 pro- 

vide the best chronic management option.


Less common causes 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 may also 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 on the 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 when inflamed 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). 

Primary Bladder Neck Obstruction. 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 be excluded 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.

Chapter 9 / Female Urinary Retention 20 1 

Fig. 4. Two different cases of 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 had high residuals and predominantly obstructive 

complaints.


Some authors have also attributed the abnormality to an increased 

number of sympathetic receptors in the bladder neck increasing sensitiv- 

ity to normal neurogenic stimulation. 

Irritative symptoms (frequency, urgency, and nocturia) often pre- 

dominate early, but may subsequently progress to a high postvoid 

residual and occasional retention in these patients. Urinary tract infec- 

tions may also complicate this disease (48-52). 

Blaivas has defined the entity in urodynarnic terms as being associ- 

ated 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 symp- 

tomatology 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 alpha- 

adrenergic 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 insulin- 

dependent diabetes mellitus (IDDM).


Diabetes is associated with segmental neuronal demyelination, axonal 

degeneration, and peripheral nervous system degeneration of the 

autonomic and somatic nervous systems in the affected population 

(16,17). It has been previously shown that reflex-evoked potentials in 

patients suffering from diabetes showed diminished conduction velocities 

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 high postvoid 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 sympa- 

thetic and parasympathetic ganglia and roots in the true pelvis. In 

women, this is most commonly seen in colon surgery (abdomino- 

perineal) resection as well as low anterior resection. Also, radical


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-pudendal distributions) 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 and highly unstable 

bladders that may have a component of poor emptying as 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 mesence- 

phalic 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 sphinc- 

ter. Subsequently, simultaneous bladder contraction and sphincteric 

activity occur resulting in high-pressure intravesical storage and empty- 

ing (75). Three patterns of dyssynergia have been described, with Type- 

I 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


(MS), transverse myelitis associated with acquired immune deficiency 

(AIDS), and other 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 no overt 

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 and is 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, which actually 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 bowel dysfunction as well as nocturnal voiding 

dysfunction and enuresis. They will also show dramatic upper-tract


urinary-tract changes such as hydronephrosis and even renal func- 

tional compromise. 

Urodynamics may reveal incomplete bladder emptying and high- 

pressure bladder storage. Fluoroscopic evaluation may show significant 

bladder trebeculation with vesicoureteral reflux and high voiding pres- 

sures (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 sudden unanticipated detrusor activity. This repre- 

sents an exaggeration of the normal reflex control (continence reflex) 

to prevent incontinence in patients who experience urgency-type symp- 

tomatology. However, once this becomes a chronic voiding habit, the 

habituation results in chronic voiding dysfunction. 

In light of this, McGuire has recommended anticholinergic medica- 

tion 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 and skeletal muscle-relaxing agents such as 

Baclofen and Diazepam (43), because these agents tend to be more 

successful with sphincteric dysfunction resulting from neurologic phe- 

nomenon. 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 such as adnexal dis- 

ease, vaginal infections, and abscesses of the glandular components in 

the periurethral area. Retention may result owing to high urethral closure 

pressures (77,78).


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 decreas- 

ing 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. Ameliora- 

tion of the inflammatory or other insulting lesion with muscle relaxants 

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 was manifested in the absence of 

overt outlet obstruction. During urodynamic evaluation, these patients 

demonstrated detrusor contractions of adequate magnitude but of poor 

duration. The authors noted that approximately one-half of all of those 

studied who had 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 in the 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 such as fecal dysfunction, 

constipation, and medication effect as being causative to the 

dysfunction.


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 bladder with early trebeculation in woman with 

urgency/frequency syndrome and sphincteric overactivity with voiding (Pseudodyssynergia).


A 

""""" 

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. Over- 

suspension or hyper-suspension of the proximal urethra and bladder 

neck due to suture tension results in these structures being positioned


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 juxta- 

urethral 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. Zim- 

mern et al. reported acute angulation of the urethra producing obstruc- 

tion 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). 

Even well-performed procedures can cause 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 sub- 

stantially altered. 

Voiding by abdominal straining or pelvic-floor relaxation when cou- 

pled with an outlet obstructive procedure may result in relative obstruc- 

tion 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 postopera- 

tively. 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 bow- 

string 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,


Fig. 7. Cystoscopic imaged in 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 image of same patient. 

Note urethral narrowing distally, not related to sphincteric activity or to dysfunctional 

voiding.


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 more associated postoperative obstructive 

phenomena than transvaginal or anterior repair-type procedures. 

Urethrolysis is the fundamental therapy for retention caused by 

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 an introital 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 accomplished by 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 performed by 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 (l 02,103). 

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 catheteriza- 

tion is to be decried and avoided if at all possible. CIC was first 

recommended by Goodman (I03b); however, Lapides (l 04) popular- 

ized 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.

II 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 method with 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 (1 09-1 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 

between this 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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N ~ LVOIDING E DYSFUNCTION


es 

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 resis- 

tance to the flow of urine. Particularly in males, bladder outlet obstruc- 

tion is a frequently encountered finding. From a diagnostic standpoint, 

the evaluation of bladder outlet obstruction relies heavily upon tradi- 

tional 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. Urolo- 

gists have also seen the treatment of bladder outlet obstruction change 

dramatically over the past decade. While transurethral prostate resection 

was the most commonly performed procedure by urologists of yester- 

year, it now competes with multiple alternative surgical and medical 



225

226 Ikeguchi et al. 

therapies. Finally, in addressing bladder outlet obstruction in males, 

more attention has been given to functional voiding disorders commonly 

seen in younger male populations. 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, uri- 

nary sepsis, or incontinence as their first sign of bladder outlet 

obstruction. 

EVALUATION 

Histo y 

Lower urinary tract symptoms (LUTS) may be divided into either 

obstructive or irritative symptoms. Patients with bladder outlet obstruc- 

tion 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 symp- 

toms may also be present. The obstructive vs irritative voiding symp- 

toms are listed below: 

Obstructive voiding symptoms: 

1. Urinary hesitancy. 

2. Dribbling/weak urinary stream. 

3. Sensation of incomplete bladder emptying. 

4. Prolonged urination. 

Irritative voiding symptoms: 

1. Urinary frequency. 

2. Nocturia.

Chapter 10 / Male Bladder Outlet Obstruction 227 

3. Urinary urgency. 

4. Urge incontinence. 

In addition, the clinician should elicit a medical history pertinent to 

the various etiologies for bladder outlet obstruction. These might 

include the presence of a split or narrow stream, 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, it may be used to monitor the progression of the disease. 

In addition, the AUA symptom index 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. 

URINE 

Lab Tests 

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 work in the case 

of bladder outlet obstruction, the clinician should bear several points 

in mind. Patients with bladder outlet obstruction may be subject to


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 age range 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). 

URINARY FLOW RATE 

Diagnostic Procedures 

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


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 under local 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 determine certain variables such as the presence or absence 

of obstruction at the level of the bladder neck, median lobe, lateral lobes, 

and measure prostatic 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 H20 during 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 ascer- 

tained. 

Provided the patient can generate an adequate detrusor contraction, 

the presence of bladder outlet obstruction is based on the combination


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 been found 

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 LUTS in 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 many different prostatic conditions may result in symptoms 

of bladder outlet obstruction, the most common cause 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 men aged 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

Chapter 10 / Male Bladder Outlet Obstruction 23 1 

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 and physical 

findings consistent with BPH, the incidence of urinary retention was 

dramatically increased with age and symptoms. The incidence of acute 

urinary retention among men in the general population in the studied 

age range was 7/1,000 person-years of follow-up. This was in contrast 

to men in their 70s that had a 1 in 10 chance of 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 under certain 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 two main 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 be correlated 

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


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 on patients 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 symp- 

toms (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. 

~inasteride was found to be no efficacious than placebo (10).

Chapter 10 I Male Bladder Outlet Obstruction 233 

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 1 a and lb (1 I). 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


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 medical therapy of BPH 

may emerge from a prophylactic standpoint, As demonstrated by 

Jacobsen et al., 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~thral Resection 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

Chapter 10 / Male Bladder Outlet Obstruction. 235 

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 in- 

clude: 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


were able to undergo voiding trial within 24 h of operation and be 

discharged home. Both peak 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 with an 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, TUP is still 

reported to improve flow rates and symptom scores better than with 

medical therapy. The most notable aspect of TUP 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 to appropriately 

select patients with mild to moderate symptoms, which generally have 

a better chance at improvement than those with more severe problems.


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: ~rans~rethr~l Needle Ablation ( ~ ~ and ~ A 

I~terstitiaZ Diode 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 ~icrowave Therapy. 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~ptomatic improvement as well as increased


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. Complications from 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 Bladder Neck 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


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-urodynamics in 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 mediated sympathetic 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 the- 

ory. 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 retrospec- 

tive 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 effi- 

cacy (31). 


Endoscopic Bladder Neck Incision and TUIP. As discussed pre- 

viously, the mainstay of therapy for primary bladder neck obstruction 

is transurethral incision of the bladder neck, and in some cases TUIP. 

Formal TURP is usually not indicated since most patients with primary 

bladder neck obstruction will have small prostates on cystoscopic exam- 

ination. Furthermore, since the majority of patients diagnosed with 

primary bladder neck obstruction are young, risks of retrograde ejacula- 

tion usually make more aggressive surgical therapies unacceptable.


Amongst men undergoing transurethral incision of the bladder neck, 

'reported success rates have been excellent. In our own experience, 

of 33 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 com- 

monly carcinoma. Furthermore, as ever before, a single effective therapy 

remains elusive. Even amongst urologists, there is relatively little con- 

sensus. Part of the problem arises from that fact that few cases of 

urethral strictures are predictably categorized to correspond to progno- 

sis. Although it is generally true that traumatic strictures are short while 

urethritis results in longer strictures, the behavior and disposition of a 

urethral stricture in any 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 tech- 

niques, 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 reten- 

tion, an indwelling Foley catheter or suprapubic catheter rnay be 

required in order to temporize before definitive therapy may be insti- 

tuted. 

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. Given the 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 (4 cm)


strictures) and 18% for longer strictures. These percentages appear to 

be consistent regardless of the location or etiology of the stricture 

disease. Furthermore, with each recurrence, the chance of stricture 

resolution with urethrotomy or dilation dwindles in an exponential 

fashion. Ultimately, the degree of urethral and spongiosa1 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 compar- 

ing the two. Among 210 men with proven urethral stricture disease, 

106 underwent filiform dilation 104 underwent internal urethrotomy. 

For all patients, there was a 12-1310 recurrence 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 cm and 

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 accomplished with minimal anesthesia and stress to the patient, 

and may be ideal for patients who are poor surgical candidates. Deploy- 

ment 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 some studies 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


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 con- 

cluded 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 psydodyssynergia generally implies a condition 

in a neurologically intact patient, similar conditions may be the 

result of a neurologic lesion (detrusor external sphincter dyssynergia, 

DESD) or in neurologically intact children (Binman’s bladder). 

Although the exact etiology of this condition is unknown, it is 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 with otherwise unremarkable prostatic examination and postvoid 

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 symptomatic improvement seen in over 80% of 

patients over a 6-m0 period (35).


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MM (1997) Natural history of prostatism: risk factors for acute urinary retention. 

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5. Chapple CR (1995) a-Adrenergic blocking drugs in bladder outflow obstruction; 

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. 

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Eur Urol 30(3):369-376. 

9. Roehrborn CG, Siege1 RL (1996) Safety and efficacy of doxazosin in benign 

prostatic hyperplasia: a pooled analysis of three double-blind, placebo-controlled 

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C, Machi M, Narayan P, Padley RJ (1996) The efficacy of terazosin, finasteride, 

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Update. Pharmacol Rev 47:267-270. 

12. Foglar R, Shibata K, Horie K, et al. (1995) Use of 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 contraction of 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 of selective and non-selective alpha 1Aadrenoreceptor 

antagonists in benign prostatic hyperplasia: studies on tamdosin in 

a fixed dose and terazosin in increasing doses. Br J Urd Oct;80(4):606-611.


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 

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Jun;157(6):2171-2178. 

17. Ginnan CJ, Kolman C, Liss CL, Bolognese JA, Binkowitz BS, Stoner E (1996) 

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a new balloon expandable prostatic endoprosthesis: the Titan stent. North American 

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MI (1996) Etiology of voiding dysfunction in men less than 50 years of age. 

Urology Jun;47(6):836-839. 

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An increase of neuropeptide Y but not nitric oxide synthase-immunoreactive


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(1996) Primary bladder neck obstruction: urodynamic findings and treatment 

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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 INCONTINEN 

TREATMENT OF POSTPROSTATECTOMY 

INCONTINENCE: A COST COMPARISON 

SUMMARY 

REFERENCES 

INTRODUCTION 

Adenocarcinoma of the prostate is the most frequently occurring 

cancer in men (I). Recently, the American Urologic Association 

released guidelines for the management of prostate cancer. These guide- 

lines confirmed that radical prostatectomy is the optimal treatment for 


Edited by: R. A. Appell 0 Humana Press Inc., Totowa, NJ

248 Scarper0 and 

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 ~ROSTA~ECTO~~ 

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-matched control, 

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.

Chapter 11 / Post-Prostatectomy Incontinence 249 

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 it is 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 male urethral sphincter consists of two anatomic zones responsible 

for continence (16) (Fig. l). The proximal ure~hral sphincter 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 (1 7). The distal urethral sphincter extends 

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

250 Scarper0 and Winters 

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 and stabilizing 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 periure- 

thral supporting structures (23). 

“W ”

Chapter l1 I Post-Prostatectomy Incontinence 25 1 

Prostatic surgery destroys the proximal urethral sphincter, and conti- 

nence 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 sphinc- 

teric 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 of the Prostate 

and Open Prostatectomy 

In many cases, prostatic hypertrophy extends beyond the verumonta- 

num (25,26) (Fig. 2). Thus, the verumontanum remains a critical land- 

mark 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 resec- 

tion should be at the verumontanum, even if 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 mini- 

mize 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 open prostatectomy 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 on too 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

252 Scarpero and Winters 

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 Retrop ubic Prosta tectomy 

Radical retropubic prostatectomy has become the most predomi- 

nately 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 preserv- 

ing 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


“anatomic factors,” such as improved visualization and preservation of 

the urethra at the prostatic apex are responsible for improved continence. 

Bladder neck preservation 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 it appears that meticulous closure of the bladder neck around 

the catheter has no influence on postoperative continence (30). Bladder 

neck preservation does appear 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 in the 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” approach to perineal prostatectomy achieved conti- 

nence rates of 97.5% after 18 MO. Several important points were stressed


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 

of Denonvillier’s fascia with the urethra attached [D], and incorporation of Denonvillier’s 

fascia into anastomotic sutures [E].) (Adapted with permission from 

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.

Chapter 11 I Post-Prostatectomy Incontinence 255 

Table 1 

Etiology of Postprostatectomy Incontinence Based on Urodynamic Findings 

~- 

No. of % Bladder % Sphincteric 

patients dysfunction incompetence % Combined 

Khan (42) et 63 al. 49.2 22.2 25.4 

Goluboff et (43) al. 56 61 5 34 

Chao and (44) 74 Mayo 4 57 39 

Winters (45) et 65 al. 1.5 70.8 27.7 

Fitispatrick (46) et 68 al. 16.2 26.5 38.2 

Yalla et al. (48) 21 38 62 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 of the prostate (43,46,47). 

Bladder dysfunction has been found preoperatively in 45% of patients 

with symptomatic bladder 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 many series 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


following radical prostatectomy in whom isolated sphincter dysfunction 

was the predominant cause (45). Detrusor instability owing to decreased 

compliance after prostatectomy has been documented to 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 in incomplete 

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 leak- 

age. When did the leakage occur after surgery, and was any leakage


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 and nighttime 

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 performed to 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 performed to 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 be detected. An important feature 

in performing cystoscopy is 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). These studies 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 VCUG also 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


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 magnitude of the urethral pressure profile varies greatly with indi- 

vidual 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 pres- 

ence 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 in the evaluation 

of incontinent patients following prostatectomy. 

T~TMENT OF 

POSTPROSTATECTOMY INCONTINENCE 

After performance of urodynamic testing to determine the exact 

etiology of postprostatectomy incontinence, appropriate treatment decisions 

can be made. The following treatment recommendations are based 

on these urodynamic findings.


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.” These conservative measures offer little prom- 

ise in the correction of severe or total urinary incontinence. 

PHARMACOLOGIC TREATMENT 

Alpha-adrenergic agents (ephedrine, pseudoephedrine, and phenylpropranolamine) 

may improve leakage 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. Polytetrafluoroeth- 

ylene (Teflon) paste was one of 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).


Table 2 

Efficacy of Collagen in the Treatment of Postprostatectomy Incontinence 

Shortliffe et al. (63) 16 3 

McGuire and Appell (64) 134 22 

Aboseif et al. (65) 88 42 

Herschorn et al. (66) 10 2 

Cumrnings et al. (67) 19 4 

Kageyama et al. (68) 10 1 

Griebling et al. (69) 25 2 

Smith et al. (70) 57 2 

Improvedl M 

No. of Social follow-up 

Cases Dry continence Failed (mo) 

5 

70 

33 

5 

7 

5 

8 

20 

7 

42 

13 

3 

8 

4 

15 

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 inflam- 

matory 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 

dry at 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

Chapter l1 I Post-Prostatectomy Incontinence 261 

Klutke et al. (72) introduced “antegrade” placement of collagen through 

a suprapubic tract. The rationale is to inject collagen into supple, well- 

vascularized 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 long- 

term outcome. From these data, it is apparent that collagen injection 

therapy is not the ideal treatment of incontinence following prostatec- 

tomy. 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). 

~RTI~ICI~L ~ R 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 moderate to severe sphincteric incompetence after prostatectomy. 

It is imperative that patients undergo urodynamic 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 mechanism is placed 

in a dependent position in the scrotum through the suprapubic incision 

(Fig. 6). The sphincter is filled with isotonic contrast medium to allow 

radiologic identification of possible leaks. The mechanism is left deacti- 

vated for 6 wk. to prevent erosion. 

Long-term success rates and patient satisfaction are well-documented 

following i~plantation of artificial sphincters. Each patient should be


Fig. 4. Perineal approach to bulbar urethra for placement 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 done again 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 reviewed the results of 156 

men implanted with a mean follow-up of 41.6 mo (76). Total continence 

was achieved in 75% of patients, and 15% were improved. The revision 

rate in this series was 19.3%. Haab et 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,


Fig. 5. The use of measuring “tape” to determine appropriate cuff size. The most 

common size cuff 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 common causes of device failure are fluid leak or urethral 

tissue atrophy. Both problems create a decrease in closing pressure of 

the cuff. Alteration in pumping mechanics may signify device malfunc- 

tion. 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 X- 

ray. 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 normally functioning device that 

starts leaking 2 6 mo after implantation. When this problem is con- 

firmed, the simplest solution is to decrease the cuff size to a smaller


Fig. 6. Schematic representation of 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 be removed. 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~mentation of the urethra


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 incon- 

tinence. Mark et al. (83) reported 26 patients with stress incontinence 

and urethrovesical stricture no longer than 2.0 cm. They found synchro- 

nous incision of the stricture and insertion of an artificial urinary sphinc- 

ter 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 implanta- 

tion (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 “retight- 

ening” 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 inconti- 

nence. 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.


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 mini- 

mized 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. 


When aggressive therapy does not control incontinence, repeat uro- 

dynamic investigation should be undertaken to document persistent 

bladder dysfunction and to evaluate sphincter function. When aggres- 

sive anticholinergic therapy does not control bladder overactivity, blad- 

der augmentation should be considered. The various procedures for 

bladder augmentation are discussed in detail in chapter 14. 

Combined Bladder Dysfinction and Sphincteric Incompetence 

The treatment of this patient group with postprostatectomy incontinence 

is most challenging. The basic approach to these patients involves 

initial behavioral and pharmacological attempts 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 on anticholinergic 

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

Chapter 1 I / Post-Prostatectomy Incontinence 267 

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 entero- 

cystoplasty (SS) indicates that this form of management may be applica- 

ble in this group of patients. These patients should be forewarned about 

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 from consideration from artificial urinary sphincter implanta- 

tion 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 colla- 

gen 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 common etiology


following radical prostatectomy and combined bladder dysfunction 

and sphincteric incompetence is the most common etiology following 

TURP. Urodynamic studies 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. 

REiFEREiNCES 

1. Boring C, Squires T, Tong T (1993) Cancer Statistics. CA Cuncer J Clin 43:7-26. 

2. Middleton R, Thompson I, Austenfeld M, et al. (1995) Prostate cancer clinical 

guidelines Panel summary report on the management of clinically localized prostate 

cancer. J Urol 154:2144-2148. 

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EN TIES


1 2 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 be treated with 

pharmacologic therapy. These voiding problems are often described in 

one of two broad categories. 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 

understood once the neuroanatomy/anatomy is first delineated. The 

major anatomic areas that are involved in micturition are the detrusor, 

the smooth muscle of the posterior urethra, the prostate, and the striated 

muscle of the external sphincter. The neuroanatomy involves the pelvic, 

hypogastric, and pudendal nerves. 



275

276 Serels and Appell 

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 be owing 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 where the 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 and the 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 on the previous discussion, it is clear that voiding dysfunction 

can be affected 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, most agents that interact with the nervous 

system lack specificity for the lower urinary tract and therefore side 

effects are common.

Chapter 12 / Clinical Pharmacology 277 

Pelvic nerve 

(parasympathetics) 

A 

Ach 

L Ac 

Hypogastric 

Ach 

N. 

(sympathetic) 

Fig. 1. Diagram showing the innervation to the bladder, bladder neck, and exter- 

nal 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 can result from spine injuries, neurologic 

diseases, or events such as pelvidperineal pain, 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 down by 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 of 25-100 mg four times daily may be used.


Bethanecol has also been used to stimulate reflex bladder contractions 

in patients who have had 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) have been used 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 (1 0-1 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 in turn 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 completely convincing (22-24). Their use is based on the 

belief that opiods inhibit the micturition reflex, though the data 

is inconclusive.

Chapter 12 I Clinical Pharmacology 279 

Medications to Decreuse Outlet Resistance 

As mentioned previously, the smooth muscle of the bladder base 

and proximal urethra 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 was the 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 been promoted 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 alphald receptor 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 works directly 

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


(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 neuron activity, 

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, tachy- 

cardia, and anxiety and should as a result be performed 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 and con- 

traction is not totally abolished. It has nevertheless been reported to 

improve voiding dysfunction caused by 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 shown to improve urinary symptoms


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. These extracts 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 evidence that it is effective 

in relieving the symptoms of BPH (48,491. The studies thus far have 

been uncontrolled or of limited follow-up. Phytotherapy does not 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).


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 can be used 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 produce the 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 gland than 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 far have shown 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 summary results 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 and shown to be effective with less side 

effects (65-67).

Chapter 12 I Clinical Pharmacology 283 

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 muscle is no exception. 

Nifedipine, a calcium channel blocker, has been shown to 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 muscle by 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 used to 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 noted to have some benefit 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), such as imipramine hydrochloride, 

decrease bladder contractility and increase outlet resistance. These 

agents have essentially three major pharmacological actions: 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).


Interestingly, the main anticholinergic effect of imipramine is systemic 

with only 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 as those 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 and pressure 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,


severe pains upon instillation, and precipitation of autonomic 

dysreflexia in some. 

Medications to Increme Outlet Resistance 

Alpha adrenergic agonists have been used to 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 and stimulates 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 be of benefit 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 respira- 

tory 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 recep- 

tor content, the function of the smooth muscle, the estrogen binding 

sites, the supporting tissues, or the mucosal seal mechanism (119-123). 

There have been others that endorsed the use of estrogens in combina- 

tion 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 be adminis- 

tered 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 estra- 

diol is being introduced for vaginal use. This new device offers a

286 Sereis and Appeli 

continuous delivery over a 90-d period and has shown to be very 

acceptable in certain women (126,127). 

Medications for InJEammutory Conditions 

of the Bladder Cuzlsing Storuge Failure 

Interstitial cystitis (IC) is a syndrome whose pathogenesis 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., glycosaminoglycans- 

GAG-). 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 and usually 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 recommended that 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 shown to 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


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 mg tid. 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 been tried but the 

data to support their use is sketchy. The assumption is 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 been used 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 used to inhibit mast-cell release (137- 

140). 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 of Failure to Store 

A synthetic antidiuretic hormone peptide analog known as DDAVP 

(l -deaminino-%" arginine vasopressin) is used to treat noctural enure- 

sis 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 are a 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


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 advance- 

ment of pharmacologic treatment of voiding dysfunction and provide 

the best future care to our patients. 

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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 incon- 

tinence. Urge incontinence is conservatively estimated to account for 

40% of all urinary incontinence patients (I). Of this population, two- 

thirds 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, biofeed- 

back, timed voiding), drug therapies, and containment devices are com- 

monly 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 



297

298 Siege1 

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. They include 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 and acceptability, 

efficacy, and suitability for a given underlying condition. The 

various forms of electrical stimulation have been used for symptoms 

of stress, urge and mixed incontinence, 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 modulate pelvic 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 compliant in 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

Chapter 13 / Treatment of Detrusor Instability 299 

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 keep the 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 be owing 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 dysfunc- 

tion is unknown, but most experts agree that the therapies work by 

producing a modulatory effect on sacral nerve reflexes (5-40). Stimula- 

tion 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

300 Siege1 

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 through direct 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 play an 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 confirmed that 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 found sensitive to low-frequency 

stimulation (6,8,13-19). Various devices are currently on the market 

utilizing these nerve paths. 

There are two main types 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 day over 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).

Chapter 13 I Treatment of Detrusor Instability 301 

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 not received 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 no effect 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 

n

302 Siege1 

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 inconti- 

nence control in treated patients (20). 

Trunsvuginul and Trunsunal Electrical Stimuhtion Devices 

Noninvasive electrical stimulation of the pelvic floor using an exter- 

nally 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 Kegel- 

type movement of the pelvic floor muscles and therefore may be useful

303

304 Siege1 

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 (2 7-29). 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 revers- 

ible. 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


malleolus just posterior to the margin of the tibia and then advanced 

to the medial edge of 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 be obtained 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 S3 sacral 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 S3 nerve 

ramus is optimal because it contains the sensory fibers from the genitals 

and perineum, afferent and efferent fibers from the anterior part of the 

levator ani and urethral sphincter, and autonomic fibers from the detru- 

sor (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 (PG) 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

306 Siege1 

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

end of the lead. 

TEST STIMULATION 

The first stage in the implantation of the device is test stimulation 

using a temporary electrode. ‘Unlike other electrical stimulation modal- 

ities, 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 func- 

tional 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 subcutaneous tissue with 1 % lidocaine, the posterior surface 

of the bony sacrum is probed with an insulated needle. Each plane of 

resistance, including the subcutaneous tissue, fascia, and posterior sacral 

surface is flooded with local anesthetic. The probing needle is oriented 

to follow the natural course of the sacral ramus through the 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 S3 pattern. Because S3 is 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


Fig. 3. Surgical Implantation of 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.

308 Siege1 

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 remain exposed 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 S3 responses 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. 

The perineum and 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, Can- 

ada, 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 conserva- 

tive forms of medical treatment. After a successful test stimulation


procedure, qualified patients were randomized into 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 am of the study upon conclusion of the delay period. Voiding 

diasies were used to collect efficacy outcome info~ation on 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 with urge 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 demonstrated clinically 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 in the domains of Physical Functioning, Vitality 

and General Health (20). 

Ur~ency~requen~y. Of the 220 patients with urgency-frequency, 

80 patients qualified for surgical implantation following a successful 

test stimulation procedure; 47 were randomized into 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 demonstrated a significant reduction in pelviclbladder discomfort 

at 6 m0 and 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 was documented at 12 and at 18 m0 

post-implant.

310 Siege1 

Six months postimplant treatment group patients demonstrated sig- 

nificant 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% demonstra- 

ting 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 force j; and increased patient 

comfort among implanted patients. Evidence of improved bladder func- 

tion 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 post- 

implant. 

At the 6-mo follow-up analysis implant patients demonstrated sig- 

nificant improvements in Bodily Pain, as measured by the SF36 and 

had more favorable perceptions of their general health transition com- 

pared 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 refrac- 

tory urge incontinence in 1997. The Food and Drug Administration 

(FDA) is currently reviewing data for expanded indications of urgency- 

frequency and urinary retention. The device has been available for 

these indications in Canada, Europe, and Australia since 1994.


Adverse events related to the therapy, the device, or implant proce- 

dure 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 irri ta- 

tion (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 (

3 12 Siege1 

therapies and surgery. While it is 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 does not 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 Health and Human Services, Public 

Health Service, Agency for Health Care Policy and Research, AHCPR Publication 

No. 96-0682, March. 

2. Fall M (1985) Electrical pelvic 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. Urd 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 Urd 140:1331. 

8. Thon W, Baskin L, Jonas U, et al. (1991) Neuromodulation of voiding dysfunction 

and pelvic pain. World J Urd 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. Chancellor MB, deGroat WC (Submitted for publication) Hypotheses on how 

sacral nerve stimulation works for the treatment of detrusor overactivity and 

urinary retention.


11. Blok BFM, van Maarseveen JTPW, Holstege G (1998) Electrical stimulation of 

the sacral dorsal gray commissure evokes relaxation of the external urethral 

sphincter in the cat. Neurosci Letters 249:68-70. 

12. Schultz-Lampel D, Jiang C, Lindstrom S, Thuroff JW (1998) Experimental results 

on mechanisms of action of electrical neuromodulation in chronic urinary retention. 

World J Urol 16:301-304. 

13. Vapnek JM, Schmidt RA (1991) Restoration of voiding in chronic urinary retention 

using the neuroprosthesis. World J Urol 9:142-144. 

14. Siegel SW (1992) Management of voiding dysfunction with an implantable neuroprosthesis. 

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 in lower 

urinary tract dysfunction: results of trial stimulation in 100 patients. J Urol 

15212071-2075. 

18. Bosch J, Groen J (1995) Sacral (S3) Segmental nerve stimulation as 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 stimulation in multiple sclerosis patients. Lancet 348:717-719. 

20. Medtronic data on file; MDT- 103. 

21. Empi (1994) The ~ndamentals of 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 urinary incontinence in 

women. Urology 50(6):934-940. 

23. Bent AE, Sand PK, Ostegard DR, Brubaker L (1993) Transvaginal electrical 

stimulation in the treatment of genuine stress incontinence and detrusor instability. 

IntE Urogynecol J 4:9-13. 

24. Sand PK, Richardson DA, Staskin DR, al. et (1 995) Pelvic floor electrical stimulation 

in the treatment of genuine stress incontinence: a multicenter, placebocontrolled 

trial. Am J Obstet Gynecol 183:72-79. 

25. Richardson DA, Miller ILL, Siegel SW, et al. (1996) Pelvic floor electrical stimulation: 

a comparison of daily and every-other-day therapy for genuine stress incontinence. 

Urology 48( 1):llO-118. 

26. Elgamasy AN, Lewis V, Hassouna ME, Ghoniern GM Effect (1996) of transvaginal 

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 treating genuine stress incontinence: a randomized clinical trial. Neurourol 

Urodyn 16543-55 1. 

29. Kulseng-Hanssen S, Kristoffersen M, Larsen E (1998) Evaluation of the subjective 

and objective effect of maximal electrical stimulation in patients complaining of 

urge incontinence. Acta Obstet Gynecol Scand 168(Suppl):12-15. 

30. Bo K (1998) Effect of electrical stimulation on stress and urge urinary incontinence. 

Clinical outcome and practical recommendations based on randomized controlled 

trials. Acta Obstet Gynecol Scand 168 (Suppl):3-11.

3 14 Siege1 

31. 

32. 

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35. 

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Davila GW, Bernier F (1995) Multimodality pelvic physiotherapy treatment of 

urinary incontinence in adult women. Intl Urogynecol J 6:187-194. 

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. 

Stoller ML (1998) Afferent nerve stimulation for pelvic floor dysfunction. 

J Endourol 12( 1):S108 (Abstract F2-6). 

Elabbady AA, Hassouna MM, Elhilali MM (1994) Neural stirnulation for chronic 

voiding dysfunctions. J Urol 152:2076-2080. 

Appell RA (1998) Electrical stimulation for the treatment of urinary incontinence. 

Urology 51 (2A Suppl):24-26. 

Shaker HS, Hassouna M (1998) Sacral nerve root neuromodulation: an effective 

treatment for refractory urge incontinence. J Urol 159: 15 16-15 19. 

Shaker HS, Hassouna M (1998) Sacral root neuromodulation in idiopathic nonob- 

structive chronic urinary retention. J UroZ 159: 1476-1478. 

Stadelmaier MKE, Hohenfellner M, Gall FP (1995) Electrical stimulation of sacral 

spinal nerves for treatment of faecal incontinence. Lancet 346(8983):1124-1.127.

l 4 Treatment 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 have failed conservative measures such as pharmacotherapy, 

behavioral techniques, and minimally invasive procedures 

such as neurornodulation. The concept of 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 primary indication 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 



315

316 aoury 

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 developed in reconstructive 

urology. Fluoroscopic multichannel urodynamics provided the scientific 

foundation for establishing the urophysiologic mechanisms through 

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 and drugs to manage urinary incontinence, there are patients 

who remain refractory 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 as interstitial 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

Chapter 14 / Augmentation Cystoplasty 3 17 

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 may be 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 performed for detrusor hyperactivity resulting 

from such entities 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 noted earlier, the 

majority of patients with bladder overactivity and/or impaired detrusor 

compliance respond 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 his- 

tory 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 what appropriate management of the ureters and outlet 

should be.

318 Khoury 

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 insuf- 

ficiency or chronic renal failure. Urinalysis and culture should be per- 

formed 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 neces- 

sary. Voiding cystography will identify bladder abnormalities that may 

influence a decision regarding bladder substitution rather than simple 

augmentation and will identify the presence and severity of vesicoure- 

teric 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, which combine electronic urody- 

namic data collection and simultaneous cystourothrography. Filling 

cystometrogram will assess compliance, stability, storage, sensation, 

and capacity. Storage after filling will further define stability and compe- 

tence of the outlet. Pressure flow studies will document voiding dysfunc- 

tion 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 fluo- 

roscopy 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

Chapter 14 / Augmentation Cystoplasty 319 

may alter the choice of the proposed reconstructive procedure. Signifi- 

cant outlet findings, urethral stricture disease, or trauma 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. Compro- 

mised renal function in the past was initially considered an absolute 

contraindication to bladder reconstruction as it could exacerbate meta- 

bolic 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 trans- 

plantation. 

A well-motivated and compliant patient is imperative as bladder 

reconstruction surgery can be fraught with relatively severe postopera- 

tive 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 be required on a routine basis and that devia- 

tion 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 high intravesicle 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.

320 Khoury 

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 of Bhdder Resection and Preparation 

The extent of bladder resection, if at all, is determined by the pathology 

of the underlying disease for which cystoplasty 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 cephalad to 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 used for bladder augmentation. Each bowel segment has its 

own advantages and disadvantages, and its own strong proponents 

(12-14). Several factors influence the type of bowel employed in reconstruction. 

These include availability, anatomic considerations, impact 

on nutrition, bowel and renal function, the need to preserve the ileocecal 

valve, particularly in patients with myelodysplasia, and finally, the

Chapter 14 I Augmentation Cystoplasty 321 

surgeon’s preference. It is my preference to use ileum for simple augmentation; 

however, in some cases, particularly in patients with myelodysplasia, 

sigmoid colon lends itself to bladder reconstruction because 

of its redundancy and proximity to the bladder. 

Bowel Sepent Reconfiguration 

The ultimate outcome in cystoplasty reconstruction is a large-capac- 

ity, low-pressure system with normal compliance. This is best accom- 

plished 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 recon- 

struction, the reflux will then resolve (19). Likewise, this has been the 

author’s experience for those patients with lower 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

322 aoury 

obstruction (22). Direct reimplantation into the augmenting bowel seg- 

ment has been favorable in those circumstances where the bladder 

remnant is either too small or pathology precludes standard reimplanta- 

tion. Examples of these include the split cuff nipple as described by 

Turner-Warwick (23), the Goodwin (24) and Carney-LeDuc (25) reim- 

plantations. 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 and magnitude of the 

incontinence, dexterity of the patient and ambulatory status. Mild bladder 

neck incompetence can be treated pharmacologically by using drugs 

such as alpha agonists to increase outlet resistance (26). For more 

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 and Mundy reported on 48 patients 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 calcium levels. Of the 28 patients, l2 were 

women between the ages of 45 and 50 and all had normal dual-photon 

absorptiometry bone scans, demonstrating no bone demineralization.

Chapter 14 / Augmentation Cystoplasty 323 

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 no dramatic changes in calcium balance or skeletal 

~in~ra~ization, the 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 complete bladder 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 be successful. 

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 common and 

should be anticipated in those patients on CIC. Pyelonephritis, however,

324 laloury 

is uncommon, and if 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 on tuberculous 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 cystoscopy with 

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 radio- 

nucleide cystography. 

Pregnancy A.er Bhdder Reconstruction 

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 monthly serum creatinines and, when indicated, renal 

ultrasonography. Hill and Gamer (38) recommend that those women

Chapter 14 I Augmentation Cystoplasty 325 

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 Cesarean section to avoid 

disruption of the underlying continence mechanism. 

1. 

2. 

3. 

4. 

5. 

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Von Mikulicz J (1899 j Zur Operation der angeborenen Blasenspalte. Zentralbe 

Chir 20:64 1-643. 

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. 

Couvelaire R (1950) La “petite vessie” des tuberculeux geniourinaires: essai 

de classification pacelore et variantesioute des cysto-intestine-plasties. J Urd 

(Paris) 56:38 1. 

Gil-Vernet JM (1965) The ileocolic segment in urologic surgery. J UroE 94:418. 

Pitts WR, Muecke EC (1979) A 20-year experience with ileal conduits: the fate 

of the kidneys. J Urol 122: 154. 

6. Schwarz GR, Jeffs RD (1975) Ilea1 conduit urinary diversion in children: computer 

analysis of followup from 2 to 16 years. J Urol 114:285. 

7. Diokno AC, Kass E, Lapides J (19’76) A new approach to myelodysplasia. 

J Urol 116:771-772. 

8. Lapides J, Diokno AC, Silber SJ, et al. Clean intermittent self-catheterization in 

the treatment of urinary tract disease. J Urol 107:458. 

9. Mulcahy JJ, James HE, McRoberts JW (1977) Oxybutynin chloride combined with 

intermittent clean catheterization in the treatment of myelomeningocele patients. 

J Urol 118:95. 

10. Wan J, McGuire EJ, Bloom DA, and Ritchey ML (1993 j Stress leak point pressure: 

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. 

12. Adams MC, Mitchell ME, Rink RC (1988) Gastrocystoplasty: an alternative 

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 on the outcome of augmentation enterocystoplasty. J Urol 136: 1201- 

1204. 

14. Kuss R (1959) Colocystoplasty rather than ileocystoplasty. J Urol 82:587. 

15. Cheng C, Whitfield HN (1990) Cystoplasty: tubularization or detubularization? 

Br J Urd 66:30-34. 

16. Hinman F (1988) Selection of 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.

326 fioury 

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. Cohen SJ (1975) Ureterozystoneostomie: eine neue antireflux 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-Warwick R (1987) Substitution cystoplasty. 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, Kaufmann JJ, 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 ureteroileal implantation 

technique: long term followup. J Urd 137:1156. 

26. Wein AJ (1987) Lower urinary tract function and pharmacologic management of 

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. Young HH (1922) An operation for the cure of incontinence associated with 

epispadias. J Urol 7: l. 

29. Dees JE (1949) Congenital epispadias with incontinence. J Urol 62:5 13. 

30. Leadbetter GW (1964) Surgical correction of total urinary incontinence. J Urol 

91:261. 

31. Strawbridge LR, Kramer SA, Castillo OA, Barrett DM (1989) Augmentation 

cystoplasty and the artificial genitourinary sphincter. J UroE 142:297-301. 

32. Nurse DE, Mundy AR (1989) Metabolic complications of cystoplasty. Br J 

Urol 63:165-170. 

33. Mundy AR, Nurse DE (1992) Calcium balance growth skeletal and mineralization 

in patients with cystoplasties. Br J Urol 69:257-259. 

34. Golomb J, Klutke CG, Lewin KJ, et al. (1989) Bladder neoplasms associated with 

augmentation cystoplasty: report of 2 cases and literature review. J Urol 142:377- 

380. 

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. 

37. Braverman RW, Leboweitz RL (1991) Perforation of the augmented urinary 

bladder in nine children and adolescents: importance of cystography. Am J Roentgenol 

1575. 

38. Hill DE, Kramer SA (1990) Management of pregnancy after augmentation 

cystoplasty. J Urol 144 (part 2): 457-459.

INDEX 

A 

5-alpha reductase inhibitors, 233-234 

ALPP, 45-46 

Abdominal examination, 3 1 

American Spinal Injury Association 

Abdominal leak-point pressure (ALPP), (ASIA) Score, 120 

45-46 

American Urologic Association Symp- 

Abdominal stoma, 100 

tom Index, 29-30 

Abdominal straining 

Anatomic etiology 

voiding, 2 l0 

female urinary retention, 198-202 

Abrams-Griffiths Nomogram, 47f Anterior vaginal wall 

Absent volitional control of the external prolapse, 198 

sphincter (AVCS), 68, 69t Anticholinergics, 73, 101, 158, 266, 

Acetylcholine (Ach), 276, 28 1-282 

28 1-282 

Acontractile bladder 

Antidepressants, 287 

female urinary retention, 204 Antihistamines, 287 

Acquired immune deficiency syndrome Antimuscarinic agents, 284 

(AIDS) 

Anuria 

female urinary retention, 205 


Activities of daily living (ADL) Areflexic bladder 

MS, 99 

LMN 

Acute urinary retention 

CIC, 127 

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, l 32 

SCI, 128 

bowel segment selection, 320-32 1 

selective vs nonselective, 233 

bladder outlet, 322 

327

328 Index 

complications, 322-325 

electrolyte disorders, 322-323 

Behavioral voiding dysfunction, 242 

Benign prostatic hyperplasia (BPH) 

incontinence, 323 

bladder outlet obstruction, 230-242 

metabolic disorders, 322-323 

pharmacological therapy, 23 1-234, 

neoplasms, 324 

pregnancy, 324-325 

280-28 1 

surgery, 234-238 

spontaneous perforation, 324 incontinence, 73 

urinary infection, 323-324 

natural history, 23 l 

voiding difficulties, 323 

Bentyl, 283 

contraindications, 3 19 

Benzodiazepines, 279-280 

detrusor instability, 3 15-325 Beta adrenergic agonists, 279 

indications, 3 17 

Beta-sitosterol, 28 1 

MS, 105-1 09 

Bethanechol chloride, 128, 145, 157-158, 

preoperative evaluation, 3 17-3 19 277-278 

cystourethroscopy, 3 18-3 19 Biofeedback 

laboratory studies, 3 18 

SUI, 166-1 68 

radiologic studies, 3 18 Bladder 

urodynamic evaluation, 3 18 endoscopy, 52-53 

surgery, 3 19 

hyperactive 

ureters, 32 1-322 

filling, 5 

Autoaugmentation, 3 16-3 17 

innervation, 277f 

Autologous fat, 170-1 7 1 

Bladder augmentation 

Autonomic dysreflexia 

cystoplasty, 320-32 l 

SCI, 132-1 33 

SCI, 130 

Autonomous neurogenic bladder, 17 lumbar disc disease, 158 

AVCS, 68,69t 

Bladder autoaugmentation 

Axonal degeneration 

MS, 105 

female urinary retention, 203 Bladder cancer 

SCI, 132 

B 

Bladder chimney, 106 

Bladder dysfunction 

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 

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 

MS, 99-100 

treatment, 10 

poststroke, 78 

Bladder filling 

Behavioral therapy 


SUI, 165-166 

facilitation, 8t

Index 329 

requirements, 4 

Bladder leak-point pressure (BLPP), 46 

Bladder neck 

endoscopic incision, 239-240 


Bladder neck obstruction 


primary 

male, 238-242 

Bladder neck suspension 

Burch 

SUI, 173-174,174f 

percutaneous, 175, 176f 

Pereyra-Raz, 174, 175f 

SUI, 173-1 76 

Bladder neoplasms, 324 

Bladder outlet 

augmentation cystoplasty, 322 

endoscopy 

female, 53-54 

male, 54 

Bladder outlet obstruction 

diagnosis, 44--45,46f 

female urinary retention, 189-1 9 1 

gynecologic causes, 198-200 

male, 225-242 

behavioral voiding dysknction, 242 

BPH. See Benign prostatic 

hyperplasia 

cystoscopy, 229 

lab tests, 227-228 

patient history, 226-227 

physical, 227 

postvoid residual, 228-229 

presentation, 226 

MS, 104 

Blood tests, 33,227-228,3 18 

BLPP, 46 

Bors-Comarr classification 

voiding dysfunction, 1 1-1 3, l 1 t 

Bowel dysfunction, 30 


Bowel neoplasms, 324 

BPH. See Benign prostatic hyperplasia 

(BPH) 

Bradley classification 

voiding dysfunction, 14-1 5 

Bulbocavernosus reflex (BCR), 88 


Burch bladder neck suspension 

SUI, 173-1 74,174f 

Capsaicin, 129, 284285 

Cardura, 74,232,279 

Catheterization, 2 14-2 15 

Cauda equina syndrome, 154-1 55 

Cerebral shock, 67 

Cerebrovascular accidents (CVA), 6344 

bladder dysfunction 

early presentation, 67 

late presentation, 67 

hemispheric dominance, 70 

patient history, 7 1-72 

urinary incontinence, 64-65 

alternative therapy, 78-79 

female, 77-78 

incidence, 66 

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 

SUI, 166 

urological evaluation, 7 l 

Bladder storage, 186 

Cervical lesions 

Bladder suspension 

urinary retention, 200 

female urinary retention, 209-2 l0 Cholinergic agonists 

Bladder transection 

SCI, 128-1 29 

c

330 Index 

Chronic continence 

Cystometrics 

incidence, 297 

bedside, 49-5 l 

Chronic indwelling catheter 

Cystometrogram (CMC), 38"43,40f, 42f 

LMN and areflexic bladder, 127 Cystometry 

Chronic urinary retention 

elderly, 72 

etiology, 199t 

Cystoplasty 

CIC. See Clean intermittent 

augmentation 

catheterization (CIC) 

MS, 105-1 09 

Cisparide, 278 

classification, 3 16-3 17 

Clean intermittent catheterization (CIC), Cystoscopic image 

74,76, 187,2 14,323 

DM, 145 

sling obstruction, 2 1 1 f 

cystoscopy 

LMN and areflexic bladder, 127 female urinary retention, 196 


Cystospaz, 266,282 


CMG, 38"43,40f, 42f 

Cystourethroscopy, 5 1-55, 194,3 18-3 19 

Cohen cross-trigonal reimplant, 32 1 

Collagen, 26O-26 1,260t 

I) 

injection, 77 


Collagenous ingrowth 

detrusor, 207 

Colon surgery 


Compliance, 4 1 

Condom catheter 


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 


Cystocystoplasty 

MS, 104 

Cystolysis 

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 

MS, 104 

detrusor hyperreflexia, 107, 108

Index 331 

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, 9 1 f-95f 

treatment, 10 1-1 02 

neurogenic 

capsaicin, 129 

SCI, 120-1 l 2 

urethral obstruction 

MS, 106-107, 108 

Detrusor instability, 4 1 

augmentation cystoplasty, 3 15-325 

DM 


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, 1 3 9 


pathophysiology, 143-145 

presentation, 139-140 

prevalence, 139 


urodynamic findings, 142-143, 142f 

Diabetic cystopathy, 14 I, 143-144 


Diabetic neurogenic bladder 


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 


Dyspareunia, 3 0 

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 1 l 

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 Index 


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 


spasticity, 207 

Extraurethral incontinence 

endoscopy, 54-55 

F 


pharmacological therapy, 277-28 1 

bladder emptying facilitation, 277- 

278 

BPH outlet obstruction, 23 1-234, 

280-28 l 

decrease outlet resistance, 279-280 


phamacological therapy, 28 1-287 

decrease bladder contractility, 

28 1-285 

increase outlet resistance, 

285-286 

inflammatory bladder conditions, 

286-287 

nocturnal enuresis, 287 

Fecal impaction 


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 

Fluid restriction 


Fluoroscopy 

elderly, 72 

pressure flow testing, 19 1-1 92 

sphincter dysfunction, 208f 

urethral obstruction, 192f-197f 

Fluxetine, 287 

Foley catheter 


Frequency, 28 

SNS, 309-3 10 

Functional etiology 


Functional system classification 

voiding dysfunction, 5t4t, 2 1-23, 

26-27 

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 


Hyoscyamine, 266,282 

Hyoscyamine sulfate, 282 

Hyperactive bladder 

filling, 5 

Hyperchloremic metabolic acidosis, 322

Index 333 

Hysterectomy 


Hytrin, 279 

IS, 5,286 

IVU, 55-56 

I 

K 

IDDM 

Kegel exercises, 167,259 


Ilia1 intesusception nipple technique, 32 1 

L 

Imipramine, 145,259,283-284 

Irnrnobility 


Impaired detrusor contractility, 207-209 

Implants 

SUI, 170-1 73 

Indigo laser prostatectomy, 75 

Indwelling Foley catheter 


In-Flow device, 76, 76f 

Ingelmann-Sundberg procedure 

MS, 102-1 03 

Injection therapy, 259-26 1 

Insterstitial diode laser, 237 

Insulin-dependent diabetic mellitus 

(IDDM) 



myelodysplasia, 126 

Internittent flow pattern, 36, 37f 

Intermittent self catheterization, 108-1 09 

International Continence 

Society Classification 

voiding dysfunction, 19-2 l, 19t 

International Prostate Symptom Score, 

29-30 

InterStim Continence Control System, 10 3 

InterStirn device, 301 

Interstitial cystitis (IS), 5, 286 

Intervertebral disc 

prolapsed, 154-1 55 

Involuntary detrusor contractions 

classification, 4 1 

Irritative voiding 

symptoms, 28 

male bladder outlet obstruction, 

226-227 

Laminectomy, 157 

Lapides classification 

voiding dysfunction, 15-1 7, 16t 

Laser sphincterotomy 

MS, 108 

Leak-point pressure, 45-46 

Learned voiding dysfunction, 205-206 

Lesions 

lower motor neuron (LMN), 1-12 


vaginal 


Levsin, 282 

Linear PURR nomogram, 48f 

LMN 

areflexic bladder 

CIC, 127 

lesion, 1-1 2 

Low bladder compliance 

MS 

male, 97f 

Lower motor neuron (LMN) 

areflexic bladder 

CIC, 127 

lesion, 1-12 

Lower urinary tract 

central innervation, 65-66 

innervation, 149-1 54, 150t 

Lower urinary tract symptoms (LUTS), 25 

male bladder outlet obstruction, 226 

Lumbar disc disease, 149-1 58 

clinical features, 154-1 55 

evaluation, 155-1 56 

neurologic features, 157t 

neuropathophysiology, 149-1 54, 15Ot 

treatment, 157-1 58

334 Index 

urodynamics, 156 bladder transection, 10 

Lumbar disc prolapse, 15 1-1 52, 152f-153f comon urodynamic patterns, 90, 

LUTS, 25 

9 f-97f l 

male bladder outlet obstruction, 226 concurrent stress incontinence, 109 

continent urinary diversion, 105-1 09 

M 

cystolysis, 104 

denervation 

Male bladder outlet 

endoscopy, 54 

Male genitals 


Male suburethral sling, 265 

Marion’s disease 


Meningocele, 123 

Metabolic disorders 


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 


detrusor areflexia, 108-1 09 

detrusor hyperreflexia 

DESD, 107-1 08 

DESD and urethral obstruction, 108 

treatment, 10 1-1 02 

urethral obstruction, 106-1 07 

detrusor myectomy, 105 

detrusor myotomy, 104 

diagnostic evaluation, 86 

etiology, 84 


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 

Minipress, 279 

Motor paralytic bladder, 16 

etiology, 123-124 

ureteral reimplantation, 32 1 

MRI, 56 

Myelomeningocele 

MS. See Multiple sclerosis (MS) 

child 

MS 800 artificial urinary sphincter, 261 

Mucosal structure disease 

female, 20 l f 

Multichannel subtracted pressure 

urodynamic study, 50f 

diagnosis, 124-1 25 

Myo-inositol 

peripheral nerves, 144 

flow testing 

N 


Multiple sclerosis (MS), 83-1 09 

ADL, 99 

alcohol injection, 103-104 


behavior modification, 99-1 00 

Nd:YAG laser 

MS, 108 

Needle electrical stimulation devices, 

304-305

Index 335 

Neoplasms 

Orthotopic cystoplasty, 3 16 


Neural tube defects 

children 

Overworked bladder, 4 1 

Oxybutynin chloride, 101, 145,266,282 


Neurogenic bladder 

P 

diabetic 



Neurogenic detrusor hyperreflexia 

capsaicin, 129 

Neurogenic dyssynergia 


Neurogenic etiology 


Neurologic evaluation, 32-33 


Neurostimulation 

SCI, 130-1 3 l 

Nifedipine, 283 

Pad test 

post-prostatectomy incontinence, 257 

urinary incontinence, 8’7 

Parasympathetic agonist agents 

pharmacologic manipulation 

female urinary retention, 2 15 

Parkinson’s disease 


Pelvic floor muscle exercises, 99-1 00, 167, 

259 

Pelvic floor relaxation 

voiding, 2 IO 

Pelvic nerve injury 

Nitric oxide (NO), 279,284 


Nocturia, 28 

Pelvic pain, 30 

selective 

elderly, 72 

Noninvasive uroflowmetry 


Non-organic urinary retention 

fernale urinary retention, 205-206 

North American Contigen 

Study Group, 172 

Pelvis 


Pentosanpolysulfate, 286-287 

Percutaneous bladder neck suspension, 

175, 176f 

Pereyra-Raz bladder neck suspension, 

174, 175f 

Peripheral nerves 

myo-inositol, 144 

0 

Peripheral nervous system degeneration 


Obstruction diagnosis 

Pessaries 

method, 187 

vaginal, 168 

Obstructive etiology 

PG, 278 


Pharmacologic manipulation 

parasympathetic agonist agents 

Obstructive voiding 


symptoms, 28 

Phenoxybenzamine, 279 

male bladder outlet obstruction, 226 Phenylpropanolamine (PPA), 170, 

Oliguria 

259,285 

female urinary retention, 198 Physiologic etiology 

Open prostatectomy, 25 1-252 


Opioid antagonists, 278 

Phytotherapeutics, 28 1,28 1 t

336 Index 

PMC, 65-66 

Pro-Banthine, 266, 282 

Pollen extract, 28 1 

Procardia, 133 

Polyneuropathy 

Prolapsed intervertebral disc, 154-1 55 

DM, 144 

Prompted voiding schedule 

Polytetrafluoroethylene (Teflon) paste, poststroke, 78 

259-260 

Propantheline, 266,282 

Pontine micturition center (PMC), 65-66 Propantheline bromide, 282 

Post-prostatectomy incontinence, 247-268 Proscar, 232-234,280-28 l 

etiology, 255-256,255t 

Prostaglandin inhibitors, 283 

evaluation, 256-258 

Prostaglandin (PG), 278 

cystourethroscopy, 257 

Prostate adenoma, 252f 

pad-weight test, 257 

Prostate gland 

patient history, 256-257 

anatomy, 249-25 1 

physical examination, 257 


RUG, 257 

Prostatic microwave therapy, 23 7-23 8 

urinalysis, 257 

Prostatic stents, 74 

urodynamic, 257-258 

Proteoglycans, 286 

VCUG, 257-258 

Proximal urethra 

VLPP, 258 

spasticity, 206-207 


Proximal urethral sphincter, 249 

open prostatectomy, 25 1-252 Prozak, 287 

radical perineal prostatectomy, Pseudodyssnergia, 242 

253-254 

Pseudoephedrine, 170,259,285 

radical retropubic prostatectomy, Psychogenic cause 

252-253,254f 


treatment, 258-267 

Pubovaginal sling, 78, 177f 

bladder dysfunction, 265-266 lumbar disc disease, 158 

bladder dysfunction/sphincteric Pumpkin seeds, 281 

incompetence, 266-267 PURR nomogram, 48f 

cost comparison, 267 

PVR, 34,228-229 

sphincteric incompetence, 

elderly, 72 

259-26 l 

Pyelonephritis, 323-324 

TUR, 25 1-252 

Pygeum africanum, 28 l 

Postvoid residual (PVR), 34,228-229 

elderly, 72 

Potassium channel openers, 283 

R 

PPA, 170,259,285 

Prazosin, 279 

Pregnancy 


Pressure flow testing 


radiographic monitoring, 19 1-1 92 

Primary bladder neck obstruction 


Radical hysterectomy 


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 337 

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 1 l 

adverse effects, 3 1 1 

clinical efficacy, 308-3 1 l 

retention, 3 10-3 1 1 

urge incontinence, 309 

urgency/frequency, 309-3 10 

surgical implantation, 308 

temporary electrode implantation, 306- 

307 

test stimulation, 306, 307f 

Sacral neuromodulation 


Saw palmetto, 28 l 

SCI. See Spinal cord injury (SCI) 

Segmental neuronal demyelination 


Selective nocturia 

elderly, 72 

Self catheterization 


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 

female urinary retention, 2 10-2 12 

Sling obstruction 

cystoscopic image, 21 If 

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 


fluoroscopy, 208f 

dyssynergia, 19 

external 


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 

artificial, 180 

Sphincteric incompetence 

post-prostatectomy 

SCI, 132 

SSEP, 120 

Stents 

urethral, 24 1-242 

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 


Sphincteric relaxation, 186 

management, 168 

Sphincterotomy 

MS, 109 

SCI, 129 

Stress urinary incontinence (SUI), 1631 8 l 

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, 170-1 80 

prevention, 13 1-1 33 

artificial urinary sphincter, 180 

detrusor sphincter dyssynergia, 

bladder neck suspension, 173-1 76 

204205 

implants, 170-1 73 

long-term urologic management, 126- sling procedures, 176-1 80, 

13 1 

177f-178f 

mortality, l 15-1 16 

treatment outcome, 163-1 65, 164t 

pharmacologic therapy, 128 

recovery phase, l 19-120 

spinal shock, 1 19 

surgery, 129 


urodynamic evaluation, 120-1 2 1 

Spinal shock, l 19 

Split cuff nipple, 322 

Spontaneous perforation 


Squamous cell carcinoma 

Striated sphincter dyssynergia, 19 

Stroke. See Cerebrovascular accidents 

Substitution cystoplasty, 3 16 

Subtrigonal phenol injection 

MS, 103-104 

SUI. See Stress urinary incontinence (SUI) 

Suprapubic catheter 


Surgery 

prio 

urinary tract function, 3 l

Index 339 

Surgical capsule, 249 

TUNA, 75,237 

Suture placement 

TUR, 236236,25 1-252 

female urinary retention, 209-2 l0 TVP, 235-236 

Suture tension 


Two-Phase Concept of Micturition, l 16 

Symmetric peripheral neuropathy 

DM, 144 

U 

T 

Ultrasonography, 56 

Unconscious incontinence, 29 

Uninhibited neurogenic bladder, 16 

Tamsulosin, 233 

Upper motor neuron (UMN) lesion, 1-12 

TCA, 10 1,283-284 

Ureteral obstruction 

Teflon injections, 259-260 


TENS, 306305 

Ureteral reimplantation 

Terazosin, 74,232,279 

augmentation cystoplasty, 32 1 

Timed voiding 

Ureters 

DM, 145 

augmentation cystoplasty, 32 1-322 

schedule 

Urethra 


female 

SUI, 165-166 

endoscopy, 54 

Tolterodine, 77, 101 , 266, 282 Urethral dilation, 240-24 l 

Transanal electrical stimulation devices, Urethral obstruction 

3 02-3 04 

detrusor hyperreflexia 

Transcutaneous electrical nerve stimula- MS, 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 

Transurethral microwave thermotherapy, 

75 

Transurethral needle ablation (TUNA), 75, 

237 

Transurethral resection (TUR), 236236, 

25 1-252 

Transvaginal denervation 

MS, 102-1 03 

Transvaginal electrical stimulation devices, 

302-304 

Transverse myelitis 


Tricyclic antidepressants (TCA), 10 l, 283- 

284 

Urethral stent, 24 1-242 

BPH, 238 

Urethral stricture disease, 240 

Urethra position 


Urethra suspension 

female urinary retention, 209-2 l0 

Urethrolysis 

clinical experience, 2 13t 

female urinary retention, 12-2 2 14 

Urge incontinence, 29 


SNS, 309 

therapy, 166 

Urgency, 28, 166 

Trigger voiding, 128 

SNS, 309-3 10 

TUIP, 236,239-240 

Urinalysis, 33, 227, 318

340 Index 

Urinary diversion 

continent 

MS, 105-1 09 

SCI, 130 

Urinary incontinence, 28-29 


child 


micturition diary and pad test, 8'7 

Urinary infection 


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, 13 1-1 32 

Urinary tract symptoms 

multiple sclerosis (MS), 84-85, 86 

Urine evacuation, 298-299 

Urine storage, 298-299 


facilitation, 8t 

failure, 2 1 

requirements, 4 

Urispas, 283 

Urodynamic 

classification 

voiding dysfunction, 18-19, 18t 


simplification, 75 

Uroflowmetry, 35-37,35f 


Urogenital diaphragm, 249 

Urolume, 75, 108 

Urosurge, 77,78f 

v 

Vagina 

examination, 3 1-32, 88-89 

urinary retention, 187-1 88 

Vaginal cones, 16'7 

Vaginal lesions 


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 


VCUG, 57 


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 


Voiding difficulties 


Voiding dysfunction, 25-57 

classification, 1&23,26-27 

Bors-Comarr, l 1-1 3, l l t 

Bradley, 14-1 5 

functional system, 5t4, 2 1-23, 

26-27

Index 341 

Hald Bradley, 13-14, 13t 

International Continence Society 

Classification, 19-2 1, 19t 

Lapides, 15-17, 16t 

urodynamic, 18-1 9, 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, 3 1-33 

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 pressure flow study, 43-45, 

45f, 51f 

Voiding function, 186 

Voiding pressure flow study, 43-45,45f, 

51f 

Voiding reflux 

inhibition, 10 

Vulvar lesions 


W 

Wertheim hysterectomy 


z 

Zoloft, 287

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