INTRODUCTION

Section 2 of 12  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

Urinary incontinence in women is not a recent medical and social phenomenon, but the relative importance attributed to urinary incontinence as a medical problem is increasing. Several factors responsible for the increased attention to incontinence can be cited, as follows:

• Women are more willing to talk openly about this disorder. Women are realizing that, in most cases, urinary incontinence is a treatable condition. Consequently, less embarrassment and fewer social stigmas are associated with the diagnosis.
• As the population ages, increased attention must be paid to incontinence. Urinary incontinence often is the chief reason for institutionalization of elderly people.
• Academic interest in urinary incontinence disorders is surging. This increased interest is arising among basic scientists, clinical researchers, and clinicians. The subspecialties of urogynecology and female urology are emerging, and structured fellowships are in the credentialing process.

As a direct result, the public is becoming more aware of the problem and more active and educated about incontinence. Patient advocacy groups provide patients access to information, incontinence products, and physicians who have interest or special expertise in these disorders. In the last decade, funding opportunities for incontinence research have increased vastly. Subspecialty professional organizations and journals are now active.

Important contributions to the understanding of the structure and functioning of the lower urinary tract include an improved understanding of the anatomy and dynamic functioning of the pelvic floor and its contribution to continence. In addition, much study has been conducted to bolster the understanding of the neurophysiology of the bladder, urethra, and pelvic floor. Finally, interest in the diagnosis and treatment of incontinence is ongoing.

The discipline of urodynamic testing is a burgeoning field but remains in its scientific infancy. Techniques of dynamic imaging of the pelvic floor and lower urinary tract, along with electrophysiologic testing, hold much promise in improving the understanding of continence mechanisms and ensuring accurate diagnoses. Exciting advances in surgical, nonsurgical, and pharmacologic treatments for incontinence are reported commonly in the literature. The future ability of physicians to diagnose and treat urinary incontinence appears to be bright.

Still, much more progress is needed. In a recent survey of primary care physicians, about 40% reported that they sometimes, rarely, or never ask patients about incontinence. More than 40% of internists and family practitioners routinely recommended absorbent pads to their patients as a solution to incontinence disorders. Continued education of the public and medical professionals is needed to improve the care rendered to individuals with urinary incontinence.

History of the Procedure

Disorders of urinary incontinence have been included in medical writing since antiquity. Lesions, such as genitourinary fistula, have been uncovered in the mummified remains of corpses dating back to 2000 BC. In the 1830s and 1840s, John Peter Mettauer first reported on the successful closure of vesicovaginal fistulas, lesions resulting in severe, debilitating urinary incontinence. However, J. Marion Sims, MD, garners much of the credit for this advancement. After countless attempts and failures, he eventually refined a technique of closure using silver wire sutures that was successful in most cases.

Sims was among the first surgeons to stress the close anatomic relationship between the genital and lower urinary tracts. In the early 1900s, Howard A. Kelly at Johns Hopkins also believed that gynecology and female urology were closely interrelated. Much of his work involved diseases of the urinary tract, and many authorities consider him an important figure in the founding of urology as a surgical specialty. Kelly is credited, along with W. A. Dunn, with the first significant surgical procedure for stress incontinence, now referred to as the Kelly plication.

Since Kelly's time, literally hundreds of procedures for the treatment of female incontinence have been devised. Only a few have stood the test of time. New procedures and modifications of older procedures continue to be developed. Few of these procedures have been subject to sufficient scientific scrutiny. The long-term efficacy of most incontinence operations is unknown. Most recently, procedures stressing minimally invasive surgical access have come to the forefront.

In addition to surgical advancements, physicians in the second half of the century have witnessed many other milestones in the study and treatment of female incontinence, including the following:

• Increased societal and medical awareness of the scope and prevalence of urinary incontinence
• Improved understanding of the diverse pathophysiology of female incontinence
• The development and refinement of urodynamics as a method of providing a diagnosis based on pathophysiology
• A greater appreciation of the contribution of certain medical conditions and lifestyle factors to the primary incontinence disorder
• The advent of nonsurgical and pharmacological therapies
• Increasing interest in research and systematic scientific study of urinary incontinence

Problem

According to the International Continence Society (ICS), urinary incontinence as a medical disorder is "a condition in which involuntary loss of urine is a social or hygienic problem and is objectively demonstrable." Urinary incontinence can be thought of as a symptom as reported by the patient, as a sign that is demonstrable on examination, and as a disorder. Urinary incontinence should not be thought of as a disease because no specific etiology exists; most individual cases are likely multifactorial in nature. The etiologies of urinary incontinence are diverse and, in many cases, incompletely understood.

In 1989, the National Institutes of Health Consensus Development Conference estimated the annual cost of urinary incontinence in the United States to be $12.4 billion. Some experts believe that this is a conservative estimate. True costs can be difficult to estimate because many individuals do not come to the attention of medical specialists. Some individuals pay out of pocket for adult incontinence undergarments, absorbable pads, skin care products, deodorants, and increased laundry expenses.

The psychosocial costs and morbidities are even more difficult to quantify. Embarrassment and depression are common. The affected individual may experience a decrease in social interactions, excursions out of the home, and sexual activity. The psychosocial impact on at-home caregivers, spouses, or family members rarely is considered. Recently, a questionnaire was developed to assess the quality of life of incontinent women. This questionnaire was easy to use, valid, and reliable. This tool may be a valuable adjunct to pretherapy and posttherapy assessment, as well as valuable in comparing the quality of life impact of different urodynamic diagnoses.

Frequency

Urinary incontinence is a common medical disorder. In the United States, an estimated 13 million adults experience significant involuntary urine loss. The precise prevalence of urinary incontinence is difficult to estimate. Part of the difficulty has been in defining the degree, quantity, and frequency of urine loss necessary to qualify as pathologic. Definitions have varied significantly among studies. The prevalence rate in females aged 15-64 years has been estimated at 10-25%, and, in males, the estimated rate is 1.5-5%. In one study of randomly chosen women aged 30-59 years, 26% reported incontinence at some time during their lives, and 14% perceived incontinence to be a social or hygienic problem.

Urinary incontinence occurs in 17-46% of community dwelling women older than 60 years. In the nursing home population, incontinence may be observed in as many as 38-83% of individuals. At any age, urinary incontinence is more than 2 times more common in females than in males. Urge incontinence constitutes over 50% of overall incontinence in men, 10-15% in younger women, and 30-40% in older women. Some studies demonstrate an increasing prevalence of urinary incontinence with age. Stress incontinence tends to be more common in women younger than 65 years. In patients older than 65 years, urge incontinence and mixed (ie, urge and stress) incontinence are more common.

Studies are not in agreement. One series by Yarnell and associates noted no significant increase in the prevalence of incontinence in women older than 35 years. Contributing factors with regard to age-related increases in urinary incontinence include a weakening of connective tissue, genitourinary atrophy due to hypoestrogenism, increased incidence of contributing medical disorders, increased nocturnal diuresis, and impairments in mobility and cognitive functioning.

Etiology

No single etiologic factor can be implicated in each case of urinary incontinence. Structural and functional disorders involving the bladder, urethra, ureters, and surrounding connective tissue can contribute. In addition, a disorder of the spinal cord or central nervous system (CNS) may be the major etiologic factor in some cases. Medical comorbidities also can be important. Finally, some cases of urinary incontinence may be pharmacologically induced. Even when examining an individual patient, one must be aware that the incontinence may have multiple etiologies, each with some degree of contribution to the overall disorder.

Understanding the risk factors for urinary incontinence helps shed some light on the underlying etiologic factors at work. Complete agreement does not exist in the literature regarding the risk factors for incontinence. The following are some of the more commonly cited risk factors:

• Female sex
• Age
• White or Japanese extraction
• Childbirth-related neuromuscular and connective tissue damage to the pelvic floor
• Episiotomy, third- and fourth-degree perineal lacerations
• Exposure to oxytocin in labor
• Prolonged labor
• Prolonged second stage of labor
• Giving birth to a large infant
• Instrumented delivery
• Obstructed labor with pressure-related necrosis of bladder base and proximal urethra (rare in developed countries)
• The pregnant state itself (ie, apart from delivery)
• Menopause, urogenital hypoestrogenism
• Prior hysterectomy
• Smoking
• Obesity
• Connective tissue disorders, congenitally weak connective tissue
• Chronic cough
• Chronic constipation
• Occupations or activities that stress the pelvic floor
• Strong osteomuscular body structure
• Lower genitourinary congenital anomalies
• Spinal cord injuries or congenital disorders
• CNS disorders - Stroke, multiple sclerosis (MS), Parkinson disease
• Diabetes
• Medications - Alpha-blockers, over-the-counter allergy medications (ie, retention and overflow), angiotensin-converting enzyme (ACE) inhibitors (ie, chronic cough)
• Previous incontinence surgery, surgery for fistula or urethral diverticula
• Urinary tract infection (UTI), especially in postmenopausal age group
• Radiation injury to the bladder
• Urinary tract stones, neoplasms, or foreign bodies

The etiology of urinary incontinence can be examined from many viewpoints. One way to classify types of incontinence by etiology is to first look at the anatomical structure(s) involved in the incontinence. A simplistic but conceptually useful method of classification emerges. Bladder-related, urethral, and ureteric etiologies of incontinence can be described.

Bladder-related incontinence consists of 2 main types, involuntary bladder contractions (ie, with or without loss of compliance) and a breach of anatomic integrity. Detrusor hyperreflexia is the urodynamic diagnosis made when involuntary bladder contractions are identified in the setting of a causative neurologic condition. Neurologic disorders such as MS, spinal cord injuries, CNS tumors, and meningomyelocele can be responsible for detrusor hyperreflexia. More commonly, involuntary bladder contractions are idiopathic in nature. The corresponding urodynamic diagnosis is detrusor instability (DI). Also, loss of bladder wall compliance due to radiation injury, outlet obstruction, overdistension (ie, overflow incontinence), and chronic severe inflammation can result in nonphasic increases in intravesical pressure. Bladder irritation, as can result from infection, inflammation, bladder stones, foreign bodies, and neoplasms, can also result in involuntary bladder contractions.

Among the disorders of bladder integrity are vesicovaginal or vesicocutaneous fistulas and untreated exstrophy of the bladder.

Urethral-related causes of incontinence include extrinsic and intrinsic types. Extrinsic urethral etiologies refer mainly to the loss of anatomic support to the proximal urethra and urethrovesical junction (UVJ), including genuine stress incontinence (GSI). In addition, some types of outlet obstruction can be placed in this class. Intrinsic urethral etiologies of incontinence can be further subdivided into anatomic and functional types. Examples of anatomic intrinsic urethral problems include fistulas, urethral diverticula, and epispadias. Examples of intrinsic functional urethral disorders are intrinsic sphincter deficiency (ISD) and urethral instability.

Ureteral etiologies of incontinence are rare and generally involve congenital anatomic abnormalities such as ectopic ureter or anatomic injuries (eg, ureterovaginal fistulas). This type of classification system, although a useful conceptual tool, is an oversimplification. For example, some types of incontinence may not fit neatly into any one category. Overflow incontinence due to sensory neuropathy can be thought of as both a neurogenic and, ultimately, a compliance problem. Outlet obstruction is usually an extrinsic urethral problem but can also be reasonably classified as a bladder-related etiology because, ultimately, the incontinence may be due to involuntary bladder contractions. DI can be thought of as a bladder problem, but, in most patients, the involuntary detrusor contraction is accompanied by urethral relaxation. In addition, mixed types of incontinence are commonly encountered, such as coexistent GSI and DI.

Another common classification system uses the type of symptomatology as an initial descriptor and then subdivides these categories by structural or functional etiology. The following are the ICS definition of the types of incontinence:

• Stress incontinence with normal detrusor, incompetent urethra - GSI, ISD, and combined GSI and ISD
• Urge incontinence with overactive detrusor, normal urethra - DI (idiopathic) and detrusor hyperreflexia (neuropathic)
• Overflow incontinence with underactive detrusor and/or overactive urethra - Neurogenic bladder, outlet obstruction, and pharmacologic incontinence
• Continuous incontinence with totally incompetent urethra and/or bladder or bypass of bladder - Urinary tract fistulas, nonfunctional urethra (ie, severe ISD), ectopic ureter, exstrophy of the bladder, and epispadias
• Functional incontinence with normal detrusor, normal urethra - Infection, inflammation, foreign bodies, stones, neoplasms, decreased mobility, behavioral, dementia, and pharmacologic

This classification system also is problematic. For example, urethral instability, a rare and poorly understood disorder, does not fit neatly into any single category. Incontinence due to urethral diverticulum is, likewise, difficult to classify. Some cases of DI may be triggered by cough or sneeze and, thus, may present with predominantly stress incontinence complaints. These classification systems, although not perfect, do assist the practitioner in placing the etiologies of incontinence into a conceptual framework, which aids in understanding the pathophysiology. A diagnosis based on an understanding of the pathophysiology should be the desired goal of any incontinence evaluation.

Pathophysiology

Stress incontinence

The pathophysiology of stress incontinence is incompletely understood and deceptively complex. During episodes of stress incontinence, the generated intra-abdominal pressure causes a coincident rise in intravesical pressure. The rise in intravesical pressure is greater than the rise in urethral pressure. Urethral resistance is overcome, resulting in leakage. Leakage ceases when bladder pressure again falls below urethral pressure.

Most cases of stress incontinence are believed to be related to damage to the neuromuscular functioning of the pelvic floor, coupled with injury, both remote and ongoing, to the connective tissue supports of the urethra and bladder neck. Loss of intrinsic urethral tone also may be involved in the pathologic picture. Neuromuscular damage to the voluntary striated urethral sphincter is believed to be the main culprit, but mucosal atrophy, hypovascularity, and local scarring also may be involved.

If the predominant mechanism of the stress incontinence is believed to be related to the loss of intrinsic urethral function, then the diagnosis is ISD. If loss of urethral support is thought to be the primary pathology, the disorder is called GSI. The degree of loss of both of these biologic parameters, urethral support and intrinsic urethral tone, probably falls in a bell-shaped distribution across stress incontinence populations; therefore, noting that most cases of stress incontinence have some degree of both types of pathology is important.

During times of increased intra-abdominal pressure, individuals with stress incontinence may display hypermobility or rotational descent of the UVJ. How this finding is linked to stress incontinence is uncertain, but many theories exist. In women without stress incontinence or urethral hypermobility, the urethra is stabilized during stress by several interrelated mechanisms.

One mechanism is reflex, or voluntary closure, of the pelvic floor. Contraction of the levator ani complex elevates the proximal urethra and bladder neck, tightens intact connective tissue supports, and elevates the perineal body, which may serve as a urethral back stop.

The second mechanism involves intact connective tissue support to the bladder neck and urethra. The pubocervicovesical or anterior endopelvic connective tissue in the area of the bladder neck is attached to the back of the pubic bone, the arcus tendineus fascia pelvis, and the perineal membrane. The pubourethral ligaments also suspend the mid urethra to the back of the pubic bone. These components form the passive supports to the urethra and bladder neck. During times of increased intra-abdominal pressure, if these supports are intact, they augment the supportive effect of muscular closure of the pelvic floor.

The third mechanism involves 2 bundles of striated muscle, the urethrovaginal sphincter and the compressor urethrae, found at the distal aspect of the striated urethral sphincter. These muscles may aid in compressing the urethra shut during stress maneuvers. These muscles do not surround the urethra like the striated sphincter but lie along the lateral and ventral aspects. The exact function and importance of these muscles are controversial. Some authors suggest that the urethrovaginal sphincter and the compressor urethrae may provide compression and increased pressure in the distal urethra during times of stress.

Damage to the nerves, muscle, and connective tissue of the pelvic floor is important in the genesis of stress incontinence. Intrapartum injury during childbirth probably is the most important mechanism. Aging, hypoestrogenism, chronic connective tissue strain due to primary loss of muscular support, activities or medical conditions resulting in long-term repetitive increases in intra-abdominal pressure, and other factors can contribute. During the intrapartum period, 3 types of lesions can occur—levator ani muscle tears, connective tissue breaks, and pudendal/pelvic nerve denervation. Any of these injuries can occur in isolation but are more likely to occur with 2 or more in combination. The long-term result may be the loss of active and passive urethral support and loss of intrinsic urethral tone.

Some believe that the loss of urethral and bladder neck support impairs urethral closure mechanisms during times of increased intra-abdominal pressure. This phenomenon can be viewed in several ways. Under normal circumstances, some hypothesize that any increase in intra-abdominal pressure is transmitted equally to the bladder and proximal urethra. This is likely due to the retropubic location of the proximal and mid urethra within the sphere of intra-abdominal pressure. At rest, the urethra has a higher intrinsic pressure than the bladder. This pressure gradient relationship is preserved if pressure transmission during acute increases in intra-abdominal pressure is equal to both organs. When the urethra is hypermobile, as it descends and rotates under the pubic bone, pressure transmission to the walls of the urethra may be diminished. Intraurethral pressure falls below bladder pressure, resulting in urine loss.

A related way of describing the mechanism of hypermobility-related stress incontinence is the hammock theory described by J. O. DeLancey, MD. Usually, in a person without incontinence, a cough or other acute increase in intra-abdominal pressure applies a downward force to the urethra. The urethra is then compressed shut against the firm support provided by the anterior vaginal wall and associated endopelvic connective tissue sheath. If the endopelvic connective tissue is detached from its normal lateral fixation points at the arcus tendineus fascia pelvis, then optimal urethral compression does not take place, possibly resulting in stress leakage.

A simple analogy is that of a garden hose (urethra) running over a pavement surface (anterior endopelvic connective tissue). A force is applied in a downward direction using the foot (increased intra-abdominal pressure). This force compresses the hose shut, occluding flow. If the same hose is run through a soft area of mud (damaged connective tissue), then the downward force does not occlude the hose but, rather, pushes the hose deeper into the mud.

Other interesting alternative theories of the mechanism of stress incontinence have been described. One description stems from research involving ultrasound visualization of the bladder neck and proximal urethra during stress maneuvers. Findings of potential importance include the following: (1) 93% of patients with stress incontinence displayed funneling of the proximal urethra with straining, and one half of these individuals also showed funneling at rest; and, (2) during stress maneuvers, the urethra did not rotate and descend as a single unit. The investigators found that the posterior urethral wall moved farther than the anterior wall.

Although mobile, the anterior urethral wall has been observed to stop moving, as if tethered, while the posterior wall continued to rotate and descend. The authors hypothesize that the pubourethral ligaments arrest rotational movement of the anterior, but not the posterior, wall. The authors believe that the resulting separation of the anterior and posterior urethral walls might open the proximal urethral lumen, thus allowing or contributing to stress incontinence.

Urge incontinence

The ICS describes the unstable bladder as one that has been shown objectively to contract spontaneously during the filling phase of cystometry, while the patient is inhibiting or attempting to inhibit voiding. If these contractions result in urinary leakage, then the term urge incontinence is used. In the patient who is nonneuropathic, this disorder is called DI. In situations where a definable causative neuropathic disorder exists, the coexisting urinary incontinence disorder is termed detrusor hyperreflexia. These disorders can be quite debilitating. Recently, a study using a quality of life assessment of women with incontinence showed that women with DI consistently had a worse quality of life than did women with other urodynamic diagnoses. In light of such data, understanding the pathophysiology of urge incontinence takes on great importance.

Detrusor instability

DI in adult patients is a disorder of unclear etiology and an incompletely understood pathophysiology. DI represents about 90% of the cases of urge incontinence/bladder instability. In most patients, a sensation of urgency occurs first, followed by the initiation of an involuntary bladder contraction, and, finally, urethral relaxation. A minority (11-42%) of patients may experience urethral relaxation first, thereby mimicking normal micturition. More rarely, urethral relaxation exists as an isolated event.

The corresponding urodynamic diagnosis for this condition is urethral instability. In some instances, DI may be triggered by such specific events as coughing, hand washing, changes in posture or position, an increase in the speed of bladder filling, orgasm, and anticipation of voiding (ie, key in lock incontinence). In other cases, initiating events may be less obvious or not identifiable. Less commonly, patients may complain of episodes of unexpected bladder emptying in the complete absence of any urgency.

Some researchers believe DI to represent the premature initiation of a normal micturition reflex. In vitro studies of bladder muscle strips of patients with DI have demonstrated an increase in response to electrical stimulation and an increased sensitivity to stimulation with acetylcholine. These findings may indicate a higher sensitivity to efferent neurologic activity or a lower threshold of acetylcholine release needed to initiate a detrusor contraction. A relative cholinergic denervation may explain some of these findings. This proposed mechanism is most plausible in cases of de novo DI, which follow hysterectomy or other pelvic surgery. The mechanism of denervation in idiopathic DI is less certain. Subtle obstruction and the effects of aging on smooth muscle and the autonomic nervous system are 2 possible contributors.

Another finding described in bladder muscle specimens from patients with DI is that of local loss of inhibitory medullary neurologic activity. Vasoactive intestinal peptide, a smooth muscle relaxant, is decreased markedly in the bladders of patients with DI. In addition, bladders of individuals with DI have been found deficient in smooth muscle–relaxing prostaglandins. A recent study proposed that urge incontinence, regardless of the triggering mechanism, may share a final common pathway of myogenic dysfunction of the detrusor. Spread of contractile signals via cell-to-cell coupling was proposed as the likely mechanism.

Another possible explanation for DI in a subgroup of patients involves the triggering of the micturition reflex by leakage of urine into a funneled and partially incompetent proximal urethra. This theory is consistent with the findings of DI caused by coughing or changing position.

Mixed incontinence is a common finding in older patients with urinary incontinence disorders. Often, stress incontinence symptoms precede urge incontinence symptoms in these individuals. Urgency without actual urge-related urine loss also is a common complaint of patients with stress incontinence. Some patients with stress incontinence have urine leakage into the proximal urethra that may, at first, trigger sensory urgency and/or bladder contractions, which initially are suppressible. Later, in a subgroup of these individuals, myopathic changes may occur in the bladder that make the spread of abnormally generated contractile signals more efficient and more difficult to suppress voluntarily. The development of clinical DI may follow.

Most recently, a comparison study was undertaken of bladder muscle strips from patients with severe idiopathic DI and from organ donors with no known urologic problems. The following are some of the findings:

• Patchy partial denervation of the detrusor with areas of normal innervation and areas of reduced innervation by fibers staining for acetylcholinesterase
• A reduced force of contraction in response to electrical field stimulation: This finding is in contrast to a previous study showing an increased sensitivity to electrical field stimulation, but the authors believe that the muscle strips may have had increased sensitivity to direct electrical stimulation (non–nerve mediated).
• Supersensitivity to potassium
• Increased electrical coupling of cells via cell-to-cell junctions
• Variability in the activity of muscle strips from the same bladder

The authors believe that the primary abnormality in idiopathic DI is at the detrusor muscle level with an increased capacity for spontaneous myogenic contractile activity and spread of electrical activity from cell to cell, resulting in tetanic contractions. Epidemiological studies have shown an association between DI and irritable bowel syndrome. Some authorities have proposed that a syndrome of smooth muscle dysfunction may exist in some individuals.

Another study demonstrated the presence of an increased ratio of abnormal-to-normal cell junctions in patients with bladder dysfunction. The increased ratio was demonstrated most markedly in patients with idiopathic DI. To a lesser degree, these changes also were observed in patients with outlet obstruction combined with DI and with idiopathic sensory urgency alone. The authors believe that idiopathic sensory urgency might represent a milder or less overt variant of DI. They feel that, in the future, bladder biopsy with structural evaluation of cell junctions might become a useful clinical tool in the diagnostic evaluation of bladder dysfunction.

Urethral instability

The diagnosis of urethral instability occasionally is made following the urodynamic workup of incontinence. The role of this entity within the realm of incontinence disorders is controversial. The diagnosis is made when a fall in urethral pressure is observed with a stable bladder pressure and coincident urinary leakage. Some investigators believe that urethral instability represents a variant of DI, where pressure equalization occurs rapidly between the bladder and urethra. Therefore, the rise in intravesical pressure indicative of DI is not observed. Other authors have commented that urethral instability does not respond reliably to conventional pharmacotherapy for DI. This finding suggests that the pathophysiology of urethral instability is different. Reports on treating urethral instability with drugs that increase urethral tone can be found in the literature.

Detrusor hyperreflexia

Detrusor hyperreflexia is a condition of uninhibited detrusor contractions in the presence of a neurologic lesion believed to be causative. In these cases, the pathophysiology of the incontinence can be traced back to a pathologic process involving the suprasacral spinal cord or CNS. Such disorders include spinal cord injuries, MS, cerebrovascular disease, stroke, Parkinson disease, dementia, and CNS/spinal neoplasia.

Spinal cord injuries interrupt the sacral reflex arc from the suprasacral spinal cord, cerebral cortex, and higher centers. These pathways are crucial for voluntary and involuntary inhibition. In the initial phase of spinal cord injury, the bladder is areflexic and overflow incontinence results. Later, detrusor hyperreflexia usually is found upon urodynamic evaluation.

The pathophysiology of MS is that of demyelinating plaques in the white matter of the cerebral cortex, cerebellum, brain stem, spinal cord, and optic nerve. Plaques involving the frontal lobe or lateral columns can produce lower urinary tract disorders. Incontinence may be the presenting symptom of MS in about 5% of the cases. Approximately 90% of individuals with MS experience urinary tract dysfunction during the course of the disease. A summary of the published series of urodynamic findings in MS demonstrated that in patients with lower urinary tract dysfunction, the most common urodynamic diagnosis is detrusor hyperreflexia (62%). Detrusor-sphincter dyssynergia (25%) and detrusor hyporeflexia (20%) also are common. Obstructive findings are much more common in males. Of note, the urodynamic diagnosis may change over time as the disease progresses.

Hemorrhage, infarction, or vascular compromise to certain areas of the brain can result in lower urinary tract dysfunction. The frontal lobe, internal capsule, brainstem, and cerebellum commonly are involved sites. Initially, urinary retention due to detrusor areflexia is observed. This may be followed by detrusor hyperreflexia. Approximately 40-70% of patients with Parkinson disease have lower urinary tract dysfunction. Controversy exists as to whether specific neurologic problems in patients with Parkinson disease lead to bladder dysfunction or if bladder symptoms simply are related to aging. The extrapyramidal system is believed to have an inhibitory effect on the micturition center; theoretically, loss of dopaminergic activity in this area could result in loss of detrusor inhibition.

In patients with dementia, incontinence and urinary tract dysfunction may be due to specific involvement of the areas of the cerebral cortex involved in bladder control. Alternatively, incontinence may be related to global deterioration of memory, intellectual capacity, and behavior. Urodynamically, both detrusor hyperreflexia and areflexia have been found. In the case of neoplasms, CNS tumors of the superior medial frontal lobe, spinal cord tumors above the conus medullaris, and cervical spondylosis can cause detrusor hyperreflexia.

Other causes of urge incontinence

Bladder outlet obstruction is rare in females and, usually, is a postincontinence surgery phenomenon. Advanced pelvic organ prolapse can cause a partial outflow obstruction. In older females with long-standing bladder control problems and pelvic organ prolapse, DI may coexist with a relatively poorly functioning detrusor. Due to poor contractility of the detrusor and partial obstruction related to advanced prolapse, the patient may experience incomplete emptying.

In males, early obstruction due to benign prostatic hyperplasia (BPH) may result in urge incontinence. BPH is a very common occurrence with aging and ongoing normal androgenic function. The pathophysiology of BPH is poorly understood. Relative obstruction develops because of mechanical factors, dynamic factors, and detrusor alterations. Androgen-induced enlargement of nodules of glandular tissue comprises the mechanical portion of the disorder. The dynamic component is related to increased alpha tone in prostatic and urethral smooth muscle. Detrusor dysfunction may consist of impaired contractility, DI, or both. In severe cases of obstruction, retention and overflow incontinence may develop, and the upper urinary tract can become damaged.

The presence of inflammation in the bladder is believed to result in bladder muscle irritability and urge incontinence in some instances (see Image 4). One study showed that approximately 8% of patients with bacterial urine infections had nonneuropathic bladder instability. If bacterial infection and DI coexist, successful treatment of the infection results in resolution of the DI in about one half of the patients. Nonbacterial inflammatory conditions of the bladder, including interstitial cystitis, have been associated with DI. Foreign bodies, including permanent sutures, bladder stones, and neoplasms, also have been linked to bladder irritability and instability.

Mixed incontinence is the term used when stress incontinence and DI coexist. Approximately 40-60% of females with incontinence have this combination. Although generally thought of as separate etiologies for incontinence, some indirect evidence may link these disorders in some instances. Some patients with mixed incontinence report stress incontinence symptoms first, followed in time with increasing urgency, and, finally, the appearance of urge incontinence. Many patients with stress incontinence alone as a urodynamic diagnosis also report urgency as a major symptom.

In some instances, surgery to support the UVJ cures the DI portion of mixed incontinence. In addition, some vaginal support devices designed to treat GSI have modest efficacy in the treatment of mixed incontinence. Some experts believe that funneling of the urethra, a lesion associated with stress incontinence, also may allow urine to contact the proximal urethra, resulting in a reflex detrusor contraction and DI. DI induced by coughing or the Valsalva maneuver frequently is observed during urodynamic evaluations, yielding the diagnosis of mixed incontinence.

Finally, the frequency with which the diagnoses of GSI and DI travel together is being studied. Several theories about the relationship between GSI and DI have been described. The most well-known theory involves urethral funneling and leakage of urine into the proximal urethra with triggering of urethral afferents. The result is the involuntary activation of the micturition reflex. The integral theory of incontinence states that a generalized laxity of the vagina and connective tissue support are at the root of most urinary incontinence. Similarly, other investigators believe that the stretching of pelvic nerves associated with pelvic organ prolapse may be involved in triggering involuntary detrusor contractions.

A shared pathophysiology between GSI and DI has not been proved, and, even if this relationship does exist, it may apply to only a subset of patients. Surgery for GSI is not contraindicated if the patient also has DI. At this time, the recommendation is that the surgical treatment of GSI in the setting of mixed incontinence be approached with caution. Both patient and physician must realize that DI may not improve and may even worsen. Participants should understand clearly that the surgery is intended to treat the stress incontinence component. One recent study demonstrated a better prognosis for surgical treatment if the urge incontinence symptoms clearly followed the stress incontinence symptoms in time. Although these findings are encouraging, for now, a conservative approach (ie, the treatment of mixed incontinence as 2 separate disorders) may be best. More research to further elucidate the relationship between stress and urge incontinence is needed.

Potential incontinence

Potential or masked incontinence refers to stress incontinence that is revealed only after a reduction of severe pelvic organ prolapse. Some believe that in these individuals, kinking of the urethra caused by the prolapse itself provides for at least part of the continence mechanism. In some patients, a history of stress incontinence with improvement and, finally, resolution coincident with worsening of the prolapse can be recounted. In diagnosing potential incontinence, the goal is to avoid new-onset incontinence following surgical correction of prolapse. In patients with potential incontinence, an incontinence procedure, such as a colposuspension or sling, should be considered. The diagnosis can be made by stress testing with the prolapse reduced or by pessary placement and pad testing. No particular method of prolapse reduction has been proved superior.

In a recent study using pessaries, 58% of the patients with severe pelvic organ prolapse had masked incontinence. These patients were treated with a pubovaginal sling, anterior colporrhaphy, and other appropriate reparative operations. Eighty-six percent of the patients with potential incontinence so treated had no postoperative stress-related urine loss. The group of patients with no demonstrable potential incontinence underwent anterior colporrhaphy and additional individualized procedures. Incontinence procedures, per se, were not performed in this group. No patients had postoperative stress incontinence. Mean follow-up was 40-50 months. This study points out that bladder neck procedures need not be performed if potential incontinence has been ruled out, even if bladder neck hypermobility is present. Indeed, incontinence procedures are not without their own morbidities and should not be performed unless necessary.

Overflow incontinence

Overflow incontinence is related most commonly to bladder neuropathy. Diabetes mellitus is a common etiology of the neurogenic bladder. Lumbosacral nerve disease from tumors, meningomyelocele, MS, and prolapsed intravertebral disks also can result in bladder neuropathy and overflow incontinence. High spinal cord injuries are another etiology. As discussed above, severe cases of outlet obstruction ultimately can cause severe retention, local neurologic injury, and overflow. In most cases, both sensory and motor neuropathy are present. The maximal physical capacity of the bladder is reached, often times without the individual realizing that this has occurred.

Incontinence occurs off the top of a chronically over-filled bladder. Effective emptying is not possible because of an acontractile detrusor muscle. In early bladder neuropathy, DI may coexist with a hypofunctioning detrusor muscle. Early in the course of diabetes-related bladder neuropathy, symptoms and the functioning of the detrusor may wax and wane. The result is periods when urinary retention and overflow incontinence are severe and periods when detrusor function and voiding effectiveness temporarily improve.

Continuous incontinence

This severe type of incontinence is characterized by constant or near constant leakage with no symptoms other than wetness. Generally, this represents some significant breech in the storage capabilities of the bladder or urethra. Urogenital fistulas are a classic example. A nonfunctioning urethra can result in continuous leakage. Scarring and fibrosis from previous surgery, partial urethral resection for vulvar cancer, and urethral sphincter paralysis due to lower motor neuron disease can cause the urethra to fail. In addition to being a possible etiology for fistula, pelvic irradiation rarely results in bladder noncompliance and continuous incontinence. Congenital malformations of the genitourinary tract, such as bladder exstrophy, epispadias, and ectopic ureters, can result in total incontinence.

Functional incontinence

Functional incontinence is a term describing the inability to hold urine due to reasons other than neuro-urologic and lower urinary tract dysfunction. In some cases, the cause is of a transient nature. In other instances, a permanent problem can be identified. The etiology of the incontinence may be iatrogenic, environmental, situational, or disease related. A commonly quoted mnemonic is helpful in remembering the functional contributors to incontinence.

D - Delirium

I - Infection, urinary

A - Atrophic urethritis or vaginitis

P - Pharmacologic agents

P - Psychiatric illness

E - Endocrine disorders

R - Reduced mobility or dexterity

S - Stool impaction

Pediatric incontinence

Pediatric incontinence disorders are classified according to cause. Primary incontinence disorders generally are due to congenital structural disorders, including ectopic ureter, exstrophy, epispadias, and patent urachus. Secondary structural causes can result from obstruction from urethral valves, congenital urethral strictures, and large ectopic ureteroceles. In addition, trauma can result in secondary structural incontinence.

Neurogenic lesions make up the next category of pediatric incontinence disorders. These include spinal dysraphism, tethered spinal cord, and spinal cord tumors. Nonstructural causes of incontinence can be related to infection and inflammation. Dysfunctional voiding habits can develop even at a young age. Some children may become so preoccupied with activities that voiding is delayed until capacity is reached and accidents result.

Some believe that certain children develop a pattern of not relaxing the pelvic floor while voiding. In some cases, this can be traced back to an infection or some other noxious stimuli. A vicious cycle of pelvic floor spasm, constipation, and urinary retention can develop. So-called giggle incontinence has been thought to represent an underlying temporal lobe seizure, but other studies do not support this theory. Vaginal voiding is a pseudoincontinence disorder, which may result from voiding with the legs too tightly together. The impeded flow of urine may fill the vagina. The vagina empties when standing.

Nocturnal enuresis is the most common pediatric incontinence disorder. The disorder occurs in 15% of children aged 5 years and in 1% of adolescents aged 15 years. Spontaneous resolution at a rate of 14-16% per year is the rule. This type of natural history makes the study of the etiology and treatment more difficult. Etiologic and pathophysiologic theories include decreased secretion of nighttime antidiuretic hormone, sleep disorders, delay in maturation of bladder control mechanisms, psychiatric disturbances, and allergies. A strong genetic component can be observed in some families. Indeed, a possible locus on chromosome arm 13q has been identified. Finally, some researchers believe that a weakness in urethral sphincteric function may exist due to poor alpha-sympathetic tone.

Integral theory

Recently, a unifying theory of the etiology of stress incontinence, DI, voiding dysfunction, and fecal incontinence has been proposed. The basis of the theory is that these disorders are the result of overstretching of the vaginal connective tissue and supporting ligaments, usually at the time of childbirth. Laxity of the pubourethral ligaments (ie, anterior zone of damage), mid vagina (ie, middle zone), and uterosacral ligaments (ie, posterior zone) make the usual tridirectional support of the vagina ineffective. With the vagina no longer properly tethered to the pelvic girdle, the usual neuromuscular actions that occur during increases in intra-abdominal pressure or pelvic floor relaxation during voiding are not translated as effectively into urethral closure and opening, respectively.

DI, according to this theory, occurs because of the premature firing of stretch receptors in the bladder base secondary to poor endopelvic connective tissue support to the filling bladder. The integral theory is attractive from the standpoint of parsimony but is complex. The theory is appreciated and understood best with the help of illustrations and diagrams showing directional force vectors. The interested reader is referred to the many publications by P. E. Petros, MD, on this subject.

Clinical

History

The clinical presentation of urinary incontinence can be varied in many respects. Patient complaints may be minor and situational or severe, constant, and debilitating. When obtaining a clinical history, determining whether the problem is a social and/or hygienic problem and the degree of disability attributable to the incontinence also is important. In addition, the following points regarding the clinical presentation should be sought when obtaining the history:

• Severity and quantity of urine lost and frequency of incontinence episodes
• Duration of the complaint and whether problems have been worsening
• Triggering factors or events (eg, cough, sneeze, lifting, bending, feeling of urgency, sound of running water, sexual activity/orgasm)
• Constant versus intermittent urine loss and provocation by minimal increases in intra-abdominal pressure, such as movement, changes in position, and incontinence with an empty bladder
• Associated frequency, urgency, dysuria, pain with a full bladder, and history of UTIs
• Concomitant symptoms of fecal incontinence or pelvic organ prolapse, such as pelvic pressure, feeling of protrusion, sacral backache, vaginal splinting for bowel movements, chronic constipation, urinary hesitancy, and poor stream
• Coexistent complicating or exacerbating medical problems, such as chronic cough, obstructive lung disease, diabetes, obesity, connective tissue disorders, postmenopausal hypoestrogenism, CNS or spinal cord disorders, chronic UTIs, and urinary tract stones
• Obstetrical history, including difficult deliveries, grand multiparity, forceps use, obstetrical lacerations, and large babies
• History of pelvic surgery, especially prior incontinence procedures, hysterectomy, or pelvic floor reconstructive procedures
• Other urologic procedures
• Spinal and CNS surgery
• Lifestyle issues, such as smoking, alcohol or caffeine abuse, and occupational and recreational factors causing severe or repetitive increases in intra-abdominal pressure
• Medications, such as cholinergic or anticholinergic drugs, alpha-blockers, over-the-counter allergy medications, estrogen replacement, beta-mimetics, sedatives, muscle relaxants, diuretics, and ACE inhibitors.

Incontinence histories can be very complex and time consuming. Most centers use some form of incontinence questionnaire as an aid. Sending the questionnaire to patients in advance so that they can give appropriate time and thought to their answers may be helpful. Part of the questionnaire should deal with the patient's quality of life, sexual and lifestyle issues, and the relationship of these factors to the incontinence disorder. The patient also should be instructed to fill out a voiding diary and to write down any questions. Voiding diaries should record the volume and type of fluid intake and the frequency and volume of voids. Episodes of nocturia should be noted. Finally, episodes of incontinence should be recorded, including an estimate of the volume; associated activities such as coughing, straining, and dishwashing; and associated symptoms such as urgency.

Voiding diaries are helpful as a pretherapy diagnostic tool, but they have also been used to measure posttherapy outcomes. Estimates of voiding frequency and amounts obtained by history alone can be unreliable. Voiding diaries are reproducible in the setting of stress incontinence, but fewer data exist regarding urge incontinence. In patients with stress incontinence, one study found that a representative and reproducible measure of incontinence episodes and mean daily voids can be obtained with a 3-day diary. A 1-day diary is probably too short. Further research is needed concerning voiding diaries in patients with urge incontinence.

Many cases of urinary incontinence present as a gradually progressive disorder. Progression from very mild symptoms to more severe and debilitating urine loss may take many years. The patient may come to medical attention only after experiencing a progressive worsening of symptoms. In other patients, symptoms may appear suddenly and may or may not be associated with a specific inciting event, such as pelvic/urinary tract surgery, trauma, and genitourinary tract infection. In these instances especially, associated symptoms such as pelvic pain, urgency, frequency, dysuria, and hematuria may point to a specific etiology. Most authorities agree that surgical therapy should not be based on history alone. A review of the role of patient history in the diagnosis of urinary incontinence showed that a history of stress incontinence carries a sensitivity of about 0.91, but specificity is only 0.51. Positive predictive values in the range of 0.75-0.87 have been reported for a history of stress incontinence.

Sensitivity and specificity are worse if the history is indicative of DI or mixed incontinence. Because some believe that many failed stress incontinence procedures are the result of incorrect or incomplete diagnoses, improving on the positive predictive value of history alone seems worthwhile.

The more difficult question to answer is which battery of tests and examinations produces a high positive predictive value at the lowest cost and inconvenience to the patient. One study looked at combining 4 factors to improve diagnostic accuracy. Patients with a predominant stress incontinence history, a postvoid residual (PVR) volume of no more than 50 mL, a positive cough stress test finding, and a functional bladder capacity of at least 400 mL underwent complex urodynamic testing. The diagnosis of stress incontinence was confirmed on urodynamic testing 97% of the time, but 15% of these patients also had coexisting DI. The positive predictive value, if one considers mixed incontinence as a separate disorder, is 82%. The essential issue seems to be the diagnosis of DI as a part of a mixed incontinence disorder; therefore, adding cystometry to the battery of necessary tests seems logical in most instances.

Physical examination

A focused physical examination should be performed. The examination is tailored somewhat in each case, based on the specifics of the patient's incontinence complaint and pertinent medical and surgical history. Each patient should have height, weight, blood pressure, and pulse recorded. Obesity is an important contributor to stress incontinence, and the presence of obesity may influence management decisions. Urinalysis and culture tests should be sent. Some practitioners have the patient arrive with a full bladder, measure the volume voided, and then catheterize the patient to obtain a PVR measurement. Others incorporate this into the urodynamics portion of the evaluation if this is to be performed.

The general physical examination is tailored to each individual patient. Medical illnesses and comorbidities that may be contributing to the overall incontinence disorder should be sought. Cardiac and pulmonary evaluation can be important. The abdomen should be examined for surgical scars, hernias, masses, and organomegaly. The presence of hernias may indicate inherent connective tissue weakness, a possible contributor to incontinence. Masses may contribute to stress incontinence and, occasionally, may cause obstructed voiding with resultant overflow incontinence. The back and costovertebral angles should be inspected and palpated. Tenderness, deformity, or the presence of surgical scars should prompt further investigation.

Because neurologic disorders can cause or exacerbate urinary incontinence, a focused neurologic examination should be a part of every incontinence evaluation.

Much information can be gained from simple conversation with the patient (eg, mental status) and observation of gait (eg, CNS, spinal cord, peripheral nervous system disease). Any abnormalities should prompt more in-depth investigations. Strength, sensation, and deep tendon reflexes of the lower extremities should be tested. Sensation of the perineum and perianal area should be tested with a soft touch and light prick. Using a cotton swab, the anal wink pelvic floor reflex can be elicited by stroking laterally to the anal canal. The bulbocavernosus reflex can be elicited by gently tapping the clitoris with a cotton swab in the female patient. The presence of these perineal reflexes ensures that a significant pudendal neuropathy does not exist. The absence of these reflexes does not diagnose neuropathy but merely raises suspicion. These reflexes may be extinguished if the patient is anxious during the examination.

The pelvic floor examination is an integral part of the incontinence evaluation. In female patients, in particular, incontinence disorders often coexist with pelvic floor relaxation. If a surgical approach to the incontinence is chosen, other pelvic floor defects of significance can be treated simultaneously. The examination begins with inspection of the external genitalia and urethral meatus. Evidence of atrophy, such as pallor and thinness of tissue, may indicate estrogen deficiency. A red, fleshy lesion of the posterior urethra, a caruncle, may be another indicator of urogenital hypoestrogenism. The suburethral area should be inspected and palpated. A suburethral mass should raise suspicion for a urethral diverticulum.

Other signs of a diverticulum might include tenderness and purulent or watery discharge upon compression. Urethral and trigonal tenderness also may indicate urethritis, urethral syndrome, or intersitial cystitis. The vaginal mucosa should be inspected for pallor, thinning, loss of rugae, and other signs of hypoestrogenism. If clinically suspected, a fistula opening may be discovered during vaginal examination. At times, pooling of fluid, exudate, or granulation tissue may indicate a nearby fistula tract.

A detailed pelvic floor examination should be performed for signs of pelvic organ prolapse. A systematic examination is conducted for cystocele, rectocele, uterine or vaginal prolapse, enterocele, and perineal laxity. A bivalve speculum should be used to visualize the cervix or vaginal apex. With the patient straining maximally, the speculum is withdrawn slowly, and any descent of the cervix or vaginal cuff is noted. The speculum is then disarticulated, and a single blade examination is performed, inspecting the anterior vaginal wall during straining with the posterior wall retracted. If a cystocele is observed, then a ring forceps or similar instrument is inserted over the speculum blade and opened to support the lateral vagina. The tips of the ring forceps should be against the bilateral ischial spines. If the cystocele is present with the patient straining and the lateral vagina supported, then a midline defect exists either in isolation or with a paravaginal defect.

Another clue to a midline defect is the loss of rugae with straining. If the cystocele is no longer present with lateral support, then a pure paravaginal defect is present. Another clue to paravaginal defects is collapsing side walls during bivalve speculum examination. If anterior wall prolapse is present with lateral support, then the next maneuver is to use the closed ring forceps to provide midline anterior vaginal support while the patient is straining again. If some cystocele is still noted, then a combined central and paravaginal cystocele is present. If no bulge is noted, then the defect is purely central.

Next, attention is turned to the posterior vaginal wall. The half speculum is used to retract the anterior wall of the vagina, while the posterior wall is examined during Valsalva maneuver. The presence or absence of a rectocele should be noted. If a double bump is observed when the patient strains, an enterocele may be present in addition to the rectocele.

Next, the perineal body is inspected. The height and thickness of the tissue is noted. A badly compromised perineal body may be short and consist of mostly skin with little or no underlying muscle. The levator muscles are palpated, and the resting tone is noted. Then, the patient is instructed to squeeze the examining fingers, and the levator strength can be appreciated. A rectovaginal examination is performed to determine the thickness of the rectovaginal septum. The patient then is asked to strain. Tissue felt sliding through the examining fingers may indicate an enterocele. Resting and squeezing rectal sphincter tone is noted. As the rectal finger is withdrawn, the external anal sphincter should be palpated between this finger and the thumb. The absence or attenuation of this body of muscle indicates a sphincter laceration. In the male patient, levator ani tone and strength can be tested during a rectal examination. The prostate should be palpated looking for tenderness, enlargement, andnodularity.

Cotton swab test

This part of the examination assesses urethral mobility. A lubricated sterile cotton swab is placed through the urethra and into the bladder. The swab is pulled back until increased resistance is met, indicating that the cotton tip is entering the urethra. At this point, the patient is asked to strain maximally. The change in angle, indicated by the arc of the wooden end of the swab, is measured with a goniometer or estimated visually. A change of greater than 30° indicates urethral hypermobility. Positive findings provide no specific diagnosis.

Hypermobility is present in most cases of stress incontinence. If hypermobility is not present and stress incontinence is diagnosed, ISD should be suspected. In this setting, an operation designed solely to stabilize the UVJ may not be the best choice. When performing the cotton swab test, having the patient put forth a maximal effort is important. The examiner should not use a posterior vaginal retractor. The labia should be parted if the tissue is touching the wooden shaft of the swab because this may impair movement during straining.

Stress testing

Stress testing should be performed with a full bladder. This author performs the test in both the lithotomy and standing positions. In either case, directly visualizing the urethra is necessary. The patient then is asked to cough forcefully and repetitively. Alternatively, the patient may perform a strong Valsalva maneuver. Urine loss directly observed from the urethral meatus at the peak of the increase in intra-abdominal pressure is strongly suggestive of stress incontinence (see Image 5).

Generally, the patient with stress incontinence displays immediate urine loss of relatively short duration. A few drops to a squirt of urine characteristically is lost. Delayed loss or prolonged loss raises the question of stress-induced DI. If no urine loss is observed, the test can be repeated in another position or repeated at another date. If more than mild pelvic organ prolapse is present, reduction of the prolapse should be performed with a half speculum, a pessary, or the examining fingers during the stress test. Care must be taken not to compress the urethra, regardless of which reduction method is used.

Positive stress test findings in the supine position with a relatively empty bladder and with position change or other minimal increases in intra-abdominal pressure raise the question of ISD. Complex urodynamic testing would be indicated. Pyridium pad testing can be used if the history strongly suggests stress incontinence, stress test findings are negative, and DI is ruled out. This particular test is discussed in detail in a subsequent section.

Marshall-Bonney test

Stress testing with support rendered to the hypermobile urethra has been used for decades to attempt to predict the success or failure of stress incontinence operations. The test has been criticized because it is imprecise and may work, in part, through urethral compression. A number of different methods have been described to perform elevation and support of the UVJ, including ring forceps, examining fingers, large cotton-tipped swabs, and specialized instruments. Data do not exist to recommend one method over another definitively. Urodynamics studies conducted while performing a modification of the Marshall-Bonney test revealed an average increase in urethral pressure of 52 cm H₂O, compared to greater than 250 cm H₂O with direct urethral compression. In this study, large cotton swab tips attached to short ring forceps were used to elevate the UVJ. Cough pressure transmission ratios increased from 64% before the test to 152% during the test.

A recent review article stated that the test may be useful if the findings are negative (ie, incontinence persists despite support to the hypermobile urethra). This author believes that these findings might dictate a more aggressive surgical approach, such as performing a sling procedure rather than a Burch retropubic urethropexy. This author also believes that this test has a place in planning incontinence therapy, although the performance of this test is purely within the realm of the art (ie, not the science) of incontinence evaluation.

Grading urinary incontinence

The results of the history and physical examination provide the clinician information that guides the ongoing evaluation. Part of the information available at this point is an estimation of the degree of incontinence experienced by the patient. In the 1970s, Stamey devised a grading system based on the degree of incontinence. Such a system, as outlined below, can prove to be useful in both the clinical and research settings.

• Grade 0 - Continent
• Grade 1 - Loss of urine with sudden increases in abdominal pressure, not in bed at night
• Grade 2 - Incontinence worsens with lesser degree of physical stress
• Grade 3 - Incontinence with walking, standing erect from sitting position, or sitting up in bed
• Grade 4 - Total incontinence occurs and urine is lost without relation to physical activity or position

INDICATIONS

Section 3 of 12  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

Nonsurgical treatment for urinary incontinence may be initiated whenever the patient believes that the problem warrants attention. Most authorities believe that treatment in these patients can be based on history, a physical examination, and urinalysis to rule out infection. A confirmation of the diagnosis by urodynamic studies need not be performed before initiating noninvasive treatment. Primary care physicians should be able to begin treatment in this way in a large number of patients. Referrals to a specialist should be reserved for patients with severe or continuous incontinence, complicated medical or surgical histories, or treatment failures and for those patients contemplating surgery.

Surgical treatment of stress urinary incontinence is indicated if the patient desires surgical correction, if the problem is perceived as a significant social and/or hygienic problem, and the incontinence is demonstrable and of a type that is amenable to surgery. The diagnosis should be based on the results of at least a minimum of studies, as follows:

• Urinalysis and culture to rule out infection
• Screening neurological examination of the lower extremities and pelvic floor
• Hypermobility of the urethra as determined by the cotton swab test or some other method
• Low PVR as demonstrated by catheterization or ultrasonography (US)
• Cystometry to rule out/in DI
• Stress testing demonstrates visible leakage of urine from the urethral meatus coincident with the peak of increase in intra-abdominal pressure
• Urogenital fistula has been ruled out by history and/or physical examination

More complicated urodynamic testing should be performed, if indicated, before surgical treatment. In particular, the diagnoses of ISD, mixed incontinence (ie, stress, urge), and voiding dysfunction should be kept in mind because any of these can influence the choice of procedure and complicate surgical management. In addition, in patients with no urinary incontinence complaints who are to undergo surgery for pelvic organ prolapse, the diagnosis of potential incontinence should be sought. Stress testing with the prolapse reduced or a trial of pessary management may reveal this diagnosis. If these test findings are positive, an incontinence procedure should be considered as part of the overall corrective surgical therapy.

Controversy exists as to whether patients should undergo a trial of nonsurgical management before consideration for incontinence surgery. Some authorities believe that nonsurgical management should be tried in most patients because the risks are minimal and the potential gains and cost savings are great. Others believe that an informed patient with a severe degree of incontinence, after appropriate workup, can be offered surgical management at the outset.

ISD, as demonstrated through urodynamic testing, generally is an indication for surgical management. ISD with a fixed or nonmobile urethra can be approached by periurethral bulking injections, an artificial sphincter, or an obstructive suburethral sling. If the urethra is simultaneously hypermobile, a suburethral sling is the ideal choice. Periurethral bulking agents also may be appropriate in this setting. GSI procedures, such as the retropubic urethropexy, may have higher failure rates when ISD also is present. The use of periurethral injections as the initial management does not preclude the use of the other described modalities if it should fail. Conversely, if satisfactory results are not obtained with a urethra-stabilizing procedure, periurethral injections can be added as a secondary procedure.

DI rarely is an indication for surgical treatment of incontinence. On occasion, in cases of mixed incontinence, the DI portion of the disorder may improve or resolve completely after a procedure for GSI. Nevertheless, the GSI diagnosis was the true indication for surgery. In rare instances, DI that is refractory to pharmaceutical, behavioral, and other nonsurgical management may be treated by surgery. Few data exist on the efficacy of surgery in this setting, and results often are less than ideal. Procedures have been described to partially denervate the bladder and to augment or autoaugment bladder capacity. Urinary diversion is a procedure of last resort. Recently, surgically implantable sacral neuromodulating devices have been used with some success in refractory cases. Urogenital fistulas usually require surgical management, especially if the fistula is more than pinpoint in size. Bladder drainage alone is successful in some cases of very small fistulas.

RELEVANT ANATOMY

Section 4 of 12  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

Anatomy of the urethra, bladder, and retropubic space

Detailed knowledge of the anatomy of the retropubic space, the potential space between the pubic bone and the bladder, must be mastered by the incontinence surgeon. Ventrally, the retropubic space is bounded by the pubic bones and the midline fibrocartilage. The floor and part of the dorsal aspect are comprised of the bladder, urethra, and the endopelvic connective tissue, which extend laterally on both sides to the pelvic side walls at the arcus tendineus fasciae pelvis (ATFP). The remainder of the dorsal wall consists of the pelvic parietal perineum and the transversalis fascia. Above the arcuate line, the posterior rectus sheath is present. As originally described by Retzius, the potential space extends in a cephalad direction to the level of the umbilicus.

The pectineal ligament, or Cooper ligament, lies on the superior-dorsal surface of the pubic ramus. A flat triangular extension of Cooper ligament, the lacunar ligament, widens as it travels medially and joins the inguinal ligament at the pubic tubercle. The anterior or ventral aspect of the bladder makes up the floor of the retropubic space. This part of the bladder wall is extraperitoneal in location.

The cephalad wall and part of the posterior wall are covered with peritoneum and can be accessed from within the peritoneal cavity. The inferior aspect of the bladder lies on the anterior vagina, cervix, and lower uterine segment. The tissue between the bladder and the muscular wall of the vagina is the endopelvic connective tissue. Lateral to the bladder and bladder neck and within the endopelvic connective tissue lies a venous plexus. These prominent veins are a frequent source of bleeding during retropubic urethropexy. The pubovesical ligaments, pubourethral ligaments, and the extrinsic muscles of the urethra also lie in the retropubic space.

The bladder wall is made up of muscle fibers extending in all directions. This configuration is well suited to decreasing the bladder size in all dimensions when contracting. At the bladder neck, the muscular bladder wall is more organized, and 3 relatively distinct layers become apparent. The inner longitudinal layer fuses with the inner longitudinal layer of the urethra. The middle circular layer is most prominent in the proximity of the bladder neck, and it fuses with the deep trigonal muscle. The outer longitudinal layer contributes some anterior fibers to what becomes the pubovesical muscles, terminating on the posterior surface of the pubic bone. These muscles may be important in bladder neck opening during micturition. Posteriorly, the outer longitudinal fibers interdigitate with deep trigonal fibers and the detrusor muscle. These fibers may aid in bladder neck closure.

The bladder mucosa is transitional epithelium, which is loosely connected to the muscular wall by way of a connective tissue layer called the lamina propria. At the trigone, the epithelium is more densely adherent to the underlying muscle. The trigone is a triangular structure formed by the internal urethral opening and the orifices of the right and left ureter. The superior border of the trigone is a raised area called the interureteric ridge. Deep to the mucosa are 2 muscular layers. The superficial layer connects to longitudinal urethral musculature. The deep muscle fuses with detrusor and Waldeyer sheath, the fibromuscular covering of the intramural ureter. The intramural ureter enters the bladder wall obliquely. The muscle fibers are longitudinal in orientation at this point. This segment of the ureter is about 1.5 cm in length.

The urethra is approximately 4 cm long in the female. It is imbedded in the connective tissue supporting the anterior vagina. The epithelium is comprised of stratified squamous cells, which variably becomes transitional as the bladder is approached. The epithelium is arranged in longitudinal folds. At the base of the folds are scattered gland openings along the entire urethral length. The epithelium is supported by a loose lamina propria consisting of collagen fibrils and elastic fibers, arranged both circularly and longitudinally. A rich network of blood vessels is in the subepithelial layer.

The smooth muscle of the urethra is arranged longitudinally and obliquely with only a few circular fibers. The nerve supply is cholinergic and alpha-adrenergic. The longitudinal muscles may contribute to shortening and opening of the urethra during voiding. The oblique and circular fibers contribute to urethral closure at rest.

The striated urethral musculature is complex, and the components and their orientation are not agreed upon universally. The voluntary urethral sphincter really is a group of circular and looplike interrelated muscle fibers, similar to that present in the anorectum. The innermost layer, which is prominent in the proximal two thirds of the urethra, is the sphincter urethrae. More distally, the compressor urethrae and urethrovaginal sphincter are predominant.

These 2 muscles emanate from the anterolateral aspect of the distal half to one third of the urethra and arch over the anterior or ventral surface. These striated muscles function as a unit. Because they are composed primarily of slow-twitch muscle fibers, these muscles serve ideally to maintain urethral tone. The muscles probably do maintain the urethral tone but contribute to voluntary closure and reflex closure of the urethra acutely during times of increased intra-abdominal pressure. The medial-most pubovisceral portion of the levator ani complex also is a major contributor to active bladder neck and urethral closure.

Histologic examination of the striated urethral sphincter indicates that, for the most part, the muscle complex surrounds the urethra in an incomplete fashion. Fibers can be observed to be deficient along the posterior aspect of the urethra. The shape of the muscle complex can be described as resembling a horseshoe or an omega symbol. Recent investigations using US imaging of the urethra also have confirmed a paucity of muscle bulk along the posterior urethra. The urethral meatus empties into the vestibule after the distal-most urethra pierces the perineal membrane. The mucosa of the meatus is continuous with that of the vulva. Support of the urethra and bladder neck is believed to be important in the maintenance of continence during sudden increases in intra-abdominal pressure. The support mechanism is complex and incompletely understood.

The posterior wall of the urethra is imbedded in and supported by the endopelvic connective tissue. This sheet of connective tissue consists of collagen, elastin, and a small amount of smooth muscle. The connective tissue envelops the anterior vagina. This supportive tissue has been likened to a sling or a hammock around the urethra and bladder neck. The endopelvic connective tissue in this area is attached to the perineal membrane ventrally and laterally to the levator ani muscles by way of the ATFP. The ATFP is a condensation of connective tissue, which extends bilaterally from the inferior part of the pubic bone along the junction of the fascia of the obturator internus and levator ani muscle group to an area near the ischial spine. This tissue provides secondary support to the urethra, bladder neck, and bladder base.

Defects in this tissue are believed to result in cystocele and urethral hypermobility. The primary support to this area and the entire pelvic floor is believed to be the levator ani muscles. At rest, the constant tone mediated by slow-twitch fibers constitutes the major supportive mechanism. With acute increases in intra-abdominal pressure, forceful contraction of the fast-twitch levator fibers elevates the pelvic floor and tightens intact connective tissue planes, thereby supporting the pelvic viscera.

The anterior distal wall of the urethra is attached to the pubic bone by the pubourethral ligaments. These ligaments consist of extensions of the perineal membrane and the caudal and ventral-most portion of the ATFP. The ligaments may limit movement of the anterior wall of the urethra during increases in intra-abdominal pressure but probably exert a lesser degree of support to the posterior wall. The previously described endopelvic connective tissue, when intact, provides support to the urethra as a whole. With increases in intra-abdominal pressure, some believe that the urethra is compressed shut against this firm support.

Deficiency in the hammocklike support of the endopelvic connective tissue, coupled with relative preservation of the preferentially anterior urethral support of the pubourethral ligaments, may partially explain the complex rotational and descending motion of the bladder neck commonly observed in association with stress incontinence. The pubourethral ligaments may serve to limit downward motion of the anterior urethral wall and provide a pivot point for rotatory motion around the pubic bone. Some theorize that this preferential anterior wall support also may serve to pull the anterior and posterior urethral walls apart during straining, thereby contributing to bladder neck incompetency and stress incontinence.

The intrinsic male urethra is considerably longer and somewhat more complex than its female counterpart. Distal to the bladder neck, the segment of the urethra that traverses the prostate is called the prostatic urethra. The epithelium is transitional. The orifices of the prostatic glands can be found here. On the floor of the prostatic urethra is an elevation called the verumontanum. This area contains a small pocket called the utricle. Distal to the utricle are the orifices of the 2 ejaculatory ducts. Continuing distally, the membranous urethra is encountered. This short segment traverses the urogenital diaphragm. Cowper glands are adjacent to the urethra. The epithelial cells become more elongated and appear as stratified columnar cells. The bulbous urethra derives its name from the bulb of the corpus spongiosum, which it traverses. The ducts of the Cowper glands empty in this location. The epithelium is comprised of pseudostratified columnar cells.

The penile urethra passes through the remainder of the corpus cavernosum urethrae and makes up more than half of the total anatomic urethral length. The epithelium is comprised of pseudostratified columnar cells, except in the fossa navicularis, the slightly widened distal part of the urethra that passes through the glans penis. In this distal-most segment, stratified squamous epithelium is present. Throughout the penile urethra, the periurethral tissue contains many small mucus-secreting glands, called the glands of Littre. These glands are much more numerous along the roof of the urethra, and they empty into small recesses called the lacunae of Morgagni. The bulbous and penile urethra together sometimes are referred to as the cavernous urethra.

Neuroanatomy of the lower urinary tract

Intact neuroanatomic and neurophysiologic functions are essential to both the storage and micturition phases of lower urinary tract function. These functions are controlled largely by the peripheral autonomic nervous system, with important modulating information contributed by sensory nerves from the bladder and urethra. Further modification is provided by higher CNS centers, which allow conscious control of lower urinary tract function. Lesions can occur anywhere along the neuroanatomic pathways, which can contribute to or cause incontinence or voiding dysfunction.

Voluntary control of detrusor activity is thought to arise in the frontal cerebral cortex. This area is in communication with the pontine mesencephalic reticular formation, which serves as the brainstem micturition center. Maturation of these and higher centers are important in the childhood acquisition of the ability to voluntarily suppress micturition. Diseases that involve this area of the brain may cause or contribute to incontinence disorders. Stroke, MS, Parkinson disease, and brain tumors are examples.

Efferent connections beginning in the pons and terminating in the sacral micturition center at the S2 to S4 levels are important to efficient detrusor functioning during micturition. Damage to these tracts (eg, spinal cord injury) results in detrusor areflexia. Neural activity within this system promotes micturition. A neural loop involving the bladder, sacral micturition center, pontine micturition center, and urethral sphincter mechanism has been described. This pathway allows the coordination of urethral and detrusor function. In other words, coordination of urethral relaxation with detrusor contraction is dependent on this neural pathway being intact.

Dysfunction in this loop may result in detrusor-sphincter dyssynergia. Direct connections between the cerebral cortex and the sacral-pudendal motor neurons are important contributors to voluntary control over the striated urethral-sphincter complex. Severe neuromuscular damage to the striated urethral muscles, along with brain and spinal cord injury, can prevent proper functioning of this system.

Healthy functioning of the lower urinary tract is partly dependent on the interplay of sympathetic (ie, adrenergic) and parasympathetic (ie, cholinergic) input to the bladder and urethra. Bladder filling normally takes place with little or no increase in intravesical pressure. This phenomenon is largely due to the predominance of sympathetic tone during the filling and storage phase. Simplistically, beta-adrenergic receptors predominate in the detrusor muscle.

Stimulation of these receptors promotes bladder relaxation. Alpha fibers also exist, in smaller numbers, in the parasympathetic ganglia supplying the bladder. Stimulation of the alpha fibers results in the inhibition of neural firing at the level of the parasympathetic ganglion, thereby inhibiting bladder contractions. Alpha-adrenergic receptors predominate in the smooth muscle of the bladder neck and urethra. Stimulation results in contraction of the structures. The sum effect of sympathetic stimulation of the bladder and urethra is the promotion of storage. Parasympathetic or cholinergic stimulation generally is micturition-promoting.

Postganglionic muscarinic fibers to the detrusor muscle promote bladder contractions when stimulated. In addition, stimulation of muscarinic receptors on alpha-adrenergic nerves to the urethra prevents norepinephrine stimulation. The resulting physiologic effect is urethral relaxation. Cholinergic agents, although generally thought of as promoters of detrusor activity, also can stimulate preganglionic sympathetic nicotinic receptors with neural connections to the urethra and bladder neck. Such stimulation promotes contraction of these structures.

Nonadrenergic, noncholinergic nerves with ATP-stimulated purinergic receptors have been found in animal models and in the human bladder. These nerves may be very important in bladder contractility. Prostaglandins also may be able to activate these receptors. Sensory afferent innervation of the bladder originates with stretch and pain receptors in the bladder wall. Stretch receptors, which are responsible for bladder proprioception, are the origin of impulses traveling via the pelvic nerve to the posterior columns ipsilaterally and, eventually, the brain stem micturition center. Connections from the brain stem to the cerebral cortex provide for conscious awareness of bladder distention.

Pain receptors are present in the bladder wall but not as densely as stretch receptors. These receptors are responsible for sensing temperature, touch, and irritative stimuli. The generated impulses travel by way of the hypogastric nerve to synapse in the posterior root ganglia. The impulses cross to the contralateral side before ascending in the spinothalamic tract and the thalamic nuclei, eventually reaching the cerebral cortex. Afferent impulses from these receptors can trigger detrusor contractions via a normally suppressed reflex arc. Under conditions of severe mucosal irritation (eg, UTI), this reflex may become unmasked. In addition, disorders resulting in the loss of conscious cerebral cortical input may be responsible for the emergence of this reflex.

Somatic efferent innervation to the striated urethral sphincter complex is from the second through the fourth sacral segments. The precise source of these fibers is controversial. Evidence suggests that the sphincter complex is innervated by way of the pelvic nerve rather than the pudendal nerve, as was once thought. The levator ani complex probably has a dual source of innervation from both the pelvic and pudendal nerves.

Estrogen receptors can be found in the musculature of the pelvic floor, bladder, bladder neck, and urethra. Estrogen stimulation increases the density of alpha-adrenergic receptors in the urethral smooth muscle. Progesterone may enhance beta-adrenergic activity. Emerging evidence of the presence of gonadotropin receptors in the lower urinary tract also exists.

CONTRAINDICATIONS

Section 5 of 12  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

Contraindications to incontinence surgery are few and, generally, are relative rather than absolute (eg, conditions that make general or regional anesthesia risky). In some instances, in the face of serious medical problems, nonsurgical therapies or minimally invasive surgical approaches, such as periurethral injections, can be substituted. Sensory and/or motor impairment of the bladder with coexisting stress incontinence should be approached with caution. Procedures that increase outlet resistance most likely make these conditions worse. Severe urinary retention may result. In these situations, if stress incontinence surgery is to be undertaken, instructing the patient in self-catheterization techniques is best conducted preoperatively. In patients with high-pressure bladders due to loss of compliance, some type of augmentation procedure should be performed at the time of incontinence surgery to reduce the potential for damage to the upper urinary tract.

WORKUP

Section 6 of 12  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

Lab Studies

• Urinalysis and urine culture
• • UTIs can cause or contribute to urinary incontinence disorders in several ways. Local inflammation can serve as a bladder irritant, causing uninhibited bladder contractions. Endotoxins produced by some bacterial strains can have an alpha-blocking effect on the urethral sphincter, thereby lowering intraurethral pressures.
  • Postmenopausal women are especially susceptible to these effects on the urethra and bladder. Hypoestrogenism may enhance the effects. UTIs may present in postmenopausal women without the classic symptoms of irritation and pain. The predominant symptom in some patients may be the onset or the worsening of urinary incontinence.
  • Colony counts of less than 10⁵ may be of significance in postmenopausal women and should be treated. Evidence of inflammation through urinalysis may be mild or entirely lacking despite bacterial growth from a culture. Women who are tested for urinary incontinence generally are recommended to have a screening urinalysis, and postmenopausal women also should have a urine culture.
• Diabetes testing: Testing for diabetes is not routine in the setting of urinary incontinence but should be considered if polyuria and polydipsia are a part of the clinical picture or if risk factors are present.
• Urine cytology: The role of urine cytology in the evaluation of urinary incontinence is unclear. Potential indications include persistent unexplained hematuria and bladder lesions and masses visible on cystourethroscopy. Routine use of urine cytology seems unwarranted.

Imaging Studies

• Ultrasonography
• • US is a readily available and versatile tool that has many potential uses in urology and urogynecology. US is noninvasive, does not use ionizing radiation, and is relatively inexpensive. US is useful in the evaluation of the upper urinary tract.
  • Visualization and evaluation of hydronephrosis, hydroureter, and urinary tract stones are useful in clinical practice. US visualization of the genitourinary system has been used in the staging of gynecologic malignancies and for the evaluation of urinary tract anomalies. Recently, US has been used as a research and clinical tool in the evaluation of urinary incontinence.
  • Research still is in the preliminary phases; like most new procedural technology, a lack of standardization of technique makes comparison of data across studies difficult. Variables such as route of scanning, type of scan head, patient position, and bladder volume need to be evaluated further to arrive at the best techniques for particular clinical situations.
  • Postvoid residual volume determinations
  • • The ability of US to visualize fluid collections clearly without the need for contrast makes it a potentially useful means of determining bladder volumes in a noninvasive way. Studies have been performed using transabdominal scanning to determine PVR volumes. Scanning is performed in the 2 perpendicular planes, transverse and sagittal. The following 3 diameters are obtained: height, width, and depth. The 3 diameters are multiplied by a correction coefficient of 0.7, which accounts for the nonspherical shape of the bladder when it is less than completely full. This formula probably is the simplest US formula for PVR volume determination.
    • Other methods and formulas have been described. The error using this formula, compared to the criterion standard of postvoid catheterization, is approximately 21%. The formula is not accurate at volumes less than 50 mL, but, in clinical applications, precise determination of PVR values of less than 50 mL usually are not needed. Some speculate that transvaginal methods may be more accurate at low bladder volumes.
    • Recently, a device called the Bladder Scan BVI 2500 (Diagnostic Ultrasound Corporation, Redmond, Wash) was introduced for the purpose of PVR volume measurements. Conflicting studies about the accuracy of this device have been reported. One study showed that the Bladder Scan underestimated true PVR volume, but the reported error was within acceptable limits. A second study reported gross underestimation of catheter-derived PVR volumes. The study found that the device was most accurate when volumes were less than 50 mL. US values were 60% of catheter-derived volumes in this setting.
    • This finding is in contrast to previous studies with standard transabdominal scanning. At greater than 150 mL, the device recorded PVR as only approximately 10% of the actual value. The authors could not explain these dismal results, but they believed that differences in calibration and user skills may have contributed, along with the possible inherent inaccuracy of the device. Researchers state that further study of the equipment and standardization of technique is needed.
  • Anatomic evaluation of the bladder neck
  • • US has been used extensively to study bladder neck anatomy in individuals who are continent and incontinent. This technique has been referred to as US cystourethrography by some authors. Using a transperineal approach, one recent study looked at ureterovesical junction mobility in young females who are continent. Mobility was present but minimal in most subjects. Researchers reported a mean vertical movement of the UVJ in relation to the inferior border of the symphysis of 5.3 mm, with a maximum of 9 mm. Researchers also reported horizontal excursion of 11.2 mm or less in 95% of the test subjects. These findings appear consistent with another investigation that demonstrated vertical movement of 7 mm in parous females who are continent, 11 mm in females with stress incontinence, and 5 mm in females with past successful colposuspension.
    • Additional work with US cystourethrography has shown that the test is comparable with video cystourethroscopy in a clinical research setting. Urethral funneling also has been observed with US in the evaluation of individuals with stress incontinence. In one study, funneling with straining was observed in most subjects, and funneling at rest was observed in a significant number and seemed to correlate with more severe degrees of incontinence. Special contrast media designed for US applications can enhance bladder neck and urethral visualization.
    • One group found that mobility of the posterior urethral wall was greater than the anterior wall with straining. This group hypothesized that this divergence of the proximal urethral walls may be important in the pathophysiology of stress incontinence. Another author documented the presence of bladder neck dilation in addition to hypermobility in women with stress incontinence. This author found the bladder neck to be the point of continence in many women, especially the nulligravida. A subset of parous but continent women may maintain continence in the mid or proximal urethra area. Further study will determine whether these interesting findings are useful in the clinical management of stress incontinence. The lack of standardization makes interpretation of study findings troublesome.
  • One of the greatest controversies in genitourinary US is which scanning technique is best for incontinence evaluation. Most authorities agree that transabdominal scanning is suboptimal. Transvaginal scanning provides good visualization but may distort the bladder neck anatomy. Some evidence shows that transvaginal scanning increases maximal urethral pressure, functional urethral length, and pressure transmission. Transrectal scanning can be used in men and women, but the bladder neck area still may be compressed with this approach. Introital and perineal techniques do not distort the anatomy and, thus, hold much promise.
  • Endoluminal urethral US is a research tool that has increased the understanding of intrinsic urethral anatomy. Reduced rhabdosphincter muscle volume has been reported in incontinent women using this technique. Endoluminal US also may be useful in the diagnosis of urethral diverticulum and, perhaps, as an intraoperative imaging tool during surgical repair. Three-dimensional US study of urethral anatomy also has been reported. Doppler US studies have been conducted focusing on the urethral submucosa/sphincter area and the bladder neck. Blood flow to the urethral submucosa is increased during high estrogen states, such as pregnancy and the luteal phase of the menstrual cycle. Blood flow is diminished with menopause and in patients with ISD. Increased blood flow to the bladder fundus also has been noted in some patients with DI. Another possible use for Doppler US is in confirming ureteral patency through observation of the ureteric jets.
  • Many other potential applications for US technology in incontinence evaluation have been suggested. Some of the following are research applications; others are more directly clinical.
  • • Real-time observation of the bladder neck and urethra during voiding
    • Study of pelvic floor muscles such as the levators
    • Observation of the effect of bladder volume on bladder neck anatomy
    • More precise diagnosis of pelvic organ prolapse, especially enterocele
    • Bladder wall thickness determinations to screen for DI
    • Patient visualization of bladder neck elevation as a biofeedback tool in pelvic floor exercise pr