A vast number of women suffer from urinary incontinence. These women often experience social embarrassment, isolation, and shame. A 1987 National Institutes of Health (NIH) consensus conference panel¹ estimated that at least 10 million US men and women suffer from urinary incontinence and that the United States spends at least $10.3 billion annually on this problem. In 1983, the Surgeon General estimated that $8 billion per year was spent for elderly patients alone.² More recent estimates by Wagner and Hu³ suggest that $26.3 billion was spent in 1995 for direct and indirect costs of incontinence in men and women over 65 years of age. This represents a cost of $35.65 for each individual with incontinence.

The exact prevalence of urinary incontinence is unknown and difficult to define because only a minority of affected patients admit that they have it. Yarnell and coworkers⁴ interviewed 1060 women older than 18 years of age in one region of South Wales. Of these women, 45% admitted to having urinary incontinence, but only 9% had consulted medical professionals about the problem. The older the age of the cohort studied, the higher the prevalence. In women older than 75 years of age, 59% were incontinent. These results are similar to those elicited by a survey of noninstitutionalized elderly women in Washtenaw County, Michigan. In this study, Diokno and associates⁵ interviewed 1955 women older than 59 years of age and found that 37.7% of the women had urinary incontinence; of these, 27% reported stress incontinence, 9% urge incontinence, and 55% mixed symptoms.

The problem is even greater in nursing homes and skilled care facilities. Ouslander and colleagues⁶ evaluated 842 patients (both men and women) older than 65 years in seven nursing homes and found 50% to be incontinent. According to the NIH consensus statement,¹ at least $3.3 billion per year is spent caring for incontinent patients in US nursing homes. Many of these people might not need to be in nursing homes if not for their urinary incontinence. Resnick and Yalla found that 41% of 605 institutionalized men and women had significant urinary incontinence necessitating therapy.⁷ Most of these women (61%) had detrusor hyperreflexia as their primary disorder.⁸

The federal government appears to have underestimated the problem significantly.¹ Based on these clinical studies, the true prevalence of urinary incontinence in the United States is probably at least 40 million people. Irritative voiding symptoms are even more prevalent, with up to 20% of adult women having urinary frequency (eight or more voidings per day), urgency, frequency, or nocturia with or without dysuria or suprapubic pain. These symptoms may often accompany or lead to urinary incontinence.

Genuine Stress Incontinence

Adult women can leak urine involuntarily for many different reasons. In our population at the Evanston Continence Center of Northwestern University, more than one half of the women evaluated for urinary incontinence have two or more conditions causing their urinary leakage. Approximately three quarters of all incontinent women are diagnosed as having genuine stress incontinence. This is defined by the International Continence Society's Committee on Terminology⁹ as a condition in which involuntary urinary loss occurs as a result of an increase in intravesical pressure that exceeds intraurethral pressure in the absence of a bladder contraction. This occurs secondary to a rise in intra-abdominal pressure, which may be associated with coughing, straining, sneezing, exercise, position change, or coitus. The diagnosis “genuine stress incontinence” should be distinguished from the symptom of “stress incontinence,” which denotes involuntary urinary loss during physical exertion. Urinary loss that is demonstrated synchronously with an increase in intra-abdominal pressure is the sign of stress incontinence.

Detrusor Instability

Detrusor instability is the second most common cause of urinary incontinence in adult women. It is an idiopathic condition in which involuntary bladder contractions occur spontaneously or on provocation during the bladder-filling phase while the patient is trying to inhibit micturition (Fig. 1).⁹ The bladder contractions are usually phasic in nature and should be distinguished from a low-compliance bladder, which is marked by a slow and abnormal rise in bladder pressure during filling even at low volumes. Unstable bladder contractions usually cause urge incontinence, when patients lose urine involuntarily before reaching the toilet when they feel the urge to go. Unstable bladder contractions also may cause urinary urgency, frequency, and suprapubic pressure, with the patient interpreting the contraction as an urge to void. These contractions without leakage may occur in young women with good, strong, smooth and skeletal sphincter function or in women with urethral obstruction secondary to prolapse or urethral diverticula. These obstructed detrusor contractions may generate high intravesical pressures (above 40 cm H₂O) secondary to detrusor hypertrophy. If these are left untreated, they may lead to urethrovesical reflux and upper tract damage. This contributes to the poor accuracy of symptoms as predictors of underlying conditions.

Detrusor Hyperreflexia

Another cause of motor urge incontinence is detrusor hyperreflexia, which should be distinguished from detrusor instability. Detrusor hyperreflexia is caused by involuntary bladder contractions secondary to underlying neurologic disease. Before making this diagnosis, the physician should ensure that the involuntary bladder contractions are causally and temporally related to the neurologic condition. Approximately 90% of women with detrusor overactivity and urge incontinence have the idiopathic condition detrusor instability. Only 10% of these women have detrusor hyperreflexia; the percentage is higher, however, in older institutionalized patients.^8,10 Because most patients with detrusor overactivity are neurologically normal, the term neurogenic bladder, used by many to denote the cause of urge incontinence, is really a misnomer.

Sensory Urge Incontinence

Some women who report symptoms of urge incontinence may be diagnosed with sensory urge incontinence. This is a poorly understood condition in which women who have a strong urge to void are overwhelmed by the afferent sensation and actually give up trying to hold back urination. This results in urinary leakage caused by an increase in afferent sensation, from the urethra and stretch receptors in the bladder, transmitted along the pudendal nerve. This may be caused by infection, trauma, atrophy, or inflammatory diseases of the bladder and urethra that may overwhelm the tonic supratentorial inhibitory input that prevents involuntary micturition. The diagnosis of sensory urge incontinence usually is made retrospectively when the cause of increased afferent stimulation has been resolved and the patient's urge incontinence symptoms cease. A common example of sensory urge incontinence may be found in the postmenopausal woman who has not received estrogen replacement therapy and who develops urinary urgency, frequency, and urge incontinence in the climacteric. The diagnosis of sensory urge incontinence is made when estrogen replacement therapy resolves the patient's urinary symptoms.

Insensate Incontinence

Other women may have no sensation before urinary loss (termed unconscious incontinence or insensible loss). This may be caused by severe detrusor hyperreflexia or uninhibited urethral relaxation, in which involuntary urinary leakage occurs secondary to a sudden decrease in urethral pressure in the absence of a bladder contraction or increased intra-abdominal pressure. Sand and coworkers¹¹ found uninhibited urethral relaxation in 2% of 534 consecutive incontinent female patients undergoing multichannel urodynamic testing.

Overflow Incontinence

Some women leak urine without having prior sensation because of overflow incontinence, a condition in which urine leaks involuntarily when the bladder becomes overdistended because of decreased afferent sensation due to peripheral neuropathy. These women often report stress incontinence with or without insensible loss. In the absence of an adequate evaluation, these patients may be mistreated with anti-incontinence surgery that compounds their problems by further increasing urethral resistance.

In 1960, Enhorning¹² first proposed the concept of inadequate transmission of intra-abdominal pressure to the proximal urethra as the cause of genuine stress incontinence. This may be referred to as the extrinsic continence mechanism.^12,13 The degree of transmission of abdominal pressure to the urethra is believed to depend on the support of the proximal urethra from the surrounding fibrous and muscular tissues. Although older literature stresses the role of anterior support of the pubourethral ligaments, DeLancey^14–16 has shown that the primary support of the urethra comes from the lateral attachments of the urethra, bladder neck, and vagina to the arcus tendineus fascia of the pelvis and the levator ani muscles. Alteration or relaxation of these supports leads to hypermobility of the urethra and reduced abdominal pressure transmission to the proximal urethra because of a loss of posterior support from the anterior vaginal wall.

Postpartum Stress Incontinence

Most investigators consider pregnancy and vaginal delivery to constitute the primary source of injury to these supporting structures—injury leading to urethral hypermobility and stress incontinence.^17–19 Postpartum stress incontinence probably is the result of physical damage to the fibromuscular supports of the urethra and vagina; this weakens the tension of the anterior vaginal wall under the urethra, creating diminished passive transmission of intra-abdominal pressure within the urethral lumen.¹⁶ Neurologic injury, resulting in diminished and slowed reflex contraction of the skeletal muscle within and around the urethra during increases in intra-abdominal pressure,^20,21 further limits increases in urethral pressure to compensate for the diminished passive pressure transmission to the urethra. This active increase in urethral pressure actually anticipates the increase in bladder pressure with coughing and Valsalva's maneuver. Therefore, this must represent an active reflex response of the striated muscle.^22,23 This response is lost in women with stress incontinence and is not restored even by successful anti-incontinence surgery.²³ Snooks and colleagues²⁰ and Allen and associates²¹ found delayed pudendal nerve conduction and neurologic damage with reinnervation patterns in most women undergoing vaginal delivery, which may account for some of these changes. Slowed or even diminished reflex levator contractions will also cause the fibrous supports of the vagina and urethra to fail over time as posterior pelvic musculature support is attenuated. These changes in pudendal motor latency are not found in women who have had a cesarean section.

Stress incontinence may also be caused by type III incontinence or intrinsic sphincteric deficiency in the absence of urethral hypermobility. Although the theoretical extrinsic continence mechanism and passive transmission of abdominal pressure to the urethra are intact, the intrinsic continence mechanism is deficient, with poor coaptation at the bladder neck, thus resulting in incontinence.

The underlying etiology of detrusor overactivity is poorly understood when it is not the result of neurologic injury (e.g. detrusor hyperreflexia). Detrusor hyperreflexia may be caused by any interruption in neurologic control over micturition; some common causes are multiple sclerosis, cerebrovascular accidents, spinal injuries or tumors, and congenital spinal cord abnormalities.

The idiopathic condition detrusor instability has no known etiology, but it is known to increase in prevalence with aging. In some cases, detrusor instability may be associated with urinary tract infection,²⁴ anti-incontinence surgery,²⁵ and urinary obstruction in men with benign prostatic hypertrophy. In most women, however, the cause is obscure.

Urinary incontinence also may be caused by urinary fistulae, diverticula, functional incontinence, and psychogenic incontinence. Functional incontinence occurs when the patient is unable to reach the toilet in a reasonable period of time secondary to deficits in cognitive or physical function (e.g. hip fracture or delirium). These causes must be carefully excluded before treatment is initiated, or else therapy will never be completely successful.

Etiology of Initiative Symptoms

Urinary urgency and frequency, with or without nocturia, may occur for various reasons. Bacterial infection should always be ruled out, even when women do not report dysuria. Dysuria may be absent in older women and pregnant women. Physiologic urgency and frequency may accompany pregnancy and other prerenal conditions (e.g. heart failure, diabetes, and diabetes insipidus) but is more commonly the result of postrenal conditions. Sensory urgency occurs in the absence of detrusor instability and may occur from habituation to frequent voiding, pelvic floor (levator) spasm, and even vulvovaginitis. Dysuria usually suggests urethral or bladder inflammation or infection. Conditions such as interstitial cystitis, chronic urethrotrigonitis, diverticula, or viral infections of the urethra should be sought. If hematuria is present, carcinoma in situ needs to be ruled out. Patients with urinary retention may also report urgency and frequency because these women reach their functional bladder capacities much sooner if they are already retaining significant volumes.

Many physicians attempt to establish the etiology of urinary incontinence based on a brief history and physical examination. This is inadequate for most incontinent women. To aid the clinician in establishing an accurate diagnosis before initiating treatment, a number of clinical tools have been developed.

Urogynecologic History

The urogynecologic history is an essential part of the evaluation of every incontinent woman. Although a history alone is inadequate to explain the patient's symptoms, it does define them. The history acts as an outline to establish what must be explained by any evaluation. To help clarify patients' understanding of the problem and to facilitate their evaluation, patients at the Evanston Continence Center are sent programmed questionnaires to fill out at home before coming to the office. This not only speeds up their evaluation, but it enables them to confirm questionable areas at home and adds to the accuracy of their responses.

Most authors have found history to be inadequate in establishing an accurate diagnosis,^10,26–31 but some have suggested that patients with isolated symptoms may be diagnosed on the basis of history alone.^32,33 Farrar and coworkers³² found history to be quite adequate for diagnosis. Of 56 women who reported having only symptoms of stress incontinence, 54 (96.4%) were found to have stable bladders on cystometry; of 100 women who reported having only urge continence, 89% were found to have detrusor instability. Hastie and Moisey³³ concluded that a history of only stress incontinence was 100% accurate in establishing genuine stress incontinence as the underlying diagnosis.

Our data are quite divergent from these findings. In a subgroup of 43 women with symptoms isolated to stress incontinence, 34.9% (16) were found to have involuntary bladder contractions on cystometry (Table 1). The continence history was found to be a poor predictor of the underlying conditions causing urinary leakage in 218 consecutive women studied. Similarly, Cardozo and Stanton²⁷ and Webster and associates²⁸ found the continence history to be inaccurate, even in patients whose reported symptoms were isolated to stress incontinence or urge incontinence. Numerous studies have shown that more than a history is necessary to evaluate the cause of a patient's symptoms. Jenson and colleagues³¹ reviewed the English literature from 1975 to 1987 and found 29 studies comparing history with diagnosis. Nineteen of these were acceptable for comparison. The data on 3092 patients evaluated for genuine stress incontinence showed the symptom of stress incontinence to have a sensitivity of 90.6% and a specificity of only 51.1%. A history of urge incontinence in 2950 patients had a sensitivity of 73.5% and a specificity of only 55.2%. Therefore, a basic clinical evaluation including a physical examination with a lumbosacral neurologic evaluation, urine culture, measurement of residual urine, assessment of urethral mobility, demonstration of urinary leakage, and cystometry is invaluable. This basic evaluation is an excellent, cost-effective screening method for all patients and is diagnostic is most cases. A good general medical history with a record of medication and drug usage as well as a history of prior surgeries also should be obtained. Prior anti-incontinence surgery may alter the usual prevalence of various etiologies of incontinence.³⁴ Women who have had a prior unsuccessful anti-incontinence operation have a higher incidence of detrusor instability, uninhibited urethral relaxation, and fistulae.

TABLE 1. Comparison of Urinary Symptoms and Conditions in 218 Consecutive Patients Undergoing Multichannel Urodynamics

The programmed questionnaire may be reviewed rapidly before the patient is examined and should be reconfirmed with the patient to augment the examiner's understanding of her problem. Women should be questioned about urinary incontinence during intercourse, which occurs in as many as 24% of patients and may adversely affect one half of all patients' sexual relations.³⁵ This is also a good time to question the patient about anal incontinence of feces or flatus. In one study,³⁶ anal incontinence was found to affect 51.1% of women reporting urinary incontinence. Anal incontinence of flatus, liquid stool, and solid waste affects many women with urinary leakage and should be looked for in all incontinent patients.

Patients are also asked to complete a 24- to 48-hour voiding diary before coming to our center for their appointment. Patients are asked to record when they void, the volume voided, when they leak urine, and the volume they drink. Review of this diary helps the examiner to confirm the patient's symptoms; however, the diary often does not correlate well with the symptoms. Although many patients with detrusor overactivity void often and in small volumes, clinical overlap with patients who do not have detrusor overactivity prevents the voiding diary from being used as a diagnostic test.³⁷ It is, however, a very accurate predictor of the degree of a patient's physical and social dysfunction, and it also serves as a useful quantitative measure of improvement during therapy for all storage phase disorders.³⁸

Physical Examination

A careful physical examination is performed on all incontinent women and should focus on the pelvic examination and neurologic evaluation of the lumbosacral nerve roots. These nerve roots are primarily responsible for the autonomic control of bladder storage and emptying. Assessment to rule out systemic diseases (e.g. cardiac, thyroid, adrenal, pancreatic, renal) that may play a role in incontinence is crucial.

PELVIC EXAMINATION.

On pelvic examination, the physician should look for signs of genital tract inflammation, infection, and atrophy that may affect the urethra and cause an increase in afferent sensation. This may lead to irritative voiding symptoms, such as urgency, urinary frequency, dysuria, and possibly urge incontinence. In addition, heavy vaginal discharge or cervical mucus may be confused by some patients as urinary incontinence. Oral phenazopyridine (Pyridium), which colors the urine orange, can be a useful means for such patients to distinguish between vaginal fluids and urine. Because the urethra and trigone are estrogen-dependent tissues, estrogen deficiency can contribute to urinary incontinence and dysfunction.³⁷ Most authors^37,39–45 agree that estrogen replacement therapy will improve irritative symptoms in many patients, but improvement in urinary incontinence has been inconsistent in clinical trials. In controlled trials, there may⁴³ or may not be improvement in urge incontinence episodes with estrogen replacement compared with placebo. Uncontrolled trials show improvement in stress incontinence,^41,42,45 but no beneficial effect of estrogen has been found in controlled trials.^45,46 Some investigators have shown significant changes in urethral closure pressure and functional length,^39,40,42 whereas others have not.^43–46 Meta-analysis of 23 trials from 1969 to 1992 showed subjective improvement (p < 0.01) and an increase in closure pressure with estrogen replacement therapy. Nearly all these studies have demonstrated improvement in pressure-transmission ratios that measure the increase in urethral pressure compared with bladder pressure during coughing.^39–42,44

Estrogen replacement therapy should be given when signs of estrogen deficit are noted before further urodynamic workup is performed. The vaginal route of administration is preferred initially because of the excellent absorption of estrogen by the thin, atrophic tissues of the vagina.⁴⁷ After these observations are made, the examiner should look for any signs of urethral deformity, such as diverticula or fistulae.

Vesicovaginal fistulae usually are found just anterior to the vaginal cuff after hysterectomy and usually leak urine continuously. Ureteral fistulae may also cause continuous leakage of urine and may exist concurrently with a vesicovaginal fistula. Ureteral fistulae should be evaluated by an intravenous pyelogram. When ureteral fistulae are an isolated injury, dye (indigo carmine or methylene blue) placed by catheter into the bladder will not stain a vaginal tampon or pack. Urethral fistulae cause leakage only when urine enters the urethra during episodes of stress incontinence, unless the fistulae have totally destroyed the functional upper urethra; there is continuous leakage of urine in such cases. If a urethral sac is observed, it should be palpated to see whether it is tender and massaged to see whether it empties urine or pus. If the diverticulum is distal, such discharge may be found at the urethral meatus; if it is in the proximal urethra, the discharge can be seen on urethroscopic examination.

Observation of the anterior vaginal wall, posterior wall, and vaginal apex may be accomplished with the Sims' speculum or posterior half of the bivalve speculum to identify associated genital prolapse. Genital prolapse can have profound effects on lower urinary tract function, often resulting in urinary retention or masking urinary incontinence. Posterior rotational descent of the anterior vaginal wall results in the formation of a cystocele, which can represent either a paravaginal detachment of the anterior lateral vaginal wall from the arcus tendineus fascia or a central defect due to weakness of the endopelvic connective tissue. Lateral defects are often associated with preservation of the vaginal rugae and can be analyzed with the use of a ring forceps or similar device to resupport the anterior lateral vaginal fornices to the level of the arcus tendinous fascia bilaterally. We prefer to use the separated blades of a Grave's speculum inserted laterally into the vagina. This method prevents overcorrection with anterior displacement of anterior lateral vaginal fornices. Regardless of the etiology, descent of the anterior vaginal wall can result in the urethra or bladder neck folding on itself. This process results in mechanical obstruction or kinking of the urethra, which can be identified during urethroscopy and on urethral closure pressure profiles.

Potential genuine stress incontinence has been found in 60% of women with cystoceles protruding to the vaginal introitus or beyond who do not leak urine with the prolapse unreduced.⁴⁸ Myers and colleagues also demonstrated that unreduced rectoceles may mask incontinence.^48a Stress testing with reduction of the prolapse using a pessary, Sims' speculum, or large cotton swabs in the standing position reveals qualitative information on patients who have potential genuine stress incontinence. Urethral closure pressure profiles can be used at rest, during Valsalva's maneuver, and during repetitive coughing to provide quantitative information about the underlying pathophysiologic effect of the prolapse.^49–51 Some of these women may have urinary retention secondary to this mechanical obstruction. Reduction of the prolapse during voiding will also enable the examiner to discover whether retention is merely the result of mechanical obstruction or of some other pathologic process. In some women, an underactive detrusor may develop if the bladder is forced to contract against a closed bladder neck chronically. However, initially the detrusor muscle will hypertrophy and may cause high-pressure overactive contractions with risk of upper tract damage, as discussed previously. All patients with prolapse to the introitus should be examined with a full bladder after reduction of the prolapse to look for leakage and to assess for retention. Those patients with residuals greater than 50 mL should undergo complete evaluation with voiding pressure studies after reduction of the prolapse.

A careful digital examination should be done to assess transvaginal urethral or bladder tenderness and to rule out pelvic pathology. Urethral or bladder base tenderness or a strong sense of urgency usually is consistent with inflammation on endoscopic evaluation, or it may be found in patients with detrusor overactivity. Much attention is often given to uterine leiomyomas causing urinary symptoms, but this is infrequently a cause of incontinence or irritative symptoms. Rectovaginal examination is an important part of this evaluation. Evaluation of possible enterocele dissection along the rectovaginal septum may be appreciated, but often may be missed until surgery. The pelvic examination may be aided in some patients by defacography, but this is an expensive and difficult test for patients to endure.⁵² Anal sphincter tone also should be assessed, but results correlate poorly with manometric assessment of anal sphincter function. Rectal prolapse and subtle rectoceles may be appreciated during this examination, but full evaluation often requires dynamic radiographic evaluation.

NEUROLOGIC EXAMINATION.

Urinary control in women involves a complex interaction of various reflexes interacting with the autonomic nervous system, which primarily controls bladder and urethral function. These are both modulated by cortical and brain stem centers. Neurologic damage in these areas can cause significant symptomatology.⁵³ Cerebrovascular disease can cause detrusor hyperreflexia. Peripheral lesions can lead to an acontractile bladder and overflow incontinence. Spinal cord lesions can cause detrusor-sphincter dyssynergia with intermittent voiding patterns and urinary retention resulting from lack of urethral relaxation during bladder contraction.

Peripheral control is primarily modulated by the pelvic (parasympathetic) and hypogastric (sympathetic) nerves.⁵⁴ The parasympathetic nervous system has axons that originate from sacral segments S2 to S4 that stimulate release of acetylcholine from postganglionic neurons in the bladder wall to affect bladder contractions. The sympathetic ganglia originate in the thoracolumbar spine (T10-L2) and course through the hypogastric nerve to terminate on the parasympathetic ganglia of the bladder wall and in the bladder and urethra, where there are receptors for both alpha and beta fibers.⁴⁹ The alpha fibers primarily cause contraction of the urethra and bladder neck, whereas the beta receptors cause detrusor relaxation but probably only at low volumes by releasing norepinephrine.⁵⁵ In addition, the sympathetic fibers ending on postganglionic parasympathetic neurons modulate and depress parasympathetic transmission. This helps to explain why storage of urine is a passive process. This sympathetic control may also be the basis for the pharmacologic success sometimes seen with alpha-adrenergic treatment of detrusor instability.

The neurologic examination of incontinent women should start with an assessment of mental status, cranial nerve integrity, and cerebellar control. Deep tendon reflexes and muscle strength should be assessed in the lower extremities to evaluate the anterior lumbosacral spinal cord. The bulbocavernosus and clitoral reflexes help to demonstrate the integrity of the sacral nerve roots (Fig. 2). Sensory function may be quickly evaluated from dermatomes L2 through S2 by testing for sensation of pinprick around the knee.

If a neurologic deficit is identified or suspected during a simple screening examination, electromyography should be performed to evaluate (1) skeletal muscle function and innervation or (2) abnormalities of the autonomic control of the lower urinary tract. Neurologic consultation can be helpful in such situations.

Evaluation of Urethral Mobility

Because part of the underlying pathophysiology of genuine stress incontinence is believed to be poor transmission of abdominal pressure to the urethra secondary to urethral hypermobility, an assessment of urethral mobility should be made. Such assessment also allows us to identify patients with stress incontinence in the presence of good anatomic support who do not have genuine stress incontinence. This assessment may be made in several ways, the simplest of which is the visual assessment of distal anterior vaginal wall mobility.

THE Q-TIP TEST.

The Q-tip test, as first described by Crystle and coworkers,⁵⁶ is an excellent means of quantitatively documenting the presence of urethral hypermobility. It is a simple, inexpensive way to assess urethral hypermobility quantitatively without exposing the patient to radiation. Although the determination of urethral hypermobility on Q-tip testing is a poor predictor of the etiology of a patient's urinary incontinence,^57–60 it remains an accurate and valuable measurement of urethral support. It is clear that many women develop urethral hypermobility early in their third and fourth decades but remain continent if their intrinsic sphincteric mechanism is capable of compensating for the negative pressure transmission to the urethra created by urethral hypermobility.⁶¹ This is why there is a tremendous overlap between stress-incontinent and continent patients in many,^58,59 but not all,^60–62 studies. The cotton-tipped applicator soaked in 2% lidocaine jelly is placed at the bladder neck; then the resting and straining angles are measured several times. Once inserted, the Q-tip should be pulled snugly back to the bladder neck so that the bladder wall will not limit its motion. The test is arbitrarily said to be positive for urethral hypermobility when the straining angle is greater than 30 to 35 degrees.^57,58,63

As described by McGuire,⁶⁴ patients with stress incontinence who do not have urethral hypermobility have intrinsic sphincteric deficiency (type III incontinence, discussed previously), in which stress incontinence is present despite adequate urethral support. These patients usually are managed with periurethral injections, obstructive sling procedures, or placement of artificial sphincters. Straining cystograms and ultrasound studies also can be used to measure urethral hypermobility, but they are far more expensive than simple Q-tip testing.

SPONTANEOUS UROFLOWMETRY.

Spontaneous uroflowmetry is used as a screening test to detect abnormalities of micturition. It is accomplished by having the patient sit on a commode and void onto a load cell or a spinning disk, which records an instantaneous velocity curve of micturition. Measurement of the maximum flow rate is more useful in men than in women because of its ability to detect physical obstruction of the urethra, a condition that is rare in women. Uroflowmetry is primarily a measure of voiding velocity and is measured in milliliters per second. Because there is little concern of physical urethral obstruction in women, the pattern of the uroflow curve is more important than the quantitative measurement of voiding velocity. Figure 3 A shows a normal uroflowmetry curve. Qualitative assessment of the bell-shaped uninterrupted curve readily identifies it as a normal study. Figure 3 B shows an abnormal uroflowmetry study with an interrupted intermittent flow pattern, which may suggest voiding dysfunction. These graphic tracings are made by electronic uroflowmeters. An average flow rate can be measured in a much simpler manner by timing the duration of urine flow and then measuring the volume voided. Simple calculation reveals the mean flow rate, and the patient can be catheterized to measure the residual urine. Residual urine volumes greater than 50 mL should be further investigated. These women should undergo further evaluation of their voiding mechanism with multichannel voiding-pressure studies.

Fantl and associates⁶⁵ showed that although flow rates did not vary significantly with age, parity, weight, height, or menstrual cycle phase, they were directly affected by bladder volume. Like Starling's law for the heart, bladder volume, within normal ranges, directly affects the velocity and efficiency of bladder emptying.^65,66 This makes it difficult to establish normal values for uroflowmetry without using a nomogram. Based on research by Fantl and colleagues,⁶⁵ the peak flow rate should be equal to or greater than 15 mL/second for volumes voided in excess of 200 mL. At this volume, these researchers found an average peak flow rate in women of 22.6 mL/second, with a standard deviation of 7.5 mL/second.

In women, the flow pattern is more important than the peak flow rate. A normal asymptomatic woman usually voids with continuous flow until voiding is completed. Intermittent flow patterns may occur occasionally in typically asymptomatic women (see Fig. 3 B) but are more common in patients with voiding dysfunction.⁶⁵ Abnormal uroflowmetry studies should be repeated because patients having to void in an unfamiliar setting can exhibit falsely abnormal voiding patterns.

Intermittent flow patterns and decreased flow rates are most often explained by functional obstruction with a failure of pelvic floor relaxation due to urethral atrophy, inflammation, pain, or fear.⁶⁶ Genital prolapse with mechanical urethral obstruction is another common cause of abnormal uroflowmetry in women. One of the most common causes of intermittent flow patterns in women is Valsalva voiding, which may be prevalent in women with genuine stress incontinence and decreased urethral resistance. Valsalva voiding allows these women to empty their bladders rapidly, with normal to high peak flow rates. After corrective surgery, however, Valsalva voiding yields inefficient or absent voiding because of restored normal pressure transmission to the urethra, and therefore can be disastrous.

Detrusor sphincter dyssynergia (a neurologic loss of coordination of the urethra and bladder) also can cause intermittent flow patterns and retention. Less commonly, underactive and acontractile bladders cause decreased flow rates, intermittent flow, and elevated residual urine. Medications (e.g. alpha-adrenergics, anticholinergics) also can have adverse affects on voiding function, and these effects can be detected on spontaneous uroflowmetry. Uroflowmetry is a simple, noninvasive test that can screen for abnormal voiding function. If studies are abnormal or voiding dysfunction is suspected, then electromyography and voiding pressure studies should be performed.

ENDOSCOPIC EVALUATION.

The Robertson urethroscope, with its 0-degree lens and closed sheath, can be used to assess the urethra and trigone in a retrograde fashion and to observe their function. Using the cystoscope to evaluate the urethra is inadequate because it is important to visualize the urethra on entry, before its normal appearance is distorted by insertion of the scope. Urethroscopy may be done with the use of carbon dioxide, water, or saline as the distending media. Although carbon dioxide is less messy and can offer a better view of the urethra than water or saline, it forms carbonic acid in the bladder, which can irritate the bladder and cause artificial detrusor contractions during filling.⁶⁷

The urethra is inspected in a retrograde fashion, and urethral color, inflammation, and the presence of the normal urethral folds and gland openings may be observed. Pathologic findings such as polyps, cysts, inflammatory fronds, increased exudate, condylomata, and diverticula all may be noted in the urethra. These findings often correlate to irritative symptoms such as dysuria, urgency, and frequency of micturition. On entry into the bladder, the trigone and ureteral orifices should be inspected. The ureteral orifices should be examined for their appearance and function; normal ejaculation of clear urine and good retraction of the ureteral orifices should be noted. After examination of the urethra and trigone, the examiner can use the urethroscope to observe the dynamic function of the urethra during filling and with various maneuvers. Dynamic urethroscopy was first described by Robertson.⁶⁸ The urethroscope is used to observe the bladder neck during filling to diagnose detrusor overactivity, and during Valsalva's maneuver and coughing to identify passive opening of the bladder neck, as seen in genuine stress incontinence. Sand and coworkers⁶⁹ and Scotti and associates,⁷⁰ however, have shown that dynamic urethroscopy, although fairly specific, is an insensitive screening test for detrusor instability and genuine stress incontinence.

Cystoscopy also can be used during the routine evaluation of incontinent women, but it is not advocated in the absence of irritative voiding symptoms or hematuria. Cystoscopic examination in symptomatic patients occasionally reveals signs of chronic cystitis, cystitis cystica or glandularis, interstitial cystitis, polyps, hemangiomas, or neoplasms that might not be identified with the urethroscope. These conditions can produce increased afferent sensation leading to sensory urge incontinence and therefore are important to rule out in women reporting symptoms of urgency, frequency, and urge incontinence.

In women with irritative daytime symptoms, nocturia, and suprapubic pain or discomfort before voiding, the diagnosis of interstitial cystitis is likely. Punctate suburothelial hemorrhages with redistention of the bladder during cystoscopy helps establish this diagnosis. We usually can observe these cystoscopic findings in the office without anesthesia. However, cystoscopy under anesthesia (general or regional) is needed to definitively rule out interstitial cystitis. A potassium test using KC1 bladder instillation has been described by Parsons as another way to help differentiate these patients with a defective glucosaminoglycans layer who will experience severe bladder pain with instillation of this solution when compared with saline.^70a This test is limited by its relatively poor (70%) sensitivity.

CYSTOMETRY.

Cystometry is an important diagnostic test used to measure the change in bladder pressure during bladder filling. Pressure measurement during bladder filling allows for the evaluation of bladder sensation, compliance, capacity, and detrusor inhibition during the storage phase. In a normal cystometry study, the bladder is compliant enough to allow for filling to capacity without any significant increase in bladder pressure, whereas the overactive detrusor will produce involuntary phasic contractions during filling, even at low volumes. Cystometry may be performed in many different ways and may be affected by many different variables (Table 2).

TABLE 2. Factors Influencing Cystometry

  Filling media

  H₂O
  Saline
  Urine
  CO₂
  Radiographic contrast

One of the simplest and least expensive ways to observe bladder filling is eyeball cystometry. This is a qualitative examination that lends itself well to examination at the bedside in the nonambulatory patient. A self-retaining catheter is placed transurethrally, and the bladder is progressively filled by pouring sterile water intermittently into an irrigation syringe attached to the catheter, 50 mL at a time. The syringe is held approximately 15 cm above the patient's pubic bone. The patient's first sensation to void and maximum cystometric capacity (the volume at which the patient notes pain or piloerection) are recorded, and involuntary bladder contractions are suggested by a rising rather than falling meniscus, associated with a strong urge to urinate or leakage around the catheter. A rising meniscus may be a reflection of increased abdominal pressure that may be aborted by asking the patient to relax or inspire. Abdominal relaxation may be confirmed by abdominal palpation. Ouslander and colleagues⁷¹ found eyeball cystometry to have a sensitivity of 75%, a specificity of 79%, and a positive predictive value of 85% in diagnosing detrusor overactivity compared with multichannel electronic cystometry in geriatric patients. This method also allows for the measurement of the residual urine with the initial catheterization. Although not a perfect screening test, its simplicity allows it to be used in situations in which testing otherwise would not be possible.

Simple quantitative assessment during bladder filling can be achieved by retrograde incremental cystometry, with the patient standing. This can be done with commercially prepared devices (Fig. 4), or a water cystometer can be constructed. First, the bladder is filled with a small amount of fluid and the baseline bladder pressure recorded. The bladder is then filled in a retrograde fashion by gravity, 50 mL at a time, stopping approximately every minute to measure the bladder pressure. The patient's first desire to void and maximum cystometric capacity are recorded with the corresponding bladder pressure at these volumes. Bladder pressure is recorded by reading the meniscus every 50 mL at rest and after provocation with coughing, heel bouncing, or hand washing. The cystometrogram is considered positive for detrusor overactivity if the bladder pressure rises by more than 15 cm H₂O during filling. This is further confirmed by the presence of involuntary leakage with removal of the catheter at maximum cystometric capacity. Stable bladders usually have pressure increases equal to or less than 10 cm H₂O during filling, with equivocal studies showing pressure increases of 10 to 15 cm H₂O. Repeating these equivocal studies has been shown to improve diagnostic accuracy.⁷²

Simple, incremental, retrograde studies are limited in their sensitivity because they miss small increases in bladder pressure that would create urinary leakage in the absence of the obstructing catheter. This can be avoided in some cases by the use of small (4-Fr) catheters without retention balloons that are taped to the patient's leg. These studies are limited in their specificity mainly by the misinterpretation of increased intra-abdominal pressure as increased detrusor pressure. This artifact can be avoided by the use of subtracted cystometry. In a prospective trial, Sand and coworkers⁷³ found standing retrograde incremental cystometry results to be reproducible in 84% of patients, with a sensitivity of 84.3% and specificity of 69.4% with one cystometrogram. The performance of two standing retrograde incremental cystometrograms on two occasions increased the sensitivity to 92.3% in 100 consecutive incontinent women when compared with multichannel urethrocystometry. These simple, inexpensive retrograde cystometers can be used quite accurately in screening incontinent women.^73–75 Subtracted cystometry can be used to improve diagnostic accuracy in the diagnosis of detrusor overactivity. Specificity is improved when both abdominal and bladder pressure are measured, allowing the urodynamicist to distinguish between abdominal pressure effects and those changes intrinsic to the bladder. Abdominal pressure can be measured through the vagina, the rectum, or suprapubically.

Instantaneous electronic subtraction of bladder pressure from abdominal pressure allows for continuous recording of the true detrusor pressure. A low-compliance bladder may be diagnosed when detrusor pressure gradually rises to 15 cm H₂O or higher during filling. Phasic pressure increases associated with symptoms of urgency or urge incontinence are indicative of detrusor overactivity. Provocative maneuvers can be used more easily and with less confusion during subtracted cystometry. This also improves the diagnostic sensitivity of the test. The easiest way to perform subtracted cystometry is to use an electronic cystometer that records two or three channels of activity. These electronic cystometers typically cost $5,000 to $20,000.

When more accuracy or information is needed regarding the bladder's ability to store urine, examiners can use urethrocystometry combined with electromyography. Monitoring urethral pressure responses and the electrical activity of the periurethral and intrinsic urethral skeletal muscle further augments our ability to understand the detrusor's reaction to bladder filling. Measurement of urethral pressure also enhances our ability to detect detrusor overactivity, which usually is preceded by urethral relaxation.

Sudden urethral pressure decline or fluctuation suggests impending involuntary detrusor contractions, signaling the urodynamicist to try to push the patient a little further. Ambulatory urodynamics are studies that allow for the performance of cystometry during normal orthograde filling from renal urine production, which can be used in the patient's own environment, rather than in the clinic setting. These are the most physiologic and sensitive studies currently available.^76–78 McInterney and associates⁷⁶ found ambulatory urodynamics to be far more sensitive in women with urge incontinence. However, van Waalwijk van Doorn and colleagues⁷⁷ showed that one third of asymptomatic volunteers had involuntary detrusor contractions during a 5-hour ambulatory study. This may profoundly limit the diagnostic accuracy of ambulatory urodynamics. These studies also are very expensive and not readily available in most centers.⁷⁸

The patient's urine is the most physiologic medium, but it is very difficult to use during retrograde cystometry; therefore most investigators use carbon dioxide, water, saline, or radiographic contrast media. Although carbon dioxide has been used widely in the past, most investigators have replaced it with liquid media.^67,78,79 Carbon dioxide is easy to use compared with liquid media, and it allows for rapid flow rates that are more provocative. It also allows cystometry to be repeated rapidly; however, as mentioned previously, it is an irritating medium that forms carbonic acid when mixed with urine.⁶⁷ Water and saline are used by many investigators interchangeably, but saline is probably more physiologic, especially when instilled at body temperature. Little has been described regarding the accuracy of radiographic solutions as media for cystometry, but most of these solutions are nonirritating and probably comparable to saline. A contrast medium such as 35% diodone, however, is quite irritating and is more likely to produce involuntary bladder contractions.⁷⁸ Contrast media should be used for cystometry when combined with videocystourethrography to allow visualization of the bladder during filling.

Cystometry can be performed with the patient in a number of positions, but standing studies are the most provocative and sensitive. In elderly or infirm patients, standing may be difficult; birthing chairs or commodes can be used for such patients in studies that allow the patient to sit upright. Movement to a standing position with assistance may be provocative in some of these patients.⁸⁰ Various provocative maneuvers can be used during cystometry (see Table 2) to help elicit involuntary bladder contractions. Although some maneuvers may not be physiologic, it should be recognized that stationery cystometry can miss involuntary detrusor contractions in up to 50% of patients reporting urge incontinence.⁷⁸ Therefore, artificial provocation may be necessary to compensate for the inherent insensitivity of these laboratory urodynamic studies. A recent study of provocative maneuvers to elicit detrusor instability by Mayer and coworkers⁸¹ showed hand washing to be the most provocative. We commonly have the patient cough and heel-bounce after every 50 to 100 mL of fluid infused and reserve hand washing and other forms of provocation until the end of the study if involuntary detrusor contractions have not been recorded.

Some involuntary detrusor contractions can be missed even with the use of electronic, continuous, multichannel, subtracted cystometric evaluations with provocation. Low-pressure detrusor contractions can be mistaken for episodes of stress incontinence in these patients unless the isometric force of these contractions can be measured. The use of stop tests in these ambiguous situations can identify isometric contractions that might otherwise go unnoticed.⁸² Voluntary interruption of the stream of urine, mechanical obstruction of the bladder neck, transurethrally with a catheter or manually through the vagina, will close the bladder neck and allow for measurement of the true isometric bladder pressure. These stop tests help to improve the sensitivity of cystometry and also can be useful during instrumented voiding studies. Bladder compliance also may be assessed during cystometry. This represents the change in volume associated with a change in pressure (Δv/Δp). Because the bladder is composed of both active elements (smooth muscle) and passive elements (collagen and elastin), the evaluation of the filling phase also must include the distensibility of viscoelastic properties of the bladder.⁸³ In the absence of phasic contractions, changes in these properties suggest the possibility of bladder injury due to inflammatory disease, radiation, or surgical trauma. In these patients, cystometry may reveal a low-compliance bladder with a slow, gradual rise in true detrusor pressure during filling.

STRESS TESTING.

Stress testing is a simple clinical test to demonstrate urinary leakage. This test is accomplished by having a patient cough, perform Valsalva's maneuver, or do whatever it normally takes to increase intra-abdominal pressure to cause her to reproduce her stress incontinence. It is most provocative with a full bladder and with the patient standing, as opposed to lying supine. Urinary leakage coincident with an increase in intra-abdominal pressure is regarded as a positive sign of stress incontinence; however, continuous urinary leakage after a sudden increase in intra-abdominal pressure may represent stress-induced detrusor contractions after provocation.⁸¹

PAD TESTING.

Pad testing is a method of documenting and quantifying urinary leakage objectively. Various methods of pad testing have been described in the literature. They are all based on the use a preweighed sanitary napkin or collecting device to measure urine loss over a period of time during planned or random activities. Twenty-minute, 40-minute, 1-hour, 2-hour, 12-hour, and 24-hour tests have all been used to document and quantify urinary incontinence. The pad test can be a useful adjunct to urodynamic evaluation when urinary leakage is not exhibited in the artificial testing environment of a physician's office or clinic.

Jorgensen and associates⁸⁴ found that the 1-hour pad test endorsed by the International Continence Society detected nearly twice the number of incontinent women as stress testing and voiding cystourethrography. Because of the variable diuresis with an oral fluid load, this is consistent with the findings of some investigators^85,86 but inconsistent with those of others.^87,88 It is preferable to use a fixed-volume 20-minute pad test in clinical trials. This test incorporates all the activities of the standard 1-hour test into a simpler, faster, and more reproducible format.^89,90 With rare exceptions (excessive perspiration or vaginal discharge), urine loss equal to or greater than 1 g/hr indicates urinary leakage on pad testing. In healthy subjects, mean pad weight increases are less than 1 g/hr.^91,92 Home pad tests spanning extended periods of time are best able to reproduce the magnitude of the patient's incontinence.⁹³ Although the correlation between 24-hour and 48-hour pad tests with the standard 1-hour test is low (r = 0.35), the reproducibility of a 24-hour pad test is quite good (r = 0.96).⁹³ Extended testing correlates better with a patient's symptoms.⁹³

These urodynamic tests allow physicians to demonstrate urinary leakage and to understand its etiology in most patients. Because of the artificial nature of the office environment and the inherent lack of sensitivity of some of these tests, not all patients will demonstrate urinary leakage during the screening examination. When the screening evaluation fails to explain the patient's symptoms, she should undergo more complex multichannel urodynamic and radiographic studies.

Multichannel Urodynamics

Initial evaluation with the simple methods described may not be sufficient to define the etiology of an incontinent woman's problem. If some aspect of the patient's symptoms remains unexplained, more sophisticated testing in a urodynamics laboratory is indicated. Other indications include previously failed anti-incontinence operations; age older than 60 years; continuous or insensible urine loss, or both; suspicion of neuropathic dysfunction; mixed incontinence symptoms; urinary retention; and women with presumed intrinsic sphincteric deficiency in the absence of urethral hypermobility.^94,95 Complex multichannel urodynamic and radiographic studies require more expensive equipment that may not always be available to the clinician. In these instances, decisions regarding referral can be difficult.

URETHROCYSTOMETRY.

The performance of urethrocystometry involves the use of pressure-measuring catheters and transducers that are placed in the urethra, bladder, and rectum or vagina to measure intra-abdominal pressure.^96–98 Analog or digital urodynamic monitors are used to measure these three pressures and the true detrusor pressure from instantaneous subtraction of abdominal from bladder pressure and urethral closure pressure that is calculated by subtraction of bladder pressure from urethral pressure. Measurement of these five pressures with or without electromyography (EMG) can be accomplished during filling to create an urethrocystometry study (Fig. 5).⁹⁰ Urethral and bladder pressures can be measured by the same microtransducer catheter. This also can be used to fill the bladder through a small infusion channel in the center of the catheter (Fig. 6). Patients are positioned on birthing chairs, x-ray tables, or urodynamic commode chairs, and a single transducer catheter is placed in either the vagina or rectum to measure the intra-abdominal pressure. The dual transducer catheter is placed in the urethra and positioned so that the proximal microtransducer, which is 6 cm from the catheter tip and distal transducer, is placed at the point of maximal urethral pressure and oriented laterally. Filling is then begun in a retrograde fashion either through the lumen of the urethral catheter or via a separate small catheter or pediatric feeding tube.⁹⁶ Cystometric parameters and changes are noted as described previously with subtracted cystometry, but urethrocystometry offers the added advantage of being able to monitor urethral pressure.

Monitoring urethral pressure during cystometry is advantageous because it allows the detection of urethral pressure decreases that normally occur before a bladder contraction, whether voluntary or involuntary, and such variations usually are associated with corresponding EMG changes. Alternatively, one may observe marked variations in urethral pressure without detrusor contractions. This urethral instability may be a forerunner of detrusor instability (Fig. 7) and often signifies an impending bladder contraction.^99–101 These pressure variations may be associated independently with symptoms of urgency and sensory urge incontinence.^99,100 Some investigators question, however, whether these pressure fluctuations have any significance at all.¹⁰² Exaggerated urethral pressure fluctuations may be directly associated with complete urethral relaxation and may cause urinary incontinence from uninhibited urethral relaxation.¹¹ Care must be taken to ensure that these urethral pressure variations are not artificial (i.e. due to patient movement, abdominal pressure changes, voluntary contraction of the levator ani muscles). Alpha blockers may relieve symptoms in some patients with urethral instability. Urethral pressure decreases preceding detrusor instability can be used as a marker for biofeedback therapy to train patients to inhibit involuntary detrusor contractions. In healthy women, filling the bladder will lead to a rise in urethral pressure secondary to increased skeletal muscle activity associated with a gradual increase in skeletal muscle EMG activity (augmentation). This may be triggered by stretch receptors in the bladder trigone.¹⁰³

Healthy volunteers have been found to have an average maximum cystometric capacity of 594 mL with the first sensation to void noted at 32% of capacity.¹⁰⁴ Ninety-five percent of the control subjects noted first desire to void before filling to 300 mL of H₂O.

URETHRAL CLOSURE PRESSURE PROFILES.

Recording urethral closure pressure profiles involves measurement of the urethral pressure all along the length of the urethra. By slowly withdrawing a dual microtransducer catheter through the urethra with an automated withdrawal arm, one can measure the urethral pressure all along the urethra. This generates a pressure-time plot called a urethral closure pressure profile (UCPP) (Fig. 8). The “pressure” in the urethra measured with this system is actually force that is generated by urethral smooth muscle, periurethral vasculature, skeletal muscle in and around the urethra, and inert collagen and elastic tissue in the urethra.^105–109 Damage or attenuation of any of these contributing factors may dramatically alter the UCPP.^105–109

The UCPP begins as the proximal or urethral pressure transducer enters the proximal urethra. At this point, the urethral pressure usually is greater than bladder pressure, resulting in an increase in closure pressure. The UCPP reaches its peak in the proximal to mid urethra, and then the closure pressure decreases until in the distal urethra, where it drops below zero because distal urethral pressure is less than bladder pressure. The profile ends when the urethral transducer reaches the urethral meatus, where the urethral pressure reaches zero (atmospheric pressure), to which it was originally calibrated. The resting profile can be adversely affected by age, surgery, vaginal delivery, and other forms of trauma.^{19,61,102,110} The patient's position,¹¹¹ the degree of patient relaxation,¹⁰⁶ the microtransducer catheter orientation, and the bladder volume¹⁰⁷ may all affect the resting UCPP. All these factors should be standardized when resting profiles are done.

Although continent women generally have higher closure pressures and functional lengths than patients with genuine stress incontinence, there is tremendous overlap between these two populations.^112–114 This makes the resting UCPP a poor diagnostic test for determining who has genuine stress incontinence.^110–115 Dynamic UCPP during Valsalva's maneuver and coughing may be more discriminant. These tests were designed to study the effects of increased intra-abdominal pressure on the sphincteric unit. Although many argue that there is no usefulness in measuring resting urethral closure pressure, this measurement allows for a graphic illustration of the functional capability of the sphincter and its internal integrity.^116,117 We have shown that women who have urethral closure pressure less than or equal to 20 cm H₂O are at increased risk of failing routine anti-incontinence surgery. This finding of a low-pressure urethra appears to be the most significant risk factor for failing anti-incontinence surgery. In these women with deficient intrinsic sphincteric mechanisms, resupporting the urethra with retropubic urethropexies and needle suspensions to improve urethral pressure transmission does not appear to be enough. Although they are anatomically corrected 97% of the time by these operations, less than 50% of these women are objectively cured of their genuine stress incontinence.¹¹⁶ These patients with low-pressure urethras also appear to have decreased success with nonoperative therapies.

Dynamic UCPPs offer the urodynamicist more information about the function of the sphincter urethrae under stress. These profiles may be done at any bladder volume and in any position, but standing with a full bladder is probably the most stressful and sensitive position for this test.^114,118 Valsalva profiles are done by withdrawing the urethral pressure catheter through the urethra after Valsalva's maneuver is initiated. During these profiles, the ability of Valsalva's maneuver to produce leakage of urine in the absence of a bladder contraction and with zero closure pressure and functional length establishes the diagnosis of genuine stress incontinence. Valsalva's maneuver appears to generate a more consistent stress compared with repetitive coughing, but cough profiles appear to be more sensitive and reproducible.¹¹⁹

Hilton and Stanton¹¹⁰ performed cough UCPPs in 120 stress-incontinent women and 20 asymptomatic women and found that despite bladder-neck opening in 25% of the controls, they all had pressure transmission ratios equal to or greater than 100% (i.e. the ratio of increase in urethral pressure with coughing to increase in bladder pressure with coughing × 100%) (Fig. 9). The stress-incontinent patients all had deficient pressure transmission ratios,¹¹⁰ as determined by cough UCPPs. Profiles are considered positive for genuine stress incontinence if urinary leakage occurs with pressure equalization. This implies not only that there is negative pressure transmission but also that each negative deflection in closure pressure with coughing descends to or below the zero closure pressure level.

LEAK POINT PRESSURE.

Recently, a new urodynamic test has been described to quantify defective sphincteric function in patients with genuine stress incontinence.¹²⁰ The leak point pressure is an indirect measure of urethral resistance to the outflow of urine. It is a simple measurement of the intra-abdominal pressure necessary to cause urinary leakage due to genuine stress incontinence and therefore is a more discriminating measure than clinical grading of the patient's symptoms.

The Valsalva leak point pressure is measured by a vaginal or anal pressure transducer catheter. Alternatively, a leak point pressure can be measured with a bladder pressure catheter. The patient is asked to perform Valsalva's maneuver with gradually increasing force. The minimum abdominal or bladder pressure that causes urinary leakage is the leak point pressure. This test has been found quite reproducible and simple to perform and is useful in monitoring therapy for genuine stress incontinence.

VOIDING PRESSURE STUDIES.

The same equipment used to analyze urethrocystometry can be used to analyze micturition. By using a dual microtransducer catheter or external transducer-catheter system, urethral and bladder pressure can be measured by placing the proximal transducer at the point of maximum urethral pressure. The abdominal pressure can be measured vaginally or rectally; EMG activity can be measured with needle, wire, patch, or ring electrodes at the anus or urethra. A load cell and funnel are placed under the patient to measure urine flow. The patient's voiding mechanism and function can be analyzed easily with this equipment. Simple uroflowmetry offers information only about voiding speed, pattern, and completeness. Men void normally only in one way: by relaxing the urethra and having a bladder contraction. Women void completely in five different ways. Like men, they may void by urethral relaxation and detrusor contraction, or by urethral relaxation alone. Either of these patterns may be augmented by the Valsalva maneuver. They may also void by Valsalva alone. Although Valsalva voiding is normal and more common in women with genuine stress incontinence,^121–123 it can cause prolonged urinary retention after surgery for genuine stress incontinence. In women with Aldrige-type suburethral sling procedures (slings connected to rectus fascia anteriorly), permanent retention can occur if Valsalva voiding persists.¹²¹

Rud and colleagues¹²¹ have shown that normal continent women usually void by urethral relaxation, followed by a detrusor contraction 3 seconds later. These two events have the cumulative effect of decreasing urethral closure pressure with the onset of urine flow 6 seconds after initial urethral relaxation. Urinary retention can be explained by (1) failure of urethral relaxation during a detrusor contraction, (2) mechanical obstruction of the urethra, (3) underactive detrusor contractions (inadequate in time or magnitude), or (4) an acontractile detrusor. All these will predispose patients to overflow incontinence. Voiding pressure studies may be used not only to assess voiding dysfunction but also preoperatively to analyze borderline voiding mechanisms that may be decompensated by surgery. These studies allow for the prediction of voiding dysfunction and retention after anti-incontinence surgery. Retropubic colposuspensions and needle suspension procedures may increase urethral resistance significantly and in some patients may cause prolonged paruresis.¹²⁴ Bhatia and Bergman¹²⁵ have shown that women with low pressure (below 15 cm H₂O) or absent detrusor contractions who use Valsalva's maneuver to void are at a 12-fold increased risk of requiring prolonged (more than 7 days) postoperative catheterization.

Klutke and coworkers¹²⁶ have shown that retropubic urethropexies, like the Burch procedure, are only successful if they increase urethral resistance during voiding. They looked at pressure flow studies in 178 women after Burch procedures and found that urethral resistance (detrusor pressure at maximum flow divided by the square of the maximum flow rate) increased in successful cases from 0.051 to 0.099, but there was no change from a baseline urethral resistance of 0.041 in those who were unsuccessful. However, Belair and associates¹²⁷ have shown that these operations, which do increase urethral resistance, are not obstructive, and instead, when compared with nomogram data, return urethral resistance to normal levels.

RADIOGRAPHIC STUDIES.

The combination of cystometry and radiographic techniques has made it possible to study the pressure changes in the lower urinary tract while monitoring its appearance with fluoroscopy or ultrasound. This type of study is called videocystourethrography. Although some find that fluoroscopy adds little to the evaluation,¹²³ many find it useful. It is rarely used, however, because of its expense and the need for dedicated space to house the fluoroscopic and urodynamic equipment. Anatomic assessment and documentation with corresponding functional analysis of urethral, detrusor, and abdominal pressures clearly make this an optimal system to analyze urinary tract pathology. The alternative is to evaluate the anatomic changes with endoscopy, pelvic examination, and Q-tip testing (described previously) separate from the multichannel urodynamic assessment and to integrate the information mentally. The major disadvantages of videocystourethrography are the radiation exposure (1 rad), cost, and need for radiology personnel and space. Fluoroscopic evaluation of the bladder may help to clarify whether low-pressure, involuntary detrusor contractions are symptomatic or whether a patient's bladder neck funnels with increases in intra-abdominal pressure. Bladder neck funneling at rest may define an incompetent bladder neck in the patient with intrinsic sphincteric deficiency or type III incontinence that should be treated with periurethral injections of glutaraldehyde cross-linked (GAX)-collagen, autologous fat or carbon-coated beads.

Postvoiding films of the bladder can be used to analyze urinary residuals and to look for urethral diverticula. Urethrograms with Tratner catheters are more sensitive at detecting these diverticula, which can cause postvoiding dribbling if located distally or sensory urge incontinence if located proximally. Voiding cystourethrograms can be used to diagnose ureterovesical reflux in patients with retention.

Cystograms can be useful in cases of suspected fistulae (see Fig. 10) and bladder tumors. Figure 10 depicts a hysterosalpingogram in a woman with a vesicouterine fistula. Cystograms also can be used to evaluate bladder neoplasms, but cystoscopy is preferable.

1. Urinary Incontinence in Adults. National Institutes of Health Consensus Development Conference Statement. Bethesda, National Institutes of Health, 1987

2. Brazda JF: Washington report. Nation's Health 13: 3, 1983

3. Wagner TH, Hu T: Economic costs of urinary incontinence in 1995. Urology 51: 355, 1998

4. Yarnell JWG, Voyle GJ, Richards CJ et al: TP: The prevalence and severity of urinary incontinence in women. J Epidemiol Community Health 35: 71, 1981

5. Diokno AC, Brock BM, Brown MB et al: Prevalence of urinary incontinence and other urological symptoms in the noninstitutionalized elderly. J Urol 136: 1022, 1986

6. Ouslander JG, Kane RL, Abrass IB: Urinary incontinence in elderly nursing home patients. JAMA 248: 1194, 1982

7. Resnick NM, Yalla SV: Management of urinary incontinence in the elderly. N Engl J Med 313: 800, 1985

8. Resnick NM, Yalla SV, Laurino E: The pathophysiology of urinary incontinence among institutionalized elderly persons. N Engl J Med 320: 1, 1989

9. Bates P, Bradley WE, Glen E et al: First report on the standardization of terminology of lower urinary tract function. Urinary incontinence: Procedures related to the evaluation of urine storage-cystometry, urethral closure pressure profile, units of measurement. Br J Urol 48: 39, 1976

10. Ouslander J, Staskin D, Raz S et al: Clinical versus urodynamic diagnosis in an incontinent geriatric female population. J Urol 137: 68, 1987

11. Sand PK, Bowen LW, Ostergard DR: Uninhibited urethral relaxation: An unusual cause of incontinence. Obstet Gynecol 68: 645, 1986

12. Enhorning GE: Closing mechanism of the female urethra. Lancet 1: 1414, 1960

13. Enhorning GE: A concept of urinary continence. Urol Int 31: 3, 1976

14. DeLancey JOL: Anatomy and embryology of the lower urinary tract. Obstet Gynecol Clin North Am 16: 717, 1989

15. DeLancey JOL: Structural aspects of the extrinsic continence mechanism. Obstet Gynecol 72: 296, 1988

16. DeLancey JOL: Structural support of the urethra as it relates to stress urinary incontinence: The hammock hypothesis. Am J Obstet Gynecol 170: 1713, 1994

17. Francis WJA: Disturbances of bladder function in relation to pregnancy. Br J Obstet Gynaecol 67: 353, 1960

18. Francis WJA: The onset of stress incontinence. Br J Obstet Gynaecol 67: 899, 1960

19. van Geelen JM, Lemmens WAJG, Eskes TKAB et al: The urethral pressure profile in pregnancy and after delivery in healthy nulliparous women. Am J Obstet Gynecol 144: 636, 1982

20. Snooks SJ, Swash M, Setchell M et al: Injury to innervation of pelvic floor sphincter musculature in childbirth. Lancet 1: 546, 1984

21. Allen RE, Hosker GL, Smith ARB et al: Pelvic floor damage and childbirth: A neurophysiological study. Br J Obstet Gynaecol 97: 770, 1990

22. Constantinou CE, Govan DE: Contribution and timing of transmitted and generated pressure components in the female urethra. In Zinnia NR, Sterling AM (eds): Female Incontinence, pp 113–120. New York, Alan R Liss, 1981

23. Rosenzweig BA, Bhatia NN: Temporal separation of cough-induced urethral and bladder pressure spikes in women with urinary incontinence. Urology 39: 165, 1992

24. Bhatia NN, Bergman A: Cystometry: Unstable bladder and urinary tract infection. Br J Urol 58: 134, 1986

25. Sand PK, Bowen LW, Ostergard DR et al: The effect of retropubic urethropexy or detrusor stability. Obstet Gynecol 71: 818, 1988

26. Sand PK, Hill RC, Ostergard DR: Incontinence history as a predictor of detrusor stability. Obstet Gynecol 71: 257, 1988

27. Cardozo LD, Stanton SL: Genuine stress incontinence and detrusor instability: A review of 200 patients. Br J Obstet Gynaecol 87: 184, 1980

28. Webster GD, Sihelnik SA, Stone AR: Female urinary incontinence: The incidence, identification, and characteristics of detrusor instability. Neurourol Urodyn 3: 235, 1984

29. Glezerman M, Glasner M, Rikover M et al: Evaluation of reliability of history in women complaining of urinary stress incontinence. Eur J Obstet Gynecol Reprod Biol 21: 159, 1986

30. LeCoutour X, Jung-Faerber S, Klein P et al: Female urinary incontinence: Comparative value of history and urodynamic investigations. Eur J Obstet Gynecol Reprod Biol 37: 279, 1990

31. Jensen JK, Nielsen FR Jr, Ostergard DR: The role of patient history in the diagnosis of urinary incontinence. Obstet Gynecol 83: 904, 1994

32. Farrar DJ, Whiteside CG, Osborne JL et al: A urodynamic analysis of micturition symptoms in the female. Surg Gynecol Obstet 141: 875, 1975

33. Hastie KJ, Moisey CU: Are urodynamics necessary in female patients presenting with stress incontinence? Br J Urol 63: 155, 1989

34. Awad SA, Flood HD, Acker KL: The significance of prior anti-incontinence surgery in women who present with urinary incontinence. J Urol 140: 517, 1988

35. Hilton P: Urinary incontinence during sexual intercourse: A common, but rarely volunteered, symptom. Br J Obstet Gynaecol 95: 377, 1988

36. Haadem K, Dahlstrom JA, Bengtsson M et al: Sphincter function in the urethra and anal canal: A comparison of women with manifest urinary incontinence. Int Urogynecol J 2: 85, 1991

37. Batra SC, Iosif CS: Female urethra: A target for estrogen action. J Urol 129: 418, 1983

38. Larsson G, Abrams P, Victor A: The frequency/volume chart in detrusor instability. Neurourol Urodyn 10: 533, 1991

39. Bhatia NN, Bergman A, Karram MM: Effect of estrogen on urethral function in women with urinary incontinence. Am J Obstet Gynecol 160: 176, 1989

40. Rud T: The effects of estrogens and gestogens on the urethral pressure profile in urinary continent and stress incontinent women. Acta Obstet Gynecol Scand 59: 265, 1980

41. Hilton P: The use of intravaginal estrogen cream in genuine stress incontinence. Br J Obstet Gynecol 90: 940, 1983

42. Faber P, Heidenreich J: Treatment of stress incontinence with estrogen in postmenopausal women. Urol Int 32: 221, 1977

43. Walter S, Wolf H, Barlebo H et al: Urinary incontinence in postmenopausal women treated with estrogens. Urol Int 33: 135, 1978

44. Karram MM, Yeko TR, Sauer MV et al: Urodynamic changes following hormonal replacement therapy in women with premature ovarian failure. Obstet Gynecol 74: 208, 1989

45. Fantl JA, Cardozo L, McClish DK et al: Estrogen therapy in the management of urinary incontinence in postmenopausal women: A meta-analysis. First report of the Hormones and Urogenital Therapy Committee. Obstet Gynecol 83: 12, 1994

46. Wilson PD, Faragher B, Butler B et al: Treatment with oral piperazine oestrone sulphate for genuine stress incontinence in post-menopausal women. Br J Obstet Gynaecol 94: 568, 1987

47. Schiff I, Tulchinsky D, Ryan KJ: Vaginal absorption of estrone and 17-beta-estradiol. Fertil Steril 28: 1063, 1977

48. Bowen LW, Sand PK, Ostergard DR: Urodynamic effects of a vaginal pessary in women with genital prolapse (abstract). Presented at the 34th Annual American College of Obstetricians and Gynecologists Meeting, New Orleans, 1986

48. Myers DL, LaSala CA, Hogan JW et al. The effect of posterior wall support defects on urodynamic indices in stress urinary incontinence. Obstet Gynecol 91:710, 1998

49. Fianu S, Kjaeldgaard A, Larsson B: Preoperative screen for latent stress incontinence in women with cystocele. Neurourol Urodyn 4: 3, 1985

50. Bergman A, Koonings PP, Ballard CA: Predicting postoperative urinary incontinence development in women undergoing operation for genitourinary prolapse. Am J Obstet Gynecol 158: 1171, 1988

51. Bump RC, Fantl JA, Hurt WG: The mechanism of urinary continence in women with severe uterovaginal prolapse: Results of barrier studies. Obstet Gynecol 3: 291, 1988

52. Kelvin FM, Maglinte DT, Benson JT: Evacuation proctography (defecography): An aid to the investigation of pelvic floor disorders. Obstet Gynecol 83: 307, 1994

53. Bradley WE, Rockswold GL, Timm GW et al: Neurology of micturition. J Urol 115: 481, 1976

54. Ostergard DR: The neurological control of micturition and integral voiding reflexes. Obstet Gynecol Surv 34: 417, 1979

55. Raz S: Adrenergic influence on the internal urinary sphincter. Isr J Med Sci 10: 608, 1974

56. Crystle CD, Charme LS, Copeland WE: Q-tip test in stress urinary incontinence. Obstet Gynecol 38: 313, 1971

57. Montz FJ, Stanton SL: Q-tip test in female urinary incontinence. Obstet Gynecol 67: 258, 1986

58. Fantl JA, Hurt WG, Bump RC et al: Urethral axis and sphincteric function. Am J Obstet Gynecol 155: 554, 1986

59. Bergman A, McCarthy TA, Ballard CA et al: Role of the Q-tip test in evaluating stress urinary incontinence. J Reprod Med 32: 273, 1987

60. Karram MM, Bhatia NN: The Q-tip test: Standardization of the technique and its interpretation in women with urinary incontinence. Obstet Gynecol Scand 6: 807, 1988

61. Rud T: Urethral pressure profile in continent women from childhood to old age. Acta Obstet Gynecol Scand 59: 331, 1980

62. Walters MD, Diaz K: Q-tip test: A study of continent and incontinent women. Obstet Gynecol 70: 208, 1987

63. Bergman A, Koonings PP, Ballard CA: Negative Q-tip test as a risk factor for failed incontinence surgery in women. J Reprod Med 34: 193, 1989

64. McGuire EJ: Urodynamic findings in patients after failure of stress incontinence operations. Prog Clin Biol Res 78: 351, 1981

65. Fantl JA, Smith PJ, Schneider V et al: Fluid weight uroflowmetry in women. Am J Obstet Gynecol 145: 1017, 1983

66. Drach GW, Ignatoff J, Layton T: Peak urinary flow rate: Observations in female subjects and comparison to male subjects. J Urol 122: 215, 1979

67. Wein AJ, Hanno PM, Dixon DO et al: The reproducibility and interpretation of carbon dioxide cystometry. J Urol 120: 205, 1978

68. Robertson JR: Dynamic urethroscopy. In Ostergard DR, Bent AE (eds): Urogynecology and Urodynamics, pp 115-21. Baltimore, Williams & Wilkins, 1991

69. Sand PK, Hill RC, Ostergard DR: Supine urethroscopic and standing cystometry as screening methods for the detection of detrusor instability. Obstet Gynecol 70: 57, 1987

70. Scotti RJ, Ostergard DR, Guillaume AA et al: Predictive value of urethroscopy as compared to urodynamics in the diagnosis of genuine stress incontinence. J Reprod Med 35: 772, 1990

70. Parsons CL: Potassium sensitivity test. Tech Urol 2: 171, 1996

71. Ouslander J, Leach G, Abelson S et al: Simple versus multichannel cystometry in the evaluation of bladder function in an incontinent geriatric population. J Urol 140: 1482, 1988

72. Brubaker L, Sand PK: Cystometry, urethrocystometry, and videocystourethrography. Obstet Gynecol 33: 324, 1990

73. Sand PK, Brubaker LT, Novak T: Simple standing incremental cystometry as a screening method for detrusor instability. Obstet Gynecol 77: 453, 1991

74. Wheeler JS, Niecestro RM, Fredian C et al: Comparison of a simple cystometer with a multichannel in females with voiding dysfunction. Int Urogynecol J 2: 90, 1991

75. Sutherst JR, Brown MC: Comparison of a single and multichannel cystometry in diagnosing bladder instability. Br Med J 288: 1720, 1984

76. McInterney PD, Vanner TF, Harris SAB, Stephenson TP: Ambulatory urodynamics. Br J Urol 67: 272, 1991

77. van Waalwijk van Doorn ESC, Zwiers W, Wetzels LLRH, Dubruyne FMJ: A comparative study between standard and ambulatory urodynamics. Neurourol Urodyn 6: 159, 1987

78. Cucchi A: Screening tests for detrusor instability in clinical urodynamics. Int Urogynecol J 2: 101, 1991

79. Low JA, Mauger GM, Dragovic J: Diagnosis of the unstable detrusor: Comparison of an incremental and continuous infusion technique. Obstet Gynecol 65: 99, 1985

80. Arnold EP: Cystometry-postural effects in incontinent women. Urol Int 29: 185, 1974

81. Mayer R, Wells T, Brink C et al: Handwashing in the cystometric evaluation of detrusor instability. Neurourol Urodyn 10: 563, 1991

82. Frigerio L, Ferrari A, Candiani GB: The significance of the stop test in female urinary incontinence. Diagn Gynecol Obstet 3: 301, 1981

83. Coolsaet B: Bladder compliance and detrusor activity during the collection phase. Neurourol Urodyn 4: 263, 1985

84. Jorgensen L, Lose F, Andersen JT: One hour pad-weighing test for objective assessment of female urinary incontinence. Obstet Gynecol 69: 39, 1987

85. Sutherst JR, Brown MC, Richmond D: Analysis of the pattern of urine loss in women with incontinence as measured by weighing perineal pads. Br J Urol 58: 273, 1986

86. Klarskov P, Hald T: Reproducibility and reliability of urinary incontinence assessment with a 60 minute test. Scand J Urol Nephrol 18: 293, 1984

87. Lose G, Gammelgaard J, Jorgensen TJ: The one-hour pad-weighing test: Reproducibility and the correlation between the test results, the start volume in the bladder, and the diuresis. Neurourol Urodyn 5: 17, 1986

88. Eadie AS, Glen ES, Rowan D: Assessment of urinary loss over a two-hour test period: A comparison between the urilos recording nappy system and the perineal pad weighing test. Urogynecologia 1: 35, 1985

89. Lose G, Rosenkilde P, Gammelgaard J et al: Pad-weighing test performed with standardized bladder volume. Urology 32: 78, 1988

90. Kinn AC, Larsson B: Pad test with fixed bladder volume in urinary stress incontinence. Acta Obstet Gynecol Scand 66: 369, 1987

91. Sutherst J, Brown M, Shower M: Assessing the severity of urinary incontinence in women by weighing perineal pads. Lancet 1: 1128, 1981

92. Walsh JB, Mills GL: Measurement of urinary loss in elderly incontinent patients. Lancet 1: 1130, 1981

93. Thind P, Gerstenberg TC: One-hour ward test vs 24-hour home pad weighing test in the diagnosis of urinary incontinence. Neurourol Urodyn 10: 241, 1991

94. Horbach NS: Problems in the clinical diagnosis of stress incontinence. J Reprod Med 35: 751, 1990

95. Bradley WE: Autonomic neuropathy and the genitourinary system. Urology 119: 299, 1978

96. Sand PK, Bowen LW, Ostergard DR: The effect of a filling catheter during urodynamics. Int Urogynecol J 1: 124, 1990

97. McCarthy TA: Validity of rectal pressure measurements as indication of intraabdominal pressure changes during urodynamic evaluation. Urology 20: 657, 1982

98. Asmussen M, Ulmsten U: Simultaneous urethro-cystometry with a new technique. Scand J Urol Nephrol 10: 7, 1976

99. Kulseng-Hanssen S: Prevalence and pattern of unstable urethral pressure in 174 gynecologic patients referred for urodynamic investigation. Am J Obstet Gynecol 146: 895, 1983

100. Vereecken RL, Das J: Urethral instability: Related to stress and/or urge incontinence? J Urol 134: 698, 1985

101. Weil A, Miege B, Rottenberg R et al: Clinical significance of urethral instability. Obstet Gynecol 68: 106, 1986

102. Tapp AJS, Cardozo LD, Versi E et al: The prevalence of variation of resting urethral pressure in women and its association with lower urinary tract function. J Urol 61: 314, 1988

103. Kiruluta HG, Downie JW, Awad SA: The continence mechanism: The effect of bladder filling on the urethra. Invest Urol 18: 460, 1981

104. Abdel-Rahman M, Coulombe A, Devroede G et al: Urorectodynamic evaluation of healthy volunteers. Urology 19: 559, 1982

105. Awad SA, Downie JW: Relative contributions of smooth and striated muscles to the canine urethral pressure profile. Br J Urol 48: 347, 1976

106. Plate P, Susset J: Studies of female urethral pressure profile: I. The normal urethral pressure profile. J Urol 123: 64, 1980

107. Constantinou CE: Resting and stress urethral pressures as a clinical guide to the mechanism of continence in the female patient. Urol Clin North Am 12: 247, 1985

108. Weil A, Reyes H, Bischof P et al: Clinical relevance of urethral stress profile using microtransducers after surgery for stress incontinence in females. Urol Int 38: 363, 1983

109. Rud T, Andersson KE, Asmussen M et al: Factors maintaining the intraurethral pressure in women. Invest Urol 17: 343, 1980

110. Hilton P, Stanton SL: Urethral pressure measurement by microtransducer: The results in symptom-free women and in those with genuine stress incontinence. Br J Obstet Gynaecol 90: 919, 1983

111. Sorensen S, Knudsen UB, Kirkeby HJ et al: Urodynamic investigations in healthy fertile females during the menstrual cycle. Scand J Urol Nephrol 114 (Suppl): 28, 1988

112. Versi E: Discriminant analysis of urethral pressure profilometry data for the diagnosis of genuine stress incontinence. Br J Obstet Gynaecol 97: 251, 1990

113. Meyer S, De Grandi P, Schmidt N et al: Urodynamic parameters in patients with slight and severe genuine stress incontinence: Is the stress profile useful? Neurourology 13: 21, 1994

114. Henriksson L, Ulmsten U, Andersson KE: The effect of changes of posture on the urethral closure pressure in stress-incontinent women. Scand J Urol Nephrol 11: 207, 1977

115. Versi E, Cardozo LK, Studd J et al: Evaluation of urethral pressure profilometry for the diagnosis of genuine stress incontinence. World J Urol 4: 6, 1986

116. Sand PK, Bowen LW, Panganiban R et al: The low pressure urethra as a factor in failed retropubic urethropexy. Obstet Gynecol 69: 399, 1987

117. Bowen LW, Sand PK, Ostergard DR et al: Unsuccessful Burch retropubic urethropexy: A case-controlled urodynamic study. Am J Obstet Gynecol 160: 452, 1989

118. Rosenzweig BA, Bhatia NN, Nelson et al: Dynamic urethral pressure profilometry pressure transmission ratio: What do the numbers really mean? Obstet Gynecol 77: 586, 1991

119. Hilton P: The urethral pressure profile under stress: A comparison of profiles on coughing and straining. Neurourol Urodyn 2: 55, 1983

120. Ghoniem GM, Roach MB, Lweis VH et al: The value of leak pressure and bladder compliance in the urodynamic evaluation of meningomyelocele patients. J Urol 144: 1140, 1990

121. Rud T, Ulmsten U, Andersson KE: Initiation of voiding in healthy women and those with stress incontinence. Acta Obstet Gynecol Scand 57: 457, 1978

122. Rud T, Ulmsten U, Westby M: Initiation of micturition: A study of combined urethrocystometry and urethrocystography in healthy and stress incontinent females. Scand J Urol Nephrol 13: 259, 1979

123. Sjoberg B, Nyman CR: Hydrodynamics of micturition in stress-incontinent women. Scand J Urol Nephrol 16: 1, 1984

124. Bhatia NN, Bergman A: Use of preoperative uroflowmetry and simultaneous urethrocystometry for predicting risk of prolonged post-operative bladder drainage. Urology 28: 440, 1986

125. Bhatia NN, Bergman A: Urodynamic predictability of voiding following incontinence surgery. Obstet Gynecol 63: 85, 1984

126. Klutke JJ, Klutke CG, Bergman J, Elia, G: Bladder neck suspension for stress urinary incontinence: how does it work? Neurourol Urodynam 8: 623, 1999

127. Belair, G, Tessier J, Bertrand PE, Schick E: Retropubic cystourethroscopy: Is it an obstructive procedure? J Urol 158: 533, 1997