Genitourinary Dysfunction

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Chapter 23 Genitourinary Dysfunction

PELVIC ORGAN PROLAPSE, URINARY INCONTINENCE, AND INFECTIONS

Christopher M. Tarnay, Narender N. Bhatia

A better understanding of the anatomic basis of pelvic relaxation defects has led to less invasive techniques and better outcomes for the treatment of female genitourinary dysfunction.

Normal Pelvic Anatomy and Supports

Anatomically, the pelvic organs, including the vagina, uterus, bladder, and rectum, are maintained within the pelvis by the bilaterally paired and posteriorly fused levator ani muscles. The anterior separation between the levator ani is called the levator hiatus. Inferiorly, the levator hiatus is covered by the urogenital diaphragm. The urethra, vagina, and rectum pass through the levator hiatus and urogenital diaphragm as they exit the pelvis. The endopelvic fascia is a visceral pelvic fascia that invests the pelvic organs and forms bilateral condensations referred to as ligaments (i.e., pubourethral, cardinal, and uterosacral ligaments). These ligaments attach the organs to the fascia of the pelvic side walls and bony pelvis. Damage to the vagina and its support system allows the urethra, bladder, rectum, and small bowel to herniate and protrude into the vaginal canal.

The perineal body is a central point for the attachment of the perineal musculature. Although the contents of the abdominal cavity bear down on the pelvic organs, they remain suspended in their relation to each other and to the underlying levator sling and perineal body.

Pelvic Organ Prolapse

Pelvic organ prolapse (POP) refers to protrusion of the pelvic organs into the vaginal canal or beyond the vaginal opening. It results from a weakness in the endopelvic fascia investing the vagina, along with its ligamentous supports. Defects in vaginal support may occur in isolation (e.g., anterior vaginal wall only) but are more commonly combined. The nomenclature of POP has evolved such that cystocele, rectocele, and enterocele have been replaced by more anatomically precise terms (Figure 23-1).

FIGURE 23-1 Diagrammatic representation of the four types of vaginal/uterine prolapse.

ANTERIOR VAGINAL PROLAPSE (CYSTOCELE)

The anterior vagina is the most common site of vaginal prolapse. Women with this type of defect describe symptoms of vaginal fullness, heaviness, pressure, and discomfort that often progress over the course of the day and are most noticeable after prolonged standing or straining. Women may have to apply manual pressure to empty their bladder completely. Other symptoms include stress urinary incontinence (SUI), urinary urgency, frequency, and nocturia. Significant anterior vaginal wall prolapse that protrudes beyond the vaginal opening (hymen) can cause urethral obstruction due to kinking, resulting in urinary retention.

POSTERIOR VAGINAL PROLAPSE (RECTOCELE AND ENTEROCELE)

Posterior vaginal defects occur when there is weakness in the rectovaginal septum. Symptoms can be indistinguishable from other types of prolapse because the discomfort, pressure, and sense of a vaginal bulge are nonspecific. However, when difficulties with bowel function and defecation occur, lower posterior vaginal prolapse is likely. Straining or the need to manually splint for complete bowel elimination may occur. Upper posterior vaginal wall prolapse is nearly always associated with herniation of the pouch of Douglas, and because this is likely to contain loops of bowel, it is called an enterocele.

APICAL VAGINAL AND UTERINE PROLAPSE

Although vaginal prolapse can occur without uterine prolapse, the uterus cannot descend without carrying the upper or apical portion of the vagina with it.

Complete procidentia (uterine prolapse through the vaginal hymen) represents failure of all the vaginal supports (Figure 23-2). Hypertrophy, elongation, congestion, and edema of the cervix may sometimes cause a large protrusion of tissue beyond the hymen, which may be mistaken for a complete procidentia. Vaginal vault prolapse or eversion of the vagina may be seen after vaginal or abdominal hysterectomy and represents failure of the supports around the upper vagina.

FIGURE 23-2 Complete uterine prolapse (procidentia). Note the lesions on either side of cervical dimple (arrows) representing pressure ulcerations from clothing/undergarments.

(Courtesy of CM Tarnay, MD, Ronald Reagan–UCLA Medical Center.)

Symptoms of POP mainly affect quality of life. However, significant sequelae of POP can occur in neglected cases of procidentia, which may be complicated by excessive purulent discharge, decubitus ulceration, bleeding, and rarely, carcinoma of the cervix.

ETIOLOGY OF PROLAPSE

The pelvic fascia, ligaments, and muscles may become attenuated from excessive stretching during pregnancy, labor, and difficult vaginal delivery, especially with forceps or vacuum assistance. Asian and black women appear less likely than white women to develop prolapse.

Increased intraabdominal pressure resulting from a chronic cough, ascites, repeated lifting of heavy weights, or habitual straining as a result of constipation may predispose to prolapse. Atrophy of the supporting tissues with aging, especially after menopause, also plays an important role in the initiation or worsening of pelvic relaxation. Iatrogenic factors include failure to adequately correct all pelvic support defects at the time of pelvic surgery, such as hysterectomy.

DIAGNOSIS

Vaginal examination is facilitated by using a single-blade speculum. While depressing the posterior vaginal wall, the patient is asked to strain down. This demonstrates the descent of the anterior vaginal wall consistent with prolapse and urethral displacement. Similarly, retraction of the anterior vaginal wall during straining will accentuate posterior vaginal defects and uncover enterocele and rectocele if present. Rectal-vaginal examination is often useful to demonstrate a rectocele and to distinguish it from an enterocele.

QUANTIFYING AND STAGING PELVIC ORGAN PROLAPSE

The preferred method to describe and document the severity of POP is the Pelvic Organ Prolapse Quantification (POP-Q) system. The extent of prolapse is evaluated and measured relative to the hymen, which is a fixed anatomic landmark. The anatomic position of the six defined points for measurement is denoted in centimeters above the hymen (negative number) or centimeters below the hymen (positive number). The plane at the level of the hymen is defined as zero (Figure 23-3).

FIGURE 23-3 Illustration showing a side view of female pelvis. Six sites (points Aa, Ba, C, D, Bp, and Ap), genital hiatus (gh), perineal body (pb), and total vaginal length (tvl) used for pelvic organ support quantitation.

(Reproduced with permission from Bump RC, et al: The standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction. Am J Obstet Gynecol 175:10, 1996.)

Stages of POP can be assigned according to the most severe portion of the prolapse after the full extent of the protrusion has been determined. An ordinal system is used for measurements of different points along the vaginal canal and allows for better communication among clinicians. This staging system enables more objective tracking of surgical outcomes (Table 23-1).

TABLE 23-1 PELVIC ORGAN PROLAPSE STAGING SYSTEM

Stage	Characteristics
0	No prolapse
0	Aa, Ba, Ap, Bp are −3 cm and C or D ≤ −(tvl −2) cm
1	Most distal portion of the prolapse −1 cm (above the level of hymen)
2	Most distal portion of the prolapse ≥ −1 cm but ≤ +1 cm (≤1 cm above or below the hymen)
3	Most distal portion of the prolapse > +1 cm but > +(tvl − 2) cm (beyond the hymen; protrudes no farther than 2 cm less than the total vaginal length)
4	Complete eversion; most distal portion of the prolapse ≥ +(tvl − 2) cm

Aa, point A of anterior wall; Ba, point B of anterior wall; Ap, point A of posterior wall; Bp, point B of posterior wall; −, above the hymen; +, beyond the hymen; tvl, total vaginal length.

Reproduced with permission from Harvey MA, Versi E: Urogynecology and pelvic floor dysfunction. In Ryan KJ, Berkowitz RS, Barbieri RL, Dunaif A (eds): Kistner’s Gynecology and Women’s Health, 7th ed. St. Louis, Mosby, 1999. Copyright © 1999 Elsevier.

MANAGEMENT

Prophylactic measures to mitigate the symptoms of POP include identifying and treating chronic respiratory and metabolic disorders, correction of constipation and intraabdominal disorders that may cause repetitive increases in intraabdominal pressure, and administration of estrogen to menopausal women. Failure to recognize and treat significant support defects at the time of concomitant gynecologic surgery may lead to progression of existing prolapse and the development of urinary incontinence or retention and urinary tract infections (UTIs).

Nonsurgical Treatment

When only a mild degree of pelvic relaxation is present, pelvic floor muscle exercises may improve the tone of the pelvic floor musculature. Pessaries, which provide intravaginal support (Figure 23-4), may be used to correct prolapse by “propping up” the vagina. They can be considered when the patient is medically unfit or refuses surgery or during pregnancy and the postpartum period. They are also useful to promote healing of a decubitus ulcer before surgery for prolapse.

FIGURE 23-4 Some types of vaginal pessaries used for prolapse: Gellhorn (A), Shaatz (B), ring (C), ring with support (D), cube (E), Smith (F), Hodge (G), Hodge with support for cystocele (H), Inflatoball (I), Gehrung (J), and doughnut (K).

Pessaries require proper fitting and selection of the appropriate type and size. They should be removed, cleaned, and reinserted every 6 to 12 weeks. They may cause vaginal irritation and ulceration. Neglect may result in serious consequences, including fistula formation, impaction, bleeding, and infection.

Urinary Incontinence

Urinary incontinence is defined as the involuntary loss of urine that is objectively demonstrable and is a social or hygienic problem. Urinary incontinence has been reported to affect 15% to 50% of women. The problem increases in prevalence with age, reaching more than 50% in elderly persons in nursing homes. It is estimated that the direct financial cost of urinary incontinence in the United States is between $10 and $15 billion per year.

ANATOMY AND PHYSIOLOGY OF THE LOWER URINARY TRACT

In the adult female, the urethra is a muscular tube, 3 to 4 cm in length, lined proximally with transitional epithelium and distally with stratified squamous epithelium. It is surrounded mainly by smooth muscle. The striated muscular urethral sphincter, which surrounds the distal two thirds of the urethra, contributes about 50% of the total urethral resistance and serves as a secondary defense against incontinence. It is also responsible for the interruption of urinary flow at the end of micturition.

The two posterior pubourethral ligaments provide a strong suspensory mechanism for the urethra and serve to hold it forward and in close proximity to the pubis under conditions of stress. They extend from the lower part of the pubic bone to the urethra at the junction of its middle and distal third.

INNERVATION

The lower urinary tract is under the control of both parasympathetic and sympathetic nerves. The parasympathetic fibers originate in the sacral spinal cord segments S2 through S4. Stimulation of the pelvic parasympathetic nerves and administration of cholinergic drugs cause the detrusor muscle to contract. Anticholinergic drugs reduce the vesicle pressure and increase the bladder capacity.

The sympathetic fibers originate from thoracolumbar segments (T10 through L2) of the spinal cord. The sympathetic system has α- and β-adrenergic components. The β-fibers terminate primarily in the detrusor muscle, whereas the α-fibers terminate primarily in the urethra. α-Adrenergic stimulation contracts the bladder neck and urethra and relaxes the detrusor. β-Adrenergic stimulation relaxes the urethra and detrusor muscle. The pudendal nerve (S2 to S4) provides motor innervation to the striated urethral sphincter.

FACTORS INFLUENCING BLADDER BEHAVIOR

Sensory Innervation

Afferent impulses from the bladder, trigone, and proximal urethra pass to S2 through S4 levels of the spinal cord by means of the pelvic hypogastric nerves. The sensitivity of these nerve endings may be enhanced by acute infection, interstitial cystitis, radiation cystitis, and increased intravesical pressure. The latter may occur in the standing or bending-forward position or in association with obesity, pregnancy, or pelvic tumors.

Inhibitory impulses, probably relayed by the pudendal nerve, also pass to S2 through S4 after mechanical stimulation of the perineum and anal canal. Their passage may explain why pain in this region can cause urinary retention.

Central Nervous System

In infancy, the storage and expulsion of urine are automatic and controlled at the level of the sacral reflex arc. Later, connections to the higher centers become established, and by training and conditioning, this spinal reflex becomes socially influenced so that voiding can be voluntarily accomplished. Although organic neurologic diseases may interrupt the influence of the higher centers on the spinal reflex arc, patterns of micturition may also be profoundly altered by mental, environmental, and sociologic disturbances.

CONTINENCE CONTROL

The bladder must store and hold urine painlessly and then, at the appropriate social setting, empty urine effectively. The normal bladder holds urine because the intraurethral pressure exceeds the intravesical pressure. The pubourethral ligaments and surrounding endopelvic fascia support the urethra so that abrupt increases in intraabdominal pressure are transmitted equally to the bladder and proximal third of the urethra, thus maintaining a pressure gradient between the two structures. In addition, a reflex contraction of the levator ani compresses the mid-urethra, decreasing the likelihood of urine loss.

Stress Urinary Incontinence

SUI is involuntary leakage of urine in response to physical exertion, sneezing, or coughing.

ETIOLOGY

The most commonly accepted theory for the pathogenesis of SUI is urethral hypermobility due to vaginal wall relaxation, displacing the bladder neck and proximal urethra downward. When this occurs, increased intraabdominal pressure from coughing, sneezing, or physical exertion is no longer transmitted equally to the bladder and proximal urethra. The normal urethral resistance is overcome by this increased bladder pressure, and leakage of urine results.

The second possible mechanism is intrinsic sphincter deficiency, where the urethra fails to close in response to increases in intraabdominal pressure. This cause of SUI is analogous to having a leaky “valve” in the urethra.

Factors that contribute to SUI include childbearing, previous urogenital surgery, pelvic radiation, estrogen deficiency (menopause), and medications such as diuretics and α-adrenergic blockers.

PELVIC EXAMINATION

Inspection of the vaginal walls should be performed with a single-blade speculum, which allows optimal visualization of the anterior vaginal wall and urethrovesical junction. Scarring, tenderness, and rigidity of the urethra from previous vaginal surgeries or pelvic trauma may be indicated by a scarred anterior vaginal wall. Because the distal urethra is estrogen dependent, the patient with urogenital atrophy also has atrophic urethritis.

DIAGNOSTIC TESTS

Stress Test

The patient is examined with a full bladder in the lithotomy position. While the physician observes the urethral meatus, the patient is asked to cough. SUI is present if short spurts of urine escape simultaneously with each cough. A delayed leakage, or loss of large volumes of urine, suggests uninhibited bladder contractions. If loss of urine is not demonstrated in the lithotomy position, the test should be repeated with the patient in a standing position.

Cotton Swab (Q-Tip) Test

This test determines the mobility and descent of the urethrovesical junction on straining and allows differentiation from anterior vaginal laxity alone. With the patient in the lithotomy position, the examiner inserts a lubricated cotton swab into the urethra to the level of the urethrovesical junction and measures the angle between the cotton swab and the horizontal. The patient then strains maximally, which produces descent of the urethrovesical junction. Along with the descent, the cotton swab moves, producing a new angle with the horizontal. The normal change in angle is up to 30 degrees. In patients with pelvic relaxation and SUI, the change in cotton swab angle ranges from 30 to 60 degrees or more (Figure 23-5).

FIGURE 23-5 Diagrammatic representation of the Q-tip (cotton swab) test, showing mobility of the urethrovesical junction in a continent patient and a patient with stress urinary incontinence.

Urethrocystoscopy

Urethrocystoscopy allows the physician to examine inside the urethra, urethrovesical junction, bladder walls, and ureteral orifices. This procedure is useful to detect bladder stones, tumors, diverticula, or sutures from prior surgeries.

Cystometrogram

Cystometry consists of distending the bladder with known volumes of water and observing pressure changes in bladder function during filling. The most important observation is the presence of a detrusor reflex and the patient’s ability to control or inhibit this reflex.

The first sensation of bladder filling should occur at volumes of 150 to 200 mL. The critical volume (400 to 500 mL) is the capacity that the bladder musculature tolerates before the patient experiences a strong desire to urinate. At this point, if the patient is asked to void, a terminal contraction may appear and is seen as a sudden rise in intravesical pressure. At the peak of the contraction, the patient is instructed to inhibit this reflex (indicated by arrows in Figure 23-6). A normal person should be able to inhibit this detrusor reflex and thereby bring down intravesical pressure (see Figure 23-6A). In a urologically or neurologically abnormal patient, the detrusor reflex may appear without the specific instruction to void, and the patient cannot inhibit it (see Figure 23-6B); this observation is referred to as an uninhibited detrusor contraction. Other terms for this disorder include overactive bladder, detrusor dyssynergia, detrusor hyperreflexia, irritable bladder, hypertonic bladder, unstable bladder, and uninhibited neurogenic bladder.

FIGURE 23-6 Water cystometrogram in a normal patient (A), a patient with detrusor hyperreflexia (B), and a patient with detrusor areflexia (hypotonic bladder) (C). Arrows in A and B indicate peak of bladder contraction.

These cystometric procedures allow differentiation between patients who are incontinent as a result of uninhibited detrusor contraction and those who have SUI. Conversely, the hypotonic bladder accommodates excessive amounts of gas or water with little increase in intravesical pressure, and the terminal detrusor contraction is absent when the patient is asked to void (see Figure 23-6C).

Urethral Pressure Measurements

A low urethral pressure may be found in patients with SUI, whereas an abnormally high urethral closing pressure may be associated with voiding difficulties, hesitancy, and urinary retention.

Urethral function can be evaluated with cystometric testing. The urethral closing pressure profile (UCPP) is a graphic record of pressure along the length of the urethra. The urethral closing pressure normally varies between 50 and 100 cm H₂O. A Valsalva maneuver or abdominal leak point pressure of less than 60 cm H₂O or urethral closure pressure of less than 20 cm H₂O are suggestive of the diagnosis of intrinsic sphincteric deficiency (ISD).

Uroflowmetry

Uroflowmetry records rates of urine flow through the urethra when the patient is asked to void spontaneously.

Voiding Cystourethrogram

In this radiologic investigation, fluoroscopy is used to observe bladder filling, the mobility of the urethra and bladder base, and the anatomic changes during voiding. The procedure provides valuable information regarding bladder size and the competence of the bladder neck during coughing. It may detect any bladder trabeculation; vesicoureteral reflux during voiding; funneling of the bladder neck, bladder, and urethral diverticula; and outflow obstruction.

Ultrasonography

Employing real-time or sector ultrasonography, information can be obtained about the inclination of the urethra, flatness of the bladder base, and mobility and funneling of the urethrovesical junction, both at rest and with a Valsalva maneuver. In addition, bladder or urethral diverticula may be identified.

Video urodynamics incorporates fluoroscopy with concurrent measurement of bladder and urethral pressures. Dynamic magnetic resonance imaging studies are employed to detect pelvic floor and relaxation defects in incontinent patients.

SUMMARY

For a significant percentage of patients with SUI, a good history and physical examination, the cotton swab test, and the cough stress test are adequate investigations. The addition of uroflowmetry, cystourethroscopy, and the cystometrogram are appropriate when more detailed information is needed for diagnosis and treatment. Additional urodynamic, electromyographic, electrophysiologic, and radiologic studies may be necessary in patients with a history of multiple previous surgeries for urinary incontinence and for patients with associated neurologic disease.

TREATMENT

Medical Therapy

In postmenopausal incontinent women, estrogens improve urethral closing pressure, vaginal epithelial thickness and vascularity, and reflex urethral function. α-Adrenergic stimulants, such as phenylpropanolamine and pseudoephedrine, may enhance urethral closure and improve continence but are unproved in placebo controlled trials. The search for an effective medication to treat SUI is still ongoing.

Physical Therapy

Pelvic floor muscle exercises (PFMEs) also known as Kegel exercises, are proven first-line therapy to improve or cure mild to moderate forms of SUI. PFMEs require diligence and willingness to practice at home and at work. Many women find them difficult, fatiguing, or time-consuming. Kegel exercises before and after delivery may help patients with postpartum urinary incontinence.

Intravaginal Devices

Larger sizes of pessaries (see Figure 23-4) have been used to elevate and support the bladder neck and urethra. They have been shown to be effective for SUI.

Surgical Therapy

Surgery is the most commonly employed treatment for SUI. The aim of all surgical procedures is to correct the pelvic relaxation defect and to stabilize and restore the normal supports of the urethra. The approach may be vaginal, abdominal, or combined abdominovaginal.

ABDOMINAL APPROACH

Abdominal retropubic urethropexy has a long-term success rate of 85% to 95%. The retropubic urethropexy is performed extraperitoneally (in the space of Retzius) by placing sutures in the fascia lateral to and on each side of the bladder neck and proximal urethra and elevating the vesicourethral junction by attaching the sutures to the symphysis pubis (Marshall-Marchetti-Krantz procedure) or to Cooper’s ligament (Burch procedure)

Postoperatively, a transurethral or suprapubic catheter is left in the bladder for continuous bladder drainage for 48 to 72 hours before instituting spontaneous voiding. Some patients (20% to 30%) may need prolonged postoperative bladder drainage (more than 7 days). An occasional patient may develop osteitis pubis after the Marshall-Marchetti-Krantz procedure.

VAGINAL APPROACH

Suburethral sling procedures have long been used to treat refractive patients or patients with severe SUI. Conventional slings often required harvesting a patient’s own fascial tissue to be placed under the bladder neck but were plagued by high rates of urinary retention.

The latest modification of the sling procedure is the use of tension-free synthetic (polypropylene) mesh made of polypropylene placed at the level of the mid-urethra. This pioneering technique, developed in Sweden, was introduced in the United States in the late 1990s. The tension-free vaginal tape was developed as a minimally invasive technique for the surgical correction of genuine SUI and has a high success rate. Traditionally, a mid-urethral sling is placed retropubically. A variation in placement for the mid-urethral sling is the transobturator approach. Rather than retropubic passage, the sling is passed through the obturator foramen laterally. The potential advantage of this approach, which avoids the space of Retzius, is reduction in bladder, bowel, or vascular injury.

SPECIAL PROCEDURES

Conventional surgical procedures for incontinence sometimes fail in patients with a diagnosis of ISD. ISD is a subtype of SUI marked by a very poorly functioning urethral sphincter. These patients are treated with a suburethral sling procedure or periurethral bulking injections to improve urethral function. A commonly used bulking material is bovine collagen (Contigen). This collagen gel causes periurethral compression after injection and becomes a fibrous network that serves as a matrix for host connective tissue. Collagen, however, is ultimately degraded by the body, and this type of therapy usually requires reinjection at frequent intervals, usually several months. A nonabsorbable bulking agent is calcium hydroxylapatite, which is nontoxic and nonantigenic and is less likely to degrade.

Urge Urinary Incontinence and Overactive Bladder

The two terms are often used interchangeably to describe a problem with bladder control that is associated with a strong desire to pass urine with a decreased ability to control it. Urge urinary incontinence (UUI) is defined as the involuntary leakage of urine accompanied by or immediately preceded by urgency. UUI can be associated with small losses of urine between normal micturitions or large volume losses with complete bladder emptying. Overactive bladder (OAB), previously described as UUI associated with detrusor muscle instability, is a more descriptive symptom-based term and more accurately encompasses the common clinical presentation. OAB is defined as “urgency, with or without urge incontinence, usually with frequency and nocturia.”OAB has become the preferred term because it comprises symptoms of urgency, urge urinary incontinence, frequency, and nocturia.

The incidence of overactive bladder increases with age, approximating 30% in the geriatric patient population. In most patients, the exact etiology of bladder instability remains unknown, but a number of risk factors are associated with its development (Box 23-1).

Classically, women with OAB describe a sudden strong urge to urinate with an inability to suppress the feeling, rushing to the bathroom, and leaking before making it to the toilet. Awakening several times a night to urinate is also a prominent feature.

TREATMENT

The optimal treatment of OAB starts with behavioral modification, adding pharmacologic and physical interventions, such as electrical stimulation, as needed. Identification of any dietary triggers, like caffeine, alcohol, or carbonated beverages, is important. The use of a self-reported bladder diary can be helpful for obtaining this information.

Behavioral Modification

Reducing fluid intake and avoiding liquids during the evening hours are good initial behavioral changes. Gradually increasing the intervals between voidings and doing pelvic floor muscle strengthening exercises, such as Kegel exercises, are effective for attaining better bladder control.

Pharmacologic Treatment

Antimuscarinics, or anticholinergics, have become the mainstays of drug treatment for OAB.

The mainstays of drug therapy include oxybutynin chloride (Ditropan) and tolterodine (Detrol). Oxybutynin chloride has been shown to improve symptoms of urinary urgency in about 70% of patients. Tolterodine also has anticholinergic activity. Because of its bladder specificity, tolterodine has a more favorable side-effect profile than oxybutynin. It is also dosed less frequently, which improves patient compliance. Both are available in immediate release and long-acting formulations. Oxybutynin is also available for delivery in a transdermal patch.

Trospium chloride, solifenacin, and darifenacin are newer agents used in the treatment of OAB. All significantly improve OAB symptoms compared with placebo. Evidence suggests that side-effect profiles will be similar or lower than the less specific antimuscarinics.

Imipramine hydrochloride is a tricyclic antidepressant that acts through its anticholinergic properties to increase bladder storage. The drug improves bladder compliance rather than counteracting uninhibited detrusor contractions. It is given in doses greatly reduced from those recommended for use as an antidepressant. It also blocks postsynaptic noradrenaline uptake and thereby increases bladder outlet resistance. With its dual action, imipramine may be effective in patients with both stress incontinence and OAB (mixed incontinence). It should be dosed in the evening because it may be sedating, and should be used with caution in elderly patients owing to potential orthostatic hypotension.

Functional Electrical Stimulation

Functional electrical stimulation offers an alternative for treating stress or urge incontinence when other treatments fail. A vaginal or rectal probe is inserted, usually twice daily for 15 to 30 minutes, to provide electrical stimulation to the pelvic floor muscles or to the nerves to these structures. Stimulation of the afferent fibers of the pudendal nerve can produce contractions of the pelvic floor and periurethral skeletal muscles, improving their tone and function in women with SUI.

Overflow Incontinence

Urinary retention and overflow incontinence may result from detrusor areflexia or a hypotonic bladder, as is seen with lower motor neuron disease, spinal cord injuries, or autonomic neuropathy (diabetes mellitus). These patients are best managed by intermittent self-catheterization.

Overflow incontinence may also occur when there is an outflow obstruction. Straining to void, poor stream, retention of urine, and incomplete emptying may indicate an obstructive disorder. Overdistention of the bladder because of unrecognized urinary retention may occur in the postoperative period. This is a temporary problem related to postoperative pain and may be managed by continuous bladder drainage for 24 to 48 hours.

Urinary Fistula

Fistulas are an uncommon cause of urinary incontinence in the United States. Obstetric fistulas, however, are a tremendous source of social and physical distress in developing countries. Obstetric injuries, once the leading cause of urinary fistulas, have almost disappeared in developed countries. They usually result from operative deliveries (e.g., forceps) rather than from neglected labor and pressure necrosis.

Pelvic surgery, irradiation, or both now account for 95% of the vesicovaginal fistulas in the United States. More than 50% occur after simple abdominal or vaginal hysterectomy. About 1% to 2% of radical hysterectomies are followed in 10 to 21 days by a urinary fistula, usually ureterovaginal. These fistulas are usually due to devascularization of the ureter rather than direct injury.

Urethrovaginal fistulas generally occur as complications of surgery for urethral diverticula, anterior vaginal wall prolapse, or SUI.

DIAGNOSIS OF A FISTULA

The usual history of painless and continuous vaginal leakage of urine soon after pelvic surgery is strongly suggestive of this problem. Instillation of methylene blue dye into the bladder will discolor a vaginal pack if a vesicovaginal fistula is present. Intravenous indigo carmine is excreted in the urine and will discolor a vaginal pack in the presence of a vesicovaginal or ureterovaginal fistula. In addition, cystourethroscopy should be performed to determine the site and number of fistulas. Most posthysterectomy vesicovaginal fistulas are located just anterior to the vaginal vault. An intravenous pyelogram or retrograde pyelogram should be undertaken to localize a ureterovaginal fistula.

FISTULA REPAIR

Most obstetric fistulas can be repaired immediately on detection. For postsurgical fistulas, it is usual to wait some weeks to allow the inflammation to settle. During this waiting period, UTI should be treated and estrogen therapy instituted in postmenopausal women. Steroids have been advocated to hasten resolution of inflammatory changes and allow early surgical intervention. Their use in this circumstance is controversial.

Vesicovaginal Fistula

The vaginal approach (Latzko’s operation) is the procedure of choice. A bulbocavernosus muscle flap or fat pad (Martius graft) may be interposed between the bladder and vagina to provide support, vascularity, and strength to the suture line, especially in patients who have had multiple previous attempted repairs and in those with a postradiation fistula. Large radiation-induced fistulas may necessitate urinary conduit for urinary diversion.

Ureterovaginal Fistula

Treatment of ureterovaginal fistula depends on its size and location. Small fistulas usually close spontaneously after placement of a ureteric stent (double J), provided the tissues have not been irradiated.

If the fistula is close to the ureterovesical junction, the ureter proximal to the fistula can be reimplanted into the bladder (ureteroneocystostomy). If the fistula is several centimeters from the bladder, a Boari flap may be useful, a segment of ileum may be interposed between the proximal ureter and the bladder, or rarely a transureteroureterostomy may be employed.

Although urinary incontinence is a common condition, the evaluation of the patient with urinary incontinence can be challenging.

Urethral Syndrome

The urethral syndrome occurs in a patient with various lower urinary tract symptoms, including acute or chronic pain (see Chapter 21), in the absence of obvious bladder or urethral abnormality, and with no evidence of UTI. Any combination of symptoms may be present, the most common being urinary frequency, urgency, dysuria, postvoid fullness, incontinence, and dyspareunia.

Diagnosis is based on a detailed history and physical examination, negative urine cultures, dynamic cystourethroscopy, and urodynamic studies.

TREATMENT

Application of vaginal estrogen cream is effective in patients with atrophic urethritis. Some patients may improve with use of tetracycline for 10 to 14 days. Internal urethrotomy and urethrolysis have also been employed with variable success.

Urinary Tract Infection

UTI is one of the most frequently diagnosed infectious diseases in medical practice. Every year in the United States, about 10% of women are diagnosed with cystitis, and this is associated with direct costs of more than $1.6 billion.

About 20% to 30% of women have at least one UTI during their lifetime, and 20% develop recurrent infections. Ninety-five percent of UTIs are symptomatic, and three fourths of these symptomatic episodes show positive urine cultures. Almost all asymptomatic patients have negative cultures.

TERMINOLOGY

The terminology surrounding UTIs is rather complex and requires some definition.

• Bacteriuria means the presence of bacteria in the urine.

• Significant bacteriuria is generally accepted as a bacterial colony count of 10⁵ or more per milliliter of urine in a properly collected clean-catch specimen in an asymptomatic patient. Lower colony counts may be accepted in symptomatic patients.

• Asymptomatic bacteriuria is significant bacteriuria with or without pyuria in a patient without symptoms of UTI.

• Pyelonephritis is a bacterial infection of the renal parenchyma and the renal pelvicaliceal system. Acute pyelonephritis is commonly associated with chills and fever, flank pain, costovertebral tenderness, urinary frequency, urgency, and dysuria. Chronic pyelonephritis denotes histologic changes of patchy interstitial nephritis, destruction of tubules, cellular infiltration, and inflammatory changes in the renal parenchyma.

• Chronic pyelonephritis is not synonymous with chronic UTI, which means only prolonged bacteriuria.

• Cystitis is an inflammation of the urinary bladder. Patients with cystitis usually have symptoms of lower urinary tract irritation, such as dysuria (burning on urination), urgency, frequency with small amounts of voided urine, nocturia, suprapubic discomfort, and at times, urinary incontinence and hematuria.

• Persistence of bacteriuria is the presence of microorganisms that were isolated at the start of treatment and continue to be isolated while the patient is receiving therapy. Persistence may be caused by several factors, including the presence of resistant organisms, inadequate drug therapy, and poor patient compliance.

• Superinfection is the appearance of a different organism while a patient is still receiving therapy. The new organism may be a different strain or a different serologic type.

• Relapse occurs with the recurrence of significant bacteriuria with the same species and serologic strain of organism. Relapse usually appears within 2 to 3 weeks of completion of therapy and most likely represents perineal colonization by the infecting organism.

• Reinfection is an infection occurring after cessation of therapy with a different strain of microorganism or a different serologic type of the original infecting strain. Typically, reinfection occurs 2 to 12 weeks after a previous episode of infection and indicates recurrent bladder bacteriuria.

• Recurrent UTI is diagnosed when two UTIs occur within 6 months or three or more occur during a single year. Women of blood group B or AB have an increased risk for recurrent UTIs.

INCIDENCE AND PREVALENCE

After the age of 1 year and throughout adulthood, females are affected more frequently than males (10:1 ratio). Asymptomatic bacteriuria increases from an incidence in preschool children of 1% to 5% to a peak of about 10% in postmenopausal women. Urologic abnormalities are found in up to 70% of children with a UTI. Box 23-2 lists the risk factors for UTIs in premenopausal and postmenopausal women.

BOX 23-2 Risk Factors for Urinary Tract Infection in Women

Data from American College of Obstetricians and Gynecologists (ACOG): Treatment of urinary tract infections in nonpregnant women. Practice Bulletin No. 91. Obstet Gynecol 111:785-794, 2008.

Postmenopausal

Vaginal atrophy

Incomplete bladder emptying

Poor perineal hygiene

Rectocele, cystocele, urethrocele, or uterovaginal prolapse

Lifetime history of urinary tract infections

Type 1 diabetes mellitus

PATHOGENESIS

Bacteria may gain entry to the urinary tract by three pathways: the ascending route, the descending or hematogenous route, and the lymphatic route.

Ascending Infection

The female is more susceptible because of the short length of the urethra, urethral contamination by rectal pathogens, introital and vestibular colonization by pathogenic bacteria, and decreased urethral resistance after menopause. Sexual intercourse is a major source of bacteriuria within 24 hours, and the relative risk is proportional to the frequency of intercourse in the past 7 days (e.g., honeymoon cystitis).

Hematogenous Infection

Urinary infection through the hematogenous route is very uncommon, but it is seen occasionally in elderly, debilitated, or immunosuppressed patients with overwhelming infections in whom kidney infection is only part of the multisystemic involvement. Renal tuberculosis is almost always acquired through the hematogenous route.

Lymphatic Infection

Experimental evidence suggests that bacterial infection spreads along lymphatic channels that connect the bowel and the urinary tract.

HOST DEFENSE MECHANISMS

Entrance of bacteria into the urinary tract does not necessarily result in infection. Natural barriers for invasion, such as the “washout” effect of normal periodic voiding, the antiseptic properties of the bladder tissues, and the high concentration of organic acids in normal urine, prevent bacterial invasion. Other factors, such as a pH of less than 5 and urea ammonium and organic acid content of the urine, all affect bacterial growth. If invasion takes place, the bacteria may remain in the bladder or may ascend to the kidney. Transient vesicoureteral reflux seen in association with severe lower UTIs may allow the infected urine to reach the kidneys.

PERPETUATING FACTORS

The following factors encourage and perpetuate UTIs:

1. Mechanical urinary obstruction. Ureteropelvic junction obstruction, ureteral stricture, urethral stenosis, and calculi are common to patients with recurrent or chronic UTIs.

2. Functional urinary obstruction abnormalities. Incomplete bladder emptying and vesicoureteric reflux encourage stasis of urine and bacterial growth. Pregnancy produces transient functional ureteral obstruction both mechanically and hormonally. Hypospadias may result in repeated infections after coitus (honeymoon cystitis).

3. Systemic factors. Diabetes mellitus, gout, sickle cell trait, cystic renal disease, and metabolic disorders, such as nephrocalcinosis, chronic potassium deficiency, and renal tubular defects, increase susceptibility to pyelonephritis.

CLINICAL CLASSIFICATION

From the point of view of pathogenesis and management, UTIs in nonpregnant females can be considered to be either uncomplicated or complicated. Uncomplicated cases account for 95% of UTIs in women and seldom produce renal damage. They are either the first episode of infection or an episode far removed in time from a previous urinary infection. Ninety percent of first infections are due to Escherichia coli. Seventy-five percent of these infective episodes do not recur for several years. Complicated UTIs occur in patients with neurologic or obstructive abnormalities or in those with underlying parenchymal disease.

INVESTIGATIONS

Urinalysis

Microscopic examination of an uncentrifuged, unstained specimen (a drop of urine on the slide covered with a coverslip) provides better than 90% accuracy in detecting significant bacteriuria when one or more bacteria are seen per high-power field. A positive Gram stain almost always correlates with a positive quantitative culture. A negative Gram stain virtually eliminates significant bacteriuria.

Pyuria is arbitrarily defined as the presence of five or more white blood cells per high-power field in the centrifuged specimen. The presence of white blood cells (pyuria) and red blood cells along with bacteriuria suggests infection. Pyuria without significant bacteria may indicate a nonbacterial inflammation or a urinary tract foreign body or tumor. It is a classic finding in urinary tuberculosis. Casts, when present, indicate renal parenchymal disease.

URINE CULTURE AND MICROBIOLOGY

A quantitative urine culture is the most important laboratory test in the diagnosis and management of complicated or uncomplicated UTIs. E. coli is the predominant organism in 80% to 85% of patients. The remaining, less common organisms are Klebsiella, Enterobacter, Proteus, Enterococcus, and Staphylococcus species and group D Streptococcus. Anaerobic fecal bacteria do not grow well in urine and are rarely seen in urinary infections. Yeast, such as Candida albicans (funguria), may be seen in patients with diabetes mellitus or in individuals receiving immunosuppressive therapy, especially in the presence of foreign bodies or indwelling catheters.

There are three techniques for urine collection: (1) the midstream clean-catch method, (2) urethral catheterization, and (3) suprapubic aspiration. The midstream clean-catch method has an 80% reliability, which increases to 95% if two consecutive specimens show a colony count of 100,000 or more of the same organism. In routine cases of uncomplicated infections, the presence of two or more species of organisms in the same specimen normally suggests contamination. Urethral catheterization provides an optimal urine specimen. A positive culture has 95% accuracy, and false-positive cultures are rare.

Suprapubic aspiration, although providing the most reliable specimen, is reserved for those in whom contamination is difficult to avoid (e.g., young children and elderly people).

RADIOLOGIC STUDIES

Imaging can be critical in the evaluation of patients whose recurrences are due to bacterial persistence (e.g., stones or infected congenital anomalies), but it is of almost no value in the 99% of patients with reinfections. Intravenous pyelography and computed tomographic urography are the main studies employed. Cystography and voiding urethrocystography may help to detect ureteric reflux, diverticula, and fistulous tracts in patients with persistent bacteriuria.

Unless physical examination and urinalysis (bacteriuria) clearly indicate urinary infection, it is advisable to withhold definite antimicrobial therapy until culture and sensitivity reports are available. As a general rule, bacteriuria should be treated, and not pyuria. General measures in the management of UTIs involve the following:

1. Rest and hydration. Hydration promotes dilution of bacterial counts, frequent bladder emptying, and reduction of medullary osmolality, which assists phagocytosis.

2. Acidification of the urine. Ascorbic acid (500 mg twice daily), ammonium chloride (12 g/day in divided doses), or apricot, plum, prune, or cranberry juices have been employed to increase the antibacterial activity of urine and to inhibit bacterial multiplication. Grapefruit juice and carbonated drinks, particularly those containing citrates, turn the urine alkaline and should be avoided.

3. Urinary analgesics. Agents such as phenazopyridine hydrochloride (Pyridium), 100 mg twice daily for 2 to 3 days, are often helpful in relieving dysuria.

Basic Principles of Antimicrobial Therapy

The drug selected should be readily available, of low cost, rapidly absorbed from the upper gastrointestinal tract with minimal irritation, and selectively excreted in the urinary tract. A high serum level of antibiotics is undesirable in the treatment of acute cystitis because it tends to alter normal bacterial flora. Nitrofurantoin (Macrodantin) produces low serum levels with a half-life of only 19 minutes, thereby minimizing the chances of alteration of intestinal and vaginal bacterial flora. Treatment with nitrofurantoin is effective against all uropathogens except Proteus species.

Single-dose therapy is an effective alternative to a 3- to 7-day course, especially in patients with acute uncomplicated cystitis. Single-dose therapy fails, however, in more than 50% of patients with an upper tract infection. Table 23-2 lists some common antibiotic regimens for uncomplicated cystitis along with their relative costs.

TABLE 23-2 COMMON TREATMENT REGIMENS FOR UNCOMPLICATED BACTERIAL CYSTITIS

Antimicrobial Agent	Dose	Relative Cost^∗
SINGLE-DOSE TREATMENTS
Ampicillin^†	2 g	1
Amoxicillin^†	3 g	1
Nitrofurantoin	200 mg	1
Fosfomycin tromethamine	3 g (powder)	3
THREE-DAY COURSE
Ampicillin^†	250 mg 4 times daily	1
Amoxicillin^†	500 mg 3 times daily	1
Trimethoprim	100 mg twice daily	2
Ciprofloxacin	250 mg twice daily	3
SEVEN– TO 10-DAY COURSE
Nitrofurantoin	100 mg at bedtime	3
Nitrofurantoin macrocrystals	50-100 mg 4 times daily	4