CHAPTER 23: Urinary Incontinence

Urinary incontinence is defined as involuntary leakage of urine. This is in contrast to urine that leaks from extraurethral sources, such as with fistulas or congenital malformations of the lower urinary tract. Although incontinence is categorized into several forms, this chapter focuses on the evaluation and management of stress and urgency urinary incontinence. Stress urinary incontinence (SUI) is the involuntary leakage of urine with increases in intraabdominal pressure. Urgency urinary incontinence (previously “urge” urinary incontinence) is the involuntary leakage accompanied or immediately preceded by a perceived strong imminent need to void. A related condition, overactive bladder, describes urinary urgency with or without incontinence and usually with increased daytime urinary frequency and nocturia (Abrams, 2009).

According to International Continence Society guidelines, urinary incontinence is a symptom, a sign, and a condition (Abrams, 2002). For example, with SUI, a patient may complain of involuntary urine leakage with exercise or laughing. Concurrent with these symptoms, involuntary leakage from the urethra synchronous with cough or Valsalva may be observed during examination by a provider. And as a condition, SUI is objectively demonstrated during urodynamic testing if involuntary leakage of urine is seen with increased abdominal pressure and absence of detrusor muscle contraction. Under these circumstances, when the symptom or sign of SUI is confirmed with objective testing, the term urodynamic stress incontinence is preferred.

With urgency urinary incontinence, women have difficulty postponing urination urges and generally must promptly empty their bladder on cue and without delay. Common triggers are hand washing, running water, or exposure to cold. Urgency urinary incontinence is sometimes objectively demonstrated during urodynamic testing to correspond temporally with spontaneous detrusor muscle contractions—a condition termed detrusor overactivity. When both stress and urgency symptoms are present, it is called mixed urinary incontinence.

In Western societies, epidemiologic studies indicate a prevalence of urinary incontinence of 25 to 51 percent and even higher among nursing home patients (Buckley, 2010; Markland, 2011). This wide range is attributed to variations in research methodologies, population characteristics, and definitions of incontinence. As part of the 2005 to 2006 National Health and Nutrition Examination Survey (NHANES), a cross-sectional group of 1961 nonpregnant, noninstitutionalized women in the United States were questioned regarding pelvic floor disorders. Urinary incontinence characterized by participants as moderate to severe leakage was identified in 15.7 percent (Nygaard, 2008). However, current available data are limited by the fact that most women do not seek medical attention for this condition (Hunskaar, 2000). It is estimated that only one in four women will seek medical advice for incontinence, due to embarrassment, limited health care access, or poor screening by health care providers (Hagstad, 1985).

Among ambulatory women with urinary incontinence, the most common type is SUI, which represents 29 to 75 percent of cases. Urgency urinary incontinence accounts for up to 33 percent of incontinence cases, whereas the remainder is attributable to mixed forms (Hunskaar, 2000). In one review, 15 percent of 64,528 women met criteria for overactive bladder with or without incontinence, and 11 percent had urgency urinary incontinence (Hartmann, 2009).

Urinary incontinence can significantly impair quality of life and lead to disrupted social relationships, embarrassment and frustration, hospitalizations due to skin breakdown and urinary tract infection (UTI), and nursing home admission. An incontinent elderly woman is 2.5 times more likely to be admitted to a nursing home than a continent one (Langa, 2002). Moreover, population projections from the U.S. Census Bureau forecast that the number of American women with urinary incontinence will increase 55 percent from 18.3 million to 28.4 million between 2010 and 2050 (Wu, 2009).

Age

The prevalence of incontinence appears to increase gradually during young adult life. For example, data from the 2005 to 2006 NHANES demonstrate a steady increase in incontinence prevalence with age: 7 percent in those aged 20 to 40 years, 17 percent for ages 40 to 60, 23 percent for ages 60 to 80, and 32 percent for those older than 80 (Nygaard, 2008).

Incontinence should not be viewed as a normal consequence of aging. However, several physiologic age-related changes in the lower urinary tract may predispose to incontinence, overactive bladder, or other voiding difficulties. First, the prevalence of involuntary detrusor contractions increases with age, and detrusor overactivity is found in 21 percent of healthy, continent community-dwelling elderly (Resnick, 1995). Both total bladder capacity and the ability to postpone voiding decreases, and these declines may lead to urinary frequency. In addition, urinary flow rates are reduced in older women and are likely due to an age-associated decrease in detrusor contractility (Resnick, 1984). In women, postmenopausal decreases in estrogen levels result in atrophy of the urethral mucosal seal, loss of compliance, and bladder irritation, which may predispose to both stress and urgency urinary incontinence. Finally, renal filtration rate and diurnal levels of antidiuretic hormone and atrial natriuretic factor change with age. These alterations shift the diurnal-predominant pattern of fluid excretion toward one with greater urine excretion later in the day (Kirkland, 1983).

Other Factors

Race may influence incontinence rates, and white women are believed to have higher SUI rates than women of other races. In contrast, urgency urinary incontinence is believed to be more prevalent among African-American women. Most reports are not population-based and thus are not the best estimate of true racial differences. However, data from the Nurses’ Health Study cohorts, which included more than 76,000 women, did support these racial differences (Townsend, 2010). It is not yet clear whether these differences are biologic, related to health-care access, or affected by cultural expectations and symptom tolerance thresholds.

Body mass index (BMI) is a significant and independent risk factor for urinary incontinence of all types (Table 23-1). Specifically, the prevalence of both urgency urinary and stress incontinence increases proportionally with BMI (Hannestad, 2003). Theoretically, the increase in intraabdominal pressure that coincides with an increased BMI results in a higher intravesical pressure. This higher pressure overcomes urethral closing pressure and leads to incontinence (Bai, 2002). Encouragingly, weight loss for many can be an effective treatment and is considered a first-line option to reduce urinary incontinence rates (Dumoulin, 2014b). The prevalence of urinary incontinence significantly declines following weight loss achieved by behavior modification or with bariatric surgery (Burgio, 2007; Deitel, 1988; Subak, 2009). Even losses of 5 to 10 percent of body weight are sufficient for significant improvement in urinary incontinence (Wing, 2010).

Menopause may have a relationship with incontinence, but studies have inconsistently demonstrated an increase in urinary dysfunction rates (Bump, 1998). In those with symptoms, separating aging changes from hypoestrogenism effects is difficult. First, high-affinity estrogen receptors are found in the urethra, pubococcygeal muscle, and bladder trigone but are infrequently found elsewhere in the bladder (Iosif, 1981). Hypoestrogenic-related collagen changes and reductions in urethral vascularity and skeletal muscle volume are factors. They are thought collectively to contribute to impaired urethral function via a decreased resting urethral pressure (Carlile, 1988). Moreover, estrogen deficiency with resulting urogenital atrophy is believed to be responsible in part for urinary sensory symptoms following menopause (Raz, 1993). Despite this current evidence, it is less clear whether estrogen therapy is useful in the treatment or prevention of incontinence. Namely, systemic estrogen replacement, compared with placebo, appears to worsen incontinence, whereas topical vaginal estrogen application may improve incontinence (Cody, 2012; Fantl, 1994, 1996; Rahn, 2014, 2015).

Childbirth and pregnancy also play a role, and urinary incontinence prevalence is higher in parous women compared with nulliparas. The effects of childbirth may result from direct injury to pelvic muscles and connective tissue attachments. In addition, nerve damage from trauma or stretch injury can lead to pelvic muscle dysfunction. Specifically, rates of prolonged pudendal nerve latency after delivery are higher in women with incontinence compared with asymptomatic puerperal women (Snooks, 1986).

Of potential obstetric factors, one large study identified that fetal birthweight >4000 g increased the risk of all urinary incontinence types (Rortveit, 2003b). These authors also noted that cesarean delivery may offer a short-term protective effect from urinary incontinence. The adjusted odds ratio for any incontinence associated with vaginal delivery compared with that with cesarean delivery was 1.7 (Rortveit, 2003a). However, the protective effect of cesarean delivery on incontinence may dissipate after additional deliveries, decreases with age, and is not present in older women (Nygaard, 2006).

Family history may alter incontinence risks, and the urinary incontinence rates may be increased in the daughters and sisters of incontinent women. In one large survey, daughters of incontinent women had an increased relative risk of 1.3 and an absolute risk of 23 percent of having urinary incontinence. Younger sisters of incontinent women also had a greater likelihood of having any urinary incontinence (Hannestad, 2004).

Chronic obstructive pulmonary disease in women older than 60 years significantly increases urinary incontinence risks (Brown, 1996; Diokno, 1990). Similarly, cigarette smoking is identified as an independent risk factor for urinary incontinence. Both current and former smokers have a two- to threefold risk of incontinence compared with nonsmokers (Brown, 1996; Bump, 1992; Diokno, 1990). In one study, investigators found an association between current and former smoking and incontinence, but only for those who smoked more than 20 cigarettes daily. Severe incontinence was weakly associated with smoking regardless of cigarette number (Hannestad, 2003). Theoretically, persistently increased intraabdominal pressures are generated from a smoker’s chronic cough, and collagen synthesis is diminished by smoking’s antiestrogenic effects.

Hysterectomy does not appear to increase urinary incontinence rates. Studies that include pre- and postoperative urodynamic testing reveal clinically insignificant changes in bladder function. Moreover, evidence does not support avoidance of clinically indicated hysterectomy or the selection of supracervical hysterectomy as measures to prevent urinary incontinence (Vervest, 1989; Wake, 1980).

Continence

The bladder has the capacity to accommodate large increases in volume with minimal or no increases in intravesical pressure. The ability to store urine coupled with convenient and socially acceptable voluntary emptying is continence. Continence requires the complex coordination of multiple components that include: muscle contraction and relaxation, appropriate connective tissue support, and integrated innervation and communication between these structures. Simplistically, during filling, urethral contraction is coordinated with bladder relaxation and urine is stored. During voiding, the urethra relaxes and the bladder contracts. These mechanisms can be challenged by uninhibited detrusor contractions, marked increases in intraabdominal pressure, and degradation or dysfunction of the various anatomic components of the continence mechanism.

Bladder Filling

Bladder Anatomy

The bladder wall is multilayered and contains mucosal, submucosal, muscular, and adventitial layers (Fig. 23-1). The bladder mucosa is composed of a transitional cell epithelium, supported by a lamina propria. With small bladder volumes, the mucosa appears as convoluted folds. However, with bladder filling, it is stretched and thinned. The bladder epithelium, termed uroepithelium, is made up of distinct cell layers. The most superficial is the umbrella cell layer, and its impermeability is thought to provide the primary urine-plasma barrier. Covering the uroepithelium is a glycosaminoglycan (GAG) layer. This GAG layer may prohibit bacterial adherence and prevents urothelial damage by acting as a protective barrier. Specifically, theories suggest that this carbohydrate polymer layer may be defective in patients with interstitial cystitis (Chap. 11).

The muscular layer, termed the detrusor muscle, is composed of three smooth-muscle layers arranged in a plexiform fashion. This unique arrangement allows for rapid multidimensional expansion during bladder filling and is a key component to the bladder’s ability to accommodate large volumes.

Innervation

Normal function of the lower urinary tract requires integration of peripheral and central nervous systems. The peripheral nervous system contains somatic and autonomic divisions (Fig. 23-2). Of these, the somatic component innervates striated muscle, whereas the autonomic division innervates smooth muscle.

The autonomic nervous system controls involuntary action and is categorized into sympathetic and parasympathetic divisions. The sympathetic system mediates its end-organ effects through epinephrine or norepinephrine acting on α- or β-adrenergic receptors (Fig. 23-3). The parasympathetic division acts through acetylcholine binding to muscarinic or nicotinic receptors. In the pelvis, autonomic fibers that supply the pelvic viscera course in the superior and inferior hypogastric plexi (Fig. 23-4).

The somatic nervous system controls voluntary movement, and the portion of this system that is most relevant to lower urinary tract function originates from Onuf somatic nucleus. This nucleus is located in the ventral horn gray matter of spinal levels S2–S4 and contains the neurons that innervate the striated urogenital sphincter complex, described next. Nerves involved with that connection include branches of the pudendal and pelvic nerves.

Urogenital Sphincter

As the bladder fills, synchronized contraction of the urogenital sphincter is integral to continence. Composed of striated muscle, this sphincter complex includes: (1) the sphincter urethrae, (2) the urethrovaginal sphincter, and (3) the compressor urethrae. The sphincter urethrae wraps circumferentially around the urethra. In comparison, the urethrovaginal sphincter and the compressor urethrae arch ventrally over the urethra and insert into the fibromuscular tissue of the anterior vaginal wall (Fig. 23-5).

These three muscles function as a single unit and contract to close the urethra. Contraction of these muscles circumferentially constricts the cephalad two thirds of the urethra and laterally compresses the distal one third. The sphincter urethrae is predominantly composed of slow-twitch fibers and remains tonically contracted, contributing substantially to continence at rest. In contrast, the urethrovaginal sphincter and the compressor urethrae are comprised of fast-twitch muscle fibers, which allow brisk contraction and urethra lumen closure when continence is challenged by sudden increases in intraabdominal pressure.

Innervation Important to Storage

The urogenital sphincter receives somatic motor innervation through the pudendal and pelvic nerves (Fig. 23-6). Thus, pudendal neuropathy, which may follow obstetric injury, can affect normal sphincter functioning. Additionally, prior pelvic surgery or pelvic radiation therapy may damage nerves, vasculature, and soft tissue. Such injury can lead to ineffective urogenital sphincter action and contribute to incontinence.

Sympathetic fibers are carried through the superior hypogastric nerve plexus and communicate with α- and β-adrenergic receptors within the bladder and urethra. β-Adrenergic receptor stimulation in the bladder dome results in smooth-muscle relaxation and assists with urine storage (Fig. 23-7). β-Agonist medication may improve overactive bladder symptoms through this mechanism of smooth muscle relaxation. In contrast, α-adrenergic receptors predominate in the bladder base and urethra. These receptors are stimulated by norepinephrine, which initiates a cascade of events that preferentially leads to urethral contraction and aids urine storage and continence. These effects of α-stimulation underlie the treatment of SUI with imipramine, a tricyclic antidepressant with adrenergic agonist properties.

Urethral Coaptation

One key to maintaining continence is adequate urethral mucosal coaptation. The uroepithelium is supported by a connective tissue layer, which is thrown into deep folds, also known as plications. A rich capillary network runs within its subepithelial layer. This vascular network aids in urethral mucosal approximation, also termed coaptation, by acting like an “inflatable cushion” (Fig. 23-8). In women who are hypoestrogenic, this submucosal vasculature plexus is less prominent. In part, hormone replacement targets this diminished vascularity and and in theory, enhances coaptation to improve continence.

Bladder Emptying

Innervation Related to Voiding

When an appropriate time for bladder emptying arises, sympathetic stimulation is reduced and parasympathetic stimulation is triggered. Specifically, neural impulses carried in the pelvic nerves stimulate acetylcholine release and lead to detrusor muscle contraction (Fig. 23-9). Concurrent with detrusor stimulation, acetylcholine also stimulates muscarinic receptors in the urethra and leads to outlet relaxation for voiding.

Within the parasympathetic division, acetylcholine receptors are broadly defined as muscarinic and nicotinic. The bladder is densely supplied with muscarinic receptors, which when stimulated lead to detrusor contraction. Of the muscarinic receptors, five glycoproteins designated M₁–M₅ have been identified. M₂ and M₃ receptor subtypes are predominantly responsible for detrusor smooth muscle contraction. Thus, treatment with muscarinic antagonist medication blunts detrusor contraction to improve continence. Continence drugs that target only the M₃ receptor maximize drug efficacy yet minimize activation of other muscarinic receptors and drug side effects.

Muscular Activity with Voiding

Smooth muscle cells within the detrusor fuse with one another so that a network of low-resistance electrical pathways extends from one muscle cell to the next. Thus, action potentials can spread quickly throughout the detrusor muscle to cause rapid contraction of the entire bladder. In addition, the plexiform arrangement of bladder detrusor fibers allows multidirectional contraction and is ideally suited for rapid concentric contraction during bladder emptying.

During voiding, all components of the striated urogenital sphincter relax. Importantly, bladder contraction and sphincter relaxation must be coordinated for effective voiding. Occasionally, the urethral sphincter fails to relax during contraction of the detrusor and retention ensues. Classically, this is a possible urinary complication of spinal cord injury termed detrusor sphincter dyssynergia and may lead to elevated bladder pressures and vesicoureteral reflux. Women with this condition are sometimes treated with α-blocking agents to help with sphincter relaxation and to lower bladder pressures during contraction, but these may aggravate hypotension. In women without known neurologic pathology but still with inappropriately contracted pelvic floor musculature, treatment with muscle relaxants may be appropriate. These drugs purportedly relax the urethral sphincter and levator ani muscles to improve coordinated voiding.

Continence Theories

Anatomic Stress Incontinence

Theories on continence vary in their supportive evidence but can simplistically be distilled into those that involve anatomic stress incontinence or those that describe decreased urethral integrity (sphincteric deficiency). These theories are not mutually exclusive and in many women, both may be contributory.

First, urethral and bladder neck support is integral to continence. This anatomic support derives from: (1) ligaments along the urethra’s lateral aspects, termed the pubourethral ligaments; (2) the vagina and its lateral fascial condensation; (3) the arcus tendineus fascia pelvis; and (4) levator ani muscles. A full anatomic description of these ligaments and muscles is found in Chapter 38.

In an ideally supported urogenital tract, increases in intraabdominal pressure are equally transmitted to the bladder, bladder base, and urethra. In women who are continent, increases in downward-directed pressure from cough, laugh, sneeze, and Valsalva maneuver are countered by supportive tissue tone provided by the levator ani muscles and vaginal connective tissue (Fig. 23-10). With loss of support, the ability of the urethra and bladder neck to close against a firm supportive “backboard” is diminished. This results in reduced urethral closing pressures, an inability to resist increases in bladder pressure, and in turn, incontinence. This mechanistic theory is the basis for surgical reestablishment of this support. Traditional procedures such as Burch and Marshall-Marchetti-Kranz (MMK) colposuspensions attempt to return this anatomic support to the urethrovesical junction and proximal urethra.

Sphincteric Deficiency

Another way to conceptualize SUI is to consider the urethra as providing continence through the combination of: urethral mucosal coaptation, the underlying urethral vascular plexus, the combined viscous and elastic properties of the urethral epithelium, and contraction of appropriate surrounding musculature. Taken together, these components contribute to urethral integrity. Defects in any or a combination of these components may lead to urine leakage and have traditionally been termed intrinsic sphincteric defect (ISD). For example, prior surgery in the retropubic space may cause denervation and scarring of the urethra and its supporting tissue. These effects subsequently prevent urethral closure and lead to incontinence. Specific causes are varied and include prior pelvic reconstructive surgeries, prior pelvic radiation therapy, diabetic neuropathy, neuronal degenerative diseases, and hypoestrogenism. Namely, in women with atrophic lower genital tracts, vascular changes within the plexus surrounding the urethra lead to poor coaptation and greater incontinence risks.

As noted earlier, nerve dysfunction following birth trauma may lead to defective urethral sphincter function. In addition, childbirth also often injures urethral fascial support. This clinical example highlights the intimate relationship between urethral support and integrity.

Treatments to restore urethral integrity include transurethral injection of bulking agents, surgical sling procedures, and pelvic floor muscle strengthening, which are all described in later sections. In brief, bulking agents are placed at the urethrovesical junction to elevate the epithelium and promote coaptation. Alternatively, sling procedures restore periurethral support anatomy or create partial urethral obstruction to enhance urethral integrity. Last, because the urethra exits through urogenital hiatus, levator ani muscle conditioning with Kegel exercises can bolster urethral integrity. These muscles can be contracted around the urethra when continence is challenged during sudden increases in intraabdominal pressures.

A consideration for surgical management of patients with ISD, particularly those younger than 50 years, is that a retropubic colposuspension procedure merely elevates and stabilizes the urethra and does not promote coaptation. This may be less likely to achieve satisfactory continence than a procedure directed at both anatomic stress incontinence and deficient urethral sphincter function and support (Sand, 1987). That said, a small trial randomizing incontinent women with ISD to Burch or sling procedures did not show differences in postoperative voiding function or in SUI cure rates (Culligan, 2003).

History

Symptom Clustering

Assessment of incontinence begins with a patient describing her urinary symptoms. These complaints may be collected through direct conversation but can be augmented with patient questionnaires. Two common forms are the Pelvic Floor Distress Inventory and the Pelvic Floor Impact Questionnaire. Both are available in long and short forms and evaluate urinary, bowel, and prolapse symptoms (Barber, 2001). Such lengthy research questionnaires may be impractical for general clinical practice. Instead, shorter validated questionnaires may easily be incorporated into the clinic setting. As shown in Table 23-2, the 3IQ has only three questions that screen for incontinence and then helps clarify the incontinence type (Brown, 2006).

During inquiry, the number of voids and pads used per day, type of pad, frequency of pad changing, and the degree of pad saturation are important. Although these specifics alone may not establish the exact type of incontinence, they do provide information regarding symptom severity and its effects on patient activities. If a woman’s symptoms do not diminish her quality of life, then simple observation is reasonable. Conversely, those with bothersome symptoms warrant further evaluation.

Specific to incontinence, information that describes the circumstances in which urine leaks and specific maneuvers that incite or provoke leakage are sought. With SUI, triggers may include increases in intraabdominal pressure such as coughing, sneezing, Valsalva maneuver, or deep penetration during intercourse. Alternatively, women with urgency urinary incontinence may describe urine loss after urge sensations that typically cannot be suppressed. Overflow incontinence was a term used in the past to refer to women who were unable to empty their bladder well but who also had involuntary, continuous urinary leakage or dribbling and often episodes of incontinence associated with urgency. Currently, however, this is considered by many to reflect another presentation of urgency urinary incontinence.

During questioning, symptoms typically cluster into those most frequently seen with SUI or with urgency urinary incontinence (see Table 23-2). Alternatively, a significant overlap of complaints may reflect coexistent SUI and urgency urinary incontinence, that is, mixed urinary incontinence. For these reasons, pattern identification is helpful as it may direct diagnostic testing and guide initial empiric therapy.

Voiding Diary

Typically, patients may not have an entirely accurate recollection of their own voiding habits. Accordingly, to obtain a thorough record, a woman ideally completes a urinary diary (Fig. 23-11). With this, the volumes and type of each oral fluid intake, volumes of urine with each void, episodes of urinary leakage, and triggers of incontinence episodes are recorded for 3 to 7 days. During each 24-hour period, women also record times of sleep and awakening to document voluntary nocturnal voiding patterns or enuresis. Three days usually suffices to determine the general trend of incontinence.

The information gained from a voiding/urinary diary is a valuable diagnostic and sometimes therapeutic tool. The first morning void is usually the largest of the day and is a good estimate of bladder capacity. Patients often can identify patterns in intake and voiding and modify behavior. For example, a patient may recognize increased urinary frequency or urgency urinary incontinence episodes after caffeine intake. Moreover, this diary information can serve as a baseline against which treatment effectiveness can be assessed.

Urinary Symptoms

Specific patient symptoms may help differentiate incontinence types. For example, most women void eight or fewer times per day. Without a history that reflects increased fluid intake, increased voiding may indicate overactive bladder, UTI, calculi, or urethral pathology and often prompts additional evaluation. In addition, urinary frequency is commonly associated with interstitial cystitis (IC). In women with IC, the numbers of voids may commonly exceed 20 per day. Nocturia may be noted in women with urgency urinary incontinence or in those with systemic fluid management disorders such as congestive heart failure. In the latter case, treatment of the underlying condition frequently leads to symptom improvement or cure of nighttime frequency.

Urinary retention may provide clues. Often incomplete emptying can result in incontinence associated with either stress or urgency. Urethral obstruction, often manifested as an inability to void or an impeded urinary stream, is uncommon in women. Its description prompts careful evaluation for pelvic organ prolapse and underscores the importance of asking about prior pelvic/vaginal surgery or trauma that could scar or obstruct the urethra.

Of other urinary symptoms, the volume of urine lost with each episode may aid diagnosis. Large volumes are typically lost following a spontaneous detrusor contraction associated with urgency urinary incontinence and may often involve loss of the entire bladder volume. In contrast, woman with SUI usually describe smaller volumes lost. Moreover, these women often are able to contract the levator ani muscles to temporarily stop their urine stream. Another symptom, postvoid dribbling, is classically associated with urethral diverticulum, which may often be mistaken for urinary incontinence (Chap. 26). Hematuria, although a common sign of UTI, may also indicate underlying malignancy and can cause irritative voiding symptoms.

Symptom onset may also prove informative. For example, problems beginning at menopause may suggest hypoestrogenism as an etiology. These patients may benefit from topical vaginal estrogen. In contrast, symptoms after hysterectomy or childbirth may reflect changes in tissue support or innervation.

Past Medical History

Obstetric trauma may be associated with damage to pelvic floor support, which may lead to SUI. Accordingly, information is sought regarding a prolonged labor, operative vaginal delivery, macrosomia, or postpartum catheterization for urinary retention. As alluded to earlier, urinary incontinence can be linked with several medical conditions or their treatments, which could be modified to improve incontinence. To help remember these potential contributors, a useful mnemonic is “DIAPPERS”: dementia/delirium, infection, atrophic vaginitis, psychological, pharmacologic, endocrine, restricted mobility, and stool impaction (Swift, 2008).

First, continence requires the cognitive ability to recognize and react appropriately to the sensation of a full bladder, motivation to maintain dryness, sufficient mobility and manual dexterity, and ready access to a toilet. Patients with dementia or significant psychological impairments often do not have the necessary cognitive ability for continence. Women with severe physical handicaps or restricted mobility may simply not have time to reach the toilet, especially in the setting of urinary urgency/overactive bladder. Thus, this so-called functional incontinence occurs in situations in which a woman cannot reach a toilet in time because of physical, psychological, or mentation limitations. Often, this group would be continent if these issues were absent. Simple interventions such as a bedside commode may be helpful in such cases.

Urinary tract infections cause bladder mucosal inflammation. This inflammation is thought to increase sensory afferent activity, which contributes to an overactive bladder. Similarly, estrogen deficiency can lead to atrophic epithelium of the vagina and urethra. These are associated with increased local irritation and greater risks of UTI and overactive bladder.

A detailed medication inventory is collected. Pertinent drugs include estrogen, α-adrenergic agonists, and diuretics, to name a few (Table 23-3).

Of endocrinopathies, diabetes mellitus can promote osmotic diuresis and polyuria if glucose control is poor. Polydipsia from diabetes insipidus or excessive caffeine or alcohol intake can also lead to polyuria or urinary frequency. Similarly, other disorders of impaired arginine vasopressin secretion or action may cause polyuria and nocturia (Ouslander, 2004). Conditions such as congestive heart failure, hypothyroidism, venous insufficiency, and the effects of certain medications all contribute to peripheral edema, leading to urinary frequency and nocturia when a patient is supine.

Last, stool impaction resulting from poor bowel habits and constipation can contribute to overactive bladder symptoms. This is perhaps from local irritation or direct compression against the bladder wall.

Physical Examination

General Inspection and Neurologic Evaluation

Initially, the perineum is inspected for evidence of atrophy, which may be noted throughout the lower genital tract. In addition, a suburethral cystic mass or dilation with transurethral expression of fluid during compression suggests a urethral diverticulum (Fig. 26-6).

Examination of an incontinent woman also includes a detailed neurologic evaluation of the perineum. Because neurologic responses may be altered in an anxious patient who is in a vulnerable setting, signs elicited during evaluation may not signify true pathology and are interpreted with caution. Neurologic testing begins with an attempt to elicit a bulbocavernosus reflex. During this test, one labium majus is stroked with a cotton swab. Normally, both labia generally contract at the same time. The afferent limb of this reflex is the clitoral branch of the pudendal nerve, whereas its efferent limb is conducted through the inferior hemorrhoidal branch of the pudendal nerve. This reflex is integrated at the S2-S4 spinal cord level (Wester, 2003). Thus, reflex absence may reflect central or peripheral neurologic deficits. Second, a normal circumferential anal sphincter contraction, colloquially called an “anal wink,” should follow cotton swab brushing of the perianal skin. External urethral sphincter activity requires at least some degree of intact S2-S4 innervation, and this anocutaneous reflex is mediated by the same spinal neurologic level. Thus, an absent wink may indicate deficits in this neurologic distribution.

Pelvic Support Assessment

Poor urethral support commonly accompanies pelvic organ prolapse. For example, women with significant prolapse are often unable to completely empty their bladder due to urethral kinking and obstruction. These women frequently must digitally elevate or reduce their prolapse to allow emptying. Thus, an external evaluation for prolapse, as described in Chapter 24, is indicated for all women with urinary incontinence. Following this evaluation for vaginal compartment defects, pelvic muscle strength is also assessed. Women with mild to moderate urinary incontinence often respond well to pelvic floor therapy, and under these circumstances, a trial of this therapy is warranted and often curative.

Lack of distal anterior vaginal wall support and resultant urethral hypermobility during increased intraabdominal pressure may help influence choice of surgical intervention in the patient reporting SUI. These patients commonly demonstrate relaxation and descent of the distal anterior vagina with resultant urethral hypermobility during increases in intraabdominal pressures. In patients with descent to the level of the hymen or beyond with Valsalva, urethral hypermobility is universal (Noblett, 2005). In those with SUI and lesser anterior vaginal wall prolapse, a Q-tip test may provide a more objective assessment of urethral hypermobility. However, it has become a less essential part of pelvic floor assessment due to its poor predictive value for antiincontinence surgery success.

When performed, the soft end of a cotton swab is placed into the urethra to the urethrovesical junction. Failure to insert the swab to this depth can lead to assessment errors. An application of intraurethral analgesia may prove helpful, and 1-percent lidocaine jelly is placed on the cotton swab prior to insertion. Following placement, a Valsalva maneuver is prompted, and the swab-excursion angle at rest and with Valsalva maneuver is measured. An angle change or a resting angle >30 degrees to the horizon suggests urethral hypermobility.

Bimanual and Rectovaginal Examination

In general, these portions of the pelvic examination provide fewer diagnostic clues to underlying incontinence causes. However, bimanual examination may reveal a pelvic mass or a uterus enlarged by leiomyomas or adenomyosis. These can create incontinence through increased external pressure transmitted to the bladder. In addition, stool impaction is easily identified with rectal examination.

Diagnostic Testing

Urinalysis and Culture

In all women with urinary incontinence, infection or urinary tract pathology must be excluded. Urinalysis and urine culture are sent at an initial visit, and infection is treated as described in Table 3-17. Persistent irritative voiding symptoms, despite appropriate antibiotic treatment, warrant additional evaluation for other conditions such as interstitial cystitis.

Postvoid Residual Volume

This volume is routinely measured during incontinence evaluation. After a woman voids, the postvoid residual (PVR) volume may be measured by transurethral catheterization or with a handheld sonographic bladder scanner. The latter is a portable 3-dimensional ultrasound device that scans the bladder and provides numeric results (Fig. 23-12). In general, they are quick, easy to use, and more comfortable for the patient. However, if using a handheld scanner, care must be taken in women with a leiomyomatous uterus or other pelvic mass as these may lead to a false report of a large PVR. In these instances, or if a scanner is not available, transurethral catheterization may be used to confirm residual bladder volume.

A large PVR volume may often reflect one of several problems including recurrent infection, urethral obstruction from a pelvic mass, or neurologic deficits. In contrast, a normally small PVR volume is often found in those with SUI. After continence surgery, PVR measurement is a helpful indicator of a patient’s ability to completely empty her bladder. Postoperative PVR determination and voiding trials are described in Chapter 42.

Urodynamic Studies

Surgical correction of incontinence is invasive and not without risk. However, the “bladder is an unreliable witness,” and historical information may not always accurately indicate the true underlying type of incontinence (Blaivas, 1996). Thus, if initial conservative management is unsuccessful or surgical treatment is anticipated, then objective assessment is pursued. In addition, if symptoms and physical findings are incongruous, then objective urodynamic studies (UDS), using simple or multichannel cystometrics, may also be indicated. For example, in a woman with mixed urinary incontinence, who has symptoms of both stress and urgency urinary incontinence, UDS may reveal that only the urgency component is responsible for her incontinence. These cases are treated with behavioral, physical, and/or pharmacologic therapy initially. Thus, if identified by UDS, these individuals can avoid unnecessary surgery. Additionally, surgical therapy may be modified if UDS reveals parameters consistent with ISD.

Despite these indications, UDS remains controversial. Leakage noted during testing is not always clinically relevant. In addition, testing may be uninformative if the original offending maneuver or situation that led to incontinence cannot be reproduced during testing. Moreover, objective confirmation of the diagnosis is not always necessary, since empiric nonsurgical therapy in women with urgency-predominant symptoms is reasonable. Also, for women with stress-predominant urinary incontinence undergoing surgical treatment, outcomes were no different 1 year later in those screened by UDS compared with those evaluated by a simple office evaluation. The office testing included demonstrable leakage during examination, urine analysis without infection, and PVR <150 mL (Nager, 2012).

Simple Cystometrics

Objective measurement of bladder function, that is, UDS, combines a battery of tests termed cystometrics, which may be simple or multichannel. Simple cystometrics allows determination of SUI and detrusor overactivity and measurement of first sensation, desire to void, and bladder capacity. This procedure is easily performed with room-temperature sterile normal saline, a 60-mL catheter-tipped syringe, and a urinary catheter, either Foley or Robnell. The urethra is sterilely prepared, the catheter is inserted, and the bladder is drained. A 60-mL syringe with its plunger removed is attached to the catheter and is filled upright with sterile water. Water is added in increments until a woman feels a sensation of bladder filling, urge to void, and bladder maximum capacity. A normal bladder capacity for most women ranges from 300 to 700 mL. Changes in the fluid meniscus within the syringe are monitored. In the absence of a cough or Valsalva maneuver that would raise intraabdominal pressure, an abrupt meniscus elevation indicates bladder contraction and suggests detrusor overactivity. Once bladder capacity is reached, the catheter is removed, and the woman is asked to perform a Valsalva maneuver or cough while standing. Leakage directly linked to these increases in intraabdominal pressure indicates SUI.

Simple cystometrics require inexpensive equipment and can typically be completed by most gynecologists. One limitation, however, is its inability to assess for ISD, which may preclude certain surgical options. Multichannel cystometrics can evaluate for ISD and thus may offer advantages. An interesting potential application of simple cystometrics is in the evaluation of the continent patient planning surgery for prolapse. With 300 mL of saline instilled in the bladder and vaginal prolapse reduced with large cotton swabs, some patients will demonstrate leakage with cough or Valsalva—perhaps when standing if not seen supine. In these women with “potential” or “occult” SUI, some may consider a prophylactic continence procedure. Currently available decision-aid tools attempt to quantify the risk of this unmasked incontinence to help patients balance concomitant continence surgery benefits and risks (Jelovsek, 2014; Wei, 2012).

Multichannel Cystometrics

This UDS type provides more information on other physiologic bladder parameters than simple cystometrics. Multichannel cystometrics more commonly is performed by urogynecologists or urologists due to the expense and limited availability of needed equipment. Testing can be performed with a woman standing or seated upright in a specialized testing chair. During evaluation, two catheters are used. One is placed into the bladder and the other into either the vagina or rectum. The vagina is preferred unless advanced prolapse is evident, as stool in the rectal vault may obstruct catheter sensors and lead to inaccurate readings. Additionally, vaginal placement for most women is more comfortable. From each of these two catheters, distinct pressure readings are obtained or calculated. These include: (1) intraabdominal pressure, (2) vesicular pressure, (3) calculated detrusor pressure, (4) bladder volume, and (5) saline-infusion flow rate. As shown in Figures 23-13 and 23-14, the various incontinence forms can be differentiated.

Initially, women are asked to empty their bladder into a commode connected to a flowmeter (uroflowmetry). After a maximal flow rate is recorded, the patient is catheterized to measure postvoid residual volume and to ensure an empty bladder prior to further testing. This test provides information on a woman’s ability to empty her bladder and can identify women with urinary retention and other types of voiding dysfunction. Presuming that a patient begins with a comfortably full bladder of 200 mL or greater, most patients can empty their bladder over 15 to 20 seconds with flow rates >20 mL/sec. Maximum flow rates <15 mL/sec, with a voided volume >200 mL, are generally considered abnormally slow. In this setting—especially if accompanied by urinary retention—voiding dysfunction is identified. This may result from obstruction from a kinked urethra in the setting of anterior vaginal wall prolapse or postoperatively after creation of antiincontinence support that is too tight. As another example, voiding dysfunction may reflect neurologic dysfunction and poor detrusor contractility, as in those with longstanding poorly controlled diabetes.

Following uroflowmetry, cystometrography is performed to determine whether a woman has urodynamic stress incontinence (USI) or detrusor overactivity (DO). Additionally, this test provides information on bladder threshold volumes at which a woman senses bladder capacity. Delayed sensation or sensation of bladder fullness only with large capacities may indicate neuropathy. Conversely, extreme bladder sensitivity may suggest sensory disorders such as interstitial cystitis.

For the cystometrogram, a catheter is inserted transurethrally into the bladder and a second catheter is inserted into the vagina or rectum (see Fig. 23-14). While the patient is seated, the bladder is filled with room-temperature sterile normal saline, and the patient is asked to cough at regular intervals. Additionally, during filling, the volumes at which a first desire to void and maximal bladder capacity is reached are noted. From pressure readings, DO and/or USI may be identified.

After cystometrography, once approximately 200 mL of saline has been instilled, an abdominal leak point pressure is measured. The patient is asked to perform a Valsalva maneuver, and the pressure generated by the effort is measured and evidence of urine leakage is sought. If leakage is seen when a pressure of <60 cm H₂O is generated, then criteria have been met for a diagnosis of ISD. At our institution, abdominal leak point pressures are measured at a bladder volume of 200 mL, using the true zero of intravesical pressure as the baseline. However, the volume at which this test is performed varies among institutions, with some choosing to use bladder capacity and others choosing to use 150 mL as the testing volume.

This evaluation usually follows cystometrography and is similar to the uroflowmetry conducted at the beginning of urodynamic testing. A woman is asked to void into a large beaker that rests on a calibrated weighted sensor. Maximum flow rate and postvoid residual volume are once again recorded. Similar to uroflowmetry, the output from the urodynamics instrumentation provides a graphical representation of the void. However, during voiding, a woman now has a microtip transducer catheter in her bladder, which provides an additional display of detrusor pressure during the void, including pressures at the point of maximum flow rate. This is particularly useful in women who may have incomplete bladder emptying, as the pressure flowmetry may suggest either an obstructive scenario (elevated maximal detrusor pressure with slow flow rate) or poor detrusor contractility (low detrusor pressure and slow flow rate).

The final part of cystometric testing is the urethral pressure profile. At our institution, we usually perform this test in the seated patient with a volume of 200 mL instilled in the bladder. However, again, this volume is often institution dependent. A catheter transducer is positioned within the bladder, and the microtip dual-sensor catheter is pulled through the urethra with the aid of an automated puller arm at a speed of 1 mm/sec. Maximum urethral closure pressure (MUCP) is determined by averaging the pressure from three pull-throughs of the thin 7F catheter. As such, the MUCP values provide important information on the intrinsic properties of the urethra and aid in diagnosis of ISD. A diagnosis of ISD is made if the MUCP is <20 cm H₂O or, as described in the last section, if the leak point pressure is <60 cm H₂O (McGuire, 1981). These terms and concepts provide the rationale for procedures aimed at correcting stress incontinence. Importantly, however, the values used to define ISD are not well standardized and have not been consistently found to influence surgical outcomes (Monga, 1997; Weber, 2001).

Conservative/Nonsurgical

Pelvic Floor Strengthening

Conservative management is a reasonable initial approach to most patients with urinary incontinence. The rationale behind conservative management is to strengthen the pelvic floor and provide a supportive “backboard” against which the urethra may close. For both SUI and urgency urinary incontinence, these fundamentals prove valuable. With SUI, pelvic floor strengthening attempts to compensate for anatomic defects. For urgency urinary incontinence, it intensifies pelvic floor muscle contractions to provide temporary continence during waves of bladder detrusor contraction. For strengthening, options include active pelvic floor exercises and passive electrical pelvic floor muscle stimulation.

Active pelvic floor muscle training (PFMT) may lessen, if not cure, urinary incontinence in women who have mild to moderate symptoms. Also known as Kegel exercises, PFMT entails voluntary contraction of the levator ani muscles. As with any muscle building, isometric or isotonic forms of exercise may be selected. Exercise sets are performed numerous times during the day, with some reporting up to 50 or 60 times each day. However, specific details in performance of these exercises are subject to provider preference and clinical setting.

If isotonic contractions are used for PFMT, a woman is asked to squeeze and hold contracted levator ani muscles. Women, however, often have difficulty isolating these muscles. Frequently, patients will erroneously contract their abdominal wall muscles rather than the levators. To help localize the correct group, an individual may be instructed to identify the muscles that are tightened when snug pants are pulled up and over her hips. Moreover, in an office setting, a provider can determine if the levator ani group is contracted by placing two fingers in the vagina while Kegel exercises are performed.

At our institution, we aim to help patients achieve a sustained pelvic floor contraction of 10 seconds. We begin with the contraction duration a patient can sustain (e.g., 3 seconds) and ask them to hold for this long and then relax for one to two times this duration (e.g., 6 seconds). This squeeze and release is repeated 10 to 15 times. Three sets are performed throughout the day for a total of approximately 45 contractions. Over a series of weeks with frequent follow-up visits, the contraction duration is steadily increased. Patients thus improve the tone of their pelvic floor muscles and are usually able to more forcefully squeeze their muscles in anticipation of sudden increases of intraadominal pressure for SUI.

Alternatively, if isometric contractions are used for PFMT, a woman is asked to rapidly contract and relax the levator ani muscles. These “quick flicks” may prove advantageous if waves of urinary urgency strike. Of note, there is no value to stopping urination midstream, and women are counseled that this practice often worsens voiding dysfunction.

To augment exercise efficacy, weighted vaginal cones or obturators may be placed into the vagina during Kegel exercises. These provide resistance against which pelvic floor muscles can work.

PFMT for women with urinary incontinence compared with no treatment, placebo or sham treatment, or other inactive control treatment has been reviewed (Dumoulin, 2014a). Although interventions vary considerably, women who performed PFMT are more likely to report cure or improved incontinence and improved continence-specific quality of life than women who did not use PFMT. The exercising women also objectively demonstrated less leakage during office-based pad testing. Prognostic indicators that may predict a poor response to PFMT for SUI treatment include severe baseline incontinence, prolapse beyond the hymenal ring, prior failed physiotherapy, a history of prolonged second-stage labor, BMI >30 kg/m², high psychological distress, and poor overall physical health (Hendriks, 2010).

As an alternative to active pelvic floor contraction, a vaginal probe may be used to deliver low-frequency electrical stimulation to the levator ani muscles. Although the mechanism is unclear, this passive electrical stimulation may be used to improve either SUI or urgency urinary incontinence (Indrekvam, 2001; Wang, 2004). With urgency urinary incontinence, traditionally a low frequency is applied, whereas for SUI, higher frequencies are used. Electrical stimulation may be implemented alone or more commonly in combination with active PFMT.

Many behavioral techniques, often considered together as biofeedback therapy, measure physiologic signals such as muscle tension and then display them to a patient in real time. In general, visual, auditory, and/or verbal feedback cues are directed to the patient during these therapy sessions. Specifically, during biofeedback for active PFMT, a sterile vaginal probe that measures pressure changes within the vagina during levator ani muscle contraction is typically used. Visual readings reflect an estimate of muscle contraction strength. Treatment sessions are individualized, dictated by the underlying dysfunction, and modified based on response to therapy. In many cases, reinforcing sessions at various subsequent intervals may also prove advantageous.

Dietary

Various food groups that may have high acidity or caffeine content can lead to greater urinary frequency and urgency. Dallosso and colleagues (2003) found consumption of carbonated drinks to be associated with development of urgency urinary incontinence symptoms. Accordingly, elimination of these dietary irritants may benefit these women. In addition, certain dietary supplements such as calcium glycerophosphate (Prelief) have been shown to decrease urgency and frequency symptoms (Bologna, 2001). This is a phosphate-based product and is thought to buffer urine acidity.

Scheduled Voiding

Women with urgency urinary incontinence may feel voiding urges as frequently as every 10 to 15 minutes. Initial goals extend voidings to half-hour intervals. Tools used to achieve this include Kegel exercises during waves of urgency or mental distraction techniques during these times. Scheduled voiding, although used primarily for urgency urinary incontinence, may also be helpful for those with SUI. For these patients, regularly scheduled urination leads to an empty bladder during a greater percentage of the day. Because some women will leak urine only if bladder volumes surpass a specific threshold, frequent emptying can significantly decrease incontinence episodes.

Estrogen Replacement

Estrogen has been shown to increase urethral blood flow and increase α-adrenergic receptor sensitivity, thereby increasing urethral coaptation and urethral closure pressure. Hypothetically, estrogen may also increase collagen deposition and increase vascularity of the periurethral capillary plexus. These are purported to improve urethral coaptation. Thus, for incontinent women who are atrophic, administration of exogenous estrogen is reasonable.

Estrogen is commonly administered topically, and many different regimens are appropriate. At our institution, we use conjugated equine estrogen cream (Premarin cream) administered daily for 2 weeks, then twice weekly thereafter. Although no data are available to address the duration of treatment, women may be treated chronically with topical estrogen cream. Alternatively, oral estrogen may be prescribed if other menopausal symptoms for which estrogen would be beneficial coexist (Chap. 22). However, despite these suggested benefits, a consensus regarding estrogen’s beneficial effects on the lower urinary tract has not been reached. Specifically, some studies have shown worsening or development of urinary incontinence with systemic estrogen administration (Grady, 2001; Grodstein, 2004; Hendrix, 2005; Jackson, 2006).

Treatment of Stress Urinary Incontinence

Medications

Pharmaceutical treatment plays a minor role in the treatment of women with SUI. However, for women with mixed urinary incontinence, a trial of imipramine is reasonable to aid urethral contraction and closure. As discussed earlier, this tricyclic antidepressant has α-adrenergic effects, and the urethra contains a high content of these receptors.

Pessary and Urethral Inserts

Certain pessaries have been designed to treat incontinence as well as pelvic organ prolapse. These “incontinence pessaries” are designed to reduce downward excursion or funneling of the urethrovesical junction (Fig. 24-16). This provides bladder neck support and thereby helps to reduce incontinence episodes. The success of pessary use in the treatment of urinary incontinence is variable, dependent on the amount of prolapse and other factors. Not all women are appropriate candidates for devices, nor will all desire long-term management of incontinence or prolapse with these.

A large prospective trial comparing incontinence pessaries and behavioral therapy for women with SUI demonstrated that 40 and 49 percent of patients were either much or very much improved at 3 months, respectively. The women randomized to behavioral therapy reported greater treatment satisfaction, and a greater percentage reported no bothersome incontinence symptoms (Richter, 2010b).

As an alternative to pessaries, urethral occlusive devices include urethral inserts (FemSoft and Reliance Urinary Control Insert) and urethral patches (CapSure and Re/Stor). Urethral inserts conform to the urethra and create a seal at the bladder neck to prevent accidental leakage. During routine bathroom visits, the insert is removed, discarded, and replaced with a fresh insert. Although data are limited on the effectiveness of inserts, adverse effects of mucosal irritation or superficial bacterial infection are generally minor. In an observational study of 150 women, Sirls and associates (2002) found significantly reduced rates of incontinence episodes with the FemSoft device. With urethral patches, a water-tight seal is created over the urethra after the patch adheres to surrounding periurethral skin using adhesive gel. Similarly, although success rates vary between 44 and 97 percent, these devices are associated with minimal adverse effects (Bellin, 1998; Versi, 1998).

Surgery

For those who are unsatisfied with or do not desire conservative management, surgery may be an appropriate next step for SUI. As noted earlier, urethral support is integral to continence. Thus, surgical procedures that recreate this support often diminish or cure incontinence. In general, these surgical procedures are believed to prevent bladder neck and proximal urethra descent during increases in intraabdominal pressure and are grouped as shown in Table 23-4. General postoperative risks for continence surgeries include lower urinary tract injury, failure to correct or recurrence of SUI, and creation of de novo voiding dysfunction such as urgency or retention.

Midurethral Slings

The therapeutic mechanism of these slings is based on the integral theory hypothesized by Petros and Ulmsten (1993). In brief, control of urethral closure involves the interplay of three structures: the pubourethral ligaments, the suburethral vaginal hammock, and the pubococcygeus muscle. Loss of these supports lead to urinary incontinence and pelvic floor dysfunction. Midurethral slings are believed to recreate this structural support.

There are different variations of these procedures, but all use a vaginal approach to place synthetic mesh beneath the midurethra. Recovery from midurethral sling placement is rapid, and many gynecologists provide this surgery on an outpatient basis. As such, these are often a popular surgical treatment for SUI. Simplistically, they are classified according to the route of placement and are subdivided into those using a retropubic or a transobturator approach.

For the retropubic approach, several commercial kits are available, and one commonly used is the tension-free vaginal tape (TVT). With this, the sling (tape) is placed through a vaginal incision to create a hammock beneath the urethra. On each side of the urethra, the sling’s arms are brought out to the lower anterior abdominal wall and affixed. For this procedure, sharp trocars traverse the retropubic space as illustrated in Section 45-3 of the atlas. Thus, bladder puncture and retropubic space vessel laceration are specific risks. Many studies attest to this procedure’s efficacy (Holmgren, 2005; Song, 2009). One prospective observational study confirmed the long-term safety and efficacy of the TVT device. At 17 years, 87 percent were subjectively cured or significantly improved (Nilsson, 2013).

For the transobturator tape (TOT) approach, various kits are also available, and sling material is directed bilaterally through the obturator foramen and underneath the midurethra. The entry point overlies the proximal tendon of the adductor longus muscle of the inner thigh as shown in Section 45-4. This approach was introduced with the intent to reduce the vascular and lower urinary tract injury risks that can be associated with traversing the retropubic space.

The TOT is indicated for primary SUI secondary to urethral hypermobility. For this, subjective success rates range from 73 to 92 percent up to 5 years after surgery (Abdel-Fattah, 2012; Laurikainen, 2014; Wai, 2013). However, abundant longer-term data regarding the efficacy of transobturator approaches are lacking. Moreover, in patients with SUI secondary to ISD, the value of TOT is unclear as results are conflicting and data are limited (Miller, 2006; O’Connor, 2006; Richter, 2010a).

In comparing these two, one multicenter randomized study of 597 found no significant differences in objective and subjective success rates at 12 months between the retropubic (80.8 and 62.2 percent) and the transobturator (77.7 and 55.8 percent) routes, respectively (Richter, 2010a). The retropubic route had a significantly higher rate of postoperative voiding dysfunction requiring reoperation, whereas the transobturator route resulted in more neurologic symptoms. Overall quality of life and satisfaction scores with the two procedures were similar. Others have found similar findings with respect to procedure–related complications. Namely, the retropubic route has a higher rate of bladder injury but required a decreased use of anticholinergic medication postoperatively (Barber, 2006; Brubaker, 2011).

Modification of the TVT and TOT procedure is seen with the minimally invasive slings, sometimes called “microslings” or “minislings.” With this technique, an 8-cm-long strip of polypropylene synthetic mesh is placed across and beneath the midurethra through a small vaginal incision. Mesh is not threaded through the retropubic space as with TVT, nor does it perforate the obturator membrane as with TOT. That said, lower urinary tract injury is not completely averted with this method. Initial results for the minislings suggested high objective and subjective cure rates (Neuman, 2008). However, in one study, the minisling group had a higher proportion of patients with more severe incontinence 1 year after surgery than those in the retropubic sling group (Barber, 2012).

In March 2013, the FDA issued an update regarding considerations about surgical mesh for SUI. In that statement, the established safety and efficacy of mesh sling procedures for the treatment of SUI were upheld for full-length multiincision operations. They further noted that the safety and effectiveness of minislings had not yet been adequately demonstrated.

Retropubic Urethropexy

This group includes the Burch and Marshall-Marchetti-Krantz (MMK) colposuspension procedures. Traditionally performed via laparotomy, these suspend and anchor the pubocervical fascia to the musculoskeletal framework of the pelvis (Section 45-2). With the advent of less invasive procedures for SUI, such as the midurethral sling, these techniques are less commonly performed. The Burch technique uses the strength of the iliopectineal ligament (Cooper ligament) to lift the anterior vaginal wall and the periurethral and perivesicular fibromuscular tissue. In contrast, during MMK surgery, the periosteum of the symphysis pubis is used to suspend these tissues. Thus, an added risk for MMK is osteitis pubis.

Retropubic urethropexy effectively treats SUI. One-year overall continence rates range between 85 and 90 percent, and the 5-year continence rate approximates 70 percent (Lapitan, 2009). As another indication, data suggest that Burch retropubic urethropexy performed concurrently with abdominal sacrocolpopexy (ASC) may significantly reduce rates of later, postoperative de novo SUI (Chap. 24) (Brubaker, 2008a). In support of this practice, a 7-year follow-up study showed that patients undergoing ASC and prophylactic Burch urethropexy still demonstrated lower de novo SUI rates than women receiving ASC alone (Nygaard, 2013).

Pubovaginal Slings

With this surgery, a strip of either rectus fascia or fascia lata is placed under the bladder neck and through the retropubic space. The ends are secured at the level of the rectus abdominis fascia (Section 45-5). This surgery has traditionally been used for SUI stemming from ISD. In addition, this procedure may also be indicated for patients with prior failed continence operations.

Urethral Bulking Agent Injection

Using cystoscopic guidance, agents can be injected into the urethral submucosa to “bulk up” the mucosa and improve coaptation. Surgical steps and agent types are illustrated in Section 45-6. This option has traditionally been indicated for women who have stress incontinence associated with ISD. However, the Food and Drug Administration (FDA) has broadened criteria for their use to include patients with less severe leak point pressures. Thus, those with leak point pressures <100 cm H₂O may also be candidates (McGuire, 2006). Additionally, this office procedure is a useful alternative for women with SUI who have multiple medical problems and are thus poor surgical candidates.

Transvaginal Needle Procedures and Paravaginal Defect Repair

In the 1960s through 1980s, needle suspension procedures such as the Raz, Pereyra, and Stamey techniques were popular operations for SUI but have now largely been replaced by other methods. In brief, these surgeries use specially designed ligature carriers to place sutures through the anterior vaginal wall and/or periurethral tissues and suspend them to various levels of the anterior abdominal wall. These rely on the strength and integrity of the periurethral tissue and abdominal wall strength to correct urethral hypermobility and prevent bladder neck and proximal urethra descent. Although initial cure rates are satisfactory, the durability of these procedures decreases with time. Success rates range from 50 to 60 percent, well below rates found with other current continence procedures (Moser, 2006). Failure stemmed largely from “pull-through” of sutures at the level of the anterior vaginal wall.

In addition, abdominal paravaginal defect repair (PVDR) is a surgical procedure that corrects lateral support defects of the anterior vaginal wall. The technique involves suture attachment of the lateral vaginal wall to the arcus tendineus fascia pelvis. Currently, PVDR is primarily a prolapse-correcting operation. Although previously used to correct SUI, long-term data show this to no longer be a superior method for primary treatment of SUI (Colombo, 1996; Mallipeddi, 2001).

Treatment of Urgency Urinary Incontinence

Anticholinergic Medications

These medications appear to work at the level of the detrusor muscle by competitively inhibiting acetylcholine at muscarinic receptors (M₂ and M₃) (Miller, 2005). These agents thereby blunt detrusor contractions to reduce the number of incontinence episodes and volume lost with each. These medications are significantly better than placebo at improving symptoms of urgency urinary incontinence and overactive bladder. However, in a Cochrane database review, Nabi and colleagues (2006) reported that the reduction in baseline urgency incontinence episodes per day reflects only a modest benefit.

Oxybutynin, Tolterodine, and Fesoterodine

These frequently used drugs competitively bind to cholinergic receptors (Table 23-5). As noted, muscarinic receptors are not limited to the bladder. Thus, drug side effects may be significant. Of these, dry mouth, constipation, and blurry vision are common, and dry mouth is a primary reason for drug discontinuation (Table 23-6). Importantly, anticholinergics are contraindicated in those with narrow-angle glaucoma.

Because of these side effects, the therapeutic goal of bladder M₃ blockade with these antimuscarinic agents is often limited. Accordingly, drug selection is tailored, and efficacy is balanced against tolerability. For example, Diokno and associates (2003) found oxybutynin to be more effective than tolterodine. However, tolterodine was associated with lower side effect rates. Tolterodine and fesoterodine have also been compared in a randomized study of 1135 patients. Fesoterodine was found to perform better than tolterodine, although once again, side effects were lowest in the tolterodine group (Chapple, 2008). A population-based study reported that only 56 percent of women felt their overactive bladder medication was effective, and half stopped taking the medication (Diokno, 2006).

Most side effects attributed to oxybutynin stem from its secondary metabolite that follows liver metabolism. Therefore, to minimize oral oxybutynin side effects, a transdermal patch was designed to decrease the “first-pass” effect of this drug. This leads to decreased liver metabolism and fewer systemic cholinergic side effects. Dmochowski and coworkers (2003) found fewer anticholinergic side effects with transdermal oxybutynin compared with long-acting oral tolterodine.

Transdermal oxybutynin (Oxytrol) is supplied as a 7.6 × 5.7 cm patch that is applied to the abdomen, hip, or buttock; worn continuously; and changed twice weekly. Each patch contains 36 mg of oxybutynin and delivers approximately 3.9 mg daily. Application-site pruritus is the most frequent side effect, and varying the application site may minimize skin reactions (Sand, 2007). A transdermal oxybutynin gel (Gelnique), available in 3- and 10-percent strengths, is applied daily to skin of the abdomen, upper arms/shoulders, or thigh, and application sites are rotated.

Imipramine

This agent is less effective than tolterodine and oxybutynin but displays α-adrenergic and anticholinergic characteristics. Therefore, it is occasionally prescribed for those with mixed urinary incontinence. Importantly, doses of imipramine used to treat incontinence are significantly lower than those used to treat depression or chronic pain. In our experience, this minimizes the theoretical risk of drug-related side effects.

Selective Muscarinic-receptor Antagonists

These drugs were introduced with the aim of reducing anticholinergic side effects. The agents are all M₃-receptor selective antagonists and include solifenacin (Vesicare), trospium chloride (Santura), and darifenacin (Enablex). Advantages of increased urgency warning time and decreased muscarinic side effects have been shown in randomized controlled studies (Cardozo, 2004; Chapple, 2005; Haab, 2006; Zinner, 2004). However, although the side-effect profiles of these drugs are potentially more attractive, they have not been proved superior in efficacy to nonselective muscarinic agents (Hartmann, 2009).

Mirabegron

More recently, a β₃-adrenergic receptor agonist, mirabegron (Myrbetriq), has been introduced into the U.S. pharmaceutical market for the treatment of urgency urinary incontinence, urgency, and frequency. Activation of these receptors results in relaxation of the detrusor smooth muscle and increased bladder capacity. Most commonly reported adverse reactions include hypertension, nasopharyngitis, UTIs, dry mouth, and headache (Herschorn, 2013).

Sacral Neuromodulation

Urine storage and bladder emptying require a complex coordinated interaction of spinal cord and higher brain centers, peripheral nerves, urethral and pelvic floor muscles, and the detrusor muscle. If any of these levels are altered, normal micturition is lost. To overcome these problems, electrical nerve stimulation, also called neuromodulation, has been used. InterStim is the only implantable neuromodulation system approved by the FDA for treatment of refractory urgency urinary incontinence and for treatment of anal incontinence. It may be also considered for those with pelvic pain, interstitial cystitis, and defecatory dysfunction, although it is not FDA-approved for these indications. Sacral neuromodulation is not considered primary therapy and is typically offered mainly to women who have exhausted pharmacologic and conservative options.

This outpatient surgically implanted device contains a pulse generator and electrical leads that are placed into the sacral foramina to modulate bladder and pelvic floor innervation. Its mode of action is incompletely understood but may be related to somatic afferent inhibition that interrupts abnormal reflex arcs in the sacral spinal cord involved in the filling and evacuation phases of micturition.

Implantation is typically a two-stage process. Initially, leads are placed and attached to an externally worn generator (Section 45-12). After placement, frequency and amplitude of electrical impulses can be adjusted and tailored to maximize effectiveness. If a 50-percent or greater improvement in symptoms is noted, then internal implantation of a permanent pulse generator is planned. This procedure is minimally invasive and is typically completed in a day-surgery setting. Surgical complications are rare but may include pain or infection at the generator insertion site.

Although its use is often reserved for those who have been unsuccessfully treated with behavioral or pharmacologic therapy, this modality is effective for urinary symptom treatment. Studies have found improvement rates ranging from 60 to 75 percent, and cure rates approximating 45 percent (Janknegt, 2001; Schmidt, 1999; Siegel, 2000). Sustained improvement from baseline incontinence parameters has been shown at long-term follow-up. One 3-year study reported a 57-percent reduction in incontinence episodes per day, and similar findings were found in a separate 5-year study (Kerrebroeck, 2007; Siegel, 2000). A systematic review of 17 case series at follow-up periods of 3 to 5 years similarly reported 39 percent of patients cured and 67 percent with greater than 50-percent improvement in incontinence symptoms (Brazzelli, 2006).

Percutaneous Tibial Nerve Stimulation

Sometimes referred to as posterior tibial nerve stimulation, percutaneous tibial nerve stimulation (PTNS) is becoming a more common therapy for refractory urgency urinary incontinence. It involves percutaneous needle electrode placement into an area cephalic to the medial malleolus of the lower extremity. Electrical pulses are sent via a generator to the tibial nerve. This nerve originates from spinal roots L4-S3_, and its stimulation leads to retrograde neuromodulation. Multicenter studies have demonstrated its efficacy compared with sham or with primary treatment with anticholinergic medication (Peters, 2009, 2010; MacDiarmid, 2010).

Botulinum Toxin A

Injection of botulinum toxin A (onabotulinumtoxinA) into the bladder wall is approved for the treatment of idiopathic detrusor overactivity. Three placebo-controlled studies showed the effectiveness of this treatment (Anger, 2010). All three used cystoscopic injection of 200 units of botulinum toxin A versus placebo, and each demonstrated significantly improved continence rates. Improvement occurred as early as 4 weeks after injection (Brubaker, 2008b; Flynn, 2009; Khan, 2010; Sahai, 2007). Urinary retention—defined a postvoid residual volume measuring > 200 mL—is a common side effect and developed in 27 to 43 percent of patients in these randomized trials. Most patients are asymptomatic, but patients receiving botulinum toxin A for overactive bladder or urgency urinary incontinence are counseled that temporary self-catheterization may be required after injection.

More recently, one double-blind, randomized trial compared oral anticholinergic therapy against injections of 100 units of botulinum toxin A in women with idiopathic urgency urinary incontinence. Investigators found comparable reductions in incontinence episodes. The botulinum toxin A group was less likely to complain of dry mouth and more likely to have complete resolution of urgency urinary incontinence (Visco, 2012). In the injection group, the rate of catheter use for urinary retention was only 5 percent. At our institution, we use 100 units for women with idiopathic overactive bladder.

A patient can expect the effects of the toxin to wane over time. In a small study describing the need for repeat injections, 20 patients from a cohort of 34 received a second injection, and nine patients received up to four injections. These repeat injections appear to be equally effective as the primary injection. Median time between injections is approximately 377 days (Sahai, 2010).