Urinary incontinence is defined by the International Continence Society (ICS) as “the complaint of involuntary leakage of urine.” The most common forms of urinary incontinence are classified as stress, urgency, and mixed urinary incontinence. The current ICS definition of stress urinary incontinence (SUI) is subjective based on symptoms perceived by the patient: “stress urinary incontinence is the complaint of involuntary leakage on effort or exertion, or on sneezing or coughing.”¹ In contrast, urgency urinary incontinence is “the complaint of involuntary leakage accompanied by or immediately preceded by urgency,” and mixed urinary incontinence is “a combination of symptoms of both stress and urgency urinary incontinence.”

The definition of SUI has evolved over time into its current subjective definition. It was previously referred to as “genuine stress incontinence (GSI)” by the 1990 ICS Standardization of Terminology of Lower Urinary Tract Function. GSI was defined as “the involuntary loss of urine occurring when, in the absence of a detrusor contraction, the intravesical pressure exceeds the maximum urethral pressure.” With the revision of the ICS terminology in 2002, GSI was replaced by the term “urodynamic stress incontinence.” Urodynamic stress incontinence is the observation during filling cystometry of involuntary leaking of urine during increased abdominal pressure, in the absence of a detrusor contraction. The evolution of the definition of SUI underlines the importance of eliciting the patients’ subjective experience of the condition.

Closure of the urethra is essential during filling and storage of urine in order to prevent leakage. If the urethral closure mechanism is incompetent, it allows leakage of urine in the absence of a detrusor contraction. Both intrinsic and extrinsic factors contribute to the symptoms of SUI. Intrinsic factors are those related to the function of the urethra, whereas extrinsic factors are secondary to influences apart from the urethra, such as patient level of activity or weight and urethral support. Increasingly rigorous investigation into the epidemiology, anatomy, physiology, and neurology of SUI has promoted the understanding of normal and incontinent states; this chapter provides an overview of current understanding of these mechanisms, as well as their limitations.

Prevalence rates for SUI are wide, with reported ranges from as low as 4% to as high as 70%,² and vary by age. SUI is common in younger women with estimated rates of 4% to 23% in women age 20 to 39 years. Prevalence rates peak by age 50 to 60 years, with estimated rates of 16% to 36% in women age 40 to 59 years.² Older women are more likely to be affected by urgency urinary incontinence and mixed urinary incontinence than SUI.

Multiple studies report different prevalence rates of urinary incontinence between different racial groups. African-American women are less affected by SUI compared to Caucasian women, with one population-based study showing prevalence rates of SUI in Caucasian women of 39.2% compared to 25.0% in African-American women³; other population studies have supported this finding.⁴ The explanation for the racial differences is unclear, but it is plausible that genetic, anatomic, social, and cultural factors contribute.

Pregnancy and childbirth appear to be risk factors for the development of SUI. Pregnancy, in and of itself, is a risk factor for urinary incontinence; however, there also appear to be differences in risk based on delivery type. Women who undergo vaginal delivery may have up to twice the risk of developing SUI symptoms compared to women who deliver by cesarean section.⁵ In a large epidemiologic study conducted in Norway, women who delivered vaginally appear to be at significantly higher risk for SUI than women delivered by cesarean section. This difference diminished over time.⁶ Most studies agree in the conclusion that cesarean delivery is not entirely protective of the development of SUI.

Both obesity and smoking are modifiable risk factors associated with SUI. Increases in body mass index (BMI) have been associated with increased symptoms of SUI.⁷ It is hypothesized that the increased weight causes chronic strain, stretching, and weakening of the pelvic floor. Weight loss can be associated with improvement in SUI symptoms and a decrease in symptom bother.⁸ Smoking is another modifiable risk factor; the mechanism behind the increased risk for stress incontinence in women who smoke is likely multifactorial and includes direct toxic effects on urinary tract tissue in combination with the increased abdominal pressures associated with chronic pulmonary conditions and coughing.

The mechanisms that allow continence, and the nature of the failures of those mechanisms, have been a source of debate for as long as the condition has been addressed scientifically. In the early twentieth century, Bonney promoted the idea of a loss of suburethral support as the underlying mechanism of incontinence,⁹ while Kelly described a more intrinsic urethral dysfunction as the cause, such as an open bladder neck and urethra.¹⁰ Although no longer used, the multifactorial nature of stress incontinence came into greater focus with the classification of various subtypes of stress incontinence, as follows:

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  Type 0: Reports of SUI, but well-supported bladder neck, no abnormality on videourodynamics. Thought to represent voluntary contraction during testing

  
  
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  Type I: Well-supported bladder neck, with mild (2 cm) descent and urethral opening during Valsalva

  
  
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  Type II: Greater than 2 cm descent of the bladder neck

  
  
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  Type III: Open bladder neck and proximal urethra at rest¹¹

The anatomy of the lower urinary tract is discussed below. In addition, we present data that illustrate the various mechanisms that contribute to continence.

The detrusor, the main structural element of the urinary bladder, is composed primarily of smooth muscle under autonomic control and connective tissue. It is lined internally by transitional urothelium, with a loose connective tissue layer referred to as the lamina propria. In the base of the bladder, the trigone is found. Its deep layer is continuous with Waldeyer sheath in the distal ureter, and is similar in its parasympathic innervation to the detrusor muscle, whereas the superficial layer of the trigone is continuous with the smooth muscle of the urethra, and has similar sympathetic predominance of innervation. During the filling phase, the detrusor exhibits remarkable compliance, with minimal increases in pressure as the bladder fills, until it approaches its capacity. SUI is a disorder of the filling phase, and is not attributed to detrusor dysfunction.

The epithelium of the proximal urethra is the same transitional urothelium as that found in the bladder; more distally, the epithelium becomes squamous, like that of the vulva. During the filling phase, the epithelium of the urethra is compressed into longitudinal rugations. These rugations, in addition to the rich venous vasculature of the underlying lamina propria, contribute to urethral coaptation and resultant urethral resistance to urine flow. Surrounding the lamina propria are two layers of smooth muscle of the urethra known as the intrinsic sphincter mechanism: an internal, longitudinally oriented layer, and an external, circumferentially oriented layer. These fibers are under autonomic control, and show predominance of α-adrenergic receptors of the sympathetic system (Figure 5-1).¹²

Surrounding these layers, the rhabdosphincter, or external urethral sphincter, is found in the proximal and midurethra. The appearance of the striated urethral sphincter of the urethra in normal, continent women on magnetic resonance imaging shows that the appearance of striated sphincter muscle decreased along the longitudinal axis, until the level of the perineal membrane, where there is no muscular content of the urethra.¹³ The axial structure of the rhabdosphincter may vary. In nulliparous women, it has been described as a continuous ring structure. Other studies, examining women as they age, and/or those with stress incontinence, demonstrate a diminution of the posterior or dorsal fibers.^14,15 Some have postulated that this finding may be a result of compressive forces of vaginal delivery on the muscle fibers of the posterior urethra. Distally, the extrinsic continence structures include two discrete bands of muscle (the compressor urethrae and the urethrovaginal sphincter muscles), contained within the anterior segment of the perineal membrane, which exert compressive forces from above the urethra (Figure 5-2).¹⁶

The bladder base and urethra are adjacent to the anterior vagina, and are supported by it. Although the connective tissue between the vaginal epithelium and the bladder base and urethra can often appear surgically as a distinct fascial layer referred to as the pubocervical fascia, histologic studies have confirmed that this tissue contains no true fascial fibers, and are more correctly referred to as the fibromuscularis of the vagina and its surrounding adventitia. Nonetheless, the connective support of the anterior sulci of the vagina to the surrounding pelvic structures plays an important role in maintaining continence.

Vaginal supports have been described in three different levels, with Level I representing posterolateral support to the vaginal apex, Level II representing lateral support of the anterior vaginal fornices, and Level III representing distal or perineal support.¹⁷ The Level II paravaginal attachments of the vagina to the arcus tendineus of the fasciae pelvis support the anterior vagina bilaterally, and the vagina thus forms a sling against which the bladder base and urethra are supported. Abdominal pressure during exertion is transmitted to the bladder, increasing bladder pressure, but simultaneously, that pressure is passively transmitted to the urethra, pushing it against the anterior vagina, resulting in coaptive pressure. As the fibers of the arcus tendineus fasciae pelvic travel distally, they merge with the inner aspects of the perineal membrane. These connective condensations have been termed pubourethral ligaments.¹⁸ More recent studies demonstrate that these structures represent the continuity of lateral support between Level II and Level III.

The perineal membrane is a complex collection of structures, formerly known as the urogenital diaphragm, and erroneously thought to consist of a sheet of striated muscle between two fascial layers, spanning the area between pubic rami and penetrated by the vagina and urethra. More recent study shows it to be comprised of a dorsal portion that covers the area between the pubic rami to the vagina/perineal body and a ventral portion, which is continuous with the paravaginal connective tissue and contains the compressor urethrae and urethrovaginal sphincter muscles.¹⁹

It is likely that the muscles of the pelvic floor play an important role in the stabilization and support of the lower urinary tract and in maintenance of continence. Women with SUI were observed to have greater acceleration and posterior displacement of the urethra, associated with a lengthening of the muscles, compared to continent controls, where shortening and stiffening of the pelvic floor muscles resulted in improved and more balanced stabilization of the urethra.²⁰

In addition to the passive support of the anterior vaginal wall to the urethra, other intrinsic and extrinsic factors that contribute to continence have been described. The circular striated muscle fibers of the sphincter urethrae are intrinsic to the urethra and extrinsic forces including structures surrounding the urethra contribute to the maintenance of continence. Together, these intrinsic and extrinsic systems as well as vagina support structures provide three different types of support and/or compression to the urethra, as seen in Figure 5-3.²¹ The observation that urethral pressures both precede (by 240 ms) and exceed vesical pressures (by up to 170%) during a cough is an indication that passive pressure transmission to the supporting structures is not sufficient explanation of continence.²² Conversely, patients with clinically adequate urethral support who still experience SUI also demonstrate that support is not the whole story. Similarly, urethral pressure measurements on their own are poor predictors of continence status.²³

Multiple intrinsic and extrinsic forces may explain some of the variability observed in urethral pressure measurements on urodynamic testing depending on the orientation of the catheter.²⁴ One study demonstrated, in a small number of women undergoing pelvic surgery, that by blocking the striated muscle of the sphincter, urethral pressure was reduced by roughly one-third. Vascular clamps were then (temporarily) applied to the iliac vessels, reducing urethral pressure by an additional one-third.²⁵ This model suggested that the striated (external) sphincter, smooth muscle (internal) sphincter, and vascular plexi of the lamina propria of the urethra contribute equally to urethral pressure in the continent woman.

Innervation of the urethra comprises somatic, sympathetic, and parasympathetic innervation via the pudendal, hypogastric, and pelvic nerves, respectively, illustrated in Figure 5-1. The pelvic nerves contain the afferent fibers that bring signals from the stretch and pressure receptors in the detrusor, as well as some nociceptive C-fibers that may contribute to inflammatory pain conditions.¹²

Two reflex pathways contribute to the storage mechanisms of the lower urinary tract. The sympathetic storage reflex, mediated through the hypogastric nerve, responds to activation of the stretch receptors in the detrusor with a postganglionic release of norepinephrine, which in turn activates β receptors in the bladder, which inhibit detrusor tone, and α receptors in the urethral smooth muscle, which increase tone. This reflex is suppressed by higher central nervous system (CNS) mechanisms during micturition. The somatic storage reflex also responds to sudden increases in bladder pressure. Efferent pathways signal a spinal reflex through Onufruwicz nucleus. Motor neurons, traveling through the pudendal nerve, then stimulate activity of the striated urethral sphincter and the perineal membrane muscles including the compressor urethrae and the urethrovaginal sphincter muscle. Similar to the sympathetic storage reflex, the somatic storage reflex is suppressed by spinal and supraspinal activity when micturition is appropriate.

Estrogens exert trophic effects on the urethral epithelium, vascular beds, and connective tissue, and have been demonstrated to increase both urethral pressure and pressure transmission ratios in experimental models.²⁶ However, clinical results from estrogen supplementation and its effects on SUI have not been supportive of its clinical efficacy, where women who were taking hormone replacement therapy reported more incontinence than those not taking hormone replacement therapy.²⁷ As previously discussed, the intrinsic sphincter mechanisms contain both striated (external urethral sphincter) and smooth muscle (internal urethral sphincter) components, both of which contribute to closure pressures. Pharmacologic studies can be used to observe the relative contributions of each component, as manipulation of either component will affect overall urethral closure pressure. Voluntary pelvic floor contraction (striated component) and pharmacologic stimulation of smooth muscle both result in increases in urethral closure pressure, whereas pharmacologic blockade of both striated and smooth muscle components result in decreases in closure pressures.^28-31

Urethral closure pressures, however, measure the tonic, or resting activity of the sphincter mechanisms. Other techniques are used to assess the contributions of the neurologic and muscle activity of the reflex mechanisms involved in continence. In a rat model, the intravenous adrenergic agonist nisoxetine enhanced the sneeze-induced reflex of increased midurethral pressure, without affecting baseline urethral tone. The intrathecal administration of the α-adrenergic antagonists prazosin and phentolamine eliminated this effect.³² The authors postulated that at least two adrenergic reflex systems are in place: one central system in the spinal cord, and another in the peripheral system. Conversely, the administration of duloxetine, a serotonin- and norepinephrine-reuptake inhibitor, enhanced both the baseline urethral pressure and the amplitude of the sneeze-induced reflex contraction.³³ This effect was observed both in normal rats, and in rats with SUI induced by the vaginal distension method. Leak point pressures in the incontinent rats were increased from 39 to 92 cm H₂O after the administration of duloxetine.

Sympathomimetic agents such as ephedrine and phenylpropanolamine have been studied for use in humans in the hopes of increasing urethral pressures.³⁴ However, their lack of specificity to the lower urinary tract has limited safety and tolerability. Phenylpropanolomine was withdrawn from the US market after being linked to increased rates of hemorrhagic stroke. In humans, duloxetine has been shown to increase the resting tone of the urethra.³⁵ In addition, it appears to lower the excitability threshold of the external urethral sphincter contractions,³⁶ and to potentiate the benefits of pelvic floor muscle rehabilitation therapy in women with SUI.³⁷ The motor neurons in Onufruwicz nucleus appear to be particularly sensitive to the effects of some medications, including duloxetine, which led to interest in its use as a therapy for SUI. Although it is currently indicated for treatment of SUI in Europe, it is not currently approved by the Food and Drug Administration for treatment of urinary symptoms in the United States.

Rat models of SUI have included the vaginal balloon catheter distension technique, which seeks to mimic tissue damage observed during vaginal delivery; this model has been shown to result in levator and bladder/urethral muscle injury, neurologic injury, as well as generalized hypoxia/reperfusion injuries similar to those experienced during human vaginal birth.^38,39 Other models include the extensive damage to the urethral support structures (urethrolysis),⁴⁰ focused transection of the puburethral supports,⁴¹ or direct nerve injury to the pudendal nerves.⁴² This latter technique demonstrates a one-third decrease in leak point pressures, with a nadir at 4 days; thereafter, some neuroregeneration, which is enhanced by estrogen, is observed. This model serves to illustrate some of the injury/recovery/compensation of the continence mechanism in response the neurologic injury.⁴³

In intact anesthetized cats, sneeze-induced continence reflex is most pronounced in the distal urethra, and lasted longer than the contractions induced in the bladder, proximal and midurethra. Unilateral pudendal nerve lesions most notably decreased this distal urethral reflex, and bilateral pudendal nerve lesions reduced this reflex contraction throughout the length of the urethra.⁴⁴

All of these types of intervention have been shown to produce durable models of SUI, as measured by suprapubic tube placement and measurement of induced leak point pressures. The variety of methods to model the condition of stress incontinence provides some insight into the likely overlapping structures and functions of the lower urinary tract continence mechanisms.

Much of our understanding of the risk factors and associations with the development of SUI comes from the comparison of women with incontinence to continent controls. The relative contributions of support and urethral function toward continence have been assessed using a variety of measurement techniques. DeLancey et al. demonstrated that reductions in urethral closure pressures were a better predictor of de novo SUI in women following vaginal delivery than loss of vesical support as measured by ultrasonography during a cough.⁴⁵ The coexistence of both variables in women, however, was able to predict only 37% of incontinence in these women, once again indicating that multiple mechanisms are involved.

The contribution of the pelvic floor to urethral support has generally been understood to represent reflexive contraction of the levator musculature secondary to stretching experienced during stress. In normal women, pelvic muscle reflexive contractions have been shown to increase with increasing intensity of cough and other increased abdominal pressures.⁴⁶ Some have postulated that this graduated response, rather than a simple on-or-off reflexes, indicates the central nervous system’s involvement in modulating the reflex arc, and the central nervous system must be “programmed” to allow for this nuanced reaction.⁴⁷ One study evaluated women undergoing a Manchester procedure for the treatment of uterovaginal prolapse, where 22% of women demonstrated stress incontinence after the procedure.⁴⁸ Analysis of preoperative and postoperative data in this cohort showed that low preoperative urethral pressures were associated with high risk for the development of stress incontinence.

Despite multiple theories and explanations of the mechanisms of continence and failures of current therapies, our understanding is incomplete. In isolation, urodynamic parameters perform poorly in distinguishing incontinent women from asymptomatic ones. Additionally, interventions known to improve symptoms of SUI demonstrate little or no change in our testing parameters. A more complete understanding of the pathophysiology almost certainly invites consideration not of a single underlying mechanism but rather multiple mechanisms acting in concert. Within any individual, the underlying problems resulting in SUI relate to the adequacy of suburethral/anterior vaginal support, thickness and vascular support of the urethral epithelium, the tone and quality of the internal (smooth muscle) sphincter mechanisms, the integrity and rapidity of response of the external urethral apparatus and that of the pelvic floor musculature as a whole, as well as the myriad peripheral and central neurologic pathways and reflex arcs.

The evaluation of patients with complaints of SUI starts with careful but directed questioning about any leakage of urine. The prevalence of incontinence in the population may lead some women to assume that some degree of leakage is normal, and not worth discussing or evaluating. Questions that may help to differentiate SUI from other forms of incontinence, including detrusor overactivity or overflow incontinence, include “do you leak with coughing, sneezing, or laughing,” “do you leak with physical activity,” and “is the leakage brief or sustained?” These and other questions may help guide the clinician to an understanding about the causes of leakage, and they may aid the patient with mixed urinary incontinence to differentiate between leakage types. This can be important in managing the patient’s expectations for treatments, as the therapies for stress and urgency incontinence are different. Other aspects of the patient history, including medical, surgical, and gynecologic issues, should be obtained. A wide variety of cardiovascular, neurologic, pulmonary, endocrine, and other health conditions may manifest as urinary incontinence. Medications may also play a role. α-adrenergic antagonists, sometimes used in the treatment of hypertension, can reduce urethral pressures and result in SUI.

The physical examination should be thorough and evaluate the developmental, structural, and neurologic components of pelvic and lower extremity anatomy. Strength and symmetry of the levator musculature and anal sphincter should be assessed, both at rest and with voluntary contraction. Defects in levator muscle may represent loss of motor units from neurologic injury. Assessment of the anal and clitoral reflexes can help identify potential underlying neurologic issues, although these have poor specificity and may be absent in neurologically intact women.

The presence and degree of prolapse in all vaginal compartments should be recorded according to the Pelvic Organ Prolapse Quantification (POP-Q) examination. Anterior vaginal prolapse can be very closely related to the pathophysiology of SUI, as described later in this chapter, but apical and posterior compartment prolapse can also affect the suburethral support in positive or negative ways. Bimanual examination of gynecologic anatomy and rectovaginal examination both provide critical information about relevant anatomic and neurologic considerations. Careful evaluation of the bladder and urethra can help identify other causes of urinary leakage, including urethral diverticula or urogenital fistula. Provocative maneuvers such as the cough stress test (CST) are important. During filling, a leak with cough represents a positive CST and confirms the finding of SUI. A positive CST after voiding is considered by many to be suggestive of intrinsic sphincter deficiency (ISD). Sustained leakage after a provocative maneuver may be indicative not of SUI, but rather of provoked detrusor overactivity.

Bladder neck mobility can be assessed with the cotton swab test, in which a lubricated cotton swab is introduced through the urethra into the bladder, then withdrawn until gentle resistance is met, signifying the location of the internal urethral meatus. The angle of the swab relative to the ground is measured at rest, and again with maximum Valsalva. A straining angle of greater than 30°, or a change from resting to straining angle of more than 30°, is considered urethral hypermobility. Other forms of assessment of urethral hypermobility included fluoroscopy and ultrasound. The importance of the assessment of urethral mobility is unclear, however, especially in primary SUI. The presence of urethral hypermobility cannot distinguish between continent and incontinent women, and midurethral slings have been shown not to change urethral mobility. SUI in the absence of hypermobility, however, may represent a different entity (Type III incontinence), which, in many reports, is a more challenging condition to correct, and results of urethral mobility testing may therefore be useful in counseling these patients. The cotton swab test may play a more important role in the assessment of recurrent SUI, or in voiding dysfunction following anti-incontinence procedures.

Objective information, including a bladder diary, provides information about frequency and amount of leakage. A three-day diary, in which a patient records all fluid intake, voiding episodes, volumes, and degree of urgency, as well as leakage episodes and the circumstances leading to them, is clinically useful. A perineal pad test, in which a collecting absorbent pad is weighed, and then worn by the patient during 1 hour of activity and then reweighed, can also be useful when assessing incontinence. Oral phenazopyridine stains urine orange-red; in conjunction with a perineal pad test, orange staining of the pad can help to distinguish leakage of urine from other forms of perineal wetness, including sweat or vaginal discharge. In circumstances where anatomic abnormalities such as urogenital fistula or ectopic ureter are suspected, phenazopyridine tampon testing can be used. If staining of the proximal end of the tampon is found, these conditions may be present, whereas transurethral leakage of urine will result in staining of the distal end of the tampon.