Which type of incontinence refers to involuntary loss of urine through an intact urethra as a result of a sudden increase in intra abdominal pressure?

The ICS defines it as involuntary urine leakage on effort or exertion, or on sneezing or coughing. In men, stress incontinence is mostly due to surgery (eg, after radical prostatectomy) or trauma to the bladder neck/urethral sphincter. The causes of stress incontinence in women are more complicated and somewhat controversial and therefore the following discussion is mostly related to female stress incontinence. The vast majority of stress incontinence occurs in women after middle age (with repeated vaginal deliveries and obstructed labor). It is usually a result of weakness/disruption of the pelvic floor muscle and ligaments leading to poor support of the vesicourethral sphincteric unit. An increase in urethral closure pressure is normally seen during bladder filling; when assuming an upright position; or in stressful events such as coughing, sneezing, or bearing down. During exertion, both passive pressure transmission from increased abdominal pressure and reflexic contraction of the sphincteric mechanism augment urethral resistance to prevent urine leakage.

Anatomy

Stress incontinence is thought to be caused by two major anatomical deficits: hypermobility of the sphincteric unit and intrinsic sphincter deficiency. In hypermobility, the assumption is that the intrinsic structure of the sphincter itself is intact. It loses closing efficiency because of excessive mobility and loss of support. Thus, the anatomic feature of stress incontinence is hypermobility or a lowering of the position of the vesicourethral segment (or a combination of the two factors) (Figure 30–1). On the other hand, some women who have undergone multiple retropubic or urethral operations have a deficient intrinsic sphincteric mechanism characterized by an open bladder neck and proximal urethra at rest with minimal or no urethral descent during stress. Nevertheless, many women maintain normal continence with hypermobility, and a recent dynamic magnetic resonance imaging (MRI) study finds no correlation between perineal descent and patients' symptoms of urinary incontinence (Broekhuis et al, 2010). Therefore, contemporary opinion suggests that all women with stress incontinence have some degree of intrinsic sphincter deficiency.

Figure 30–1.

Lateral cystograms in a 53-year-old woman with stress incontinence. A: Preoperative, relaxed. Note slightly low-lying vesicourethral junction. The posterior vesicourethral angle is near normal. B: With straining, excessive downward and posterior mobility of the vesicourethral segment is shown. Posterior angle almost disappears.

The relationships between the urethra, the bladder base, and various bony points have been the object of much study. For many years, the posterior vesicourethral angle has been considered a key factor indicating the presence of anatomic stress incontinence. Some authors, however, have emphasized the axis of inclination, that is, the angle between the urethral line and the vertical plane. Other investigators stress bony landmarks in the pelvis in their descriptions of the relationship of the bladder base and the vesicourethral junction to the sacrococcygeal inferior pubic point (Figure 30–2).

Figure 30–2.

Diagrammatic representation of (A) the angles considered when assessing adequacy of bladder support (posterior vesicourethral angle; angle of inclination) and (B) the “SCIPP line” (sacrococcygeal inferior pubic point) and its relationship to the bladder base and the vesicourethral segment as a reference to adequate pelvic support.

These descriptions illustrate that abnormal anatomic position and excessive mobility are essential elements in the diagnosis of stress incontinence due to hypermobility. To evaluate this aspect of incontinence, a simplified cystographic study (a lateral cystogram with a urethral catheter in place) is recommended. With the patient lying on the flat x-ray table, a lateral film is obtained, first at rest to determine the position of the vesicourethral segment in relation to the pubic bone and then with straining to ascertain its degree of mobility (Figures 30–3 and 30–4). Normally, the vesicourethral junction is opposite the lower third of the pubic bone and moves 0.5–1.5 cm with straining. This demonstration of abnormal position or excessive mobility of the vesicourethral segment is helpful in identifying the cause of existing urinary incontinence.

Figure 30–3.

Lateral cystograms in two continent women in the relaxed state. A perpendicular line from the anterior vesicourethral angle over the long axis of the pubic bone crosses the bone near the junction of the middle and lower thirds.

Figure 30–4.

Lateral cystograms in two young continent women. A: Relaxed state, 28-year-old woman. B: With straining, the vesicourethral segment is displaced 0.5 cm downward and posteriorly. C: Relaxed state, 34-year-old woman. D: With straining, the vesicourethral segment is displaced 0.8 cm downward and 1 cm posteriorly.

The urethral pressure profile is a measure of the activity of the external sphincter. A static profile demonstrates the resting tonus of both components of the sphincteric mechanism (see Figure 30–5); a dynamic profile gives the responses of these sphincteric elements to various activities, such as an increase in bladder volume, assumption of the upright position (Figure 30–6), the prolonged stress of bearing down, or the sudden stress of coughing and sneezing (Figure 30–7). Normally, the urethral closure pressure—the net difference between the intraurethral and intravesical pressures—is maintained or augmented during stress.

Figure 30–5.

Normal urethral pressure. Closure pressure at the level of the internal meatus is very low; the pressure rises progressively to reach its maximum at approximately the middle third of the urethra—the site of maximal condensation of striated muscle.

Figure 30–6.

Urethral pressure profile for a patient in sitting and upright positions. An approximately 50% increase in urethral closure pressure occurs when the patient assumes the upright position. Urethral functional length is well sustained.

Figure 30–7.

A: Intravesical and urethral pressure responses to the stresses of coughing, bearing down, and the hold maneuver. Note the sharp increase in intra-abdominal pressure reflected in intravesical pressure with coughing and the simultaneous greater increase in urethral pressure. The response is similar with bearing down. Closure pressure is maintained and even augmented during these periods of stress. The hold maneuver (recording membrane is in the proximal urethra) produces a minimal response in closure pressure of the proximal urethra. B: Recording comparable with that in A, but the membrane is in the midurethra. Note again the sustained closure pressure as a result of coughing and bearing down and the marked pressure increase in the midurethral segment with the hold maneuver.

Detailed research of the role of smooth and striated components of the bladder and urethra were performed in animal experiments in the 1980's. Electrical stimulation of the pelvic nerve induces contraction of the smooth muscle of the bladder and urethra (Figure 30–8) while stimulation of the sacral nerve contracts smooth muscle of the bladder and urethra as well as striated muscle of the external sphincter (Figure 30–9). The contribution of smooth and striated muscle to urethral opening/closure pressure is further demonstrated in Figures 30–10, 30–11, and 30–12.

Figure 30–8.

A: Response to pelvic nerve stimulation. Note the simultaneous, equal pressure rise in the bladder, proximal urethra (U1), and midurethra (U2). B: Vesical and sphincteric responses to an injection of the parasympathetic drug methacholine chloride. Note again the simultaneous rise in pressure at the bladder, proximal urethra (U1), and midurethra (U2).

Figure 30–9.

Response of the striated component to sacral nerve stimulation. Note that bladder pressure does not change and proximal urethral pressure (U1) rises only slightly, compared with the sharp and sustained increase in midurethral pressure (U2).

Figure 30–10.

A: The resistance required to force the urethra open, overcoming both voluntary and involuntary sphincteric elements. With progressively increasing pressure, the urethra opens at the critical opening pressure (in this recording, about 85 mm Hg). Once the urethra is forced open, the resistance to flow drops precipitously and becomes sustained at the level of sustained urethral resistance (in this recording, roughly 50 mm Hg). B: A similar recording obtained after administration of curare, which completely blocks voluntary sphincteric responses. Note the appreciable drop in both critical opening pressure and sustained resistance. C: Recording after administration of both curare and atropine (a combination that eliminates the activity of smooth and voluntary sphincteric elements). The critical opening pressure drops markedly and is now equal to the sustained resistance; both are very low. D: An overlap of the three recordings shows the contribution of each muscular element: the voluntary component contributes roughly 50% of the total resistance, while the smooth component contributes the other 50%. The minimal residual resistance is a function of the collagen elastic element of the urethral wall; this collagen element has no sphincteric significance.

Figure 30–11.

Urethral pressure profile. A: At rest. B: Stimulation of both the pudendal and the pelvic nerves incites the maximal response from both smooth and voluntary sphincteric elements. C: Pudendal stimulation alone demonstrates the contribution of the voluntary component. D: Pelvic nerve stimulation shows the response of the smooth-muscle component alone. Bottom tracings: Total maximal pressure profile obtained by stimulation of pelvic and pudendal nerves depicted by overlapping the profile of simultaneous stimulation of both nerves. The contribution and anatomic distribution of each element are clearly seen. Their summation results in the overall total responses recorded in B above.

Figure 30–12.

Urethral pressure profile at rest and after subjecting an experimental animal to progressively increasing extrinsic pressure applied around the abdomen—not involving any muscular activity. A: Extrinsic pressure was increased by 25-mm Hg increments. Note the sharp increase in urethral closure pressure with each increment, marked after 25 and 50 mm Hg, less so after 75 and 100 mm Hg. The increase in urethral closure pressure is far higher than the increase in extrinsic pressure, which denotes not simple transmitted pressure but active muscular function. B: Curare administration demonstrates that much of the rise in closure pressure recorded in A results from the activity of the voluntary sphincter, which is lost after blockade by curare.

The high rate of success from midurethral sling surgery led some to believe that the midurethral support is the key element in preventing stress incontinence and raise doubts about the relevance of the cystographic study. Petros and Ulmstem (1990) proposed that support of the anterior vaginal wall is provided by three separate but synergistic mechanisms: the anterior pubococcygeus muscle; the bladder neck; and the pelvic floor musculature, which acts like a hammock to help close the bladder neck during stress. Laxity of the anterior vaginal wall causes dissipation of all of three forces, resulting in stress incontinence. Delancey (1994) proposes that the stability of the supporting layer rather than the position of the urethra determines stress continence. During rises in intra-abdominal pressure, the urethra is compressed against the supporting structures, which act like a backboard and prevent loss of urine. The fact that both bladder neck and midurethral slings have been shown to be successful in treating stress incontinence supports the above-mentioned theories (Novara et al, 2010; Ulmsten et al, 1998).

A recent report of a clinical study concludes that low urethral closure pressure is the best predictor of SUI in women (DeLancey et al, 2008). An MRI study also revealed that the striated urogenital sphincter in women with stress incontinence was 12.5% smaller than that in asymptomatic continent women (Morgen et al, 2009). A study on duloxetine, a serotonin and norepinephrine reuptake inhibitor, showed that it elevates both baseline urethral pressure (adrenergic innervation on the smooth muscle) and active pressure rise with sneezing (Onuf' nucleus activated striated muscle contraction (Miyazato et al, 2008). These observations reaffirm the original observation by Tanagho that smooth muscle, striated muscle, and mucosa and submucosal vessels each contribute about one-third of the urethral closure pressure and all are important in sphincter function.

Diagnosis

A detailed history is important, including the degree of leakage; its relation to activity, position, and state of bladder fullness; the timing of its onset; and the course of its progression. Knowledge of past surgical and obstetric history, medications taken, dietary habits, and systemic diseases (eg, diabetes) can be helpful in the diagnosis. A micturition diary that records the time of micturition, voided volume, and type of incontinence is recommended by the ICS as a useful supplement (Abrams et al, 2010). A pad test over 1 hour or 24 hours has also been recommended. In addition, history should also include the degree of bother and effect on quality of life. Many questionnaires and diaries are available for clinical and research use.

Physical examination is essential especially if urine leakage is witnessed by the examiner. In women, the pelvic examination demonstrates laxity of pelvic support, presence of any degree of prolapse, cystocele, rectocele, and mobility of the anterior vaginal wall. A neurologic examination should be done if neuropathy is suspected. Cystographic study for demonstration of the anatomic abnormality is helpful, as is urodynamic study to confirm the classic features of urinary incontinence and determine its cause. The goals of cystographic and urodynamic study are, first, to demonstrate the anatomic abnormality and its extent and, second, to assess the activity of the sphincteric mechanism and hence the potential for improvement by correcting the anatomic abnormality. The degree of hypermobility in women can also be assessed by a simple Q-tip test (Swift et al, 2010). This is done by inserting a well-lubricated sterile cotton-tipped applicator gently through the urethra into the bladder and then pulling it back to the level of the bladder neck. The angle from the horizontal at rest and after straining is recorded. Hypermobility is defined as a resting or straining angle >30° from the horizontal.

Urodynamic Characteristics of Stress Incontinence

Urethral Pressure Profile

The ICS defines urodynamic stress incontinence as the involuntary leakage of urine during increased abdominal pressure, in the absence of a detrusor contraction (Abrams et al, 2003). As would be expected, most patients with stress incontinence have a low urethral pressure profile with reduced closure pressure. This factor varies with the severity of the sphincteric impairment. Not infrequently, this weakness of the pressure profile is not demonstrable when the bladder is relatively empty. It becomes more significant when the bladder has been distended (Figure 30–13). Also, the pressure profile may appear normal when the patient is in the resting (sitting) position; when he or she assumes the upright position in the dynamic pressure profile, the weakness becomes apparent (Figure 30–14).

Figure 30–13.

Urethral pressure profile with minimally filled bladder. Bladder pressure remains constant, but urethral pressure drops progressively. Closure pressure becomes minimal at the end of bladder filling.

Figure 30–14.

Urethral pressure profile in moderately severe stress incontinence: closure pressure with patient in the sitting position with half-distended bladder, then after the upright position is assumed. Note that closure pressure is close to 75 cm H2O with the patient in the sitting position but decreases to approximately 35 cm H2O with the upright position. Note also the marked shortening of functional urethral length once the upright position is assumed.

Functional Urethral Length

The anatomic length of the urethra is usually maintained, yet the functional length is shorter due to loss in the proximal urethral segment (Figure 30–15). Although it might not appear funneled on the cystogram, this segment has very low closure efficiency and its pressure is almost equal to intravesical pressure. The functional shortening might be minimal or it might involve more than one-half of the length of the urethra. It is important to note that the functional length, like the pressure profile, might appear normal when the bladder is not filled or the patient is in the sitting position.

Figure 30–15.

Urethral pressure profile in a female patient with moderate urinary stress incontinence. Note the relatively low closure pressure, the short functional urethral length, and the loss of closure pressure of the proximal 1.5 cm of urethra.

Response to Stress

With the sustained stress of bearing down or the sudden stress of coughing or sneezing, the net urethral closure pressure is reduced, depending on the degree of sphincteric weakness. In severe urinary stress incontinence, any strain or increase in intravesical pressure leads to urinary leakage (Figure 30–16).

Figure 30–16.

Urethral pressure profile in moderate stress incontinence. Note that, with the bladder relatively empty, closure pressure is close to the normal range. At the start of bladder filling, resting pressure is again normal; as filling progresses, bladder pressure remains stable and urethral closure pressure decreases progressively to a minimum with full bladder distention.

Voluntary Increase in Urethral Closure Pressure

Patients with mild stress incontinence might be capable of activating their external sphincter maximally and generating a high urethral closure pressure. However, with progression of the anatomic problem and hypermobility, this voluntary increase progressively diminishes.

Response to Bladder Distention and Change in Position

It must be emphasized that, although the features described might be normal in the resting position with minimal bladder filling, all of them can become aggravated with a full bladder or the upright position (Figures 30–14 and 30–17).

Figure 30–17.

Effect of bladder filling and emptying on urethral pressure. Top: Effect of progressive filling, which leads to a gradual drop in urethral pressure. At the end of filling, urethral closure pressure is only a fraction of the relatively normal initial closure pressure. Bottom: At the start, the bladder is full. With gradual emptying, note the progressive buildup in urethral resistance and closure pressure.

Abdominal Leak Point Pressure

Abdominal leak point pressure (ALPP) is defined as the intravesical pressure at which urine leakage occurs because of increased abdominal pressure in the absence of a detrusor contraction (Abrams et al, 2003). This test assesses the intrinsic urethral function, and thus the lower the ALPP, the weaker the sphincter.

Treatment

In mild and moderate cases, the ICS recommends lifestyle interventions, such as weight loss, caffeine reduction, pelvic floor muscle training, or duloxetine, a serotonin and norepinephrine reuptake inhibitor that has been approved in many countries but not in the United States. Electrical stimulation, vaginal devices, and urethral inserts may also help some women.

If the initial management fails, the principal surgical treatment of female urinary stress incontinence is to provide proper support of the vesicourethral segment or the midurethra.

There are numerous approaches to restoring the normal position and providing adequate support—some vaginal, others suprapubic. The suprapubic approach was popularized by the classic Marshall-Marchetti-Krantz (MMK) retropubic suspension described in 1949, in which periurethral tissue is attached to the back of the pubic symphysis. A modification was introduced by Burch in 1961, in which the anterior vaginal wall is fixed to Cooper's ligament. Many urologic surgeons today have found that the latter technique, with modifications, provides the most lasting results (Drouin et al, 1999; Kulseng-Hanssen and Berild, 2002) (Figures 30–18 and 30–19).

Figure 30–18.

A: Diagrammatic depiction of the retropubic space after mobilization of the anterior vaginal wall and placement of sutures, two on either side and far from the midline laterally. Distal sutures are opposite the midurethra, while proximal sutures are at the end of the vesicourethral junction. Sutures are attached to Cooper's ligament. B: Side view of suture placement with one side tied. The anterior vaginal wall acts as a broad sling, supporting and lifting the vesicourethral segment. The urethra is free in the retropubic space.

Figure 30–19.

Top: Cross section shows the urethra free in the retropubic space with the anterior vaginal wall lifting and supporting it. Bottom: The urethra is compressed against the pubic bone when vaginal sutures are applied close to the urethra and fixed to the symphysis pubis. The vaginal suspension has various forms; in some, the tissue is gathered behind the bladder neck (eg, the Kelly procedure), while others rely on sutures in the paravaginal tissues that are passed bluntly to the suprapubic area by a needle to be tied over the rectus sheath. This technique was originally described by Pereyra in 1959 and subsequently was modified—in 1973 by Stamey, who added endoscopic confirmation of suture placement and the degree of compression, and in 1981 by Raz. Most of these techniques have a high initial success rate; however, there is some concern about the long-term results. Hence, the retropubic approach remains the recommended procedure.

The other approach is to suspend the bladder neck or support the midurethra with an abdominal or transobturator sling. Numerous sling materials are being used: for example, cadaveric fascia lata and various synthetic materials. Tension-free vaginal tape (TVT) has been gaining popularity. Early results for TVT with follow-up to 11 years demonstrate comparable or improved versus traditional surgical approaches (suburethral slings, urethropexy, colposuspension, or injectable bulking agents) and reported success rates of up to 77% (Fong and Netti, 2010; Novara et al, 2010). Potential complications include bladder injury, infection, urinary retention, hemorrhage or hematoma, erosion (vaginal or urethral), and dyspareunia.

In patients with significant intrinsic sphincteric damage, local injection of bulking material, such as hyaluronic acid/dextranomer gel, polydimethylsiloxane (Macroplastique), pyrolytic carbon-coated beads suspended in a water-based carrier gel (Durasphere®), and collagen, is used to increase the bladder outlet resistance for patients in whom vesicourethral mobility is not excessive and whose primary problem is intrinsic sphincteric weakness (Ghoniem et al, 2010; Lightner et al, 2009). Recently, myoblast, fibroblast, and adult stem cells have been injected into periurethral tissue with very promising results (Carr et al, 1988; Mitterberger et al, 2007, 2008; Yamamoto et al, 2010). Besides the bulking effect, the injected stem cells seem to be able to stimulate local tissue proliferation (smooth muscle, collagen and elastic fibers) and thus improve the competence of the sphincter (Lin et al, 2010).

Which type of incontinence refers to involuntary loss of urine through an intact urethra?

Which of the following types of incontinence refers to involuntary loss of urine through an intact urethra as a result of a sudden increase in intra abdominal pressure?

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