Urinary incontinence affects an estimated 13 million adults in the United States, 85% of whom are women. The problem is especially common among nursing home residents, affecting 50%, and older women, affecting 15% to 30% of women over 65 years old who live in retirement communities. An estimated $15 to $20 billion is spent on this problem each year in the United States alone.
|ANATOMY OF FEMALE URINARY CONTINENCE MECHANISMS|
NORMAL ANATOMY OF URINARY CONTINENCE
In both sexes, the urethral wall contains smooth muscle cells that constitute an intrinsic urethral sphincter. These cells surround the submucosa and are arranged in an inner longitudinal layer and a thinner outer circular layer.
In males, an internal urethral sphincter is formed by a ring of smooth muscle near the bladder neck, which receives sympathetic input and prevents the retrograde passage of semen during ejaculation.
In both sexes, the urethra is also surrounded by rings of striated muscle that form an external urethral sphincter. In males, this muscle is located around the membranous urethra. In females, it is located primarily around the middle third of the urethra, and it receives ﬁbers from the compressor urethrae and sphincter urethrovaginalis muscles located just above the perineal membrane. The compressor urethrae muscles arise from the ischiopubic rami, with ﬁbers from each side interdigitating anterior to the urethra. Meanwhile, the sphincter urethrovaginalis muscles arise from the perineal body, pass along the lateral walls of the vagina, and then also interdigitate anterior to the urethra.
The pressures exerted by the urethral sphincters alone are sufﬁcient to maintain continence in most circumstances. During acute increases in intraabdominal pressure, however, the proximal urethra requires additional support to resist the resulting increase in intravesical pressure. In females, such support comes from a “hammock” of connective tissue against which the bladder neck and proximal urethra are compressed. The hammock is formed by the pubocervical fascia, which connects to the tendinous arch of the pelvic fascia on each side (which is itself attached to the levator ani muscles).
NEURAL CONTROL OF BLADDER FILLING AND VOIDING
Both ﬁlling and voiding require coordinated action of the detrusor muscle and urethral sphincters. During ﬁlling, mild distention of the bladder produces afferent signals that travel in pelvic nerves to the spinal cord. These signals trigger spinal reﬂexes that increase sympathetic outﬂow along the hypogastric nerves, causing relaxation of the detrusor muscle and contraction of the ureteral smooth muscle. In addition, these reﬂexes stimulate neurons originating in Onuf nucleus, located in the sacral spinal cord, which travel along the pudendal nerve to stimulate contraction of the external urethral sphincter. This response, known as the “guarding reﬂex,” prevents incontinence during bladder ﬁlling.
When bladder distention reaches a set point, intense afferent signals from the bladder activate ascending spinobulbospinal pathways that stimulate the pontine micturition center (PMC, also known as the Barrington nucleus). Activation of the PMC inhibits sympathetic outﬂow to the bladder and urethra, inhibits pudendal input to the external urethral sphincter, and promotes parasympathetic input to the detrusor along the pelvic splanchnic nerves. The net effect is relaxation of the urethral sphincters followed by contraction of the detrusor, which leads to voiding.
In adults, the PMC can be consciously suppressed until voiding is desired. Such suppression depends on inputs from cortical areas that include the prefrontal cortex, anterior cingulate cortex, and periaqueductal gray. In infants, primitive sacral reﬂexes promote voiding without the involvement of higher brain areas, such as the PMC. These reﬂexes eventually become subjected to the control of the PMC and modulatory inputs from the prefrontal cortex.
1. Neuropathic dysfunction
2. Stress urinary incontinence
3. Urge urinary incontinence
Of note, overﬂow incontinence often occurs secondary to neuropathic dysfunction or chronic outlet obstruction, and it is thus not considered a primary form of incontinence.
|NEURAL CONTROL OF BLADDER FILLING AND VOIDING|
Patients with neuropathic dysfunction have aberrations in the neural control of ﬁlling and voiding. Lesions at different levels in the relevant neural pathways cause different symptom patterns. Thus the speciﬁc level of the lesion must be inferred as precisely as possible based on history and urodynamic data.
With suprapontine lesions (i.e., cerebrovascular accident, Parkinson disease), cortical inhibition of the PMC is eliminated, causing the detrusor to become overactive. Because spinal cord connections remain intact, however, synergy persists between bladder contraction and urethral sphincter relaxation. In Parkinson disease, however, opening of the striated sphincter may be delayed, which could be misinterpreted as dyssynergia.
With lesions of between the pons and spinal cord segment S2 (i.e., multiple sclerosis, trauma), there is initial areﬂexia of the bladder, but intrinsic spinal reﬂexes (typically inactive since infancy) slowly emerge and cause the detrusor to become overactive. The voiding is often inefﬁcient, however, because interruption of spinal circuits can lead to detrusor-external sphincter dyssynergia (DESD).
With lesions of the peripheral pelvic nerves (i.e., diabetes mellitus, pelvic surgery), patients lose afferent sensations from the bladder, and the bladder often becomes hypoactive or even areﬂexic, leading to urinary retention.
A thorough history, neurologic examination, and urodynamic evaluation (see Plate 8-4) often elucidates the speciﬁc site of the lesion. The treatment strategy depends on the speciﬁc kind of dysfunction.
If the detrusor is overactive, pharmacologic agents are the ﬁrst-line treatment. Anticholinergic drugs, for example, can block parasympathetic input to the bladder. Oxybutynin is a tertiary amine antimuscarinic drug commonly used for this indication; common adverse effects include dry mouth, facial ﬂushing, dry skin, and drowsiness. Tolterodine tartarate is another common agent that generally has fewer adverse effects than oxybutynin. Additional antimuscarinics include solifenacin, darifenacin, trospium, and fesoterodine. In select patients with refractory detrusor overactivity, a sacral nerve stimulator with an implantable electrode can be placed. In others, injection of botulinum toxin into the detrusor muscle may be helpful.
In cases of urinary retention, clean intermittent catheterization is the mainstay of conservative management. Catheterization every 4 to 6 hours can prevent leakage associated with bladder overﬂow (i.e., overﬂow incontinence). An indwelling Foley or suprapubic catheter may be required for patients who do not have the manual dexterity or resurces to perform clean intermittent catheterization.
STRESS URINARY INCONTINENCE
As described above, urethral support from the pelvic ﬂoor is essential for maintenance of continence during increases in intraabdominal pressure. In response to aging, multiple vaginal deliveries, chronic cough, or obesity, these supports may become damaged or weakened. As a result, the urethra becomes hypermobile and, during episodes of “stress” (i.e., coughing, straining), undergoes rotation and opening that permits leakage of urine. This phenomenon is known as stress urinary incontinence (SUI).
As described previously, the urethral sphincters also protect against incontinence in response to increased intravesical pressure via the guarding reﬂex. Although these sphincters were once thought to be normal in SUI, it is now known they may exhibit a variable degree of dysfunction that contributes to urine leakage. Signiﬁcant dysfunction of the external urethral sphincter may reﬂect pudendal neuropathy, which can result from aging or prior pregnancy.
A pelvic examination may be remarkable for laxity of the pelvic musculature, while vaginal examination may demonstrate anterior wall weakness, cystocele, or rectocele. During the Valsalva maneuver, urinary leakage may be noted while the patient is in the lithotomy position. The degree of urethral mobility may be assessed by the Q-tip test, in which a well-lubricated, sterile cotton tipped applicator is inserted into the urethra to the level of the bladder neck. The resting, horizontal angle of the Q-tip and the angle after maximum strain are both recorded. Hypermobility is deﬁned as a resting or straining angle of greater than 30 degrees.
The various treatment options for SUI attempt to restore support to the urethra. Pelvic ﬂoor rehabilitation is an intensive program in which patients perform Kegel exercises and other routines to engage and strengthen the pelvic ﬂoor. Up to 40% to 50% of patients will be satisﬁed with the results of this therapy and avoid an operation. Thus noninvasive management should be the ﬁrst line of therapy for appropriately selected and motivated patients.
Surgery is indicated in (1) patients with severe symptoms, (2) patients with signiﬁcant pelvic organ prolapse that may need to be simultaneously corrected, (3) those who are highly motivated to achieve continence because of physical or occupational stress, and (4) those with good pelvic ﬂoor function who likely have a signiﬁcant degree of intrinsic sphincter dysfunction.
Both suprapubic and vaginal approaches have been developed to restore urethral support. In the Marshall-Marchetti-Krantz procedure, which takes a suprapubic approach, the periurethral tissues are attached to the posterior surface of the pubic symphysis. This operation was subsequently modiﬁed to become the Burch procedure, in which the anterior vaginal wall is ﬁxed to the Cooper ligament, turning it into a substitute for the normal fascial “hammock” against which the urethra can be compressed.
A vaginal approach is much more common in contemporary times, especially among women with intrinsic sphincteric deﬁciency or signiﬁcant pelvic muscle weakness. In one procedure, known as transobturator tension-free vaginal tape, a synthetic piece of polypropylene mesh is passed behind the urethra using a device that crosses through the obturator membranes. In this way, the mesh affords posterior support to the urethra, although its ends are not tethered to the pubic bone. The tape may also be constructed using other organic materials, such as cadaveric fascia lata.
If patients have intrinsic sphincter weakness, injection of bulking material into the urethra is sometimes performed. Such materials include collagen, silicone, or polydimethylsiloxane (solid silicone elastomer).
|STRESS URINARY INCONTINENCE|
URGE URINARY INCONTINENCE
Urge incontinence is typiﬁed by the sudden, intense desire to urinate to prevent leakage. In this condition, the detrusor has spontaneous, abnormal contractions, often in the setting of normal anatomy and, in some cases, neural function. Nonneurogenic urge incontinence commonly occurs in patients with cystitis or signiﬁcant bladder outlet obstruction with a resulting decrease in compliance. The distinction between stress and urge incontinence is important because urge incontinence may result from a secondary pathologic process and is best managed with anticholinergics rather than surgical intervention.
OTHER FORMS OF URINARY INCONTINENCE
Although not as prevalent as the forms of incontinence described previously, other mechanisms of urinary incontinence may occur. Fistulous communication between the bladder and the vagina or rectum, commonly a result of prior surgery or neoplasm, can result in total incontinence.
Surgical damage to the urinary sphincter may also result in incontinence. Finally, among the pediatric population, incontinence may result from ectopic ureteral insertion or urethral attachments, as well as other urogenital anomalies that affect the de elopment of the external sphincter, such as epispadias.