VOIDING DYSFUNCTION
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.
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| 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.
VOIDING
DYSFUNCTION
Voiding
dysfunctions reflect abnormalities in either the normal anatomy or neural
control of the lower urinary tract. The major causes
of chronic voiding dysfunction can be broadly classified as:
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.
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| NEURAL CONTROL OF BLADDER FILLING AND VOIDING |
NEUROPATHIC
DYSFUNCTION
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).
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| 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.
