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Even in an individual patient, urinary incontinence may have multiple

etiologies, with varying degrees of contribution to the overall disorder.
Structural and functional disorders involving the bladder, urethra, ureters,
and surrounding connective tissue can contribute. In addition, a disorder of
the spinal cord or central nervous system (CNS) may be the major etiologic
factor in some cases. Medical comorbidities also can be important. Finally,
some cases of urinary incontinence may be pharmacologically induced. [29]
The most common cause of stress incontinence in women is urethral
hypermobility secondary to poor anatomic pelvic support. Women may lose
this pelvic support with postmenopausal estrogen loss, childbirth, surgery,
or certain disease states that affect tissue strength. A less common cause
of stress incontinence is intrinsic sphincter deficiency, which can result from
the aging process, pelvic trauma, surgery
(eg, hysterectomy, [30] urethropexy, pubovaginal sling), or neurologic
The most common cause of intrinsic sphincter deficiency in men is radical
prostatectomy for prostate cancer or transurethral resection of
the prostatefor benign prostatic hyperplasia. A less common cause of
intrinsic sphincter deficiency is trauma to the bladder neck or prostate,
resulting from pelvic fracture due to high-impact deceleration injuries.
Contributing factors with aging-related urinary incontinence include a
weakening of connective tissue, genitourinary atrophy due to
hypoestrogenism, increased incidence of contributing medical disorders,
increased nocturnal diuresis, and impairments in mobility and cognitive
functioning. [9, 31]
Other factors that may increase the risk of developing incontinence include
obesity, straining at stool as a child or young adult, heavy manual
labor, chronic obstructive pulmonary disease, and smoking. [32, 33] In many
cases of incontinence that are due to detrusor overactivity, the problem is
idiopathic in nature.
In a prospective cohort study of 5,391 young women from the Australian
Longitudinal Study on Women's Health, depressive symptoms were
associated with 37% higher odds of having urinary incontinence after
adjustment for sociodemographic factors, body mass index, health
behaviors, and reproductive factors. Having physician-diagnosed
depression was associated with 42% higher odds. [34]
A review of women with type 1 diabetes mellitus who participated in the
Diabetes Control and Complications Trial (DCCT) and its observational
follow-up study, the Epidemiology of Diabetes Interventions and
Complications (EDIC), found that incident urinary incontinence was
associated with higher hemoglobin A1c levels, independent of other
recognized risk factors. Thus, improved glycemic control might reduce the
risk of urinary incontinence in such patients. [35]
Less frequent causes of urinary incontinence include complications of
urologic procedures or pelvic radiation therapy. In the pediatric population,
it includes enuresis and congenital abnormalities of the genitourinary
Transient causes
Transient urinary incontinence is often seen in both elderly and hospitalized
patients. The mnemonic DIAPPERS is a good way to remember most of
the reversible causes of incontinence, as follows [25] :
D: Delirium or acute confusion
I: Infection (symptomatic UTI)
A: Atrophic vaginitis or urethritis
P: Pharmaceutical agents
P: Psychological disorders (depression, behavioral disturbances)
E: Excess urine output (due to excess fluid intake, alcoholic or
caffeinated beverages, diuretics, peripheral edema, congestive heart
failure, or metabolic disorders such as hyperglycemia or hypercalcemia)
R: Restricted mobility (limits ability to reach a bathroom in time)
S: Stool impaction
In addition to urinary tract infection, conditions such as bladder
cancer, bladder stones, and foreign bodies can irritate the bladder, resulting
in involuntary bladder contractions and incontinence. Less common
infectious causes of overflow incontinence include AIDS, genital herpes
affecting the perineal area, and neurosyphilis. Stones or neoplasms may
also result in incontinence due to obstruction.
Neurological causes
Cortical lesions (eg, from strokes, tumors, aneurysms, or hemorrhages)
can lead to inappropriate voiding secondary to depressed social
awareness, decreased sensation, and/or inappropriate urethral sphincter
relaxation. [25]Cerebrovascular disease doubles the risk for urinary
incontinence in older women.
Spinal cord lesions can alter sympathetic and parasympathetic tone,
resulting in urinary incontinence. Peripheral nerve disease such as diabetic
peripheral neuropathy can cause urinary incontinence through a contractile
dysfunction of the bladder.
Metastatic carcinoma can cause epidural spinal cord compression. Back
pain is the initial symptom in most cases. Almost 20% of cases involve the
lumbosacral spine. If the sacral cord is involved, urinary incontinence or
retention can be expected. Urinary incontinence symptoms represent an
unfavorable prognostic indicator in this patient population. Early diagnosis
and treatment of spinal cord compression is extremely important.
Paraplegia or quadriplegia can develop within hours or days after the first
neurologic deficit appears.
S2-S5 nerve root injury (herniation) can cause bladder dysfunction. Cauda
equina syndrome can develop in patients with a large centrally protruding
disk. Symptoms include bilateral leg pain and weakness, saddle
anesthesia, urinary retention or incontinence, and fecal retention or
incontinence. It is important to recognize this syndrome early because
there is a high risk for chronic neurologic deficits if treatment is delayed.
Hemicauda equina syndrome (from a herniated lumbar disk) can also
manifest as urinary incontinence. It presents as unilateral leg pain,
unilateral sensory deficit in the S1-S5 dermatomes, and urinary
incontinence or urinary retention. These patients require urgent
neurosurgical consultation for emergency surgery.
Multiple sclerosis should be considered in any patient without evidence of
urinary tract infection who has episodic or rapid onset of urinary symptoms.
Urinary incontinence may occur by itself or may be accompanied by other
vague neurological symptoms.
Patients with a neurogenic disorder such as myelomeningocele may have
an open bladder neck that results in severe intrinsic sphincter deficiency
and urinary loss.
Pharmacologic causes
Many medications contribute to urinary incontinence, directly or indirectly.
Medications must always be considered as the cause of new-onset urinary
incontinenceespecially in elderly persons, in whom polypharmacy is often
encountered. [36, 25]
Medication may result in incontinence through the following mechanisms:
Drugs with anticholinergic properties or side effects (eg,
antipsychotics, antidepressants) - Urinary retention and thus overflow
Alpha-adrenergic agonists - Urinary retention and thus overflow
urinary incontinence
Alpha-antagonist - Urethral relaxation
Diuretics Overwhelming of bladder capacity in elderly persons
Calcium channel blockers - Decreased smooth muscle contractility in
the bladder, causing urinary retention with overflow incontinence
Sedative-hypnotics - Immobility secondary to sedation, leading to
functional incontinence
Angiotensin-converting enzyme (ACE) inhibitors Diuretic effect, as
well as side effect of cough with relaxation of pelvic floor musculature,
can exacerbate incontinence
Antiparkinson medications - Urinary urgency and constipation
Micturition requires coordination of several physiological processes.
Somatic and autonomic nerves carry bladder volume input to the spinal
cord, and motor output innervating the detrusor, sphincter, and bladder
musculature is adjusted accordingly. The cerebral cortex exerts a
predominantly inhibitory influence, whereas the brainstem facilitates
urination by coordinating urethral sphincter relaxation and detrusor muscle
As the bladder fills, sympathetic tone contributes to closure of the bladder
neck and relaxation of the dome of the bladder and inhibits
parasympathetic tone. At the same time, somatic innervation maintains
tone in the pelvic floor musculature as well as the striated periurethral
When urination occurs, sympathetic and somatic tones in the bladder and
periurethral muscles diminish, resulting in decreased urethral resistance.
Cholinergic parasympathetic tone increases, resulting in bladder
contraction. Urine flow results when bladder pressure exceeds urethral
resistance. Normal bladder capacity is 300-500 mL, and the first urge to
void generally occurs between bladder volumes of 150 and 300 mL.
Incontinence occurs when micturition physiology, functional toileting ability,
or both have been disrupted. [9] The underlying pathology varies among the
different types of incontinence (ie, stress, urge, mixed, reflex, overflow, and
functional incontinence).
Stress incontinence pathophysiology
During episodes of stress incontinence, an increase in intra-abdominal
pressure (eg, from laughing, sneezing, coughing, climbing stairs) raises
pressure within the bladder to the point where it exceeds the urethras
resistance to urinary flow. [2, 3, 4] Leakage ceases when bladder pressure
again falls below urethral pressure.
The major cause of stress incontinence is urethral hypermobility due to
impaired support from pelvic floor. A less common cause is an intrinsic
sphincter deficiency, usually secondary to pelvic surgeries. In either case,
urethral sphincter function is impaired, resulting in urine loss at lower than
usual abdominal pressures.
In women with stress urinary incontinence, either or both mechanisms may
be present, although some authors hold that stress incontinence does not
develop in patients with poor pelvic support unless intrinsic sphincter
deficiency is also present. Intrinsic sphincter deficiency, resulting from loss
of function of both the internal and the external sphincter mechanism, is the
only cause of stress incontinence in males.
Urethral hypermobility
Urethral hypermobility is related to impaired neuromuscular functioning of
the pelvic floor coupled with injury, both remote and ongoing, to the
connective tissue supports of the urethra and bladder neck. When this
occurs, the proximal urethra and the bladder neck descend to rotate away
and out of the pelvis at times of increased intra-abdominal pressure.
Because the bladder neck and proximal urethra move out of the pelvis,
more pressure is transmitted to the bladder. During this process, the
posterior wall of the urethra shears off the anterior urethral wall to open the
bladder neck when intrinsic sphincter deficiency is present.
In women without urethral hypermobility, the urethra is stabilized during
stress by three interrelated mechanisms. One mechanism is reflex, or
voluntary, closure of the pelvic floor. Contraction of the levator ani complex
elevates the proximal urethra and bladder neck, tightens intact connective
tissue supports, and elevates the perineal body, which may serve as a
urethral backstop.
The second mechanism involves intact connective tissue support to the
bladder neck and urethra. The pubocervicovesical or anterior endopelvic
connective tissue in the area of the bladder neck is attached to the back of
the pubic bone, the arcus tendineus fascia pelvis, and the perineal
membrane. The pubourethral ligaments also suspend the middle portion of
the urethra to the back of the pubic bone.
These connective-tissue components form the passive supports to the
urethra and bladder neck. During times of increased intra-abdominal
pressure, if these supports are intact, they augment the supportive effect of
muscular closure of the pelvic floor.
The third mechanism involves 2 bundles of striated muscle, the
urethrovaginal sphincter and the compressor urethrae, found at the distal
aspect of the striated urethral sphincter. These muscles may aid in
compressing the urethra shut during stress maneuvers. These muscles do
not surround the urethra, as the striated sphincter does, but lie along the
lateral and ventral aspects.
The exact function and importance of these muscles are controversial.
Some authors suggest that the urethrovaginal sphincter and the
compressor urethrae may provide compression and increased pressure in
the distal urethra during times of stress.
Damage to the nerves, muscle, and connective tissue of the pelvic floor is
important in the genesis of stress incontinence. Injury during childbirth
probably is the most important mechanism. Aging, hypoestrogenism,
chronic connective tissue strain due to primary loss of muscular support,
activities or medical conditions resulting in long-term repetitive increases in
intra-abdominal pressure, and other factors can contribute.
During childbirth, 3 types of lesions can occur: levator ani muscle tears,
connective tissue breaks, and pudendal/pelvic nerve denervation. Any of
these injuries can occur in isolation but 2 or more in combination are more
likely to occur. The long-term result may be the loss of active and passive
urethral support and loss of intrinsic urethral tone.
The loss of urethral and bladder neck support may impair urethral closure
mechanisms during times of increased intra-abdominal pressure. This
phenomenon can be viewed in several ways.
Some hypothesize that under normal circumstances, any increase in intra-
abdominal pressure is transmitted equally to the bladder and proximal
urethra. This is likely due to the retropubic location of the proximal and mid
urethra within the sphere of intra-abdominal pressure. At rest, the urethra
has a higher intrinsic pressure than the bladder. This pressure gradient
relationship is preserved if acute increases in intra-abdominal pressure are
transmitted equally to both organs.
When the urethra is hypermobile, pressure transmission to the walls of the
urethra may be diminished as it descends and rotates under the pubic
bone. Intraurethral pressure falls below bladder pressure, resulting in urine
A related way of describing the mechanism of hypermobility-related stress
incontinence is the hammock theory posited by DeLancey. [14] Normally, an
acute increase in intra-abdominal pressure applies a downward force to the
urethra. The urethra is then compressed shut against the firm support
provided by the anterior vaginal wall and associated endopelvic connective
tissue sheath. If the endopelvic connective tissue is detached from its
normal lateral fixation points at the arcus tendineus fascia pelvis, optimal
urethral compression does not take place.
A simple analogy is that of a garden hose (urethra) running over a
pavement surface (anterior endopelvic connective tissue). A force is applied
in a downward direction using the foot (increased intra-abdominal
pressure). This force compresses the hose shut, occluding flow. If the same
hose is run through a soft area of mud (damaged connective tissue), then
the downward force does not occlude the hose but, rather, pushes the hose
deeper into the mud.
An alternative theory of the mechanism of stress incontinence stems from
research involving ultrasound visualization of the bladder neck and
proximal urethra during stress maneuvers. This research found that 93% of
patients with stress incontinence displayed funneling of the proximal
urethra with straining, and half of those individuals also showed funneling
at rest. [15] In addition, during stress maneuvers, the urethra did not rotate
and descend as a single unit; rather, the posterior urethral wall moved
farther than the anterior wall.
Although mobile, the anterior urethral wall has been observed to stop
moving, as if tethered, while the posterior wall continued to rotate and
descend. Possibly, the pubourethral ligaments arrest rotational movement
of the anterior wall but not the posterior wall. The resulting separation of the
anterior and posterior urethral walls might open the proximal urethral
lumen, thus allowing or contributing to stress incontinence.
Intrinsic sphincter deficiency
Intrinsic sphincter deficiency is a condition in which the urethral sphincter is
unable to coapt and generate enough resting urethral closing pressure to
retain urine in the bladder. The anatomic support of the urethra may be
Intrinsic sphincter deficiency is due to devascularization and/or denervation
of the bladder neck and proximal urethra. The urethral sphincter may
become weak after pelvic surgery (eg, failed bladder suspension surgery)
because of nearby nerve damage or excessive scarring of the urethra and
surrounding tissues. Additional causes of urethral dysfunction include pelvic
radiation or neurologic injury, including myelomeningocele.
Women with severe intrinsic sphincter deficiency do not always have the
usual urethral hypermobility during a Valsalva maneuver. Paradoxically, the
urethra appears well supported. This results in so-called lead pipe urethra,
where the urethra remains open at rest. Whenever intra-abdominal
pressure exceeds proximal urethral pressure, involuntary urine loss
ensues. Because the urethra cannot remain closed, the patient
experiences almost continuous urinary incontinence.
Female urethral function is influenced by estrogen. The lack of estrogen at
menopause leads to atrophy and replacement of submucosa (ie, vascular
plexus) by fibrous tissue. When estrogen is administered to
postmenopausal women with atrophic vaginitis, the mucosa regains its
turgor, with simultaneous up-regulation of alpha-receptors and
angiogenesis of vascular plexus. Lack of estrogen is a risk factor for
developing intrinsic sphincter deficiency, but estrogen replacement may
reverse its effects.
Occult stress incontinence
Stress incontinence on prolapse reduction (previously termed latent stress
incontinence) is a term used to describe stress incontinence observed only
after reduction of pelvic prolapse. Some believe that kinking of the urethra
caused by the prolapse itself provides for at least part of the continence
mechanism. These patients may have a history of stress incontinence that
improved and finally resolved as their prolapse worsened.
In diagnosing occult incontinence, the goal is to avoid new-onset
incontinence following surgical correction of prolapse. This may be
accomplished through the use of an incontinence procedure, such as a
colposuspension or sling. The diagnosis can be made by stress testing with
the prolapse reduced or by pessary placement and pad testing. No
particular method of prolapse reduction has been proved superior.
In a study of continent women with severe pelvic organ prolapse, reduction
of the prolapse with a pessary revealed occult incontinence in 58% of
cases.[16] These patients were treated with a pubovaginal sling, anterior
colporrhaphy, and other appropriate reparative operations. Eighty-six
percent of the patients with potential incontinence so treated had no
postoperative stress-related urine loss.
The group of patients with no demonstrable occult incontinence underwent
anterior colporrhaphy and additional individualized procedures.
Incontinence procedures, per se, were not performed in this group. No
patients had postoperative stress incontinence. Mean follow-up was 40-50
This study points out that bladder neck procedures need not be performed
if potential incontinence has been ruled out, even if bladder neck
hypermobility is present. Indeed, incontinence procedures are not without
their own morbidities and should not be performed unless necessary.
Urge incontinence pathophysiology
Urge incontinence is involuntary urine loss associated with a feeling of
urgency. The corresponding urodynamic term is detrusor overactivity, which
is the observation of involuntary detrusor contractions during filling
cystometry. [17, 18] These contractions may be voluntary or spontaneous and
may or may not cause symptoms of urgency and/or urgency incontinence.
However, a study using a quality of life assessment of women with
incontinence showed that women with urge incontinence from detrusor
overactivity consistently had a worse quality of life than did women with
other urodynamic diagnoses.
Urge incontinence may be a result of detrusor myopathy, neuropathy, or a
combination of both. When the identifiable cause is unknown, it is termed
idiopathic urge incontinence. When a definable causative neuropathic
disorder exists, the coexisting urinary incontinence disorder is
termed neurogenic detrusor overactivity. Symptoms of overactive bladder
or urge incontinence in the absence of neurologic causes are known
as detrusor instability.
The term overactive bladder describes a syndrome of urinary urgency,
usually accompanied by frequency and nocturia, with or without urgency
urinary incontinence, in the absence of urinary tract infection or other
obvious pathology. Overactive bladder in adults is a disorder of unclear
etiology and incompletely understood pathophysiology. For discussion of
this topic, see the article Overactive Bladder.
Some researchers believe that detrusor overactivity represents the
premature initiation of a normal micturition reflex. In vitro studies of bladder
muscle strips from patients with detrusor overactivity have demonstrated an
increase in response to electrical stimulation and an increased sensitivity to
stimulation with acetylcholine. [19] These findings may indicate a higher
sensitivity to efferent neurologic activity or a lower threshold of
acetylcholine release needed to initiate a detrusor contraction.
A relative cholinergic denervation may explain some of these findings. This
proposed mechanism is most plausible in cases of de novo detrusor
overactivity, which follow hysterectomy or other pelvic surgery. The
mechanism of denervation in idiopathic detrusor overactivity is less certain.
Subtle obstruction and the effects of aging on smooth muscle and the
autonomic nervous system are 2 possible contributors.
Another finding described in bladder muscle specimens from patients with
detrusor overactivity is local loss of inhibitory medullary neurologic activity.
Vasoactive intestinal peptide, a smooth muscle relaxant, is decreased
markedly in the bladders of patients with detrusor overactivity. In addition,
bladders of individuals with detrusor overactivity have been found deficient
in smooth musclerelaxing prostaglandins.
Mills and colleagues conducted a comparison study of bladder muscle
strips from patients with severe idiopathic detrusor overactivity and from
organ donors with no known urologic problems. [17] The following are some
of the findings:
Patchy partial denervation of the detrusor with areas of normal
innervation and areas of reduced innervation by fibers staining for
A reduced force of contraction in response to electrical field
stimulation: This finding is in contrast to a previous study showing an
increased sensitivity to electrical field stimulation, but the authors believe
that the muscle strips may have had increased sensitivity to direct
electrical stimulation (nonnerve mediated).
Supersensitivity to potassium
Increased electrical coupling of cells via cell-to-cell junctions
Variability in the activity of muscle strips from the same bladder
The authors believe that the primary abnormality in detrusor overactivity is
at the detrusor muscle level with an increased capacity for spontaneous
myogenic contractile activity and spread of electrical activity from cell to
cell, resulting in tetanic contractions. Epidemiological studies have shown
an association between detrusor overactivity and irritable bowel
syndrome. [20]Some authorities have proposed that a syndrome of smooth
muscle dysfunction may underlie this association.
Another study demonstrated the presence of an increased ratio of
abnormal-to-normal cell junctions in patients with bladder dysfunction. The
increased ratio was demonstrated most markedly in patients with detrusor
overactivity. To a lesser degree, these changes also were observed in
patients with outlet obstruction combined with detrusor overactivity and with
idiopathic sensory urgency alone. [21]
These authors concluded that idiopathic sensory urgency might represent a
milder or less overt variant of detrusor overactivity. They suggested that, in
the future, bladder biopsy with structural evaluation of cell junctions might
become a useful clinical tool in the diagnostic evaluation of bladder
dysfunction. [21]
One study proposed that urge incontinence, regardless of the triggering
mechanism, may share a final common pathway of myogenic dysfunction
of the detrusor. [22] Spread of contractile signals via cell-to-cell coupling was
proposed as the likely mechanism.
Another possible explanation for detrusor overactivity in a subgroup of
patients involves the triggering of the micturition reflex by leakage of urine
into a funneled and partially incompetent proximal urethra. This theory is
consistent with the findings of detrusor overactivity caused by coughing or
changing position.
In males, early obstruction due to benign prostatic hyperplasia (BPH) may
result in urge incontinence. [23] The pathophysiology of BPH is poorly
understood. Relative obstruction develops because of mechanical factors,
dynamic factors, and detrusor alterations.
Androgen-induced enlargement of nodules of glandular tissue comprises
the mechanical portion of the disorder. The dynamic component is related
to increased alpha tone in prostatic and urethral smooth muscle. Detrusor
dysfunction may consist of impaired contractility, detrusor overactivity, or
both. In severe cases of obstruction, retention and overflow incontinence
may develop, and the upper urinary tract can become damaged.
The presence of inflammation in the bladder is believed to result in bladder
muscle irritability and urge incontinence in some instances, as depicted in
the image below. One study showed that approximately 8% of patients with
bacterial urinary tract infections had nonneuropathic bladder instability. If
bacterial infection and detrusor overactivity coexist, successful treatment of
the infection results in resolution of the detrusor overactivity in about one
half of the patients.
A cystoscopic view of the bladder
mucosa reveals shallow ulcerations and petechial hemorrhages-findings
consistent with bacterial cystitis.
View Media Gallery
Nonbacterial inflammatory conditions of the bladder, including interstitial
cystitis, have been associated with detrusor overactivity. Foreign bodies,
including permanent sutures, bladder stones, and neoplasms, also have
been linked to bladder irritability and instability.
Mixed incontinence pathophysiology
Mixed incontinence is urinary incontinence resulting from a combination of
stress and urge incontinence. [2, 9] Approximately 40-60% of females with
incontinence have this combination. Although it is generally defined as
detrusor overactivity and impaired urethral function, the actual
pathophysiology of mixed urinary incontinence is still being investigated.
While generally thought of as separate etiologies for incontinence, some
indirect evidence may link these disorders in some instances.
In mixed incontinence, the bladder outlet is weak and the detrusor is
overactive. A classic example of mixed incontinence is a patient with
meningomyelocele and an incompetent bladder neck with a hyperreflexic
detrusor; however, a combination of urethral hypermobility and detrusor
instability is a more common scenario.
Mixed incontinence is a common finding in older patients with urinary
incontinence disorders. Often, stress incontinence symptoms precede urge
incontinence symptoms in these individuals. Urgency without actual urge-
related urine loss also is a common complaint of patients with stress
Some patients with stress incontinence have urine leakage into the
proximal urethra that may, at first, trigger sensory urgency and/or bladder
contractions, which initially are suppressible. Later, in a subgroup of these
individuals, myopathic changes may occur in the bladder that make the
spread of abnormally generated contractile signals more efficient and more
difficult to suppress voluntarily.
Reflex incontinence pathophysiology
Reflex incontinence is due to neurologic impairment of the central nervous
system. Common neurologic disorders associated with reflex incontinence
include stroke, Parkinson disease, and brain tumors. Reflex incontinence
also occurs in patients with spinal cord injuries and multiple sclerosis.
When patients with suprapontine or suprasacral spinal cord lesions present
with symptoms of urge incontinence, this is known as detrusor
Spinal cord injuries interrupt the sacral reflex arc from the suprasacral
spinal cord, cerebral cortex, and higher centers. These pathways are
crucial for voluntary and involuntary inhibition. In the initial phase of spinal
cord injury, the bladder is areflexic and overflow incontinence results. Later,
detrusor hyperreflexia usually is found upon urodynamic evaluation.
In multiple sclerosis (MS), demyelinating plaques in the frontal lobe or
lateral columns can produce lower urinary tract disorders. Incontinence
may be the presenting symptom of MS in about 5% of cases.
Approximately 90% of individuals with MS experience urinary tract
dysfunction during the course of the disease.
A summary of the published series of urodynamic findings in MS
demonstrated that in patients with lower urinary tract dysfunction, the most
common urodynamic diagnosis is detrusor hyperreflexia (62%). Detrusor-
sphincter dyssynergia (25%) and detrusor hyporeflexia (20%) also are
common. Obstructive findings are much more common in males. Of note,
the urodynamic diagnosis may change over time as the disease
Hemorrhage, infarction, or vascular compromise to certain areas of the
brain can result in lower urinary tract dysfunction. The frontal lobe, internal
capsule, brainstem, and cerebellum commonly are involved sites. Initially,
urinary retention due to detrusor areflexia is observed. This may be
followed by detrusor hyperreflexia.
Approximately 40-70% of patients with Parkinson disease have lower
urinary tract dysfunction. Controversy exists as to whether specific
neurologic problems in patients with Parkinson disease lead to bladder
dysfunction or if bladder symptoms simply are related to aging. The
extrapyramidal system is believed to have an inhibitory effect on the
micturition center; theoretically, loss of dopaminergic activity in this area
could result in loss of detrusor inhibition.
In patients with dementia, incontinence and urinary tract dysfunction may
be due to specific involvement of the areas of the cerebral cortex involved
in bladder control. Alternatively, incontinence may be related to global
deterioration of memory, intellectual capacity, and behavior.
Urodynamically, both detrusor hyperreflexia and areflexia have been found.
CNS neoplasms may result in incontinence. Tumors of the superior medial
frontal lobe, spinal cord tumors above the conus medullaris, and cervical
spondylosis can cause detrusor hyperreflexia.
Overflow incontinence pathophysiology
The major contributing factor to overflow incontinence is incomplete
bladder emptying secondary to impaired detrusor contractility or bladder
outlet obstruction. [2, 9] Impaired detrusor contractility is typically neurogenic
in nature; causes include diabetes mellitus, lumbosacral nerve disease
from tumors, meningomyelocele, MS, prolapsed intravertebral disks, and
high spinal cord injuries. Less common causes of overflow incontinence
include AIDS, genital herpes affecting the perineal area, and neurosyphilis.
In most cases, both sensory and motor neuropathies are present. The
maximal storage capacity of the bladder is reached, oftentimes without the
individual realizing that this has occurred. Incontinence occurs off the top of
a chronically over-filled bladder. Effective emptying is not possible because
of an acontractile detrusor muscle.
Common causes of bladder outlet obstruction in men include benign
prostatic hyperplasia (BPH), vesical neck contracture, and urethral
strictures. In women, urethral obstruction after anti-incontinence surgery
such as a sling or bladder neck suspension can result in iatrogenically
induced overflow incontinence.
Functional incontinence
Functional incontinence is seen in patients with normal voiding systems but
who have difficulty reaching the toilet because of physical or psychological
impediments. [2] In some cases, the cause is transient or reversible. In
others, a permanent problem can be identified. The etiology of the
incontinence may be iatrogenic, environmental, situational, or disease
related. The following common mnemonic, DIAPPERS, is helpful in
remembering the functional contributors to incontinence [25] :
D - Delirium
I - Infection, urinary
A - Atrophic urethritis or vaginitis
P - Pharmacologic agents
P - Psychiatric illness
E - Endocrine disorders
R - Reduced mobility or dexterity
S - Stool impaction
Integral theory
A unifying theory of the etiology of stress incontinence, urge incontinence,
voiding dysfunction, and fecal incontinence in women has been proposed.
The basis of the theory is that these disorders are the result of
overstretching of the vaginal connective tissue and supporting ligaments,
which usually occurs during childbirth.
Laxity of the pubourethral ligaments (ie, anterior zone of damage), mid
vagina (ie, middle zone), and uterosacral ligaments (ie, posterior zone)
make the usual tridirectional support of the vagina ineffective. With the
vagina no longer properly tethered to the pelvic girdle, the usual
neuromuscular actions that occur during increases in intra-abdominal
pressure or pelvic floor relaxation during voiding are not translated as
effectively into urethral closure and opening, respectively.
Detrusor overactivity, according to this theory, occurs because of the
premature firing of stretch receptors in the bladder base secondary to poor
endopelvic connective tissue support to the filling bladder.
The integral theory is attractive from the standpoint of parsimony but is
complex. The theory is best appreciated and understood with the help of
illustrations and diagrams showing directional force vectors.
Continuous incontinence
This severe type of incontinence is characterized by constant or near
constant leakage with no symptoms other than wetness. Generally, this
represents a significant breech in the storage capabilities of the bladder or
urethra. Urogenital fistulas are a classic example.
A nonfunctioning urethra can result in continuous leakage. Scarring and
fibrosis from previous surgery, partial urethral resection for vulvar cancer,
and urethral sphincter paralysis due to lower motor neuron disease can
cause the urethra to fail.
Pelvic irradiation may not only cause urogenital fistula but in rare cases
causes bladder noncompliance that results in continuous incontinence.
Congenital malformations of the genitourinary tract, such as bladder
exstrophy, [27] epispadias, and ectopic ureters, can result in total
Pediatric urinary incontinence
Pediatric incontinence disorders are classified according to cause. Primary
incontinence disorders generally are due to congenital structural disorders,
including ectopic ureter, exstrophy, epispadias, and patent urachus.
Secondary structural causes can result from obstruction from urethral
valves, congenital urethral strictures, and large ectopic ureteroceles. In
addition, trauma can result in secondary structural incontinence.
Neurogenic lesions make up the next category of pediatric incontinence
disorders. These include spinal dysraphism, tethered spinal cord, and
spinal cord tumors.
Nonstructural causes account for most cases of pediatric
incontinence. [28]Infection and inflammation may be the source.
Dysfunctional voiding habits can develop even at a young age. Some
children may become so preoccupied with activities that voiding is delayed
until capacity is reached and accidents result.
Some believe that certain children develop a pattern of not relaxing the
pelvic floor while voiding. In some cases, this can be traced back to an
infection or some other noxious stimuli. A vicious cycle of pelvic floor
spasm, constipation, and urinary retention can develop.
So-called giggle incontinence has been thought to represent an underlying
temporal lobe seizure. Other studies do not support this theory, however.
Vaginal voiding is a pseudoincontinence disorder, which may result from
voiding with the legs held too tightly together. The impeded flow of urine
may fill the vagina. The vagina empties when the child stands.
Nocturnal enuresis is the most common pediatric incontinence disorder. For
discussion of this topic, see Enuresis.

The precise prevalence of urinary incontinence is difficult to estimate. Part

of the difficulty has been in defining the degree, quantity, and frequency of
urine loss necessary to qualify as pathologic, with varying definitions
among studies. Consequently, the prevalence of urinary incontinence
reported in the literature is varied.

In addition, urinary incontinence is underdiagnosed and underreported. An

estimated 50-70% of women with urinary incontinence fail to seek medical
evaluation and treatment because of social stigma. Only 5% of incontinent
individuals in the community and 2% in nursing homes receive appropriate
medical evaluation and treatment. People with incontinence often live with
this condition for 6-9 years before seeking medical therapy.

In a Swedish study of 9197 nulliparous women aged 25-64 years, the rate
of urinary incontinence increased from 9.7% in the youngest women with a
body mass index <25 kg/m2 to 48.4% among the oldest women with a body
mass index 35 kg/m2. [37] In a Dutch study of 1257 adults, the prevalence of
urinary incontinence was 49.0% in women versus 22.6% in men. In both
men and women, the prevalence of urinary incontinence increased with
aging. [38, 39]

Urinary incontinence has been estimated to affect 10-13 million people in

the United States and 200 million people worldwide. The cost of treating
urinary incontinence in United States alone is $16.3 billion, 75% of which is
spent on treatment of women. Urinary incontinence can result in prolonged
hospital admission, urinary tract infections, contact dermatitis, and falls.
Urinary incontinence is a leading cause of admission to a nursing home
when families find it too difficult to care for a relative with incontinence.

Sex- and age-related patterns

Age is the single largest risk factor for urinary incontinence, although at any
age, urinary incontinence is more than 2 times more common in females
than in males. Urinary incontinence affects up to 7% of children older than
5 years, 10-35% of adults, and 50-84% of the elderly persons in long-term
care facilities. [1] The incidence of urinary incontinence is 1.4% of adults
aged 15-24 years and 2.9% of those aged 55-64 years. [2]

In a cross-sectional analysis of women who participated in the 2005-2006

National Health and Nutrition Examination Survey (NHANES), Nygaard et
al demonstrated that the prevalence of urinary incontinence increased with
age, but reported a lower overall prevalence than other researchers. The
prevalence was 6.9% in women aged 20-39 years, 17.2% in those aged
40-59 years, 23.3% in those aged 60-79 years, and 31.7% in women older
than 80 years. [40]

An age-related pattern also appears in the predominant type of urinary

incontinence experienced. In general, studies have shown that stress
urinary incontinence tends to be more common in women younger than 65
years, while urge urinary incontinence and mixed urinary incontinence is
more common in women older than 65 years.

Stress incontinence affects 15-60% of womenboth young and old

individuals. More than 25% of nulliparous young college athletes
experience stress incontinence when participating in sports.

Race-related factors

Although data concerning urinary incontinence in people of different races

are sparse, reports are emerging that race may play an important role in
the prevalence and likelihood of reporting of incontinence. In addition,
differences in anatomic morphology of the urinary sphincter mechanism in
people of different races may affect the likelihood of developing

Fultz et al found that 23.02% of white women reported incontinence,

compared with 16.17% of black women. [41] In a study by Anger et al, based
on the 1999-2000 NHANES data, the prevalence of urinary incontinence
was higher in non-Hispanic white women (41%) than in non-Hispanic black
(20%) or Mexican American women (36%). [42] In contrast, Freeman et al
found that black women were significantly more likely than white women to
report menopausal symptoms (46% vs 30%), urinary incontinence, and
vaginal dryness. [43]

Howard et al described functional and morphologic differences in the

urethral sphincteric and support system of nulliparous black and white
women. Black women demonstrated a 29% higher average urethral closure
pressure during a maximum pelvic muscle contraction. Paradoxically, a
36% greater bladder neck hypermobility was present as measured with the
cotton-swab test (black women at 49 vs white women at 36). [38]

Sears et al reported that, among patients with incontinence, urge

incontinence was more common in black women (51.5%), whereas stress
incontinence was statistically significantly more common in white women
(66.2%). [44] Daneshgari et al found that Hispanic women reported stress
incontinence and mixed incontinence more often than did non-Hispanic
white women. However, the increased prevalence of incontinence in
Hispanic women is likely due to higher prevalences of obesity,
hysterectomy, and parity than in white women. [45]

Nygaard et al examined the prevalence of symptomatic pelvic floor

disorders in women in the United States and found no difference among
non-Hispanic whites (16%), Hispanics (15.9%), non-Hispanic blacks
(13.8%), and other races(15%). [40] These authors did not differentiate urge
from stress incontinence.
Urinary incontinence is defined by the International Continence Society as
the involuntary loss of urine that represents a hygienic or social problem to
the individual. [7] Urinary incontinence can be thought of as a symptom as
reported by the patient, as a sign that is demonstrable on examination, and
as a disorder.
Urinary incontinence should not be thought of as a disease, because no
specific etiology exists; most individual cases are likely multifactorial in
nature. The etiologies of urinary incontinence are diverse and, in many
cases, incompletely understood.
Patients with urinary incontinence should undergo a basic evaluation that
includes a history, physical examination, and urinalysis (see Presentation).
Additional information from a patient's voiding diary, cotton-swab test,
cough stress test, measurement of postvoid residual (PVR) urine volume,
cystoscopy, and urodynamic studies may be needed in selected patients
(see Workup).
Videourodynamic studies are reserved to evaluate complex cases of stress
urinary incontinence. Videourodynamic studies combine the radiographic
findings of a voiding cystourethrogram and multichannel urodynamics. Go
to Urodynamic Studies for Urinary Incontinence for more information on this
Types of urinary incontinence
Four types of urinary incontinence are defined in the Clinical Practice
Guideline issued by the Agency for Health Care Policy and Research:
stress, urge, mixed, and overflow. Some authors include functional
incontinence as a fifth type of incontinence. [2, 8, 9, 4]
Stress incontinence is characterized by urine leakage associated with
increased abdominal pressure from laughing, sneezing, coughing, climbing
stairs, or other physical stressors on the abdominal cavity and, thus, the
bladder. [2, 3, 4] Urge urinary incontinence is involuntary leakage accompanied
by or immediately preceded by urgency. Mixed urinary incontinence is a
combination of stress and urge incontinence; it is marked by involuntary
leakage associated with urgency and also with exertion, effort, sneezing or
Functional incontinence is the inability to hold urine due to reasons other
than neuro-urologic and lower urinary tract dysfunction.
Other terms describing urinary incontinence are as follows:
Enuresis - Involuntary loss of urine
Nocturnal enuresis - Loss of urine occurring during sleep
Continuous urinary incontinence - Continuous leakage
Successful treatment of urinary incontinence must be tailored to the
specific type of incontinence and its cause (see Treatment). The usual
approaches are as follows:
Stress incontinence - Pelvic floor physiotherapy, anti-incontinence
devices, and surgery
Urge incontinence - Changes in diet, behavioral modification, pelvic-
floor exercises, and/or medications and new forms of surgical
Mixed incontinence - Pelvic floor physical therapy, anticholinergic
drugs, and surgery
Overflow incontinence - Catheterization regimen or diversion
Functional incontinence - Treatment of the underlying cause
Historical context
Urinary incontinence in women is not a recent medical and social
phenomenon, but the relative importance attributed to urinary incontinence
as a medical problem is increasing. Several factors responsible for the
increased attention to incontinence can be cited.
First, women are more willing to talk openly about this disorder. Women are
realizing that, in most cases, urinary incontinence is a treatable condition.
Consequently, less embarrassment and fewer social stigmas are
associated with the diagnosis.
Second, as the population ages, incontinence becomes a more frequent
concern. Urinary incontinence often is the chief reason for
institutionalization of elderly people.
Third, interest in urinary incontinence disorders within the medical
community is surging. This increased interest is arising among basic
scientists, clinical researchers, and clinicians. The subspecialties of
urogynecology and female urology are emerging, and structured
fellowships are in the credentialing process. A Female Pelvic Medicine and
Reconstructive Surgery fellowship is now accredited as a subspecialty by
the American Board of Obstetrics and Gynecology (ABOG) and the
American Board of Urology (ABU).
As a direct result of this increased interest, the public is becoming more
aware of the problem and more active and educated about incontinence.
Patient advocacy groups provide patients access to information,
incontinence products, and physicians who have interest or special
expertise in these disorders. In the last decade, funding opportunities for
incontinence research have increased vastly. Subspecialty professional
organizations and journals are now active.
Important contributions to the understanding of the structure and
functioning of the lower urinary tract include an improved understanding of
the anatomy and dynamic functioning of the pelvic floor and its contribution
to continence. In addition, much study has been conducted to bolster the
understanding of the neurophysiology of the bladder, urethra, and pelvic
floor. Finally, interest in the diagnosis and treatment of incontinence is
An estimated 50-70% of women with urinary incontinence fail to seek
medical evaluation and treatment because of social stigma. Only 5% of
individuals who are incontinent and 2% of nursing home residents who are
incontinent receive appropriate medical evaluation and treatment. Patients
who are incontinent often cope with this condition for 6-9 years before
seeking medical therapy.
In a 1997 survey of primary care physicians, about 40% reported that they
sometimes, rarely, or never ask patients about incontinence. More than
40% of internists and family practitioners routinely recommended absorbent
pads to their patients as a solution to incontinence disorders. [10] Continued
education of the public and medical professionals is needed to improve the
care rendered to individuals with urinary incontinence.
In 1989, the National Institutes of Health Consensus Development
Conference estimated the annual cost of urinary incontinence in the United
States to be $12.4 billion. Some experts believe that this is a conservative
estimate. True costs can be difficult to estimate because many individuals
do not come to the attention of medical specialists.
A 2009 survey of women in a managed care population found that the
prevalence of undiagnosed urinary incontinence was 53% in the preceding
year. [11] Some individuals pay out of pocket for adult incontinence
undergarments, absorbable pads, skin care products, deodorants, and
increased laundry expenses.
The psychosocial costs and morbidities are even more difficult to quantify.
Embarrassment and depression are common. The affected individual may
experience a decrease in social interactions, excursions out of the home,
and sexual activity.
The psychosocial impact on at-home caregivers, spouses, or family
members rarely is considered. Kelleher et al developed a questionnaire to
assess the quality of life of women with incontinence. [12] This questionnaire
has proven to be easy to use, valid, and reliable. This tool may be a
valuable adjunct to pretherapy and posttherapy assessment, as well as
valuable in comparing the quality of life impact of different urodynamic
Several other questionnaires are available for urge incontinence, stress
incontinence, and quality of life. Many have been validated in many
languages, presurgery and postsurgery. The questionnaires most often
used are the Urinary Distress Inventory (UDI)6, Incontinence Quality of
Life (IQoL) Questionnaire, Incontinence Impact Questionnaire (IIQ)7, UDI,
Overactive Bladder Symptom and Health-Related Questionnaire (OAB-Q),
and Kings Health Questionnaire KHQ). [13]
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The sling procedure, or suburethral sling procedure, refers to a particular kind of
surgery using ancillary material to aid in closure of the urethral sphincter function of
the bladder. It is performed as a treatment of severe urinary incontinence. The sling
procedure, also known as the suburethral fascial sling or the pubovaginal sling, has
many forms due to advances in the types of material used for the sling. Some
popular types of sling material are Teflon (polytetrafluoroethylene), Gore-Tex , and

rectus fascia (fibrous tissue of the rectum). The surgery can be done through the
vagina or the abdomen and some clinicians perform the procedure using a
laparoscopea small instrument that allows surgery through very small incisions in
the belly button and above the pubic hairline. The long-term efficacy and durability of
the laparoscopic suburethral sling procedure for management of stress incontinence
are undetermined. A new technique, the Tension-Free Vaginal Tape Sling Procedure
(TVT), has gained popularity in recent years and early research indicates high
success rates and few postoperative complications. This procedure is done under
local anesthetic and offers new opportunities for treatment of stress incontinence.
However, TVT has not been researched for its long-term effects. Finally, there are
many surgeons who use the sling procedure for all forms of incontinence.

Incontinence is very common and not fully understood. Generally defined as the
involuntary loss of urine, incontinence comes in many forms and has many
etiologies. Four established types of incontinence, according to the Agency for
Health Care Policy and Research, affect approximately 13 million adultsmost of
them older women. Actual prevalence may be higher because incontinence is widely
underreported and underdiagnosed. The four types of incontinence are: stress
incontinence, urge incontinence (detrusor overactivity or instability), mixed
incontinence, and overflow incontinence. There are also other types of incontinence
tied to specific conditions, such as neurogenic bladder in which neurological signals
to the bladder are impaired.

Stress incontinence is the most frequently diagnosed form of incontinence and

occurs largely with physical activity, laughter and coughing, and sneezing. The
inability to hold urine can be due to weakness in the internal and external urinary
sphincter or due to a weakened urethra. These two conditions, intrinsic sphincter
deficiency (ISD) and urethral hypermobility or genuine stress incontinence (GSI),
pertain to the inability of the "gatekeeper" sphincter muscles to stay taut and/or the
urethra failing to hold urine under pressure from the abdomen. In women, as the
pelvic structures relax due to age, injury, or illness, the uterus prolapses and the
urethra becomes hypermobile. This allows the urethra to descend at an angle that
permits loss of urine and puts pressure upon the sphincter muscles, both internal
and external, allowing the mouth of the bladder to stay open.

Urge incontinence, the other frequent type of incontinence, pertains to overactivity of

the sphincter in which the muscle contracts frequently, causing the need to urinate.
Stress incontinence is often allied with sphincter overactivity and is often
accompanied by urge incontinence.

Severe stress incontinence occurs most frequently in women younger than 60 years
old. It is thought to be due to the relaxation of the supporting structures of the pelvis
that results from childbirth, obesity, or lack of exercise . Some researchers believe
that aging, perhaps due to estrogen deficiency, is a major cause of severe urinary
incontinence in women, but no link has been found between incontinence and
estrogen deficiency. Surgery for stress or mixed incontinence is primarily offered to
patients who have failed, are not satisfied with, or are unable to comply with more
conservative approaches. It is often performed during such other surgeries as
urethra prolapse, cystocele surgery, urethral reconstruction, and hysterectomy .

The sling procedure gets its name from the tissue attached under the mid- or
proximal urethra and sutured at its ends onto a solid structure like the rectus sheath,
pubic bone, or pelvic side walls. The procedure is used in the severest cases of
stress incontinence, particularly those that have a concomitant sphincter inadequacy
(ISD). The sling supports the urethra as it receives pressure from the abdomen and
helps the internal sphincter muscles to keep the urethral opening closed. The
procedure is the most popular because it has the highest success rate of all surgical
remedies for severe stress incontinence related to sphincter inadequacies in both
men and women.

Urinary incontinence (UI) plagues 1035% of adults and at least half of the million
nursing home residents in the United States. Other studies indicate that between
10% and 30% of women experience incontinence during their lifetimes, compared to
about 5% of men. One reason that more women than men have incontinent episodes
is the relatively shorter urethras of women. Women have urethras of about 2 in (5
cm) and men have urethras of 10 in (25.4 cm). Studies have documented that about
50% of all women have occasional urinary incontinence, and as many as 10% have
regular incontinence. Nearly 20% of women over age 75 experience daily urinary
incontinence. Incontinence is a major factor in individuals entering long term care
facilities. Women at highest risk are those who have given birth to more than three
children and women who were given oxytocin to induce labor. Oxytocin puts more
pressure on the pelvic muscles than does ordinary labor. Women who smoke have
twice the rate of incontinence, according to one study of 600 women. Those women
who do high-impact exercises are at much higher risk for incontinence. According to
the medical literature, those at highest risk for urinary leakage are gymnasts,
followed by softball, volleyball, and basketball players. Finally, women who have
diabetes or are obese have higher rates of incontinence. Women who require sling
procedures have often had other surgeries for incontinence, necessitating sling
procedure to treat intrinsic sphincter deficiency caused by operative trauma. A rarer
cause of stress incontinence in older women is urethral instability. In men, stress
incontinence is usually caused by sphincter damage after surgery on the prostate.

Anti-incontinence surgery is used to address the failure of two parts of female urinary
continence: loss of support to the bladder neck or central urethra and intrinsic
sphincter deficiency (ISD). The surgery does not restore function to the urethra or to
the ability for closure to the sphincter. It replaces the mechanism for continence with
supporting and compressive aids. Stabilizing the supporting elements of the urethra
(ligaments, fascia, and muscles) was thought for many years to be the most
important factor in curing incontinence. Called anatomic or genuine stress urinary
incontinence (SUI), retropublic procedures, like the Burch procedure, sought only to
restore the urethra to a fixed position. However, it became clear with the high failure
rate of these procedures that ISD was present and unless surgery could confer some
added compressive ability to the closure of the bladder, SUI would persist.

The urethral sling procedure is effective in the treatment of the severest types of
incontinence (Types II and III) by re-establishing the "hammock effect" of the
proximal or central point of the urethra during abdominal straining. The surgery
involves the placement of a piece of material under the urethra at its arterial or
vesical juncture and anchoring it on either side of the pubic bone or to the abdominal
wall or vaginal wall. This technique involves the creation of a sling from a strip of
tissue from the patient's own abdominal fascia (fibrous tissue) or from a cadaver.
Synthetic slings also are used, but some are prone to break down over time.

The urethral sling procedure is most often performed as open surgery, which
involves entering the pelvic area from the abdomen or from the vagina while the
patient is under general or regional anesthesia. Broad-spectrum antibiotics are
offered intravenously. If the patient is fitted with a urethral catheter, ampicillin and
gentamicin are administered instead. The patient is placed in stirrups. Surgery takes
place as a 6-to-9-cm by 1.5-cm sling is harvested from rectal tissue and sutured
under the urethra at each end within the retropubic space (the area that undergirds
the urethra). Synthetic tissue or fascia from a donor may also be used.

The goal of the surgery is to create a compression aid to the urethra. This involves
an individualized approach to the tension needed on the sling. While the sling
procedure is relatively easy to complete, the issue of tension on the sling is hard to
determine and involves the use of tests during surgery for determining the
compression effect of the sling on the urethra. Some manual tests are performed or a
more sophisticated urodynamic test, like cystourethrography, may determine tension.
It is important for the surgeon to test tension during surgery because of the high rate
of retention of urine (inability to void) after surgery associated with this procedure
and the miscalculation of the required tension.

Candidates for surgical treatment of incontinence must undergo a full clinical,
neurological, and radiographic evaluation before there can be direct analysis of the
condition to be treated and the desired outcome. Both urethral and bladder functions
are evaluated and there is an attempt to determine the conditions associated with
stress incontinence. In many women, incontinence may be due to vaginal prolapse.
Stress incontinence can be identified by observation of urine during pelvic
examination or by a sitting or standing stress test where patients are asked to cough
or strain and evidence of leakage is obtained. Gynecologists often use a Q-tip test to
determine the angle and change in the position of the urethra during straining. Other
tests include subtracted cystometry to measure how much the bladder can hold, how
much pressure builds up inside the bladder as it stores urine, and how full it is when
the patients feels the urge to urinate.

The frequency of stress incontinence as measured by typical symptoms ranges

between 33% and 65%. The frequency of stress incontinence is around 12% when
measured or defined by cystometric findings. The ability to distinguish SUI as the
cause of incontinence, as opposed to ISD, becomes more complicated; but it is a
very important factor in the decision to have surgery. A combination of pelvic
examination for urethral hypermoblity and leak point pressure as measured by
coughing or other abdominal straining has been shown to be very effective in
distinguishing ISD, and identifying the patient who needs surgery.
IV ketorolac and oral and intravenous pain medication are administered, as are
postoperative antibiotics. A general diet is available usually on the evening of
surgery. When the patient is able to walk, usually the same day, the urethral catheter
is removed. The patient must perform self-catheterization to check urine volume
every four hours to protect the urethral wall. If the patient is unwilling to perform
catheterization, a tube can be placed suprapubically (in the back of the pubis) for
voiding. Catheterization lasts about eight days, with about 98% of patients able to
void at three months. Patients are discharged on the second day postoperatively,
unless they have had other procedures and need additional recovery time. Patients
may not lift heavy objects or engage in strenuous activity for approximately six
weeks. Sexual intercourse may be resumed in the fourth week following surgery.
Follow-up visits are scheduled for three to four weeks after surgery

Although the sling treatment has a very high success rate, it is also associated with a
prolonged period of voiding difficulties, intraoperative bladder or urethra injury,
infections associated with screw or staple points, and rejection of sling material from
a donor or erosion of synthetic sling material. Patients should not be encouraged to
undergo a sling procedure unless the risk of long-term voiding difficulty and the need
for intermittent self-catheterization are understood. Fascial slings seem to be
associated with the fewest complications for sling procedure treatment. Synthetic
slings have a greater risk of having to be removed due to erosion and inflammation.

Normal results
Regardless of the procedure used, a proportion of patients will remain incontinent.
Results vary according to the type of sling procedure used, the type of attachment
used for the sling, and the type of material used for the sling. Normal results for the
sling procedure overall are recurrent stress incontinence of 312% after bladder sling
procedures. In general, reported cure rates are lower for second and subsequent
surgical procedures. A recent qualitative study published in the American Journal of
Obstetrics and Gynecology of 57 patients who underwent patient-contributed fascial
sling procedures indicates good success with fascial sling procedures. At a median
of 42 months after the procedure, the postoperative objective cure rate for stress
urinary incontinence was 97%, with 88% of patients indicating that the sling had
improved the quality of their lives. Eighty-four percent of patients indicated that the
sling relieved their incontinence long term, and 82% of patients stated that they
would undergo the surgery again. The study also found that voiding function was a
common side effect in 41% of the patients.

Morbidity and mortality rates

The most common complications of sling procedures are voiding problems (10.4%),
new detrusor instability (727%), and lower urinary tract damage (3%). Some of the
complications depend upon tension issues as well as on the materials used for the
sling. There are recent and well-designed studies of patient fascia and donor fascia
used for slings in five centers with follow-up from 30 to 51 months that report no
erosions or vaginal wall complications in any patients. Prolonged retention or voiding
issues occurred in 2.3% of patients and de novo or spontaneous urge incontinence
developed in 6%. These figures relate only to a large study utilizing patient or donor
fascia and one that did not control for other factors like techniques of anchoring. In
general, studies of the sling procedure are small and have many variables. There are
no long term studies (over five years) of this most popular procedure.

Alternatives to anti-incontinent sling procedure surgery depend upon the severity of
the incontinence and the type. Severe stress incontinence with intrinsic sphincter
deficiency can benefit from bulking agents for the urethra to increase compression,
as well as external devices like a pessary that is placed in the vagina and holds up
the bladder to prevent leakage. Urethral inserts can be placed in the urethra until it is
time to use the bathroom. The patient learns to put the insertion in and take it out as
needed. There are also urine seals that are small foam pads inserted in garments.
Milder forms of incontinence can benefit from an assessment of medication usage,
pelvic muscle exercises, bladder retraining, weight loss, and certain devices that
stimulate the muscles around the urethra to strengthen them. For mild urethral
mobility, procedures for tacking or stabilizing the urethra at the neck called Needle
Neck Suspension, as well as procedures to hold the urethra in place with sutures,
like the Burch method, are alternative forms of surgery.

"Urologic Surgery." In Campbell's Urology, edited by M. F. Campbell, et al., 8th ed.
Philadelphia: W. B. Saunders, 2002.

Lobel, B., A. Manunta, and A. Rodriguez. "The Management of Female Stress
Urinary Incontinence Using the Sling Procedure." British International Journal of
Urology 88, no. 8 (November 2001): 832.

Melton, Lisa. "Targeted Treatment for Incontinence Beckons." Lancet 359, no. 9303,
(January 2002): 326.

Richter, H. R. "Effects of Pubovaginal Sling Procedure on Patients with Urethral

Hypermobility and Intrinsic Sphincteric Deficiency: Would They Do it
Again?" American Journal of Obstetrics and Gynecology 184, no. 2 (January 2001):

American Foundation for Urologic Disease/The Bladder Health Council. 1128 North
Charles St., Baltimore, MD 21201. (410) 468-1800. Fax: (410) 468-1808. admin@ .

The Simon Foundation for Continence. P.O. Box 835, Wilmette, IL 60091. (800) 23-
simon or (847) 864-3913. .

National Kidney and Urological Diseases Information Clearinghouse. Bladder
Control in Women. Intellihealth. April 17, 2003 [cited June 25,
d=dmtContent .

"Urinary Incontinence." MD Consult Patient Handout. [cited June 25,

2003]. .

Nancy McKenzie, Ph.D.


The surgery is performed by a urological surgeon who has trained specifically for this
procedure. The surgery takes place in a general hospital.


Do I have a urethral closure problem as a part of my incontinence?

How many sling procedures have you performed?

How soon will I be able to tell if I am going to have urine retention difficulties?

If this surgery does not work, are there other procedures that will allow me a
better quality of life?

Is patient satisfaction a formal part of your evaluation of the success of the

procedure you use?

What type of material do you use for the sling and why do you choose this

Read more:

Retropubic suspension refers to the surgical procedures used to correct incontinence
by supporting and stabilizing the bladder and urethra. The Burch procedure, also
known as retropubic urethropexy procedure or Burch colosuspension, and Marshall-
Marchetti-Krantz procedure (MMK) are the two primary surgeries for treating stress
incontinence. The major difference between these procedures is the method for
supporting the bladder. The Burch procedure uses sutures to attach the urethra and
bladder to muscle tissue in the pelvic area. MMK uses sutures to attach these organs
to the pelvic cartilage. Laparoscopic retropubic surgery can be performed with a
video laparoscope through small incisions in the belly button and above the pubic

The urinary system expels a quart and a half of urine per day. The amount of urine
produced depends upon diet and medications taken, as well as exercise and loss of
water due to sweating. The ureters, two tubes connecting the kidneys and the
bladder, pass urine almost continually and when the bladder is full the brain sends a
signal to the bladder to relax and let urine pass from the bladder to the urethra.
People who are continent control the release of urine from the urethra via the
sphincter muscles. These two sets of muscles act like rubber bands to keep the
bladder closed until a conscious decision is made to urinate. The intrinsic sphincter
or urethral sphincter muscles keep the bladder closed and the extrinsic sphincter
muscles surround the urethra and prevent leakage. Incontinence is common when
either the urethra lacks tautness and stability (genuine stress urine incontinence,
SUI) and/or the sphincter muscles are unable to keep the bladder closed (intrinsic
sphincter deficiency, ISD).

Incontinence occurs in many forms with four primary types related to anatomic,
neurological, dietary, or disease, or injury.

Stress incontinence
The most frequent form of incontinence is stress incontinence. This relates to
leakage of the urethra with activity that puts stress on the abdominal muscles. The
primary sign of stress incontinence is this leakage at sneezing, coughing, exercise,
or other straining activities, which indicates a lack of support for the urethra due to
weakened muscles, fascia, or ligaments. Pressure from the abdomen with
movement, like exercising, uncompensated by tautness or stability in the urethra,
causes the urethra to be displaced or mobile leading to leakage. Essentially,
this hypermobility of the urethra is an indication that it is moving down or herniating
through weakened pelvic structures.

To diagnose incontinence and determine treatment, three grades of severity for

stress incontinence are used.

Type I: Moderate movement of the urethra, with no hernia or cystocele.

Type II: Severe or hypermobility in the urethra of more than 0.8 in (2 cm), with
or without decent of the urethra into pelvic structures.

Type III: Hypermobility of the urethra where the primary source of

incontinence is the inability of the sphincter muscles to keep the bladder
closed. This is due to weakness or deficiency in the intrinsic sphincter

Urge incontinence
Urge incontinence relates to the frequent need to urinate and may involve going to
the bathroom every two hours. Accidents are common when not reaching a

Weak pelvic floor muscles (A) can cause stress incontinence. In a retropubic suspension, the neck
of the bladder is elevated and stitched to the pubic bone to hold it in place (B). (
Illustration by GGS Inc.

in time. Urge incontinence is not due to general changes in the urethra or supporting
muscles. It is often linked to other disorders that produce muscle spasms in the
bladder, such as infections. Urge incontinence can also be due to underlying
illnesses like stroke, spinal cord injury, multiple sclerosis and Alzheimer's disease,
which cause detrusor hyperflexiathe contracting of the bladder muscle responsible
for sending urine from the bladder to the urethra. Urge incontinence is very common
in the elderly, especially those in long term care facilities.

Mixed incontinence
Mixed incontinence is a combination of stress incontinence and urge incontinence,
especially in older women. Since each form of incontinence pertains to different
functions or anatomy, it is very important to distinguish which part of the incontinence
is to be treated by surgery.

Overflow incontinence
Overflow incontinence results in leakage from a bladder that never completely
empties due to weakened bladder muscles. Overflow incontinence is involuntary and
not accompanied by the urge to urinate. Many causes exist for overflow incontinence,
including weak bladder muscles due to diabetes, nerve damage, or a blocked
urethra. Men are more frequently affected than women.

Over 15 million Americans have urinary incontinence and women comprise 85% of
all cases. It affects 25% of women of reproductive age and 50% of women past
menopause. Due to the female anatomy, women have twice the risk for stress
incontinence compared to men. In addition, childbirth places pressure and burden on
the pelvic muscles that often weaken with age, thereby weakening urethra stability.
Women are more prone to surgeries for urological changes than men and severe
urinary incontinence is often associated with these surgeries as well as
hysterectomies. The majority of women with incontinence have stress incontinence
or mixed incontinence. Male incontinence occurs primarily in response to blockage in
the prostate or after prostate surgery. It is usually treated with implants and/or an
artificial sphincter insert.

There are a variety of retropubic suspension surgeries available to treat stress
incontinence. The variations differ by the types of structures used to support the
urethra and bladder. In all procedures, parts of the pelvic anatomy (pubic bone,
ligaments) serve as an anchor or wall upon which the urethra is tacked for stability.
The surgery is called a suspension surgery because it stabilizes the urethra from
tilting by suspending it against a part of the pelvic anatomy. The Burch procedure is
often performed when other surgery is needed such as repair of the urethra for
cystoceles and urethral reconstruction. However, this procedure is the most difficult of
the anti-incontinent surgeries and is more common in mild forms of stress
incontinence where intrinsic sphincter deficiency is not present.

The Burch procedure can be done through open abdominal surgery, which requires a
long incision at the bikini line, or surgery performed through the vagina. The patient,
in stirrups, receives general anesthesia. Within the retropubic area, the anterior
vaginal wall is separated from the bladder manually. The bladder neck is identified
and old adhesions or fatty tissues are removed. The neck of the bladder is sutured to
pubic ligaments where it will form adhesions and thereby gain stability. The surgeon
examines for bladder injury and the surgery is completed. Urethral position is tested
by placing a cotton-tipped swab in the urethra and measuring the angle. With
abdominal surgery or vaginal surgery a catheter may be put in place by the surgeon
for postoperative voiding and to decrease the risks of infection. A suction drain may
be placed in the retropubic space for bleeding. The drain is removed one to three
days after surgery.

Recently, laparoscopic surgery has been used to perform retropubic suspensions.

Laparoscopic surgery requires only three or four 0.25-in (0.6-cm) incisions in the
belly button, pubic hairline, or groin area and uses small instruments without opening
the abdominal cavity. Shorter healing time is involved with this procedure, the
hospital stay is usually not more than 24 hours and recovery to normal activities
takes about seven to 14 days. However, the Burch procedure performed using
laparoscopic techniques requires great skill on the part of the surgeon and research
indicates that the results may not be as long lasting as those developed with
abdominal or vaginal surgery.

A patient with incontinence may have multiple factors that induce transient or chronic
incontinence. It is crucial that the physician obtain a complete history, physical,
clinical, neurological, and medication evaluation of the patient, as well as a
radiographic assessment before continuing urological tests aimed at a surgical
solution. The specific indications for the Burch colosuspension procedure or its
variants is the correction of stress urinary incontinence. This can be a patient who
also requires abdominal surgery that cannot be performed vaginally,
like hysterectomy or sigmoid surgery, as well as patients who have SUI without ISD.

A urodynamic study with a point pressure leak test will allow a diagnosis to be made
that can distinguish the patient who has a hypermobile urethra from the patient who
also has ISD. The point pressure leak test, also known as the Valsalva leak test,
measures the amount of abdominal pressure required to induce leakage. The patient
is asked to cough or strain in order to encourage leakage. The point at which the
patient leaks helps determine if stress incontinence with ISD contribution is present.
Obese patients and patients that engage in high impact exercise regimens are not
considered good candidates for retropubic suspension.

Patients with open retropubic procedures are given pain medication postoperatively
that is tapered down over the next two days. A suprapubic catheter stays in place for
approximately five days with voiding difficulties encountered initially in many patients.
Patients with laparoscopic suspensions are reported to have less blood loss during
surgery, less postoperative narcotic requirements, and shorter hospital stays.
Patients are expected to refrain from strenuous activity for three months and to have
a follow-up visit within three weeks after surgery.

As with any major abdominal or pelvic surgical procedures, complications that may
occur after a retropubic suspension include bleeding; injury to the bladder, urethra,
and ureters; wound infection; and blood clots. Specific to the Burch procedure are
complications that involve urethral obstruction because of urethral kinking due to
elevation of the vagina or bladder base. Postoperative voiding difficulties are
common and depend upon the suture tension of the urethral axis. Corrective surgery
and the release of the urethra to a more anatomic position resolves voiding issues
with a very high rate of success. Vaginal prolapse is also a risk of this procedure.

Normal results
The patient can expect more than 8090% cure or great improvement in their
incontinence. There is a large body of literature documenting the success of the
Burch procedure. Published research shows a cure rate ranging from 6393%,
according to the actual version of colosuspension used. Laparoscopic surgery has
not produced the long term results that open surgery has and there is the possibility
that the fibrosis (adhesion) necessary for a successful outcome does not occur as
easily with the laparoscopic procedure. Patients not carefully screened out for ISD
will not have a high level of success with the Burch procedure since the source of the
incontinence will not have been treated. Sling procedures are recommended for
patients with ISD instead of colosuspension surgery.

Morbidity and mortality rates

The Burch procedure may aggravate vaginal wall weakness or vaginal prolapse. This
incident varies between 3% and 17%. Research on the Marshall-Marchetti-Krantz
procedure pertaining to 2,712 patients found a complication rate of 21%, with wound
complications and infections making up the majority, 5.5% and 3.9% respectively.
Direct wound injury occurred in 1.6% and obstructions in 0.3% overall.

General or simple severe stress incontinence related primarily to weakening of the
urethral support can be remedied with changes in diet, weight loss, and certain
behavioral and rehabilitative measures. These include:

Regular, daily exercising of the pelvic muscles called Kegel exercises,

requiring 30200 contractions a day for eight weeks.

Biofeedback to gain awareness and control of pelvic muscles.

Vaginal weight training in which small weights are inserted in the vagina to
tighten vaginal muscles.

Mild electrical stimulation to increase contractions in pelvic muscles.

Bladder retraining in which the patient is taught how to resist the urge to
urinate and expand the intervals between urinations.
There are also medications that can facilitate continence for those experiencing
stress or urge incontinence. These include some kinds of antidepressants, although
the mechanism of action is not quite understood, as well
as antispasmodic medication and estrogen therapy. Finally, should behavioral,
rehabilitative, and surgical procedures fail, there remain alternatives through the use
of vaginal cones and urethral plugs that can be inserted and removed by the patient.

See also Needle neck suspension ; Sling procedure .


Walsh, Patrick. Campbell's Urology. 8th ed. Elsevier Science, 2000.

Liu, C. Y. "Laparoscopic Treatment of Stress Urinary Incontinence." Obstetrics and Gynecology
Clinics of North America 26, no. 1 (March 1999): 149-67.

Melton, Lisa. "Targeted Treatment for Incontinence Beckons." Lancet 359, no. 9303 (January 2002):

Smoger, S. H., T. L. Felice, and G. H. Kloecker. "Urinary Incontinence Among Male Veterans
Receiving Care in Primary Care Clinics." Annals of Internal Medicine 132, no. 7 (April 4, 2000): 547-

Stoffel, J. T., J. Bresette, and J. J. Smith. "Retropubic Surgery for Stress Urinary
Incontinence." Urologic Clinics of North America 29, no. 3 (August 2002).

Weber, A. M., and M. D. Walters. "The Burch and Sling Procedures are Similarly Effective for Surgical
Treatment of Genuine Stress Urinary Incontinence." Evidence-based Obstetrics & Gynecology 4, no. 1
(March 2002).

American Foundation for Urologic Diseases. The Bladder Health Council, 1128 North Charles Street,
Baltimore, MD 21201. (410) 468-1800. .

National Kidney and Urologic Diseases Information Clearinghouse. 3 Information Way, Bethesda, MD

(800) 891-5390 or (301) 654-4415. .

The Simon Foundation for Continence, P.O. Box 835, Wilmette, IL 60091. (800) 23-SIMON or (847)
864-3913. .

Bladder Control in Women. National Kidney and Urologic Disease Information
Clearinghouse. NIH Publication no. 97-4195. May 2002 [cited May 12,
2003]. .

Ginsberg, David. "Trends in Surgical Therapy for Stress Urinary Incontinence." American Urological
Association 97th Annual Meeting, WebMD Conference Coverage. 2002 [cited May 12,
2003]. .

Hendrix, Susan L., and S. Gene McNeeley. "Urinary Incontinence and Menopause: Update on
Evidence-Based Treatment." Medscape, October 28, 2002 [cited May 12,
2003]. .

Nancy McKenzie, PhD



Retropubic suspension procedures are performed by a urological surgeon specially

trained in incontinence surgeries. Surgery is performed in a general hospital.


Which retropubic suspension procedure is recommended?

What is your cure rate with this procedure?

What is your injury rate for this procedure?

Could my incontinence be treated just as well with the sling procedure?

Do you perform laparoscopic surgeries to treat incontinence?

Read more:

Artificial sphincter insertion surgery is the implantation of an artificial valve in the
genitourinary tract or in the anal canal to restore continence and psychological well
being to individuals with urinary or anal sphincter insufficiency that leads to severe
urinary or fecal incontinence.

This procedure is useful for adults and children who have severe incontinence due to
lack of muscle contraction by either the urethral sphincter or the bowel sphincter. The
primary work of the lower urinary tract and the colon is the storage of urine and
waste, respectively, until such time as the expulsion of urine or feces is appropriate.
These holding and expelling functions in each system require a delicate balance of
tension and relaxation of muscles, especially those related to conscious control of
the act of urination or defecation through the valve-like sphincter in each system.
Both types of incontinence have mechanical causes related to reservoir adequacy
and sphincter, or "gatekeeper" control, as well as mixed etiologies in the chemistry,
neurology, and psychology of human makeup. The simplest bases of incontinence lie
in the mechanical components of reservoir mobility and sphincter muscle tone.
These two factors receive the most surgical attention for both urinary and fecal

Urinary sphincter surgery

There are four sources of urinary incontinence related primarily to issues of tone in
pelvic, urethral, and sphincter muscles. Most urinary incontinence is caused by
leakage when stress is applied to the abdominal muscles by coughing, sneezing, or
exercising. Stress incontinence results from reduced sphincter adequacy in the ability
to keep the bladder closed during movement. Stress incontinence can also be
related to the mobility of the urethra and whether this reservoir for urine tilts, causing
spilling of urine. The urethral cause of stress incontinence is treated with other
surgical procedures. A second form of incontinence is urge incontinence. It relates to
sphincter overactivity, or sphincter hyperflexia, in which the sphincter contracts
uncontrollably, causing the patient to urinate, often many times a day. Finally, there is
urinary incontinence due to an inadequately small urethra that causes urine overflow.
This is known as overflow incontinence and can often be treated with augmentation
to the urethra to increase its size.

Only severe stress incontinence related to sphincter adequacy can benefit from the
artificial urinary sphincter.

Normally, the anal sphincter muscles maintain fecal continence (A). In cases of incontinence, an
artificial sphincter may be inserted, which can open and close to mimic the function of the natural
sphincter (B). Once implanted, the patient uses a pump under the skin to inflate and deflate the anal
cuff (C). (
Illustration by GGS Inc.

This includes conditions that result in the removal of the sphincter. Sphincter
deficiency can result directly from pelvic fracture; urethral reconstruction; prostate
surgeries; spinal cord injury; neurogenic bladder conditions that include sphincter
dysfunction; and some congential conditions. Each can warrant consideration for a
sphincter implant.
Implantation surgery related to urinary sphincter incompetence is also called artificial
sphincter insertion or inflatable sphincter insertion. The artificial urinary sphincter
(AUS) is a small device placed under the skin that keeps pressure on the urethra
until there is a decision to urinate, at which point a pump allows the urethra to open
and urination commences. Since the 1990s, advances in prostate cancer diagnosis
and surgery have resulted in radical prostatectomies being performed, with urinary
incontinence rates ranging from 360%. The AUS has become a reliable treatment
for this main source of urinary incontinence in men. Women with intrinsic sphincter
deficiency, or weakened muscles of the sphincter, also benefit from the AUS.
However, the use of AUS with women has declined with advances in the use of the
sub-urethral sling due to its useful "hammock" effect on the sphincter and its high
rates of continence success. Women with neurologenic incontinence can benefit
from the AUS.

Artificial anal sphincter surgery

Fecal incontinence is the inability to control bowel function. The condition can be the
result of a difficult childbirth, colorectal disease such as Crohn's disease, accidents
involving neurological injuries, surgical resection for localized cancer, or by other
neurological disorders. Severe fecal incontinence may, depending upon the
underlying disease, require surgical intervention that can include repair of the anal
sphincter, colostomy , or replacement of the anal sphincter. Artificial anal sphincter
is a very easy-to-use device implanted under the skin that mimics the function of the
anal sphincter.


Artificial urinary sphincter surgery

According to the Agency for Health Care Policy and Research, urinary incontinence
affects approximately 13 million adults. Men have incontinence rates that are much
lower than women, with a range of 1.55%, compared to women over 65 with rates
of almost 50%. In older men, prostate problems and their treatments are the most
common sources of incontinence. Incontinence is a complication in nearly all male
patients for the first three to six months after radical prostatectomy. A year after the
procedure, most men regain continence. Stress incontinence occurs in 15% of men
after the standard treatment for severe benign prostatic hyperplasia.

Artificial anal sphincter surgery

According to the National Institute of Diabetes & Digestive & Kidney Diseases
(NIDDK), more than 6.5 million Americans have fecal incontinence. Fecal
incontinence affects people of all ages. It is estimated that over 2% of the population
is affected by fecal incontinence. Many cases are never reported. Community-based
studies reveal that 30% of patients are over the age of 65, and 63% are female.
According to one study published in the American Journal of Gasteronology, only
34% of incontinent patients have ever mentioned their problem to a physician, even
though 23% wear absorbent pads, 12% are on medications, and 11% lead lives
restricted by their incontinence. Women are more than five times as likely as men to
have fecal incontinence, primarily due to obstetric injury, especially
with forceps delivery and anal sphincter laceration. Fecal incontinence is frequent in
men who have total and subtotal prostatectomies. Fecal incontinence is not a part of
aging, even though it affects people over 65 in higher numbers than other


Artificial urinary sphincter surgery

The artificial urinary sphincter is an implantable device that has three components:

an inflatable cuff

a fluid reservoir (balloon)

a semiautomatic pump that connects the cuff and balloon

Open surgery is the major form of surgery for the implant. Infections are minimized
by sterilization of the urine preoperatively and preoperative bowel preparation. The
pelvic space is entered from the abdomen or from the vagina, with
general anesthesia for the patient. Broad-spectrum antibiotics are given
intravenously and at the site of small incisions for the device. A urinary catheter is put
into place. The cuff is implanted around the bladder neck and secured and passed
through the rectus muscle and anterior fascia to be connected later to the pump. A
space is fashioned to hold the balloon in the pubic region, and a pump is placed in a
pouch below the abdomen. The artificial urinary sphincter is activated only after six
to eight weeks to allow healing from the surgery. The patient is trained in the use of
the device by understanding that the cuff remains inflated in its "resting state," and
keeps the urethra closed by pressure, allowing continence. Upon the decision to
urinate, the patient temporarily deflates the cuff by pressing the pump. The urethra
opens and the bladder empties. The cuff closes automatically.

Artificial anal sphincter surgery

The artificial anal sphincter is an implantable device that has three components:

an inflatable cuff

a fluid reservoir (balloon)

a semiautomatic pump that connects the cuff and balloon

In open abdominal surgery, the implant device is placed beneath the skin through
small incisions within the pelvic space. One incision is placed between the anus and
the vagina or scrotum, and the inflatable cuff is put around the neck of the anal
sphincter. A second incision at the lower end of the abdomen is used to make a
space behind the pubic bone for placement of the balloon. The pump is placed in a
small pocket beneath the labia or scrotum, using two incisions. The artificial anal
sphincter is activated only after six to eight weeks to allow healing from the surgery.
The patient is trained in the use of the device by understanding that the anal cuff
remains inflated in its "resting state," and keeps the anal canal closed by pressure,
allowing continence. Upon the decision to have a bowel movement, the patient
temporarily deflates the cuff by pressing the pump and fecal matter is released. The
balloon re-inflates after the movement.


Artificial urinary sphincter surgery

Patients must be chosen carefully, exhibit isolated sphincter deficiency, and be
motivated and able to work with the device and its exigencies. To characterize the
condition to be treated and to determine outcomes, full clinical, urodynamic, and
radiographic evaluations are necessary. The ability to distinguish mobility of the
urethra as the cause of incontinence from sphincter insufficiency is difficult, but very
important in the decision for surgery. A combination of pelvic examination for
urethral hypermobility and a leak-point pressure as measured by coughing or other
abdominal straining has been shown to be very effective in identifying the patient
who needs the surgical implant. Visual examination of the bladder with
a cystoscope is very important in the preoperative evaluation for placement of the
sphincter. Urethral and bladder conditions found by the examination should be
addressed before implantation. Previous reconstruction or repair of the urethra may
prevent implantation of the cuff. In open abdominal surgery, the implant surgery uses
preventive infection measures that are very important, including sterilization of the
urine preoperatively with antibiotics, the cleansing of the intestines from fecal matter
and secretions through laxatives immediately prior to surgery, and antibiotic
treatment and vigorous irrigation of the wound sites.

Artificial anal sphincter surgery

Since only a limited number of patients with fecal incontinence would benefit from an
artificial sphincter, it is very important that a thorough examination be performed to
distinguish the causes of the incontinence. A medical history and physical, as well as
documented entries or an incontinence diary are crucial to the diagnosis of fecal
incontinence. The physical exam usually includes a visual inspection of the anus and
the area lying between the anus and genitals for hemorrhoids, infections, and other
conditions. The strength of the sphincter is tested by the doctor probing with a finger
to test muscle strength.

Medical tests usually include:

Anorectal manometry. This is a long tube with a balloon on the end that is
inserted in the anus and rectum to measure the tightness of the anal sphincter
and the ability to respond to nerve firings.

Anorectal ultrasonography. This test also includes an insertion of a small

instrument into the anus with a video screen that produces sound waves,
picturing the rectum and anus.

X rays. A substance called barium is used to make the rectum walls visible to
x ray. This liquid is swallowed by the patient before the test.

Anal electromyography. This test uses the insertion of tiny needle electrodes
into muscles around the anus and tests for nerve damage.

Artificial urinary sphincter surgery
Surgery requires a few days of hospitalization. Oral and intravenous pain
medications are administered, along with postoperative antibiotics. A general diet is
available, usually on the evening of surgery. When the patient is able to walk, the
urethral catheter is removed. Patients are discharged on the second day
postoperatively, unless they have had other procedures and need extra recovery
time. Patients may not lift heavy objects or engage in strenuous activity for
approximately six weeks. After six to eight weeks, the patient returns to the physician
for training in the use of the implant device.

Artificial anal sphincter surgery

Surgery hospitalization requires a few days with dietary restrictions and anti-diarrheal
medicine to bind the bowels. Antibiotics are administered to lower the risk of
infection, and skin incisions are cleaned frequently. Patients may not lift heavy
objects or engage in strenuous activity for approximately six weeks. After the body
has had time to heal over six to eight weeks, the patient returns to the physician for
training in the use of the pump. Two or three sessions are required and after the
training, the patient is encouraged to lead as normal a life as possible.

Normal results

Artificial urinary sphincter surgery

One problem with the urinary sphincter implant is failure. If the device fails, or the cuff
erodes, the surgery must be repeated. In a study published in 2001, 37% of women
had the implant after an average of seven years, but 70% had the original or a
replacement and 82% were continent. Studies on men report similar findings.
Malfunction has improved with advances in using a narrower cuff. In one large study
encompassing one surgeon over 11 years, the re-operative rate of AUS related to
malfunction in men was 21%. Over 90% of patients were alive with a properly
functioning device.

Another problem with the surgery is urinary voiding. This may be difficult initially due
to postoperative edema caused by bruising of the tissue. In the majority of cases,
urination occurs after swelling has receded.
AUS is a good alternative for children. The results of AUS in children range from 62
90%, with similar rates for both girls and boys.

Artificial anal sphincter surgery

Anal sphincter implant surgery has been successfully performed for many years. The
device most often used has a cumulative failure rate of 5% over 2.5 years. The long-
term functional outcome of artificial anal sphincter implantation for severe fecal
incontinence has not been determined. However, adequate sphincter function is
recovered in most cases, and the removal rate of the device is low. Most of the good
results are dependent upon careful patient selection and appropriate surgical and
operative management with a highly experienced surgical team .

Morbidity and mortality rates

Artificial urinary sphincter surgery

Infection has been a frequent and serious complication of surgery, not only because
of the infection per se, but also because infection can cause erosion of the urethra or
bladder neck under the implant. The infection may actually worsen the incontinence.
The overall infection rate with AUS implants is 13%. Because of interactions
between the host and the foreign body represented by the implant, infections can
occur soon after the surgery, or months and even years later. New techniques using
antibiotics and skin preparations have improved infection rates considerably.

Artificial anal sphincter surgery

This surgery is for a limited number of patients who have isolated sphincter
deficiency. Patients must be chosen who have little co-morbidity (serious illnesses)
and can be trained in the use of the pump. Although it is a fairly simple operation,
some researchers report a 30% infection rate.

Artificial urinary sphincter surgery
Milder forms of urinary incompetence can be treated with changes in diet, evaluation
of medications, and the use of antidepressants and estrogen replacement, as well as
bladder training and pelvic muscle strengthening. However, sphincter deficiency,
unlike incontinence caused by urethral mobility, requires a substitute for the sphincter
contraction by implant or by auxiliary tissue. If AUS cannot treat sphincter deficiency,
the sling or "hammock" procedure is a good second choice. It brings tightness to the
sphincter by using tissue under the urethra to increase contractual function.
The sling procedure is already preferred over the AUS for women.

Artificial anal sphincter surgery

Milder forms of fecal incontinence are being treated by changes in diet and the use of
certain bowel-binding medications. For some forms of mild fecal incontinence,
special forms of exercise can help to strengthen and tone the pelvic floor muscles,
along with providing biofeedback to train the muscles to work with an appropriate
schedule. Only after these measures have been tried, including the use of pads, is
the patient counseled on the benefits of an anal sphincter implant.


Walsh, P., et al. Campbell's Urology, 8th Edition. St. Louis: Elsevier Science, 2000.

Michot, F. "Artificial Anal Sphincter in Severe Fecal Incontinence: Outcome of
Prospective Experience with 37 Patients in One Institution." Annals of Surgery, Vol.
237, No. 1 (January 1, 2003): 5256.

Rotholtz, N. A., and S. D. Wexner. "Surgical Treatment of Constipation and Fecal

Incontinence." Gastroenterology Clinics, Vol. 30, No. 01 (March 2001).

American Society of Colon and Rectal Surgeons. 85 W. Algonquin Rd., Suite 550,
Arlington Heights, IL 60005. .
National Institute of Diabetes and Digestive and Kidney Diseases. (800) 891-5390
(kidney); (800) 860-8747 (diabetes); (800) 891-5389 (digestive
diseases). .

National Association of Incontinence. .

Fecal Incontinence. National Institute of Diabetes & Digestive & Kidney Diseases
(NIDDK). .

Incontinence in Men. Health and Age. http://www.healthand .

Urinary Incontinence. WebMD Patient Handout. .

Urinary Incontinence in Women. National Institute of Diabetes & Digestive & Kidney
(NIDDK). .

Nancy McKenzie, PhD



Implantation surgery is performed in a hospital operating room by urologic

surgeons specially trained for implantation of the artificial sphincter in the urinary or
anal tracts. Successful surgery depends upon very experienced surgeons.


How many implantation surgeries have you performed?

What is your rate of device removal in the patients you have treated?

How likely is infection after surgery?

How likely is infection to occur long term?

Read more:
Sacral nerve stimulation, also known as sacral neuromodulation, is a procedure in
which the sacral nerve at the base of the spine is stimulated by a mild electrical
current from an implanted device. It is done to improve functioning of the urinary
tract, to relieve pain related to urination, and to control fecal incontinence.

As a proven treatment for urinary incontinence, sacral nerve stimulation (SNS) has
recently been found effective in the treatment of interstitial cystitis, a disorder that
involves hyperreflexia of the urinary sphincter. SNS is also used to treat pelvic or
urinary pain as well as fecal incontinence.

A person's ability to hold urine or feces depends on three body functions:

a reservoir function represented by the urethra/bladder or colon

a gatekeeping function represented by the urethral or anal sphincter

the brain's ability to control urination, defecation, and nerve sensitivity

A dysfunction or deficiency in any of these components can result in incontinence.

The most common forms of incontinence are stress urinary incontinence and urge
incontinence. Stress incontinence is related to an unstable detrusor muscle that
controls the urinary sphincter. When the detrusor muscle is weak, urine can leak out
of the bladder from pressure on the abdomen caused by sneezing, coughing, and
other movements. Urge incontinence is characterized by a sudden strong need to
urinate and inability to hold urine until an appropriate time; it is also associated with
hyperactivity of the urinary sphincter. Both conditions can be treated by SNS. SNS
requires an implanted device that sends continuous stimulation to the sacral nerve
that controls the urinary sphincter. This treatment has been used with over 1500
patients with a high rate of success. It was approved in Europe in 1994. The Food
and Drug Administration (FDA) approved SNS for disturbances that are usually
treated by augmentation of the sphincter muscle or implanting an artificial sphincter
can benefit from electrical stimulation of the sacral nerve. Although the mechanism
of SNS is not completely clear, researchers believe that the patient's control of the
pelvic region is restored by the stimulation or activation of afferent fibers in the
muscles of the pelvic floor.
Urinary incontinence affects between 15% and 30% of American adults living in the
community, and as many as 50% of people confined to nursing homes . It is a
disorder that affects women far more frequently than men; 85% of people suffering
from urinary incontinence are women. According to the chief of geriatrics at a Boston
hospital, 25 million Americans suffer each year from occasional episodes of urinary
or fecal incontinence.

Interstitial cystitis is less common than urinary or fecal incontinence but still affects
700,000 Americans each year. The average age of IC patients is 40; 25% of patients
are younger than 30. Although 90% of patients diagnosed with IC are women, it is
thought that the disorder may be underdiagnosed in men.

Sacral nerve stimulation (SNS) is conducted through an implanted device that
includes a thin insulated wire called a lead and a neurostimulator much like a cardiac
pacemaker. The device is inserted in a pocket in the patient's lower abdomen. SNS
is first tried on an outpatient basis in the doctor's office with the implantation of a test
lead. If the trial treatment is successful, the patient is scheduled for inpatient surgery.

Permanent surgical implantation is done under general anesthesia and requires a

one-night stay in the hospital. After the patient has been anesthetized, the surgeon
implants the neurostimulator, which is about the size of a pocket stopwatch, under
the skin of the patient's abdomen. Thin wires, or leads, running from the stimulator
carry electrical pulses from the stimulator to the sacral nerves located in the lower
back. After the stimulator and leads have been implanted, the surgeon closes the
incision in the abdomen.

Incontinence significantly affects a patient's quality of life; thus patients usually
consult a doctor when their urinary problems begin to cause difficulties in the
workplace or on social occasions. A family care practitioner will usually refer the
patient to a urologist for diagnosis of the cause(s) of the incontinence. Patients with
urinary and fecal incontinence are evaluated carefully through the taking of a
complete patient history and a physical examination . The doctor will use special
techniques to assess the capacity of the bladder or rectum as well as the functioning
of the urethral or anal sphincter in order to determine the cause or location of the
incontinence. Cystoscopy , which is the examination of the full bladder with a scope
attached to a small tube, allows the physician to rule out certain disorders as well as
plan the most effective treatment. These extensive tests are especially important in
diagnosing interstitial cystitis because all other causes of urinary urgency, frequency,
and pain must be ruled out before surgery can be suggested. Cystoscopy is done
under anesthesia and often works as a treatment for IC. Once the doctor has made
the diagnosis of urinary incontinence due to sphincter insufficiency, he or she will
explain and discuss the surgical implant with the patient. SNS may be tried out on a
temporary basis. The same pattern of diagnosis and treatment is used for patients
with IC and fecal incontinence. Temporary implants can help eliminate those patients
who will not benefit from a permanent implant.

Following surgery, the patient remains overnight in the hospital. Antibiotics may be
given to reduce the risk of infection and pain medications to relieve discomfort. The
patient will be given instructions on incision care and follow-up appointments before
he or she leaves the hospital.

Aftercare includes fine-tuning of the SNS stimulator. The doctor can adjust the
strength of the electrical impulses in his or her office with a handheld programmer.
The stimulator runs for about five to 10 years and can be replaced during an
outpatient procedure. About a third of patients require a second operation to adjust
or replace various elements of the stimulator device.

In addition to the risks of bleeding and infection that are common to surgical
procedures, implanting an SNS device carries the risks of pain at the insertion site,
discomfort when urinating, mild electrical shocks, and displacement or dislocation of
the leads.

Normal results
Patients report improvement in the number of urinations, the volume of urine
produced, lessened urgency, and higher overall quality of life after treatment with
SNS. Twenty-two patients undergoing a three to seven-day test of sacral nerve
stimulation on an outpatient basis reported significant reduction in urgency and
frequency, according to the American Urological Association. Studies have indicated
complete success in about 50% of patients. Sacral nerve stimulation is being used to
treat fecal incontinence in the United States and Europe, with promising early
reports. As of 2003, SNS is the least invasive of the recognized surgical treatments
for fecal incontinence.

Morbidity and mortality rates

Sacral nerve stimulation has been shown to be a safe and effective procedure for the
treatment of both urinary and fecal incontinence. Two groups of researchers, in
Spain and the United Kingdom respectively, have reported that "the effects of
neuromodulation are long-lasting and associated morbidity is low." The most
commonly reported complications of SNS are pain at the site of the implant (15.3%
of patients), pain on urination (9%), and displacement of the leads (8.4%).

There are three types of nonsurgical treatments that benefit some patients with IC:

Behavioral approaches. These include biofeedback, diet modifications,

bladder retraining, and pelvic muscle exercises.

Medications. These include antispasmodic drugs, tricyclic antidepressants,

and pentosan polysulfate sodium, which is sold under the trade name Elmiron.
Elmiron appears to work by protecting the lining of the bladder from bacteria
and other irritating substances in urine.

Intravesical medications. These are medications that affect the muscular

tissues of the bladder. Oxybutynin is a drug that is prescribed for patients who
are incontinent because their bladders fail to store urine
properly. Capsaicin and resiniferatoxin are used to treat hyperreflexia of the
detrusor muscle.

Surgical alternatives to SNS are considered treatments of last resort for IC because
they are invasive, irreversible, and benefit only 3040% of patients. In addition, some
studies indicate that these surgeries can lead to long-term kidney damage. They
include the following procedures:
Augmentation cystoplasty. In this procedure, the surgeon removes the
patient's bladder and replaces it with a section of the bowelin effect creating
a new bladder. The patient passes urine through the urethra in the normal

Urinary diversion. The surgeon creates a tube from a section of the patient's
bowel and places the ureters (tubes that carry urine from the kidneys to the
bladder) in this tube. The tube is then attached to a stoma, or opening in the
abdomen. Urine is carried into an external collection bag that the patient must
empty several times daily.

Internal pouch. The surgeon creates a new bladder from a section of the
bowel and attaches it inside the abdomen. The patient empties the pouch by
self-catheterization four to six times daily.


Walsh, Patrick C., MD, et al., eds. Campbell's Urology , 8th ed. Philadelphia: W. B.
Saunders Company, 2002.

Elliott, Daniel S., MD. "Medical Management of Overactive Bladder." Mayo Clinic
Proceedings 76 (April 2001): 353-355.

Ganio, E., A. Masin, C. Ratto, et al. "Short-Term Sacral Nerve Stimulation for
Functional Anorectal and Urinary Disturbances: Results in 40 Patients: Evaluation of
a New OPtion for Anorectal Functional Disorders." Disorders of the Colon and
Rectum 44 (September 2001): 1261-1267.

Kenefick, N. J., C. J. Vaisey, R. C. Cohen, et al. "Medium-Term Results of Permanent

Sacral Nerve Stimulation for Faecal Incontinence." British Journal of Surgery 89 (July
2002); 896-601.

Linares Quevedo, A. I., M. A. Jiminez Cidre, E. Fernandez Fernandez, et al.

"Posterior Sacral Root Neuromodulation in the Treatment of Chronic Urinary
Dysfunction. [in Spanish] Actas urologicas espanolas 26 (April 2002): 250-260.
American Urological Association (AUA). 1120 North Charles Street, Baltimore, MD
21201. (410) 727-1100. .

National Association for Continence (NAFC). P. O. Box 1019, Charleston, SC 29402-

1019. (843) 377-0900. .

National Kidney Foundation. 30 East 33rd Street, Suite 1100, New York, NY 10016.
(800) 622-9010 or (212) 889-2210. .

National Kidney and Urologic Diseases Information Clearinghouse (NKUDIC). 3

Information Way, Bethesda, MD 20892-3580.

Interstitial Cystitis Association. Sacral Nerve Stimulation Can Relieve Interstitial
Cystitis, Studies
Suggest .

Mayo Clinic. Sacral Nerve Stimulation .


Nancy McKenzie, PhD



SNS devices are implanted under general anesthesia by urologists, who are
physicians specializing in treating disorders of the urinary tract. The procedure is
usually performed in a hospital.


Am I likely to benefit from SNS?

How many stimulators have you implanted?

How many of your patients consider SNS a successful treatment?

What side effects have your patients reported?

Read more:

Bladder augmentation, also known as augmentation cystoplasty, is reconstructive
surgery to increase the reservoir capacity of the bladder. The procedure is very
common and involves tissue grafts (anastomosis) from a section of the small
intestine (ileum), stomach, or other substitutes that are attached to the urinary
bladder by sewing or stapling. Whether due to chronic obstructive bladder damage,
birth defects that resulted in small reservoir capacity, or dysfunction due to nerve
innervation of the bladder muscle (sphincter), surgery is chosen only after a thorough
medical work-up that involves assessment of the lower urinary tract, functional
physiological evaluation, and anatomic assessment. Some laparoscopic methods
(surgery with a fiber-optic instrument inserted through the abdomen) of bladder
augmentation have been tried, but reports indicate that these are technically arduous
and may not have the long-lasting effects of open surgery.

Bladder dysfunction and incontinence may be due to problems with the reservoir
capacity of the bladder or with the "gatekeeping" muscle (the sphincter), which,
instructed by the brain, allows urine to build up or to be released. Bladder
augmentation is used to treat serious and irreversible forms of incontinence and to
protect the upper urinary tract (kidney function) from reflexia (urine back up to the
kidneys). Many candidates for the surgery are highly compromised individuals with
other serious conditions like spinal cord injuries and multiple sclerosis, as well as
patients likely to undergo kidney transplantation . Patients who undergo bladder
augmentation must be free of bowel and urethral disease and be able to perform
self-catheterization (able to place a urinary tube into their urethra).

Standard augmentation involves segments of the bowel used to create a pouch or
wider wall for the bladder in order to enhance its reservoir capacity. Often this
reconstruction surgery is accompanied by procedures that tighten the neck of the
bladder, as well. Milkulicz performed the first clinical augmentation cystoplasty using
abdominal tissue in 1898. Couvelaire, in the 1950s, popularized bladder
augmentation for the treatment of the contracted bladder due to tuberculosis. Until
the 1970s it was thought that those with bladder dysfunction could be treated with
bladder diversion, and that this procedure offered a simple and safe means of
emptying the bladder. However, it was soon discovered that pressure from the
bladder caused irreparable damage to the kidneys, with 50% of patients exhibiting
such deterioration. The new diagnostic assessment of the bladder as well as the
need for a new medical intervention for patients with severe bladder dysfunction
opened the way for urinary tract reconstruction. Today, many techniques are
available, along with new types of grafting substitutions.

The basic procedure involves open abdominal surgery with resection of a 1020 in
(2530-cm) segment of ileum, cecum (first part of the large intestine), or the
ileocecum (the junction of small and large intestines) cut down the middle
(detubularized), and shaped into a U-configuration with a pouch at the bottom. This
opening or pouch will be the "patch" for the bladder. During surgery, the bladder itself
is also opened at the dome and cut at right angles to

During a bladder augmentation procedure, an incision is made in the abdomen to expose the
intestines and bladder (A). A section of ileum (small intestine) is removed and opened (B). After
being sterilized, it is grafted onto the bladder to increase its capacity (C). The appendix and cecum
(large intestine) may also be used (D). (
Illustration by GGS Inc.
create a clam-like shape. The open bowel "patch" is then attached to the bladder
with sutures or stapling.

Patients selected for bladder augmentation are chosen after they undergo a thorough
physical exam, x-ray tests, and bladder physiology tests, as well as a renal and
bladder ultrasound for any dilation of the kidneys or ureters or kidney obstruction. A
VCUG (holding and voiding urine) test is performed to assess the contour of the
bladder and to assess for ureteral reflux (back up of urine to the kidneys). Finally, a
CMG (cystometrogram) is performed in the physician's office to judge the pressure
and volume levels at which the urine leakage occurs. Once the tests, as well as the
history and physical exam are completed, treatment plans commence.

The patient should plan for up to two weeks in the hospital. The patient will have
been on a low-residue diet for a few days before admission. Surgery will take place
two to three days after hospital admittance. In the hospital, a general examination will
be performed and blood taken. The bowel will need to be cleaned in preparation.
Clear fluids will be given, as well as a strong laxative prior to surgery.

Early complications of surgery include cardiovascular, thrombo-embolic (blood clot),
gastrointestinal, and respiratory complications associated with major abdominal
surgery. Many patients require three months after surgery to allow their augmented
bladder to establish itself. This involves a special diet for a few months as well as
patient familiarity with the fact that the augmented bladder empties after the native
bladder. Two weeks after surgery tests are performed to ensure that the patch is leak
proof. Once a watertight reservoir is demonstrated, the catheters and drains that
were introduced for surgery are removed.

Long term risks of the procedure include peptic ulceration of the bladder and
perforation of the gastric segment. Spontaneous perforation is rare but it is life
threatening and has a 25% mortality rate. Other risks include bacterial infections,
metabolic changes, urinary tract infections, and urinary tract stones. Nocturnal
incontinence is sometimes a problem after the surgery.

Normal results
Although some patients recover spontaneous voiding function, this does not occur
with reliable predictability. Preoperatively, patients should be prepared for the
likelihood that they will have to perform lifelong intermittent catherization and
irrigation of the augmented bladder. Other effects are a special diet for up to three
months and pain after surgery.

Morbidity and mortality rates

Reported surgical risks include 35.7% rate of adhesive small bowel obstruction
requiring operative intervention, 56% incidence of wound infection, 03%
reoperation rate for bleeding. Long term complications include a 50% unchanged
bladder compliance and renal deterioration. No reduction in growth in children has
been reported, but the procedure is not recommended for children who have not
reached puberty, unless there is the threat of kidney damage.

Bladder augmentation is a medical treatment of last resort for those patients unable
to avoid incontinence through medical alternatives. Other surgeries may be indicated
if the individual is not a candidate for self-catherization or has other medical or
psychological conditions that would rule out bladder augmentation.


Dewan, P., and M. E. Mitchell, eds. Bladder Augmentation. Oxford Press, 2000.

Abrams, P., S.K. Lowry, et al. "Assessment and Treatment of Urinary
Incontinence." Lancet 355 (June 2000): 215358

Fantl, J. A., D. K. Newman, J. Colling, et al. "Urinary Incontinence in Adults: Acute

and Chronic Management. Clinical Practice Guideline, Number 2, 1996." Agency for
Health Policy and Research Publications (March 1996).

Greenwell, T. J., S. N. Venn, and A. R. Mundy. "Augmentation Cystoplasty." British

Journal of Urology International 88, no. 6 (October 2001): 511534.

Qucek, M. I., and D. A. Ginsberg. "Long-term Urodynamics Follow-up of Bladder

Augmentation for Neurogenic Bladder." Urology 169 (January 2003): 195198.

Rackley, R. R., and J. B. Abdelmalak. "Radical Prostatectomy: Laparoscopic

Augmentation Cystoplasty." Urological Clinics of America 28 (August 2001).

National Association for Continence. P.O. Box 8310 Spartanburg, SC 29305. (800)
BLADDER, (252-3337). .

National Kidney and Urologic Diseases Information Clearing-house. 3 Information

Way, Bethesda, MD 20892-3580. (301) 654-4415. .

The Simon Foundation for Continence. P.O. Box 835 Wilmette, IL 60091. (800)
23SIMON (237-4666). .

"Bladder Augmentation." Dr. Rajhttp. [cited April
2003]. .

Carr, Michael, and M. E. Mitchell. "Bladder Augmentation." Digital Urological

Journal. [cited April 2003]. .

"Neurogenic Bladder." [cited April

2003]. .

Nancy McKenzie, Ph.D.


A urological surgeon who is an MD with advanced training in urology and special
surgical training for this type of surgery. Surgery takes place in a general hospital.


How many bladder augmentation surgeries do you perform a year?

What complications of this surgery do you think are the most likely and/or

Are there other patients with my underlying medical conditions who have had
this surgery that I could contact?

Is there a pre-op patient group with this hospital that could help me
understand my rehabilitation and help with the compliance with the diet and

Read more:

Needle bladder neck suspension, also known as needle suspension, or paravaginal
surgery, is performed to support the hypermobile, or moveable urethra using sutures
to attach it to tissues covering the pelvic floor. Of the three popular surgical
procedures for urethral instability and its results in urinary stress incontinence,
needle bladder neck suspension is the quickest and easiest to perform. It has many
variants, such as the Raz, Stamey, modified Pereyra, or Gattes procedures, but its
long-term results are less impressive than other, more extensive, anti-incontinent

Fifty years of surgical attempts to treat incontinence, especially in women, has
resulted in three types of surgery tied to essentially three causes of a particular type
of incontinence related to muscle weakening of the urethra and the "gate-
keeping" sphincter muscles. Stress urinary incontinence, the uncontrollable leakage
of urine when pressure is put on the bladder during sneezing, coughing, laughing, or
exercising, is very common in women, and is estimated to affect 50% of elderly
women in long-term care facilities. The inability to hold urine has two causes. One
has to do with support for the urethra and bladder, known as genuine stress
incontinence (GSI), and the other is related to the inability of sphincter muscles, or
intrinsic sphincter deficiency (ISD), to keep the opening of the bladder closed.

In GSI, weak muscles supporting the urethra allow it to be displaced and/or descend
into the pelvic-floor fascia (connective tissues) and create cystoceles, or pockets.
The goal of surgery for GSI is to stabilize the suburethral fascia to prevent the urethra
from being overly mobile during increased abdominal pressure.

The other major source of stress incontinence is due to weakening of the internal
muscles of the sphincter, as they affect closure of the bladder. These muscles, called
the intrinsic sphincter muscles, regulate the opening and closing of the bladder when
a decision is made to urinate. Deficiency of the intrinsic sphincter muscles causes
the opening to remain open and thus leads to chronic incontinence. ISD is a source
of severe stress incontinence and may be combined with urethral hypermobility.

The challenge of surgery for stress incontinence is to adequately evaluate the actual
source of incontinence, whether GSI or ISD, and also to determine the likelihood of
cystoceles that may need repair. Under good diagnostic conditions, surgery for stress
incontinence will utilize a suprapubic (above the pubic area) procedure, or Burch
procedure, to secure the hypermobile urethra and stabilize it in a neutral position.
Surgery for ISD uses what is known as a sling procedure , or "hammock" effect,
that uses auxiliary tissue to undergird the urethra and provide contractive pressure to
the sphincter. Most stress incontinence surgeries fall into one of these two
procedures and their variants.

Needle neck bladder suspension, the third most utilized procedure for stress
incontinence, simply attempts to attach the urethra neck to the posterior pelvic wall
through the vagina or abdomen in order to stabilize the urethra. It is, however,
considered a poor choice in comparison to the other two procedures because of its
lack of long-term efficacy and its high incidence of urinary retention as an operative

More than 13 million people in the United States, both males and females, have
urinary incontinence. Women experience it twice as often as men due to pregnancy,
childbirth, menopause, and the structure of the female urinary and gynecological
systems. Anyone can become incontinent due toneurological injury, birth defects,
cardiac conditions, multiple sclerosis, and chronic conditions in later life.
Incontinence does not naturally accompany old age but is associated with many
chronic conditions that occur as age increases. Incontinence is highly associated
with obesity and lack of exercise . As many as 1530% of adults over 60 have some
form of urinary incontinence. Stress incontinence is, by far, the most frequent form of
incontinence and is the most common type of bladder control problem in younger
and middle-age women.

Needle bladder neck suspension surgery can be performed as open abdominal or
vaginal surgery, or laproscopically, which allows for small incisions, video
magnification of the operative field, and precise placement of sutures. Under a
general anesthetic, the patient is placed in a position on her back with legs in stirrups
allowing access to the suprapubic area. A Foley catheter is inserted into the bladder.
The open procedure involves the passage of a needle from the suprapubic area to
the vagina with multiple sutures through looping. Cytoscopic monitoring (using an
endoscope passed into the urethra) prevents passage of the needle through the
bladder or the urethra. The laproscopic method allows visualization of the needle
pass made from the suprapubic area to the vagina and the looping technique. The
vagina and the surrounding areas are thoroughly irrigated with an antibiotic solution
throughout the procedure. The patient is discharged the same evening or the next
morning with the catheter in place. She is kept on antibiotics and examined on the
fourth day after surgery with the removal of the catheter. The follow-up examination
includes wound inspection and a evaluation of residual urine. A pelvic examination is
performed to check for bleeding or injury.

Stress urinary incontinence can have a number of causes. It is important that
patients confer with their physicians to rule out medication-related, psychological,
and/or behavioral sources of incontinence as well as physical and neurological
causes. This involves complete medical history, as well as medication, clinical,
neurological, and radiographic evaluations. Once these are completed, urodynamic
tests that evaluate the urethra, bladder, flow, urine retention, and leakage, are
performed and allow the physician to determine the primary source of the stress
incontinence. Patients who are obese and/or engage in high-impact exercise are not
good candidates for this surgery. Patients with ISD may not be cured with this
procedure, since it is primarily intended to treat the hypermobile urethra.

Morbidity and mortality rates

Urologic surgery has inherent morbidity and mortality risks related primarily
to general surgery , with lung conditions, blood clots, infections, and cardiac events
occurring in a small percentage of surgeries, independent of the type of procedure.
In addition, the American Urological Association (AUA) has concluded that needle
suspension surgery has a number of complications related directly to suturing in the
suprapulic area. These complications include:

a 5% incidence of bladder injury

urethral injury, although rare, in a small percentage of cases

bleeding, with an incidence of 35%, primarily from the area below the pubic
nerve entrapment (816% of cases) due to lateral placement of the sutures
into the fascia at the back of the suprapubic area (This has improved with a
change in the placement of sutures.)

wound infections in about 7% of cases, with higher rates among those with
diabetes or obesity

These operative complications, coupled with the procedure's high rate (10%) of
reported pain after surgery, and its relatively high rate (5%) of urinary retention
lasting longer than four weeks, have resulted in needle neck suspension having a
limited role in the management of stress urinary incontinence.

Normal results
Despite modifications in the needle suspension procedure, the long-term outcome of
the procedure does not indicate its lasting efficacy. According to a recent report by
the AUA, a study of the effects of needle suspension found only a 67% cure, or "dry
rate," after 48 months, with delayed failures of sutures in a very high percentage (33-
80%) of cases.

See also Sling procedure .


"Urologic Surgery." In Campbell's Urology. 8th edition, edited by P. Walsh, et al.
Philadelphia: W. B. Saunders, 2000.

Bodell, D. M. and G. E. Leach. "Needle Suspension Procedures for Female
Incontinence." Urologic Clinics 29 (August 2002).

Liu, C. Y. "Laproscopic Treatment of Stress Urinary Incontinence." Obstetrics and

Gynecology Clinics 26 (March 1999).

Takahashi, S., et al. "Complications of Stamey Needle Suspension for Female Stress
Urinary Incontinence." Urology International 86 (January 2002): 148151.
American Foundation for Urologic Diseases. The Bladder Health Council. 300 West
Pratt Street, Suite 401, Baltimore, MD 21201.

American Urological Association. 1120 North Charles Street, Baltimore, MD 21201.

(410) 727-1100. Fax: 410-223-4370. .

The Simon Foundation for Continence. P.O. Box 835, Wilmette, IL 60091. (800) 237-
simon or (800) 237-4666. Voice - Toll-free: (847) 864-3913. Voice: (847) 864-9758.

"Urinary Incontinence." MD Consult Patient Handout. January 2, 2003 [cited July 7,
2003]. .

Nancy McKenzie, PhD



Surgery is performed by a urological surgeon who has a medical degree with

advanced training in urology and in surgery. Surgery is performed in a general


Is surgery my only alternative to living with urinary incontinence?

Are there other surgical procedures that are more effective for my

Can you recommend any literature I can read that explains my surgical
options for incontinence?
Can you explain why this procedure is preferable to what is known as a "sling

Read more:

Urologic surgery is the integration of surgical activities for the pelvisthe colon,
urogenital, and gynecological organsprimarily for the treatment of obstructions,
dysfunction, malignancies, and inflammatory diseases. Common urologic operations

renal (kidney) surgery

kidney removal ( nephrectomy )

surgery of the ureters, including ureterolithotomy or removal

of calculus (stones) in the ureters

bladder surgery

pelvic lymph node dissection

prostatic surgery, removal of the prostate

testicular (scrotal) surgery

urethra surgery

surgery to the penis

Conditions that commonly dictate a need for urologic surgery include neurogenic
sources like spinal cord injury; injuries to the pelvic organs; chronic digestive and
urinary diseases; as well as prostate infections and inflammations. There are many
other common chronic and malignant diseases that can benefit from resection,
surgical augmentation, or surgery to clear obstructions. These conditions impact the
digestive, renal, and reproductive systems.

Most organs are susceptible to cancer in the form of tumors and invasion of the
surrounding tissue. Urologic malignancies are on the rise. Other conditions that are
seen more frequently include kidney stones, diseases and infections; pancreatic
diseases; ulcerative colitis; penile dysfunction; and infections of the genitourinary
Urologic surgery has been revolutionized by striking advances in urodynamic
diagnostic systems. Changes in these areas have been particularly beneficial for
urologic surgery: laparascopy, endoscopic examination for colon cancer, implantation
procedures, and imaging techniques. These procedural and imaging advances have
brought the field of urology to a highly active and innovative stage, with new surgical
options created each year.

According to the National Kidney Foundation, kidney and urologic diseases affect at
least 5% of the American population, and cause over 260,000 deaths. As the
population ages, these conditions are expected to increase, especially among ethnic
minorities who have a disproportionate share of urologic diseases. Major urologic
surgery includes radical and partial resections for malignant and benign conditions;
and implantation and diversion surgeries.

Prostate cancer is the most common cancer affecting males in the United States.
One in 10 men will have the disease at some time in his life. It is, however, treated
successfully with surgery.

According to the Urological Foundation, more than 50,000 new cases of bladder
cancer are detected each year. In the United States, bladder cancer is the fourth
most common cancer in men and the ninth most common for women.

Kidney cancer occurs in 30,000 patients per year, with about 11,000 deaths. It is the
eighth most common cancer in men and the tenth most common cancer in
women. Renal cell carcinoma makes up 85% of all kidney tumors. In adults ages 50
70 years, kidney cancer occurs twice as often in men as women. At the time of
diagnosis, metastasis is present in 2530% of patients with renal cell carcinoma.

Other conditions
Enlarged prostate (benign prostate hyperplasia, or BPH) is very common, and often
treated with surgery. Interstitial cystitis (bladder infection of unknown origin) often
affects women with severe pain and incontinence. The condition, like other forms of
severe incontinence, requires surgery.
Incontinence is an increasingly diagnosed problem among the aging population in
the United States, and is gaining recognition for its highly debilitating effects both in
its fecal and urinary forms. According to the National Institute of Diabetes & Digestive
& Kidney Diseases (NIDDK), more than 6.5 million Americans have fecal
incontinence. Fecal incontinence affects people of all ages; many cases are never
reported. Women are five times more likely than men to have fecal incontinence. This
is primarily due to obstetric injury, especially with forceps delivery and anal sphincter

More than 13 million people in the United States experience urinary incontinence.
Community based studies reveal that 30% of patients are over the age of 65, and
63% are female. According to one study published in the American Journal of
Gastroenterology, only 34% of incontinent patients have ever mentioned their
problem to a physician, even though 23% wear absorbent pads, 12% take
medications, and 11% lead lives restricted by their incontinence.

Many surgical procedures are now available to correct both fecal and urinary
incontinence. They include retropubic slings for urinary incontinence, artificial
sphincter implants for urinary and fecal incontinence, and bladder and colon
diversion surgeries for restoration of voiding and waste function with an outside
appliance called an ostomy. Kidney surgery and transplantation account for a large
segment of urologic surgery. Benign conditions include sexual dysfunction, kidney
stones, and fertility issues.

Until the late twentieth century, urological operations usually involved open
abdominal surgery with full incision, lengthy hospital stays, and long recovery
periods. Today, surgery is less traumatic, with shortened hospitalizations. Minimally
invasive surgeries are the norm in many cases, with new laparascopic procedures
developed each year. Laparascopic surgery is effective for many kidney tumors and
kidney removal (nephrectomy), lymph node excision, prostate and ureteral cancers,
as well as incontinence, urological reconstruction, kidney stones, and some cases of
bladder dysfunction.

Testing is often required to determine if a patient is better suited for open or
laparscopic surgery. Blood tests for some cancers, as well as function tests for the
affected organs, will be required. Radiographic or ultrasound techniques are helpful
in providing images of abnormalities.

Cystoscopy is often used with bladder and urethra surgery. In this procedure, a thin
telescope-like instrument is inserted directly into the bladder. Disorders of the colon
may be studied with endoscopes, imaging instruments inserted directly into the
colon. Urodynamic studies of the bladder and sphincter determine how the bladder
fills and empties. Digital rectal exams diagnose prostatic disorders. In this procedure,
the physician feels the prostate with a gloved, lubricated finger inserted into the

Hospital stays range from one day to one week, depending upon the level of organ
involvement and type of urologic surgery (open versus laparoscopic). Major urologic
surgeries may require stents (temporary diversion of urine or feces) and catheters
that are removed after surgery. Some surgeries are staged in two parts to
accommodate the removal of diseased tissue, and the augmentation or
reconstruction to replace function. Laparoscopic surgery patients benefit from shorter
hospital stays, more rapid recovery, and possibly lower morbidity rates than open
surgery procedures. This is increasingly true for prostate cancer surgeries.

The risks of urologic surgery vary with the type of surgical procedure (open or
laparacopic), and the extent of organ involvement. According to one study of 2,407
urologic surgeries in four centers, the overall complication rate was 4.4%, with a
mortality rate of 0.08%.

Open surgery poses the standard surgery and anesthetic risks associated with strain
on the heart and lungs. Risks of infection at the wound site accompany all surgeries,
open and laparoscopic. The risk of injury to adjacent organs is higher in laparoscopic
surgery. Kidney removal and transplantation have many risks because of the extent
of the surgery, as do surgeries of the colon, bladder, and prostate.

Significant gains have been made in prostate surgery. Urinary control issues
following prostate surgery, especially radical prostatectomy, have improved. However,
postoperative urinary incontinence remains a significant risk, with 27% of patients in
one study reporting the need for some kind of leakage protection. In the same study,
only 14.2% of previously potent men reported the ability to achieve and maintain a
postoperative erection that is sufficient for sexual intercourse. Urologic surgeons are
well versed in the risks and benefits of the surgeries they perform, and they expect to
be asked questions related to these issues.

Normal results
The expected surgery result is a topic that the urologic surgeon and patient should
address prior to surgery. It is important that the patient understands the issues of
recovery, rehabilitation, training or retraining, and the limitations surgery may offer for
basic daily functions and enjoyment. Results of urologic surgery are individual, and
depend upon the health of the patient and his or her motivation to deal with
postoperative recovery issues and changes to organ function brought about by the

Many urological diseases can be dealt with through diet, weight loss, and lifestyle
changes. These modifications are especially significant in preventing and treating
conditions of the urinary tract. Obesity and nutrition play a significant role in urologic
diseases, and impact many urologic cancers, inflammatory and ulcerative conditions,
incontinence, and sexual dysfunction.

Medical interventions are another form of treatment, particularly for infectious and
inflammatory urologic conditions. They are particularly useful along with special
adjunctive surgical procedures for the treatment of incontinence and painful bladder
and kidney conditions. While many cancers must be treated surgically, prostate
cancer is often treated with a "wait and see" approach due to its slow rate of growth.
There is an increasing trend for men with slow-growing prostate cancers to have
regular check-ups instead of immediate treatment.

See also Open prostatectomy ; Transurethral resection of the

prostate ; Ureterostomy .

Walsh, P. Campbell's Urology. 8th ed. Elsevier Science, 2002.

Hedican, S.P. "Laparoscopy in Urology." Surgical Clinics of North America 80, no.5
(October 1, 2000): 1465-85.

Leng, W. and E.J. McGuire. "Reconstructive Urology Surgical Craft: Laparoscopic

Live Donor Nephrectomy." Urologic Clinics of North America 26, no.1 (February

Leung, A.K.H., "Critical Care and the Urologic Patient." Critical Care Clinics 19,
no.1 (January 2003).

American Society of Nephrology. 1725 Eye Street, NW Suite 510,Washington, DC
20006. (202) 659-0599. Fax: (202) 659-0709.

American Society of Transplantation. 236 Route 38 West, Suite 100, Moorestown, NJ

08057. (856) 608-1104. Fax: (856) 608-1103. .

National Institute of Diabetes and Digestive and Kidney Diseases. National Institutes
of Health, Information Office. 31 Center Drive, MSC 2560, Building 31, Room 9A-
04,Bethesda, MD 20892-2560. (800) 860-8747, (800) 891-5389, (800) 891-5390,
(301) 496-3583. Fax: (301) 496-7422. .

National Kidney Foundation. Director of Communications, 30 East 33rd Street, New

York, NY 10016. (800) 622-9010, (212) 889-2210. Fax: (212) 689-
9261. .

"Resource Guide: Prostate Cancer." American Foundation for Urologic

Nancy McKenzie, Ph.D.


Urologic surgery is performed by surgeons who specialize in the treatment of

urologic conditions. Surgery is performed in a general hospital, regional center, or
clinic, depending upon the type of procedure.


How many procedures does this physician and hospital perform compared to
other facilities?

What are the urination and sexual intercourse risks of this surgery?

Does this condition offer alternatives to surgery without risks of exacerbating

the condition?

How often are patients dissatisfied with their outcomes?

Read more:

A cystocele is the protrusion or prolapse of the bladder into the vagina. A number of
surgical interventions are available to treat cystoceles.

A prolapse occurs when an organ falls out of its normal anatomical position. The
pelvic organs normally have tissue (muscle, ligaments, etc.) holding them in place.
Certain factors, however, may cause those tissues to weaken, leading to prolapse of
the organs. A cystocele may be the result of a central or lateral (side) defect. A
central defect occurs when the bladder protrudes into the center of the anterior (front)
wall of the vagina due to a defect in the pubocervical fascia (fibrous tissue that
separates the bladder and vagina). The pubocervical fascia is also attached on each
side to tough connective tissue called the arcus tendineus; if a defect occurs close to
this attachment, it is called a lateral or paravaginal defect. A central and lateral defect
may be present simultaneously. The location of the defect determines what surgical
procedure is performed.

Factors that are linked to cystocele development include age, repeated childbirth,
hormone deficiency, menopause, constipation, ongoing physical activity, heavy
lifting, and prior hysterectomy . Symptoms of bladder prolapse include stress
incontinence (inadvertent leakage of urine with physical activity), urinary frequency,
difficult urination, a vaginal bulge, vaginal pressure or pain, painful sexual
intercourse, and lower back pain. Urinary incontinence is the most common symptom
of a cystocele.

Surgery is generally not performed unless the symptoms of the prolapse have begun
to interfere with daily life. A staging system is used to grade the severity of a
cystocele. A stage I, II, or III prolapse descends to progressively lower areas of the
vagina. A stage IV prolapse descends to or protrudes through the vaginal opening.
Surgery is generally reserved for stage III and IV cystoceles.

Approximately 22.7 out of every 10,000 women will undergo pelvic prolapse surgery.
The rate is highest among women between 60 and 69 years of age (42 per 10,000);
the mean age of patients is 54.6. White women undergo pelvic prolapse surgery at a
rate of 19.6 per 10,000 and a mean age of 54.3, while 6.4 per 10,000 African
American women have surgery at a mean age of 49.3.

A 2002 study indicated cystocele repair accounts for 8% of all prolapse repair
surgeries; in 1997, approximately 18,500 cystocele repairs were performed.
Cystocele repair was combined with rectal prolapse repair in 10% of prolapse
surgeries, with hysterectomy (surgical removal of the uterus) in 6%, and with both
procedures in 16%.

The goals of cystocele repair are to relieve a patient's symptoms, to improve or
maintain urinary and sexual function, to return pelvic structures to their original
position, and to prevent the formation of new defects. The anatomical structures
involved in a cystocele may be approached vaginally, abdominally, or

Vaginal repair
Anterior colporrhaphy is the most common procedure to repair a central defect. The
patient is first given general or regional anesthesia. A speculum is inserted into the
vagina to hold it open during the procedure. An incision is made into the vaginal skin
and the defect in the underlying fascia is identified. The vaginal skin is separated
from the fascia and the defect is folded over
In this cystocele repair by anterior colporrhaphy, a speculum is used to hold open the vagina, and
the cystocele is visualized (A). The wall of the vagina is cut open to reveal an opening in the
supporting structures, or fascia (B). The defect is closed (C), and the vaginal skin is repaired (D). (
Illustration by GGS Inc.

and sutured (stitched). Any excess vaginal skin is removed and the incision is closed
with stitches.
Lateral defects may be repaired vaginally or abdominally. During a vaginal
paravaginal repair, the approach and initial incision are similar to anterior
colporrhaphy. The defect to the fascia is located and reattached to the arcus
tendineus using sutures. The incision may then be stitched closed.

Abdominal and laparoscopic repair

A cystocele caused by a lateral defect may be treated through an abdominal incision
made transversely (from side to side) just above the pubic hairline. The space
between the pubic bone and bladder is identified and opened and the pubocervical
fascia reattached to the arcus tendineus using methods similar to the vaginal
paravaginal repair. In some cases, a retropubic colposuspension is performed during
the same surgery. Also called a Burch procedure, colposuspension treats urinary
incontinence by suspending the bladder neck to nearby ligaments with sutures.
Other surgical treatments for incontinence may be combined with paravaginal repair.

A lateral defect may also be repaired by laparoscopy , a surgical procedure in which

a laparoscope (a thin, lighted tube) and various instruments are inserted into the
abdomen through small incisions. A patient's recovery time following laparoscopic
surgery is shorter and less painful than following a traditional laparotomy (a larger
surgical incision into the abdominal cavity).

Physical examination is most often used to diagnose a cystocele. A speculum is
inserted into the vagina and the patient is asked to strain or sit in an upright position;
this increase in intra-abdominal pressure maximizes the degree of prolapse and aids
in diagnosis. The physician then inspects the walls of the vagina for prolapse or

In some cases, a physical examination cannot sufficiently diagnose pelvic prolapse.

For example, cystography may be used to determine the extent of a cystocele; the
bladder is filled by urinary catheter with contrast medium and then x rayed.
Ultrasound ormagnetic resonance imaging may also be used to visualize the pelvic

Women who have gone through menopause may be given six weeks of estrogen
therapy prior to surgery; this is thought to improve circulation to the vaginal walls and
thus improve recovery time. Antibiotics may be administered to decrease the risk of
postsurgical infection. An intravenous (IV) line is placed and a Foley catheter is
inserted into the bladder directly preceding surgery.

A Foley catheter may remain for one to two days after surgery. The patient is given a
liquid diet until normal bowel function returns. The patient also is instructed to avoid
activities for several weeks that cause strain on the surgical site; these include lifting,
coughing, long periods of standing, sneezing, straining with bowel movements, and
sexual intercourse.
Risks of cystocele repair include potential complications associated with anesthesia,
infection, bleeding, injury to other pelvic structures, dyspareunia (painful intercourse),
recurrent prolapse, and failure to correct the defect.

Normal results
A woman usually is able to resume normal activities, including sexual intercourse, in
about four weeks after the procedure. After successful cystocele repair, symptoms
recede, although a separate procedure may be needed to treat stress incontinence.

Morbidity and mortality rates

The risk of cystocele recurrence following surgical repair depends on the procedure
used to treat it. Anterior colporrhaphy is associated with a 020% rate of recurrence;
this rate is higher when colporrhaphy is combined with other surgical procedures.
Abdominal paravaginal repair results in a 5% chance of recurrence, while vaginal
paravaginal repair has the highest recurrence rate (722%).

Surgery is generally reserved for more severe cystoceles. Milder cases may be
treated by a number of medical interventions. The physician may recommend that
the patient do Kegel exercises, a series of contractions and relaxations of the
muscles in the perineal area. These exercises are thought to strengthen the pelvic
floor and may help prevent urinary incontinence.

A pessary, a device that is inserted into the vagina to help support the pelvic organs,
may be recommeded. Pessaries come in different shapes and sizes and must be
fitted to the patient by a physician. Hormone replacement therapy may also be
prescribed if the woman has gone through menopause; hormones may improve the
quality of the supporting tissues in the pelvis.

Ryan, Kenneth J., et al. Kistner's Gynecology and Women's Health. 7th ed. St. Louis,
MO: Mosby, Inc., 1999.

Walsh, Patrick C., et al. Campbell's Urology. 8th ed. Philadelphia: Elsevier Science,

Brown, Jeanette S., L. Elaine Waetjen, Leslee L. Subak, David H. Thom, Stephen
Van Den Eeden, and Eric Vittinghoff. "Pelvic Organ Prolapse Surgery in the United
States, 1997." American Journal of Obstetrics and Gynecology 186 (April 2002):

Cespedes, R. Duane, Cindy A. Cross, and Edward J. McGuire. "Pelvic Prolapse:

Diagnosing and Treating Cystoceles, Rectoceles, and Enteroceles." Medscape
Women's Health eJournal 3 (1998).

Viera, Anthony, and Margaret Larkins-Pettigrew. "Practice Use of the

Pessary." American Family Physician 61 (May 1, 2000): 27192726.

American Board of Obstetrics and Gynecology. 2915 Vine Street, Dallas, TX 75204.
(214) 871-1619. .

American Urological Association. 1120 North Charles Street, Baltimore, MD 21201.

(410) 727-1100. .

"Cystocele (Fallen Bladder)." National Kidney and Urologic Diseases Information
Clearinghouse. March 2002 [cited April 11,
2003]. .

Miklos, John. "Vaginal Prolapse Relaxation." . 2002 [cited April 11,
vagprolapse .
Stephanie Dionne Sherk



Cystocele repair is usually performed in a hospital operating room by a

gynecologist, urologist, or urogynecologist. A gynecologist is a medical doctor who
specializes in the areas of women's general and reproductive health, pregnancy, and
labor and childbirth. A urologist is a medical doctor who specializes in the diagnosis
and treatment of diseases of the urinary tract and genital organs. A urogynecologist
studies aspects of both fields.


What defect is causing the cystocele?

What surgical procedure is recommended for treatment?

Will other procedures be performed to treat urinary incontinence (e.g. Burch


What nonsurgical alternatives are available?

How soon after surgery may normal activities be resumed?

Read more:

Colporrhaphy is the surgical repair of a defect in the vaginal wall, including a
cystocele (when the bladder protrudes into the vagina) and a rectocele (when the
rectum protrudes into the vagina).

In this anterior colporrhaphy, a speculum is used to hold open the vagina, and the cystocele is
visualized (A). The wall of the vagina is cut open to reveal an opening in the supporting structures,
or fascia (B). The defect is closed (C), and the vaginal skin is repaired (D). (
Illustration by GGS Inc.

A prolapse occurs when an organ falls or sinks out of its normal anatomical place.
The pelvic organs normally have tissue (muscle, ligaments, etc.) holding them in
place. Certain factors, however, may cause those tissues to weaken, leading to
prolapse of the organs. A cystocele is defined as the protrusion or prolapse of the
bladder into the vagina; a urethrocele is the prolapse of the urethra into the vagina.
These are caused by a defect in the pubocervical fascia (fibrous tissue that
separates the bladder and vagina). A rectocele occurs when the rectum prolapses
into the vagina, caused by a defect in the rectovaginal fascia (fibrous tissue that
separates the rectum and vagina). When a part of the small intestine prolapses into
the vagina, it is called an enterocele. Uterine prolapse occurs when the uterus
protrudes downward into the vagina.

Factors that are linked to pelvic organ prolapse include age, repeated childbirth,
hormone deficiency, ongoing physical activity, and prior hysterectomy . Symptoms
of pelvic organ prolapse include stress incontinence (inadvertent leakage of urine
with physical activity), a vaginal bulge, painful sexual intercourse, back pain, and
difficult urination or bowel movements.

Approximately 50% of women report occasional urinary incontinence, with 10%
reporting regular incontinence. This percentage increases with age; daily
incontinence is experienced by 20% of women over the age of 75. According to a
recent study, approximately 16% of women ages 45 to 55 experience mild pelvic
organ prolapse, while only 3% experience prolapse severe enough to warrant
surgical repair.

Colporrhaphy may be performed on the anterior (front) and/or posterior (back) walls
of the vagina. An anterior colporrhaphy treats a cystocele or urethrocele, while a
posterior colporrhaphy treats a rectocele. Surgery is generally not performed unless
the symptoms of the prolapse have begun to interfere with daily life.

The patient is first given general, regional, or local anesthesia. A speculum is

inserted into the vagina to hold it open during the procedure. An incision is made into
the vaginal skin and the defect in the underlying fascia is identified. The vaginal skin
is separated from the fascia and the defect is folded over and sutured (stitched). Any
excess vaginal skin is removed and the incision is closed with stitches.

Physical examination is most often used to diagnose prolapse of the pelvic organs.
A speculum is inserted into the vagina, and the patient is asked to strain or sit in an
upright position. The physician then inspects the anterior, posterior, upper (apex),
and side (lateral) walls of the vagina for prolapse or bulging. In some cases, a
physical examination cannot sufficiently diagnose pelvic prolapse. For example,
cystogram may be used to determine the extent of a cystocele; the bladder is filled by
urinary catheter with contrast medium and then x-rayed.

The patient will be asked to refrain from eating or drinking after midnight on the day
of the procedure. The physician may request that an enema be administered the
night before the procedure if posterior colporrhaphy will be performed.

A Foley catheter may remain for one to two days after surgery. The patient will be
given a liquid diet until normal bowel function returns. The patient will be instructed to
avoid activities for several weeks that will cause strain on the surgical site, including
lifting, coughing, long periods of standing, sneezing, straining with bowel
movements, and sexual intercourse.

Risks of colporrhaphy include potential complications associated with anesthesia,
infection, bleeding, injury to other pelvic structures, dyspareunia (painful intercourse),
recurrent prolapse, and failure to correct the defect. A fistula is a rare complication of
colporrhaphy in which an opening develops between the vagina and bladder or the
vagina and rectum.

Normal results
A woman will usually be able to resume normal activities, including sexual
intercourse, about four weeks after the procedure. After successful colporrhaphy, the
symptoms associated with cystocele or rectocele will recede, although a separate
procedure may be needed to treat stress incontinence. Anterior colporrhaphy is
approximately 66% successful at restoring urinary continence.

Morbidity and mortality rates

There is approximately a 1% risk of serious complications associated with
colporrhaphy; the procedure is generally viewed to be safe with a very low rate of
overall complications.
Surgery is generally reserved for more severe cases of pelvic organ prolapse. Milder
cases may be treated by a number of medical interventions. The physician may
recommend that the patient do Kegel exercises, a series of contractions and
relaxations of the muscles in the perineal area. These exercises are thought to
strengthen the pelvic floor and may help prevent urinary incontinence. One study
showed an decrease of 62% in the amount of urine leakage among women ages 35
to 75 who performed Kegel exercises regularly for 16 weeks.

A pessary, a device that is inserted into the vagina to help support the pelvic organs,
may be recommended. Pessaries come in different shapes and sizes and must be
fitted to the patient by a physician. Hormone replacement therapy may also be
prescribed if the woman has gone through menopause; hormones may improve the
quality of the supporting tissues in the pelvis.


Cespedes, R. Duane, Cindy A. Cross, and Edward J. McGuire. "Pelvic Prolapse:
Diagnosing and Treating Cystoceles, Rectoceles, and Enteroceles." Medscape
Women's Health eJournal 3, no. 4 (1998).

Viera, Anthony, and Margaret Larkins-Pettigrew. "Practice Use of the

Pessary." American Family Physician 61 (May 1, 2000): 271926.

American Academy of Family Physicians. 8880 Ward Parkway, Kansas City, MO
64114. (816) 333-9700. .

American Board of Obstetrics and Gynecology. 2915 Vine Street, Dallas, TX 75204.
(214) 871-1619. .

American Urological Association. 1120 North Charles Street, Baltimore, MD 21201.

(410) 727-1100. .
"Cystocele (Fallen Bladder)." National Kidney and Urologic Diseases Information
Clearinghouse, March 2002 [cited March 20,
2003]. .

Jelovsek, Frederick R. "Cystocoele, Rectocoele, and Pelvic Support

Surgery." Society of Gynecologic Surgeons, 2001 [cited March 20,
2003]. pro002.html .

Miklos, John R., and Robert D. Moore. "Prolapse Treatment." Atlanta Center for
Laparoscopic Urogynecology, 2002 [cited March 20,
2003]. .

Stendardo, Stef. "Urinary Incontinence: Assessment and Management in Family

Practice." American Academy of Family Physicians, 2002 [cited March 20,
2003]. .

"Surgical Treatment of Genuine Stress Incontinence." Royal College of Obstetricians

and Gynaecologists, August 2002 [cited March 20,
2003]. .

Stephanie Dionne Sherk



Colporrhaphy is usually performed in a hospital operating room by a gynecologist

or urologist. A gynecologist is a medical doctor who specializes in the areas of
women's general and reproductive health, pregnancy, and labor and childbirth. A
urologist is a medical doctor who specializes in the diagnosis and treatment of
diseases of the urinary tract and genital organs.


Why is colphorrhaphy recommended in my case?

What non-surgical options are available to treat pelvic organ prolapse?

How long after surgery may I resume normal activity?

Read more:

Kedudukan ginjal terletak dibagian belakang dari kavum abdominalis di belakang peritonium pada
kedua sisi vertebra lumbalis III, dan melekat langsung pada dinding abdomen.

Bentuknya seperti biji buah kacang merah (kara/ercis), jumlahnaya ada 2 buah kiri dan kanan, ginjal
kiri lebih besar dari pada ginjal kanan.

Pada orang dewasa berat ginjal 200 gram. Dan pada umumnya ginjal laki laki lebih panjang dari
pada ginjal wanita.

Satuan struktural dan fungsional ginjal yang terkecil di sebut nefron. Tiap tiap nefron terdiri atas
komponen vaskuler dan tubuler. Komponen vaskuler terdiri atas pembuluh pembuluh darah yaitu
glomerolus dan kapiler peritubuler yang mengitari tubuli. Dalam komponen tubuler terdapat kapsul
Bowman, serta tubulus tubulus, yaitu tubulus kontortus proksimal, tubulus kontortus distal, tubulus
pengumpul dan lengkung Henle yang terdapat pada medula.

Kapsula Bowman terdiri atas lapisan parietal (luar) berbentuk gepeng dan lapis viseral (langsung
membungkus kapiler golmerlus) yang bentuknya besar dengan banyak juluran mirip jari disebut
podosit (sel berkaki) atau pedikel yang memeluk kapiler secara teratur sehingga celah celah antara
pedikel itu sangat teratur.

Kapsula bowman bersama glomerolus disebut korpuskel renal, bagian tubulus yang keluar dari
korpuskel renal disabut dengan tubulus kontortus proksimal karena jalannya yang berbelok belok,
kemudian menjadi saluran yang lurus yang semula tebal kemudian menjadi tipis disebut ansa Henle
atau loop of Henle, karena membuat lengkungan tajam berbalik kembali ke korpuskel renal asal,
kemudian berlanjut sebagai tubulus kontortus distal.

a. Bagian Bagian Ginjal

Bila sebuh ginjal kita iris memanjang, maka aka tampak bahwa ginjal terdiri dari tiga bagian, yaitu
bagian kulit (korteks), sumsum ginjal (medula), dan bagian rongga ginjal (pelvis renalis).

1. Kulit Ginjal (Korteks)

Pada kulit ginjal terdapat bagian yang bertugas melaksanakan penyaringan darah yang disebut
nefron. Pada tempat penyarinagn darah ini banyak mengandung kapiler kapiler darah yang
tersusun bergumpal gumpal disebut glomerolus. Tiap glomerolus dikelilingi oleh simpai bownman,
dan gabungan antara glomerolus dengan simpai bownman disebut badan malphigi

Penyaringan darah terjadi pada badan malphigi, yaitu diantara glomerolus dan simpai bownman. Zat
zat yang terlarut dalam darah akan masuk kedalam simpai bownman. Dari sini maka zat zat
tersebut akan menuju ke pembuluh yang merupakan lanjutan dari simpai bownman yang terdapat di
dalam sumsum ginjal.

2. Sumsum Ginjal (Medula)

Sumsum ginjal terdiri beberapa badan berbentuk kerucut yang disebut piramid renal. Dengan
dasarnya menghadap korteks dan puncaknya disebut apeks atau papila renis, mengarah ke bagian
dalam ginjal. Satu piramid dengan jaringan korteks di dalamnya disebut lobus ginjal. Piramid antara 8
hingga 18 buah tampak bergaris garis karena terdiri atas berkas saluran paralel (tubuli dan duktus
koligentes). Diantara pyramid terdapat jaringan korteks yang disebut dengan kolumna renal. Pada
bagian ini berkumpul ribuan pembuluh halus yang merupakan lanjutan dari simpai bownman. Di
dalam pembuluh halus ini terangkut urine yang merupakan hasil penyaringan darah dalam badan
malphigi, setelah mengalami berbagai proses.
3. Rongga Ginjal (Pelvis Renalis)

Pelvis Renalis adalah ujung ureter yang berpangkal di ginjal, berbentuk corong lebar. Sabelum
berbatasan dengan jaringan ginjal, pelvis renalis bercabang dua atau tiga disebut kaliks mayor, yang
masing masing bercabang membentuk beberapa kaliks minor yang langsung menutupi papila renis
dari piramid. Kliks minor ini menampung urine yang terus kleuar dari papila. Dari Kaliks minor, urine
masuk ke kaliks mayor, ke pelvis renis ke ureter, hingga di tampung dalam kandung kemih (vesikula

b. Fungsi Ginjal:

1. Mengekskresikan zat zat sisa metabolisme yang mengandung

nitrogennitrogen, misalnya amonia.
2. Mengekskresikan zat zat yang jumlahnya berlebihan (misalnya gula dan
vitamin) dan berbahaya (misalnya obat obatan, bakteri dan zat warna).
3. Mengatur keseimbangan air dan garam dengan cara osmoregulasi.
4. Mengatur tekanan darah dalam arteri dengan mengeluarkan kelebihan asam
atau basa.

Terdiri dari 2 saluran pipa masing masing bersambung dari ginjal ke kandung kemih (vesika
urinaria) panjangnya 25 30 cm dengan penampang 0,5 cm. Ureter sebagian terletak dalam
rongga abdomen dan sebagian terletak dalam rongga pelvis.

Lapisan dinding ureter terdiri dari :

Dinding luar jaringan ikat (jaringan fibrosa)

Lapisan tengah otot polos
Lapisan sebelah dalam lapisan mukosa

Lapisan dinding ureter menimbulkan gerakan gerakan peristaltik tiap 5 menit sekali yang akan
mendorong air kemih masuk ke dalam kandung kemih (vesika urinaria).

Gerakan peristaltik mendorong urin melalui ureter yang dieskresikan oleh ginjal dan disemprotkan
dalam bentuk pancaran, melalui osteum uretralis masuk ke dalam kandung kemih.

Ureter berjalan hampir vertikal ke bawah sepanjang fasia muskulus psoas dan dilapisi oleh
pedtodinium. Penyempitan ureter terjadi pada tempat ureter terjadi pada tempat ureter meninggalkan
pelvis renalis, pembuluh darah, saraf dan pembuluh sekitarnya mempunyai saraf sensorik.

3. VESIKULA URINARIA ( Kantung Kemih )

Kandung kemih dapat mengembang dan mengempis seperti balon karet, terletak di belakang simfisis
pubis di dalam ronga panggul.
Bentuk kandung kemih seperti kerucut yang dikelilingi oleh otot yang kuat, berhubungan ligamentum
vesika umbikalis medius.

Bagian vesika urinaria terdiri dari :

1. Fundus, yaitu bagian yang mengahadap kearah belakang dan bawah, bagian ini
terpisah dari rektum oleh spatium rectosivikale yang terisi oleh jaringan ikat duktus
deferent, vesika seminalis dan prostate.
2. Korpus, yaitu bagian antara verteks dan fundus.
3. Verteks, bagian yang maju kearah muka dan berhubungan dengan ligamentum
vesika umbilikalis.
4. Dinding kandung kemih terdiri dari beberapa lapisan yaitu, peritonium (lapisan
sebelah luar), tunika muskularis, tunika submukosa, dan lapisan mukosa (lapisan
bagian dalam).

Proses Miksi (Rangsangan Berkemih).

Distensi kandung kemih, oleh air kemih akan merangsang stres reseptor yang terdapat pada dinding
kandung kemih dengan jumlah 250 cc sudah cukup untuk merangsang berkemih (proses miksi).
Akibatnya akan terjadi reflek kontraksi dinding kandung kemih, dan pada saat yang sama terjadi
relaksasi spinser internus, diikuti oleh relaksasi spinter eksternus, dan akhirnya terjadi pengosongan
kandung kemih.

Rangsangan yang menyebabkan kontraksi kandung kemih dan relaksasi spinter interus dihantarkan
melalui serabut serabut para simpatis. Kontraksi sfinger eksternus secara volunter bertujuan untuk
mencegah atau menghentikan miksi. kontrol volunter ini hanya dapat terjadi bila saraf saraf yang
menangani kandung kemih uretra medula spinalis dan otak masih utuh.

Bila terjadi kerusakan pada saraf saraf tersebut maka akan terjadi inkontinensia urin (kencing keluar
terus menerus tanpa disadari) dan retensi urine (kencing tertahan).

Persarafan dan peredaran darah vesika urinaria, diatur oleh torako lumbar dan kranial dari sistem
persarafan otonom. Torako lumbar berfungsi untuk relaksasi lapisan otot dan kontraksi spinter interna.

Peritonium melapis kandung kemih sampai kira kira perbatasan ureter masuk kandung kemih.
Peritoneum dapat digerakkan membentuk lapisan dan menjadi lurus apabila kandung kemih terisi
penuh. Pembuluh darah Arteri vesikalis superior berpangkal dari umbilikalis bagian distal, vena
membentuk anyaman dibawah kandung kemih. Pembuluh limfe berjalan menuju duktus limfatilis
sepanjang arteri umbilikalis.

Uretra merupakan saluran sempit yang berpangkal pada kandung kemih yang berfungsi menyalurkan
air kemih keluar.

Pada laki- laki uretra bewrjalan berkelok kelok melalui tengah tengah prostat kemudian
menembus lapisan fibrosa yang menembus tulang pubis kebagia penis panjangnya 20 cm.

Uretra pada laki laki terdiri dari :

1. Uretra Prostaria
2. Uretra membranosa
3. Uretra kavernosa

Lapisan uretra laki laki terdiri dari lapisan mukosa (lapisan paling dalam), dan lapisan submukosa.
Uretra pada wanita terletak dibelakang simfisis pubisberjalan miring sedikit kearah atas, panjangnya
3 4 cm. Lapisan uretra pada wanita terdiri dari Tunika muskularis (sebelah luar), lapisan spongeosa
merupakan pleksus dari vena vena, dan lapisan mukosa (lapisan sebelah dalam).Muara uretra
pada wanita terletak di sebelah atas vagina (antara klitoris dan vagina) dan uretra di sini hanya
sebagai saluran ekskresi.
C. Urine (Air Kemih)
1. Sifat sifat air kemih

Jumlah eksresi dalam 24 jam 1.500 cc tergantung dari masuknya (intake)

cairan serta faktor lainnya.
Warna bening muda dan bila dibiarkan akan menjadi keruh.
Warna kuning terantung dari kepekatan, diet obat obatan dan sebagainya.
Bau khas air kemih bila dibiarkan terlalu lama maka akan berbau amoniak.
Berat jenis 1.015 1.020.
Reaksi asam bila terlalu lama akan menjadi alkalis, tergantung pada diet (sayur
menyebabkan reaksi alkalis dan protein memberi reaksi asam).

2. Komposisi air kemih

Air kemih terdiri dari kira kira 95 % air

Zat zat sisa nitrogen dari hasil metabolisme protein asam urea, amoniak dan
Elektrolit, natrium, kalsium, NH3, bikarbonat, fosfat dan sulfat
Pigmen (bilirubin, urobilin)

3. Mekanisme Pembentukan Urine

Dari sekitar 1200ml darah yang melalui glomerolus setiap menit terbentuk 120 125ml filtrat (cairan
yang telah melewati celah filtrasi). Setiap harinyadapat terbentuk 150 180L filtart. Namun dari
jumlah ini hanya sekitar 1% (1,5 L) yang akhirnya keluar sebagai kemih, dan sebagian diserap

4. Tahap tahap Pembentukan Urine

a. Proses filtrasi

Terjadi di glomerolus, proses ini terjadi karena permukaan aferent lebih besar dari permukaan aferent
maka terjadi penyerapan darah, sedangkan sebagian yang tersaring adalah bagian cairan darah
kecuali protein, cairan yang tersaring ditampung oleh simpai bowman yang terdiri dari glukosa, air,
sodium, klorida, sulfat, bikarbonat dll, diteruskan ke seluruh ginjal.

b. Proses reabsorpsi

Terjadi penyerapan kembali sebagian besar dari glukosa, sodium, klorida, fosfat dan beberapa ion
karbonat. Prosesnya terjadi secara pasif yang dikenal dengan obligator reabsorpsi terjadi pada
tubulus atas. Sedangkan pada tubulus ginjal bagian bawah terjadi kembali penyerapan dan sodium
dan ion karbonat, bila diperlukan akan diserap kembali kedalam tubulus bagian bawah,
penyerapannya terjadi secara aktif dikienal dengan reabsorpsi fakultatif dan sisanya dialirkan pada
pupila renalis.

c. Augmentasi (Pengumpulan)

Proses ini terjadi dari sebagian tubulus kontortus distal sampai tubulus pengumpul. Pada tubulus
pengumpul masih terjadi penyerapan ion Na+, Cl-, dan urea sehingga terbentuklah urine
Dari tubulus pengumpul, urine yang dibawa ke pelvis renalis lalu di bawa ke ureter. Dari ureter, urine
dialirkan menuju vesika urinaria (kandung kemih) yang merupakan tempat penyimpanan urine
sementara. Ketika kandung kemih sudah penuh, urine dikeluarkan dari tubuh melalui uretra.

4. Mikturisi

Peristiwa penggabungan urine yang mengalir melalui ureter ke dalam kandung kemih., keinginan
untuk buang air kecil disebabkan penambahan tekanan di dalam kandung kemih dimana
saebelumnmya telah ada 170 23 ml urine.

Mikturisi merupakan gerak reflek yang dapat dikendalikan dan dapat ditahan oleh pusat pusat
persyarafan yang lebih tinggi dari manusia, gerakannya oleh kontraksi otot abdominal yang menekan
kandung kemih membantu mengosongkannya.

5. Ciri ciri Urine Normal

Rata rata dalam satu hari 1 2 liter, tapi berbeda beda sesuai dengan jumlah cairan yang masuk.
Warnanya bening oranye pucat tanpa endapan, baunya tajam, reaksinya sedikit asam terhadap
lakmus dengan pH rata rata 6.
Fisiologi miksi dan dasar fisiologi kelainan pada proses berkemih ini masih
banyak menimbulkan ketidakpastian. Berkemih pada dasarnya
merupakan refleks spinal yang akan difasilitasi dan dihambat oleh pusat-
pusat susunan saraf yang lebih tinggi, seperti defekasi, kasilitasi dan
inhibisi bersifat volunter.
Urine yang memasuki vesika tidak begitu meningkatkan tekanan
intravesika sampai telah terisi penuh. Selain itu, sepert juga jenis otot
polos lainnya otot vesika memiliki sifat plastis, bila diregang ketegangan
yang mula-mula timbul tidak akan dipertahankan. Hubungan anatara
takanan intravesilukar dan volume vesikula dapat dipelajari dengan
catatan tekanan saat vesika diisi oleh air atau udara dengan penambahan
50 ml setiap kali (sistometri).
Selama proses berkemih, otot-otot perineum dan spingter uretra eksterna
relaksasi. Otot detrussor berkontraksi dan urine akan mengalir melalui
uretra. Susunan otot polos pada kedua uretra ternyata tidak memegang
peran pada proses berkemih dan fungsinya yang utama mungkin untuk
mencegah refluks semen kedalam vesika selama ejakulasi.
Mekanisme awal yang menimbulkan proses miksi volunter belum
diketahui dengan pasti. Salah satu peristiwa awal ialah relaksasi otot-otot
dasar panggul dan hal tu mungkin menimbulkan tarikan ke bawah yang
cukup besar pada otot detrusor untuk merangsang kontraksi. Kontraksi
otot-otot perinium dan spingter eksterna dapat dilakukan secara volunter,
sehingga mencegah urine untuk mengalir melewati uretra atau
menghentikan aliran urine saat sedang berkemih. Melalui proses belajar
seorang dewasa dapat mempertahankan kontraksi spingter eksterna
sehingga mampu menunda berkemih sampai saat yang tepat. Setelah
berkemih, urine di uretra wanita akan dikeluarkan oleh pengaruh gravitasi
urine sisa di uretra pria dikeluarkan oleh beberapa kontraksi m.

Selam kandung kemih terisi, banyak yang menyertai kontraksi berkemih

mulai tampak seperti yang diperlihatkan oleh gelombang tajan dengan
garis putus-putus. Keadaan ini disebabkan oleh reflek peregangan yang
dimulai oleh resertor regang sensorik pada dinding kandung kemih.
Khususnya oleh reseptor pada uretra posterior, ketika daerah ini terisi
urine pada tekanan kandung kemih yang lebih tinggi. Sinyal sensori dari
reseptor regangan kandung kemih dihantarkan ke segment sakral medula
spinalis melalui nervus pelvikus ddan kemudian secara reflek kembali
kandung kemih melalui sistem saraf parasimpatis melalui saraf yang
Ketika kadung kemih hanya terisi sebagian, kontraksi berkemih ini
biasanya secara spontan berelaksasi setelah beberapa detik, otot
detruson berhenti berkontraksi dan tekanan turun kembali ke garis basal
karena kandung kemih menjadi bertambah sering dan menyebabkan
kontraksi otot detrusos lebih kuat.
Sekali refleks berkemih mulai timbul, reflek ini akan menghilang sendiri.
Artinya kontraksi awal kandung kemih selanjutnya akan mengaktifkan
reseptor regangan untuk menyebabkan peningkatan selanjutnya pada
impuls sensorik ke kandung kemih dan uretra posterior, yang
menimbulkan peningkatan reflek kontraksi kandung kemih lebih lanjut;
jadi, siklus ini berulang dan berulang lagi sampai kandung kemih
mencapai kontraksi yang kuat. Kemudian, setelah beberapa detik sampai
lebih dari semenit, reflek yang menghilang sendiri ini mulai melemah dan
siklus regeneratif dari refleks miksi itu berhenti, menyebabkan kandung
kemih berelaksasi.
Jadi, rekleks berkemih adalah suatu siklus tunggal lengkap dari (1)
peningkatan tekanan yang cepat dan progresif, (2) periode tekanan
dipertahankan, dan (3) kembalinya tekanan ke tonus basal kandung
Sekali refleks berkemih terjadi tetapi tidak berhasil mengosongkan
kandung kemih, elemen saraf dari reflek ini biasanya tetap dalam keadaan
terinhibisi selama beberapa menit sampai satu jam atau lebih sebelum
refleks berkemih lainnya terjadi. Karena kandung kemih menjadi semakin
terisi, refleks berkemih menjadi semakin sering dan semakin kuat.
Sekali refleks berkemih menjadi cukup kuat, hal ini juga menimbulkan
refleks lain, yang berjalan melalui nervus pudendalke sfingter
eksternus untuk menghambatnya. Jika inhibisi ini lebih kuat dalam otak
dari pada sinyal konstriktor volunter ke sfingter eksterna, berkemihpun
akan terjadi. Jika tidak, bekemih tidak akan terjadi sampai kandung kemuh
menjadi kuat.