أ.م. د. وضاح المرزوك
كلية الطب /جامعة بابل
9102
Urinary Incontinence.
Involuntary loss of urine in sufficient amount or frequency to constitute
a social and/or health problem. Urinary incontinence is a major health
issue that affects more than 200 million people worldwide. In fact, it is a
manifestation of an underlying disease; occasionally it is transient and
resolves spontaneously, but most often it is chronic and progressive.
It has been estimated only 32% of primary care physicians routinely ask
about incontinence, in addition 50-75% of patients never describe
symptoms to physicians.
It is important to know that about 80% of urinary incontinence can be
cured or improved.
Risk Factors.
Age
Parity
Obesity
Vaginal delivery
Episiotomy
Diabetes
Stroke
Estrogen depletion
Genitourinary surgery and radiation
Types:
Transient Incontinence
Transient urinary incontinence is a relatively common disorder it affect
about 30% community dweller and up to 50% of inpatients it is more
common in those who use anti – cholinergic, diuretics or those with
worsening mobility.
The risk factors for transient incontinence can be illustrated by the world
DIAPPERS:
D-Delirium
I-Infection
A-Atrophic Urethritis/vaginitis
P-Pharmaceuticals
P-Psychological (rare)
E-Excessive urine output
R-Restricted mobility
S-Stool impaction
CHRONIC URINARY INCONTINENCE
Types:
Stress incontinence
Urge incontinence
Neuropathic incontinence
Congenital incontinence
False (overflow) incontinence
Posttraumatic or iatrogenic incontinence
Fistulous incontinence
STRESS INCONTINENCE.
Stress incontinence is the involuntary loss of urine with any factor that is
suddenly increases intra-abdominal pressure, it is often seen in women
after middle age (with repeated pregnancies and vaginal deliveries),
urinary stress incontinence is usually a result of weakness of the pelvic
floor and poor support or hypermobility of the vesicourethral sphincteric
unit.
Some authors like to classify urinary incontinence in various stages.
Stages I and II depend on the degree of hypermobility and usually relate
to the amount of urinary leakage. Stage III, which most often is not
associated with hypermobility, is usually due to intrinsic sphincteric
damage most often iatrogenic.
Diagnosis
A detailed history is important, including the degree of leakage; its
relation to activity, position, and state of bladder fullness; the timing of its
onset; and the course of its progression. Knowledge of past surgical and
obstetric history, medications taken, dietary habits, and systemic diseases
(eg, diabetes) can be helpful in the diagnosis.
Physical examination is essential. The pelvic examination demonstrates
laxity of pelvic support, presence of any degree of prolapse, cystocele,
rectocele, and mobility of the anterior vaginal wall. A neurologic
examination should be done if neuropathy is suspected.
Investigation which include cystographic study for demonstration of the
anatomic abnormality is important, as is urodynamic study to confirm the
classic features of urinary incontinence and determine its cause.
Indirect evidence of the degree of sphincteric weakness can be obtained
by measurement of what is called the leak pressure (ie, by measuring the
intra-abdominal pressure through a rectal transducer during the Valsalva
maneuver and noting at what pressure the first leakage of urine occurs). A
low reading indicates a severe degree of sphincteric weakness.
Treatment
The principal treatment of urinary stress incontinence is proper
suspension and support of the vesicourethral segment in a normal
position.
There are numerous approaches to restoring the normal position and
providing adequate support some vaginal, others suprapubic. The
suprapubic approach:
Marshall-Marchetti-Krantz (MMK) retropubic suspension
Burch colposuspension
Sling procedures (rectus sheath, cadaveric fascia lata and various
synthetic materials. Most recently, tension-free vaginal tape (TVT) has
been gaining popularity)
local injection of bulking material, such as hyaluronic acid/detranomer,
polydimethylsiloxan (Macroplastique), and collagen, is used to increase
the bladder outlet resistance for patients in whom vesicourethral mobility
is not excessive and whose primary problem is intrinsic sphincteric
weakness.
URGE INCONTINENCE
UI is defined as involuntary loss of urine, accompanied or
immediately preceded by urgency. The basic feature of UI is detrusor
instability and the loss of urine while attempting to inhibit micturition.
Sphincteric instability is less common.
Neurogenic, myogenic, or urothelial bladder dysfunction can lead to UI
or the constellation of symptoms which define OAB. OAB, with or
without UI, is common in both men and women and can result from
neuropathic injuries (spinal cord injury), obstruction, inflammation
(interstitial cystitis), diabetes, benign prostatic hyperplasia (BPH), and so
on, or be iatrogenic. Bladder hypersensitivity may originate from the
urothelium or the detrusor muscle or altered neural activation at various
points of the micturition cycle (eg, persistent smooth muscle activation
during filling).
Diagnosis
Assessment of patients with symptoms of UI, or OAB, should include
detailed history, including an assessment of the impact of the disorder on
daily life, physical examination, urinalysis, and identification of
modifiable causes such as impaired mobility. A sudden urge with
uncontrolled loss of urine not associated with physical activity and leak
of urine prior to reaching the bathroom are common patient complaints.
Treatment
Behavioral techniques.
Lifestyle modification includes fluid management, as large volumes can
exacerbate urinary incontinence, and bladder training to correct voiding
patterns, improve the ability to suppress urge, and increase bladder
capacity. Maneuvers included pelvic muscle training, scheduled voiding,
and relaxation techniques. The International Consultation on Continence
recommends an initial voiding interval of 1 hour during waking hours,
with weekly increases of 15–30 minutes until a 2–3 hour interval is
achieved .
Medical treatment.
Anticholinergic agents, such as tolteridone, oxybutynin, and trospium, are
considered first-line therapy for UI, suppressing or reducing involuntary
bladder contractions, and also addressing the symptoms of idiopathic
detrusor overactivity (OAB).
Intravesical botulinum toxin A has shown significant initial promise for
UI, OAB, and neurogenic detrusor overactivity.
Resiniferatoxin (an intravesical vanilloid) and oral beta-adrenergic
agonists (nonspecific smooth muscle relaxants) are two other agents
currently under investigation for UI and OAB treatment.
MIXED URINARY INCONTINENCE.
Mixed urinary incontinence (MUI) refers to the occurrence of stress-
related incontinence with symptomatic urinary urgency and UI. About
one thirds of incontinent patients have both UI linked to idiopathic
overactivity and genuine SUI. Some experts now believe that MUI is now
the predominant symptom grouping, with rates >50% reported in large
population studies.
Diagnosis
The diagnostics steps for MUI are the same as for SUI In those
individuals with equal bother (UI and SUI), or difficulty defining their
symptoms, urodynamics may help define dysfunction and therapy.
Treatment
The presenting symptoms serve as a guide to initial therapeutic approach.
The most bothersome aspect, SUI versus UI, is usually addressed first. If
both types of incontinence are equally bothersome, treatment of the urge
component is preferred in most cases.
OVERFLOW INCONTINENCE
Overflow incontinence (OI) is defined as the involuntary loss of urine
associated with bladder over distension.
Two primary processes are involved: urinary retention caused by bladder
outlet obstruction or inadequate bladder contractions. Outflow obstruction
may be secondary to BPH, bladder neck contracture or urethral stricture,
or less commonly, prostate cancer in men, and due to cystocele, pelvic
organ prolapse, or previous incontinence surgery in females. Impaired
bladder emptying caused by decreased detrusor contractility may be the
result of medications, spinal or peripheral nerve injuries, or due to long-
standing over distension. Diabetic cystopathy can result in OI as both
sensory and contractile functions may be compromised.
Diagnosis.
Specific to OI, overflow bladder is detected by measuring post-void
residual urine volume with ultrasonography (preferred) or urethral
catheterization immediately after the patient urinates. Normally, <50 mL
of urine will remain in the bladder immediately following voiding and
residual volumes of more than 200 mL indicate overflow bladder.
Urodynamic testing and cystourethroscopy are used to determine the
underlying cause, or differentiate OI from other incontinence states.
Treatment.
Overflow incontinence due to obstructive cause treated by treating the
original obstruction ( BPH, cystocele, urethral stricture etc.)
If the cause of incontinence is non-obstructive the first step is to
decompress the bladder with an indwelling catheter or clean intermittent
catheterization (CIC) for 7–14 days, while addressing potential reversible
causes such as medications, infection, or constipation. An alpha-blocker
may be initiated during this time period. Should voiding trials fail
repeatedly in the patient with an acontractile detrusor, CIC is the
treatment of choice versus a permanent indwelling catheter.
NEUROPATHIC INCONTINENCE
Neuropathic incontinence can be divided into 2 broad classifications:
active and passive. Active neuropathic incontinence (neurogenic
detrusor overactivity) is found in patients who have a spastic lesion but in
whom the sphincteric mechanism, although not under voluntary control,
still exerts adequate closure pressure.
Passive neuropathic incontinence occurs when the sphincteric
mechanism is weakened or completely lacking. Even without abnormally
high intravesical pressures, any increase in intra-abdominal pressure
results in urinary leakage.
BLADDER STONES
Bladder calculi are either secondary which occur as a manifestation of an
underlying pathologic condition, including voiding dysfunction or a
foreign body. Voiding dysfunction may be due to a urethral stricture,
benign prostatic hyperplasia, bladder neck contracture, or flaccid or
spastic neurogenic bladder, all of which result in static urine. Foreign
bodies such as Foley catheters and forgotten double-J ureteral catheters
can serve as nidi for stones . Most bladder calculi are seen in men.
Primary bladder calculi usually occur in developing countries, they are
frequently found in prepubescent boys.
Stone analysis frequently reveals ammonium urate, uric acid, or calcium
oxalate stones. A solitary bladder stone is the rule, but there are numerous
stones in 25% of patients .
Patients present with irritative voiding symptoms, intermittent urinary
stream, urinary tract infections, hematuria, or pelvic pain. Physical
examination is unrevealing. A large percentage of bladder stones are
radiolucent (uric acid).
Ultrasound of the bladder identifies the stone with its characteristic
shadowing. The stone moves with changing body position. They
frequently are non-obstructive.
The mode of stone removal for bladder stones should be directed by the
underlying cause. Simple mechanical crushing devices are still used
today. Mechanical lithotrites should be used with caution to prevent
bladder injury when the jaws are closed. Cystolitholapaxy allows most
stones to be broken and subsequently removed through a cystoscope.
Electrohydraulic, ultrasonic, laser, and pneumatic lithotrites are effective.
Cystolithotomy can be performed through a small abdominal incision
VESICAL FISTULAS
Vesical fistulas are common. The bladder may communicate with the
skin, intestinal tract, or female reproductive organs. The primary disease
is usually not urologic. The causes are as follows: (1) primary intestinal
disease—diverticulitis, 50–60%; cancer of the colon, 20–25%; and Crohn
disease, 10% . (2) primary gynecologic disease—pressure necrosis during
difficult labor; advanced cancer of the cervix; (3) treatment for
gynecologic disease following hysterectomy, low cesarean section, or
radiotherapy for tumor; and (4) trauma whether external or iatrogenic.
5.Malignant tumors of the small or large bowel, uterus, or cervix may
invade and perforate the bladder.
Clinical Findings
A. VESICOINTESTINAL FISTULA
Symptoms arising from a vesicointestinal fistula include vesical
irritability, the passage of feces and gas through the urethra, and usually a
change in bowel habits (eg, constipation, abdominal distention, diarrhea)
caused by the primary intestinal disease. Signs of bowel obstruction may
be elicited; abdominal tenderness may be found if the cause is
inflammatory. The urine is always infected.
Diagnosis
A barium enema, upper gastrointestinal series, or sigmoidoscopic
examination may demonstrate the communication. Following a barium
enema, centrifuged urine should be placed on an x-ray cassette and an
exposure made. The presence of radiopaque barium establishes the
diagnosis of vesicocolonic fistula. Cystograms may reveal gas in the
bladder or reflux of the opaque material into the bowel. Cystoscopic
examination, the most useful diagnostic procedure, shows a severe
localized inflammatory reaction from which bowel contents may exude.
B. VESICOVAGINAL FISTULA
The constant leakage of urine is most distressing to the patient. Pelvic
examination usually reveals the fistulous opening, which also can be
visualized with the cystoscope. It may be possible to pass a ureteral
catheter through the fistula into the vagina. Vaginography often
successfully shows ureterovaginal, vesicovaginal, and rectovaginal
fistulas. Biopsy of the edges of the fistula may show carcinoma.
C. VESICOUTERINE FISTULA.
The classical feature is cyclical hematuria ( hematuria occur at time of
menstruation).
Treatment
A. VESICOINTESTINAL FISTULA
If the lesion is in the rectosigmoid, treatment consists of proximal
colostomy. When the inflammatory reaction has subsided, the involved
bowel may be resected, with closure of the opening in the bladder. The
colostomy can be closed later. Some authors recommend that the entire
procedure be performed in one stage, thus avoiding the need for
preliminary colostomy.
B. VESICOVAGINAL FISTULA
Tiny fistulous openings may become sealed following the introduction of
an electrode into the fistula. As the electrode is withdrawn, the fistula is
coagulated with the electrosurgical unit to destroy the epithelium of the
tract. An indwelling catheter should be left in place for 2 weeks or more.
Occasionally, good results are noted in cases of small vesicovaginal
fistulas treated by inserting a metal screw through the vaginal end of the
fistula. It is moved up and down to act as a curet. The vaginal mucosa is
then closed and an indwelling catheter placed for 3 weeks. Larger fistulas
secondary to obstetric or surgical injuries respond readily to surgical
repair, which may be done either through the vagina or transvesically.
BLADDER DIVERTICULA
Most vesical diverticula are acquired and are secondary to either
obstruction distal to the vesical neck or the upper motor neuron type of
neurogenic bladder. Increased intravesical pressure causes vesical mucosa
to insinuate itself between hypertrophied muscle bundles, so that a
mucosal extravesical sac develops. Often this sac lies just superior to the
ureter and causes vesicoureteral reflux. The diverticulum is devoid of
muscle and therefore has no expulsive power; residual urine is the rule,
and infection is perpetuated. If the diverticulum has a narrow opening that
interferes with its emptying, transurethral resection of its neck will
improve drainage. Carcinoma occasionally develops on its wall.
Therefore authors stress the need for visualizing the interior of diverticula
during endoscopy. At the time of open prostatectomy, resection of a
diverticulum should be considered.