URINARY
INCONTINENCE
Prevalence
and Cost
Incontinence affects approximately13
million Americans. Reported prevalence
rates vary considerably; among the population between 15 and 64 years old, the prevalence
of UI in men ranges from 1-5%, in women from 10-30%. For the non-institutionalized elderly, prevalence estimates range
from 15-35% with women having at least twice the prevalence of men. The prevalence in nursing homes is greater
that 50%.
Cost estimates for caring for
incontinent adults are in the billions.
About one billion is spent annually on incontinence products (diapers,
etc.) alone.
Incontinence often ruins or distorts
patients’ lifestyles. Patients are
quite distressed by and will go to great lengths to avoid the associated
embarrassment.
Anatomy
and Physiology of the Bladder and Urethra
Basically the bladder is a
muscular bag (The detrusor) with a sphincter.
The bladder has a serosal layer, a muscle layer, and a mucosal layer of
transitional epithelium.
The
urethra extends from the bladder neck to the meatus, a distance of 4 cm in
women, and 20 cm in men. Two smooth
muscles run longitudinally along the urethra and form a functional internal
sphincter. The striated external sphincter
allows voluntary interruption of voiding.
In women the geometry of the urethrovesical junction and the proximal
urethra is important in maintaining continence. Normally, the pelvic floor muscles, especially the levator ani,
are in a constant state of contraction and support the bladder neck so that
there is a 90 Degree angle.
The neuroanatomy is complicated (see
Figure), but can be reduced to the following two clinically important details.
i)
The
detrusor muscle has Acetylcholine receptors; when these are stimulated the
detrusor contracts.
ii)
The
sphincter muscles have a alpha-1 adrenergic receptors; when stimulated, the
sphincters constrict.
In
more detail: Three sets of nerves
control the bladder. The
parasympathetic originate from the spinal cord at S2-4 and travel to the
bladder via the pelvis nerves. These
nerves synapse with cholinergic receptors in the bladder wall, bladder outlet
and urethra. They cause detrusor contraction
and inhibit sympathetic activity. The
sympathetics originate from T11-L2 and travel via the hypogastric nerves. They stimulate alpha-adrenergic receptors
located in the bladder outlet and the urethra (internal sphincter
contraction). They also stimulate
beta-receptors in the detrusor, which cause bladder relaxation. Somatic nerve fibers arising from S2-4
travel via the pudenal nerve and supply the external sphincter (voluntary
control) and the pelvic floor.
In the brain, there are two important
loci. The pontine micturion center
(PMC) coordinates the relaxation of the sphincters with the contraction of the
bladder. The frontal lobe provides
tonic inhibition of the PMC.
NORMAN MICTURITION
Initially, urine accumulates
in the bladder at low intravesicular pressures. As the volume of urine approaches 25-300 ml, the pressure begins
to rise sharply. Bladder afferents
travel through the pelvic nerves to the spinal cord bearing the message
“Bladder full.” This message ascends
via the spinal cord to the PMC and the frontal lobe, at which point the person
becomes aware of the need to void. The
frontal lobe inhibits the PMC until an appropriate place to urinate
The voluntary effort of voiding begins
with cessation of inhibition from the frontal lobe. The PMC coordinates increased parasympathetic activity and
inhibited sympathethic activity. This
results in bladder contraction and relaxation of the sphincters.
NORMAL CONTINENCE
There are several levels
which need to be intact to maintain normal continence.
Sometimes
if there is a problem at one level, the others can compensate but usually not.
The PMC must receive inhibition from
the frontal lobe. Strokes, dementia,
and delirium can affect this. Without
frontal lobe inhibition, the patient urinates the full bladder volume when the
pressure begins to distend it.
The spinal cord must be intact to
transmit all these signals.
Spontaneous bladder contractions must
be inhibited by the sympathetics.
Sympathetically medicated sphincter
contraction must be present.
The ureterovesical angle must be
preserved by the pelvic floor muscles.
TYPES OF
ESTABLISHED URINARY INCONTINENCE
The types discussed here are all
examples of established, chronic incontinence in ambulatory
patients. We will discuss causes of transient/new
incontinence and incontinence in demented/institutionalized patients
elsewhere.
Stress Incontinence
This is the second most common cause of incontinence in
women but rare in men (except when the internal sphincter is damaged by
surgery). Stress UI is defined as the involuntary loss of
urine occurring when the intravesical pressure exceeds urethral pressure in the
absence of detrusor contraction. This
usually occurs when intra-abdominal pressure abruptly increases, often with
position change, coughing, sneezing and laughing. This loss of thickness-together with the loss of the
urethrovesical 90 degree angle resulting from laxity of the pelvic floor
muscles (from aging, multiparity, surgery) – lead to stress UI. The potential targets of therapy are apparent-estrogen
deficiency, pelvic floor muscle tone, bladder position, and sphincter tone.
Urge Incontinence
This is the most common cause of incontinence. The essential problems here are uninhibited
bladder contractions of strength sufficient to overcome urethral
resistance. The pathogenesis is not
entirely worked out. But basically, as
the bladder ages, the innervation of the detrusor becomes less dense and
effective, particularly the sympathetically medicated inhibition
contractions. Spontaneous contractions
medicated by reflex are through the spinal cord start to occur at bladder
volumes of 250cc or so. Normally these
are inhibited by inputs from the PMC, but in aging bladder they may not be and
thus a full bladder contraction may occur when the patient doesn’t want it
to. This is called Detrusor
Instability. It’s sort of like a PVC of the bladder. Therapies are targeted at maintaining
voluntary control over the sphincter and inhibiting the bladder PVC’s.
Overflow Incontinence
Involuntary
loss of urine associated with over distention of the bladder. Usually results from prolonged bladder
outlet obstruction, most often from BPH.
To continue the cardiologic analogy, this is sort of like aortic
stenosis of the bladder. Eventually the
bladder (like the left ventricle) hypertrophie and dilates; the “ejection
fraction” drops, and the bladder fails.
At this point the bladder is chronically full and slowly and
continuously leaks through the stenosis.
Overflow incontinence can also result from detrusor hypotonia (analogous
to a primary cardiomyopathy) usually from diabetic neuropathy. Therapy is directed at relieving the
obstruction or increasing bladder contractility.
Incontinence Associated with
CNS Disease
Strokes,
dementia, and other CNS disease can result in loss of frontal lobe inhibition
of the PMC. Therapy is primarily
behavioral and directed at keeping the bladder empty through scheduled frequent
toileting.
TRANSIENT CAUSES
OF INCONTINENCE
Transient Incontinence occurs in up to
one third of the community dwelling elderly and up to half of acutely
hospitalized elderly patients. Whenever
a diagnosis of incontinence is made, a search for these reversible causes should
be undertaken. One mnemonic for remembering
the causes of transient incontinence is:
Delirium
Infection
Atrophic Vaginitis
Pharmaceuticals- diuretics,
alpha blockers, calcium channel blockers,
anticholinergics sedatives, alcohol
Excess urine output –from
diabetes or diuretics ( including coffee and EtOH)
Restricted Mobility- continence
is a functional behavior-e.g. an ankle fracture may make a patient with previously marginal continence
incontinent by slowing them down.
Stool Impaction- the rectal mass may stimulate bladder
contractions
DIAGNOSIS
Diagnosis is mostly by
history and physical. If further
testing is needed, urodynamic testing can be performed. Usually the incontinence can be classified
(as stress, urge, or mixed) on basis of H & P alone and appropriate treatment
initiated.
History
An
accurate voiding history is essentialindetermining the etiology of
incontinence. Ask about:
Volume of urine loss
Body position in which the urine loss
occurred
Aggravating conditions such as cough,
sneeze, exertion
Urgency, frequency, dysuria, nocturia,
hesitancy, straining, dribbling
Warning
Other medical history- menstrual,
parity, CHF, DM, CNS disease, meds
The
typical history for pure stress incontinence is loss of small amounts of urine precipitated
by cough, sneeze, laugh or strain. The
typical history for urge incontinence is sudden loss of large amounts of urine
(full bladder volume) preceded by an urge to void and inability to make it to
the toilet fast enough. Often patients
report urinating at the sound of running water or in association with other
toileting cues. The typical history for
overflow incontinence is of near constant dribbling of small amounts of urine
associated with sensation of abdominal fullness and incomplete emptying; the
patient is usually not aware that the urine is leaking. Many patients have mixed incontinence with
features of both urge and stress.
Physical Exam
In
addition to route exam, an abdominal exam to rule bladder distention, a pelvic
exam (looking for atrophic vaginitis, pelvic floor laxity, cystocele), a rectal
exam (to rule out stool impaction) and neurologic exam are indicated.
Post Void Residual Volume
The volume of urine
remaining in the bladder after the patient voids voluntarily. This is high with BPH/overflow incontinence
and low otherwise. It can be checked by
inserting a foley catheter or by sonogram (order bladder ultrasound, specify
“estimate PVR”).
Urinalysis/Urine Culture
To rule out infection, glycosuria
Urodynamics
Functional
exam of bladder performed when above do not yield clear diagnosis or attempts
at therapy are unsuccessful. Usually
performed by specialists (urology or gynecology), but can be easily done by the
motivated internist.
A foley is inserted and sterile saline
is used to fill the bladder while measuring instilled volume and measuring
pressure. Threshold volumes for first
desire to void, strong desire to void, detrusor contractions, and bladder
capacity are recorded. The catheter is
then removed and provocative tests for stress incontinence are performed – the
patient stands up and coughs or strains as a paper towel is held under to see
if drops of urine leak out.
TREATMENT
Behavioral, pharmacologic,
and surgical treatments are available for all types of incontinence. In general, they are roughly equally
efficacious. In weighing the options,
the usual pros and cons apply; Behavioral
approaches require motivated patients.
The drugs have significant systemic side effects. Surgery has its risks, costs, complications
and failures.
Stress Incontinence
Behavioral therapy is
primarily pelvic floor training, most commonly with Kegel exercises (see
attached). The goal of pelvic floor exercises
is to the increase the strength of the levator ani muscle in order to maintain
the urethrovesical angle – see the attachment.
Biofeedback can also be used to help the patient get started. The exercises work – the majority of
motivated patients will require no additional treatment.
Pharmacologic therapy is directed at
enchancing the function of the internal sphincter. Estrogen, administered intravaginally or orally, can reverse the
thinning of the urethral mucosa. Alpha
agonists can tighten up the sphincter – commonly used meds are low dose
tricyclics (imiprmine or amitriptyline, both of which have anticholinergic
activity as well) and psudoephedrine.
Surgery aims to restore the proper
architecture of the pelvis. There are
various procedures for resuspending or slinging the bladder; different surgeons
favor different operations.
Intraurethral injections of collagen are also done.
Urge Incontinence
Behavioral therapy for UUI
consists of both pelvic floor training as described above and various forms
bladder training. The idea behind
bladder training is to restore a normal pattern of voiding and normal bladder
function. Initially the patient is
instructed to void at fixed intervals, usually every 30-60 minutes regardless
of whether or not the urge to void is present.
(The initial interval can be determined using a voiding diary.) If an urge to void occurs prior to the next
schedule time, the patient is instructed to suppress the urge by attempting to
relax (often with a relaxation technique) or to distract herself. Each week the interval is increased until
contractions and can increase bladder capacity over the interval is increased
until a normal voiding pattern is stained.
As with Stress UI, the motivated get good results.
Pharmacologic therapy is
anticholinergics, which suppress involuntary bladder contractions and can
increase bladder capacity over the long term.
Anticholinergics are reasonably effective but side effects (dry mouth,
urinary retention, constipation, blurred vision, propantheline (probanthine 15
mg tid or qid), oxybutinin (ditropan 2.5mg bid or oxybutinin XL 5 qd), and
tolterodine (detrol 1 mg bid). Increase
dose as tolerated. Generally, it takes
weeks to realize full benefit of the drug.
There are no good surgical options.
Overflow Incontinence
Treatment consists of relieving the obstruction if one is
present and trying to enhance bladder contractility with pro-cholinergic oral
meds (urocholine). /this is often
ineffective and placement of a suprapubic tube may be necessary.
Incontinence Associated with
CNS Disease
The only available treatment is behavioral. Showing the patient to the bathroom and
prompting them to void at regular intervals can reduce the frequency and
severity of incontinence episodes. Remember
to ask the caregivers about incontinence.
They may not mention it and it’s often one of the factors that drives
otherwise motivated caregivers to institutionalize their family members. Prescribe adult diapers, plastic underpants,
chux, non-sterile gloves, and mattress liners and provide support to the
caregivers.
