The normal function of the urinary bladder is to store and
expel urine in a coordinated, controlled fashion. This coordinated
activity is regulated by the central and peripheral nervous systems.
Neurogenic bladder is a term applied to a malfunctioning urinary bladder
due to neurologic dysfunction or insult emanating from internal or
external trauma, disease, or injury.
Symptoms of neurogenic bladder range from detrusor
underactivity to overactivity, depending on the site of neurologic
insult. The urinary sphincter also may be affected, resulting in
sphincter underactivity or overactivity and loss of coordination with
bladder function. The appropriate therapy and a successful outcome are
predicated upon accurate diagnosis through a careful medical and voiding
history together with a variety of clinical examinations, including
urodynamics and selective radiographic imaging studies.
Neuroanatomy
Normal voiding essentially is a spinal reflex that is
modulated by the central nervous system (brain and spinal cord), which
coordinates the functions of the bladder and urethra. The bladder and
urethra are innervated by 3 sets of peripheral nerves arising from the
autonomic nervous system (ANS) and somatic nervous system. The central
nervous system is composed of the brain, brain stem, and the spinal
cord.
Brain
The brain is the master control of the entire urinary system.
The micturition control center is located in the frontal lobe
of the brain. The primary activity of this area is to send tonically
inhibitory signals to the detrusor muscle to prevent the bladder from
emptying (contracting) until a socially acceptable time and place to
urinate is available.
Certain lesions or diseases of the brain, including stroke,
cancer, or dementia, result in loss of voluntary control of the normal
micturition reflex.
The signal transmitted by the brain is routed through 2
intermediate stops (the brainstem and the sacral spinal cord) prior to
reaching the bladder.
Brainstem
The brainstem is located at the base of the skull. Within the
brainstem is a specialized area known as the pons, a major relay center
between the brain and the bladder. The pons is responsible for
coordinating the activities of the urinary sphincters and the bladder so
that they work in synergy. The mechanical process of urination is
coordinated by the pons in the area known as the pontine micturition
center (PMC). The PMC coordinates the urethral sphincter relaxation and
detrusor contraction to facilitate urination. See the image below.
The pons is a major relay center between the
brain and the bladder. The mechanical process of urination is
coordinated by the pons in the area known as the pontine micturition
center (PMC).
The conscious sensations associated with bladder activity are
transmitted to the pons from the cerebral cortex. The interaction of a
variety of excitatory and inhibitory neuronal systems is the function of
the PMC, which is characterized by its inborn excitatory nature. The
PMC functions as a relay switch in the voiding pathway. Stimulation of
the PMC causes the urethral sphincters to open while facilitating the
detrusor to contract and expel the urine.
The PMC is affected by emotions, which is why some people may
experience incontinence when they are excited or scared. The ability of
the brain to control the PMC is part of the social training that
children experience during growth and development. Usually the brain
takes over the control of the pons at age 3-4 years, which is why most
children undergo toilet training at this age.
When the bladder becomes full, the stretch receptors of the
detrusor muscle send a signal to the pons, which in turn notifies the
brain. People perceive this signal (bladder fullness) as a sudden desire
to go to the bathroom. Under normal situations, the brain sends an
inhibitory signal to the pons to inhibit the bladder from contracting
until a bathroom is found.
When the PMC is deactivated, the urge to urinate disappears,
allowing the patient to delay urination until finding a socially
acceptable time and place. When urination is appropriate, the brain
sends excitatory signals to the pons, allowing the urinary sphincters to
open and the detrusor to empty.
Spinal cord
The spinal cord extends from the brainstem down to the
lumbosacral spine. It is located in the spinal canal and is protected by
the cerebrospinal fluid, meninges, and a vertebral column. It is
approximately 14 inches long in an adult. Along its course, the spinal
cord sprouts off many nerve branches to different parts of the body.
The spinal cord functions as a long communication pathway
between the brainstem and the sacral spinal cord. When the sacral cord
receives the sensory information from the bladder, this signal travels
up the spinal cord to the pons and then ultimately to the brain. The
brain interprets this signal and sends a reply via the pons that travels
down the spinal cord to the sacral cord and, subsequently, to the
bladder.
In the normal cycle of bladder filling and emptying, the
spinal cord acts as an important intermediary between the pons and the
sacral cord. An intact spinal cord is critical for normal micturition.
If spinal cord injury has occurred, the patient will
demonstrate symptoms of urinary frequency, urgency, and urge
incontinence but will be unable to empty his or her bladder completely.
This occurs because the urinary bladder and the sphincter are both
overactive, a condition termed detrusor sphincter dyssynergia with
detrusor hyperreflexia (DSD-DH).
The sacral spinal cord is the terminal portion of the spinal
cord situated at the lower back in the lumbar area. This is a
specialized area of the spinal cord known as the sacral reflex center.
It is responsible for bladder contractions. The sacral reflex center is
the primitive voiding center.
In infants, the higher center of voiding control (the brain)
is not mature enough to command the bladder, which is why control of
urination in infants and young children comes from signals sent from the
sacral cord. When urine fills the infant bladder, an excitatory signal
is sent to the sacral cord. When this signal is received by the sacral
cord, the spinal reflex center automatically triggers the detrusor to
contract. The result is involuntary detrusor contractions with
coordinated voiding.
A continuous cycle of bladder filling and emptying occurs,
which is why infants and young children are dependent on diapers until
they are toilet trained. As the child's brain matures and develops, it
gradually dominates the control of the bladder and the urinary
sphincters to inhibit involuntary voiding until complete control is
attained. Voluntary continence usually is attained by age 3-4 years. By
this time, control of the voiding process has been relinquished by the
sacral reflex center of the sacral cord to the higher center in the
brain.
If the sacral cord becomes severely injured (eg, spinal tumor,
herniated disc), the bladder may not function. Affected patients may
develop urinary retention, termed detrusor areflexia. The detrusor will
be unable to contract, so the patient will not be able to urinate and
urinary retention will occur.
Peripheral nerves
Peripheral nerves form an intricate network of pathways for
sending and receiving information throughout the body. The nerves
originate from the main trunk of the spinal cord and branch out in
different directions to cover the entire body. Nerves convert the
internal and external environmental stimuli to electrical signals so
that the human body can understand stimuli as one of the ordinary senses
(ie, hearing, sight, smell, touch, taste, equilibrium). The bladder and
the urethral sphincters are under the influence of their corresponding
nerves.
The ANS lies outside of the central nervous system. It
regulates the actions of the internal organs (eg, intestines, heart,
bladder) under involuntary control. The ANS is divided into the
sympathetic and the parasympathetic nervous system.
Under normal conditions, the bladder and the internal urethral
sphincter primarily are under sympathetic nervous system control. When
the sympathetic nervous system is active, it causes the bladder to
increase its capacity without increasing detrusor resting pressure
(accommodation) and stimulates the internal urinary sphincter to remain
tightly closed. The sympathetic activity also inhibits parasympathetic
stimulation. When the sympathetic nervous system is active, urinary
accommodation occurs and the micturition reflex is inhibited.
The parasympathetic nervous system functions in a manner
opposite to that of the sympathetic nervous system. In terms of urinary
function, the parasympathetic nerves stimulate the detrusor to contract.
Immediately preceding parasympathetic stimulation, the sympathetic
influence on the internal urethral sphincter becomes suppressed so that
the internal sphincter relaxes and opens. In addition, the activity of
the pudendal nerve is inhibited to cause the external sphincter to open.
The result is facilitation of voluntary urination.
Like the ANS, the somatic nervous system is a part of the
nervous system that lies outside of the central spinal cord. The somatic
nervous system regulates the actions of the muscles under voluntary
control. Examples of these muscles are the external urinary sphincter
and the pelvic diaphragm. The pudendal nerve originates from the nucleus
of Onuf and regulates the voluntary actions of the external urinary
sphincter and the pelvic diaphragm. Activation of the pudendal nerve
causes contraction of the external sphincter and the pelvic floor
muscles, which occurs with activities such as Kegel exercises. Difficult
or prolonged vaginal delivery may cause temporary neurapraxia of the
pudendal nerve and cause stress urinary incontinence. Conversely,
suprasacral-infrapontine spinal cord trauma can cause overstimulation of
the pudendal nerve, resulting in urinary retention.
Physiology and Pathophysiology
Physiology
During the course of a day, an average person will void
approximately 4-8 times. The urinary bladder is in storage mode for most
of the day, allowing an individual to engage in more important
activities than urination.
Normal bladder function consists of 2 phases—filling and
emptying. The normal micturition cycle requires that the urinary bladder
and the urethral sphincter work together as a coordinated unit to store
and empty urine. During urinary storage, the bladder acts as a
low-pressure receptacle, while the urinary sphincter maintains high
resistance to urinary flow to keep the bladder outlet closed. During
urine elimination, the bladder contracts to expel urine while the
urinary sphincter opens (low resistance) to allow unobstructed urinary
flow and bladder emptying.
Filling phase
During the filling phase, the bladder accumulates increasing
volumes of urine while the pressure inside the bladder remains low. The
pressure within the bladder must be lower than the urethral pressure
during the filling phase. If the bladder pressure is greater than the
urethral pressure (resistance), urine will leak out.
The filling of the urinary bladder depends on the intrinsic
viscoelastic properties of the bladder and the inhibition of the
parasympathetic nerves. Thus, bladder filling primarily is a passive
event.
Sympathetic nerves also facilitate urine storage in the following ways:
-
Sympathetic nerves inhibit the parasympathetic nerves from triggering bladder contractions.
-
Sympathetic nerves directly cause relaxation and expansion of the detrusor muscle.
-
Sympathetic nerves close the bladder neck by constricting the
internal urethral sphincter. This sympathetic input to the lower urinary
tract is constantly active during bladder filling.
As the bladder fills, the pudendal nerve becomes excited.
Stimulation of the pudendal nerve results in contraction of the external
urethral sphincter. Contraction of the external sphincter, coupled with
that of the internal sphincter, maintains urethral pressure
(resistance) higher than normal bladder pressure. The combination of
both urinary sphincters is known as the continence mechanism.
The pressure gradients within the bladder and urethra play an
important functional role in normal micturition. As long as the urethral
pressure is higher than that of the bladder, patients will remain
continent. If the urethral pressure is abnormally low or if the
intravesical pressure is abnormally high, urinary incontinence will
result.
As the bladder initially fills, a small rise in pressure
occurs within the bladder (intravesical pressure). When the urethral
sphincter is closed, the pressure inside the urethra (intraurethral
pressure) is higher than the pressure within the bladder. While the
intraurethral pressure is higher than the intravesical pressure, urinary
continence is maintained.
During some physical activities and with coughing, sneezing,
or laughing, the pressure within the abdomen rises sharply. This rise is
transmitted to both the bladder and urethra. As long as the pressure is
evenly transmitted to both the bladder and urethra, urine will not
leak. When the pressure transmitted to the bladder is greater than
urethra, urine will leak out, resulting in stress incontinence.
Emptying phase
The storage phase of the urinary bladder can be switched to
the voiding phase either involuntarily (reflexively) or voluntarily.
Involuntary reflex voiding occurs in an infant when the volume of urine
exceeds the voiding threshold. When the bladder is filled to capacity,
the stretch receptors within the bladder wall signal the sacral cord.
The sacral cord, in turn, sends a message back to the bladder indicating
that it is time to empty the bladder.
At this point, the pudendal nerve causes relaxation of the
levator ani so that the pelvic floor muscle relaxes. The pudendal nerve
also signals the external sphincter to open. The sympathetic nerves send
a message to the internal sphincter to relax and open, resulting in a
lower urethral resistance.
When the urethral sphincters relax and open, the
parasympathetic nerves trigger contraction of the detrusor. When the
bladder contracts, the pressure generated by the bladder overcomes the
urethral pressure, resulting in urinary flow. These coordinated series
of events allow unimpeded, automatic emptying of the urine.
A repetitious cycle of bladder filling and emptying occurs in
newborn infants. The bladder empties as soon as it fills because the
brain of an infant has not matured enough to regulate the urinary
system. Because urination is unregulated by the infant's brain,
predicting when the infant will urinate is difficult.
As the infant brain develops, the PMC also matures and
gradually assumes voiding control. When the infant enters childhood
(usually at age 3-4 years), this primitive voiding reflex becomes
suppressed and the brain dominates bladder function, which is why toilet
training usually is successful at age 3-4 years. However, this
primitive voiding reflex may reappear in people with spinal cord
injuries.
Delaying voiding or voluntary voiding
Bladder function is automatic but completely governed by the
brain, which makes the final decision on whether or not to void. The
normal function of urination means that an individual has the ability to
stop and start urination on command. In addition, the individual has
the ability to delay urination until a socially acceptable time and
place. The healthy adult is aware of bladder filling and can willfully
initiate or delay voiding.
In a healthy adult, the PMC functions as an on-off switch that
is activated by stretch receptors in the bladder wall and is, in turn,
modulated by inhibitory and excitatory neurologic influences from the
brain. When the bladder is full, the stretch receptors are activated.
The individual perceives the activation of the stretch receptors as the
bladder being full, which signals a need to void.
When an individual cannot find a bathroom nearby, the brain
bombards the PMC with a multitude of inhibitory signals to prevent
detrusor contractions. At the same time, an individual may actively
contract the levator muscles to keep the external sphincter closed or
initiate distracting techniques to suppress urination.
Thus, the voiding process requires coordination of both the
ANS and somatic nervous system, which are in turn controlled by the PMC
located in the brainstem.
Pathophysiology
If a problem occurs within the nervous system, the entire
voiding cycle is affected. Any part of the nervous system may be
affected, including the brain, pons, spinal cord, sacral cord, and
peripheral nerves. A dysfunctional voiding condition results in
different symptoms, ranging from acute urinary retention to an overactive bladder or to a combination of both.
Urinary incontinence results from a dysfunction of the
bladder, the sphincter, or both. Bladder overactivity (spastic bladder)
is associated with the symptoms of urge incontinence, while sphincter
underactivity (decreased resistance) results in symptomatic stress
incontinence. A combination of detrusor overactivity and sphincter
underactivity may result in mixed symptoms.
Brain lesion
Lesions of the brain above the pons destroy the master control
center, causing a complete loss of voiding control. The voiding
reflexes of the lower urinary tract—the primitive voiding reflex—remain
intact. Affected individuals show signs of urge incontinence, or spastic
bladder (medically termed detrusor hyperreflexia or overactivity). The
bladder empties too quickly and too often, with relatively low
quantities, and storing urine in the bladder is difficult. Usually,
people with this problem rush to the bathroom and even leak urine before
reaching their destination. They may wake up frequently at night to
void.
Typical examples of a brain lesion are stroke, brain tumor, or Parkinson disease. Hydrocephalus,
cerebral palsy, and Shy-Drager syndrome also are brain lesions.
Shy-Drager syndrome is a rare condition that also causes the bladder
neck to remain open.
Spinal cord lesion
Diseases or injuries of the spinal cord between the pons and
the sacral spinal cord also result in spastic bladder or overactive
bladder. People who are paraplegic or quadriplegic have lower extremity
spasticity. Initially, after spinal cord trauma, the individual enters a
spinal shock phase where the nervous system shuts down. After 6-12
weeks, the nervous system reactivates. When the nervous system becomes
reactivated, it causes hyperstimulation of the affected organs. For
example, the legs become spastic.
These people experience urge incontinence. The bladder empties
too quickly and too frequently. The voiding disorder is similar to that
of the brain lesion except that the external sphincter may have
paradoxical contractions as well. If both the bladder and external
sphincter become spastic at the same time, the affected individual will
sense an overwhelming desire to urinate but only a small amount of urine
may dribble out. The medical term for this is detrusor-sphincter
dyssynergia because the bladder and the external sphincter are not in
synergy. Even though the bladder is trying to force out urine, the
external sphincter is tightening to prevent urine from leaving.
The causes of spinal cord injuries include motor vehicle and
diving accidents. Multiple sclerosis (MS) is a common cause of spinal
cord disease in young women. Those with MS also may exhibit visual
disturbances, known as optic neuritis.
Children born with myelomeningocele may have spastic bladders and/or an
open urethra. Conversely, some children with myelomeningocele may have a
hypocontractile bladder instead of a spastic bladder.
Sacral cord injury
Selected injuries of the sacral cord and the corresponding
nerve roots arising from the sacral cord may prevent the bladder from
emptying. If a sensory neurogenic bladder is present, the affected
individual may not be able to sense when the bladder is full. In the
case of a motor neurogenic bladder, the individual will sense the
bladder is full and the detrusor may not contract, a condition known as
detrusor areflexia. These individuals have difficulty eliminating urine
and experience overflow incontinence; the bladder gradually overdistends
until the urine spills out. Typical causes are a sacral cord tumor,
herniated disc, and injuries that crush the pelvis. This condition also
may occur after a lumbar laminectomy, radical hysterectomy, or
abdominoperineal resection.
Some teenagers suddenly develop an abnormal voiding pattern
and often are evaluated for tethered cord syndrome, a neurologic
condition in which the tip of the sacral cord is stuck near the sacrum
and cannot stretch as the child grows taller. Ischemic changes of the
sacral cord associated with the tethering cause the manifestation of
dysfunctional voiding symptoms.
Peripheral nerve injury
Diabetes mellitus and AIDS
are 2 of the conditions causing peripheral neuropathy resulting in
urinary retention. These diseases destroy the nerves to the bladder and
may lead to silent, painless distention of the bladder. Patients with
chronic diabetes lose the sensation of bladder filling first, before the
bladder decompensates. Similar to injury to the sacral cord, affected
individuals will have difficulty urinating. They also may have a
hypocontractile bladder.
Other diseases manifesting this condition are poliomyelitis,
Guillain-Barré syndrome, severe herpes in the genitoanal area,
pernicious anemia, and neurosyphilis (tabes dorsalis).
Summary of definitions
Neurogenic bladder is a malfunctioning bladder due to any type of neurologic disorder.
Detrusor hyperreflexia refers to overactive bladder symptoms
due to a suprapontine upper motor neuron neurologic disorder. External
sphincter functions normally. The detrusor muscle and the external
sphincter function in synergy (in coordination).
DSD-DH refers to overactive bladder symptoms due to neurologic
upper motor neuron disorder of the suprasacral spinal cord.
Paradoxically, the patient is in urinary retention. Both the detrusor
and the sphincter are contracting at the same time; they are in
dyssynergy (lack of coordination).
Detrusor hyperreflexia with impaired contractility (DHIC)
refers to overactive bladder symptoms, but the detrusor cannot generate
enough pressure to allow complete emptying. The external sphincter is in
synergy with detrusor contraction. The detrusor is too weak to mount an
adequate contraction for proper voiding to occur. The condition is
similar to urinary retention, but irritating voiding symptoms are
prevalent.
Detrusor instability refers to overactive bladder symptoms
without neurologic impairment. External sphincter functions normally, in
synergy.
Overactive bladder refers to symptoms of urinary urgency, with
or without urge incontinence, usually associated with frequency and
nocturia. The cause may be neurologic or nonneurologic.
Detrusor areflexia is complete inability of the detrusor to
empty due to a lower motor neuron lesion (eg, sacral cord or peripheral
nerves).
Urinary retention is the inability of the urinary bladder to empty. The cause may be neurologic or nonneurologic.
Types of Neurogenic Bladders
Supraspinal Lesions
Supraspinal lesions refer to those lesions of the central
nervous system involving the area above the pons. They include
cerebrovascular accident, brain tumor, Parkinson disease, and Shy-Drager
syndrome.
Cerebrovascular accident
After a stroke, the brain may enter into a temporary acute
cerebral shock phase. During this time, the urinary bladder will be in
retention—detrusor areflexia. Almost 25% of affected individuals develop
acute urinary retention after a stroke.
After the cerebral shock phase wears off, the bladder
demonstrates detrusor hyperreflexia with coordinated urethral sphincter
activity. This occurs because the PMC is released from the cerebral
inhibitory center. When the patient manifests symptoms of detrusor
hyperreflexia, the individual will complain of urinary frequency,
urgency, and urge incontinence.
The treatment for the cerebral shock phase is indwelling Foley
catheter or clean intermittent catheterization (CIC). When the bladder
becomes hyperreflexic, institute therapies to facilitate bladder filling
and storage with anticholinergic medications.
Brain tumor
Detrusor hyperreflexia with coordinated urethral sphincter is
the most common observed urodynamic pattern associated with a brain
tumor.
When the patient manifests symptoms of detrusor hyperreflexia,
the individual complains of urinary frequency, urgency, and urge
incontinence. First-line treatment for detrusor hyperreflexia includes
anticholinergic medication.
Parkinson disease
This is a degenerative disorder of pigmented neurons of
substantia nigra. It results in dopamine deficiency and increased
cholinergic activity in the corpus striatum.
Patients with Parkinson disease manifest symptoms of
bradykinesia, skeletal muscle tremor, cogwheel rigidity, and masked
facies. Symptoms specific to the urinary bladder include urinary
frequency, urgency, nocturia, and urge incontinence.
Typical urodynamic findings for Parkinson disease are most
consistent with detrusor hyperreflexia and urethral sphincter
bradykinesia. The striated urethral sphincter often demonstrates poorly
sustained contraction.
Similar to other supraspinal lesions, the treatment for
Parkinson disease is to facilitate bladder filling and promote urinary
storage with anticholinergic agents.
If patients with Parkinson disease exhibit symptoms of bladder
outlet obstruction (BOO) due to benign prostatic enlargement (BPE), the
diagnosis of BOO should be confirmed by multichannel urodynamic
studies. The most common cause of postprostatectomy incontinence in the
patient with Parkinson disease is detrusor hyperreflexia.
If transurethral resection of the prostate (TURP) is performed
without urodynamic confirmation of obstruction, the patient may become
totally incontinent after the TURP procedure.
Shy-Drager syndrome
Shy-Drager syndrome is a rare, progressive, and degenerative
disease affecting the ANS with multisystem organ atrophy. In addition to
Parkinson-like symptoms, cerebellar ataxia and autonomic dysfunction
are common. Affected individuals demonstrate orthostatic hypotension,
anhidrosis, and urinary incontinence.
Degeneration of the nucleus of Onuf results in denervation of
the external striated sphincter. Sympathetic nerve atrophy causes
nonfunctional bladder and an open bladder neck.
Urodynamic evaluation often reveals detrusor hyperreflexia,
although a few individuals may have detrusor areflexia or poorly
sustained bladder contractions. Often, the bladder neck (internal
sphincter) will be open at rest, with striated sphincter denervation.
The treatment for Shy-Drager syndrome is to facilitate urinary
storage with anticholinergic agents coupled with CIC or indwelling
catheter. Patients with Shy-Drager syndrome should avoid undergoing TURP
because the risk of total incontinence is high.
Spinal Cord Lesions
Spinal cord injury
When an individual sustains a spinal cord injury from a diving
accident or motor vehicle injury, the initial response from the nervous
system is spinal shock. During this spinal shock phase, the affected
individual experiences flaccid paralysis below the level of injury, and
the somatic reflex activity is either depressed or absent.
The anal and bulbocavernosus reflex typically is absent. The
autonomic activity is depressed, and the individual experiences urinary
retention and constipation. Urodynamic findings are consistent with
areflexic detrusor and rectum. The internal and external urethral
sphincter activities, however, are normal.
The spinal shock phase typically lasts 6-12 weeks; it may be
prolonged in some cases. During this time, the urinary bladder must be
drained with CIC or indwelling urethral catheter.
When the spinal shock phase wears off, bladder function
returns but the detrusor activity increases in reflex excitability to an
overactive state—detrusor hyperreflexia. Depending on the level of the
lesion, the individual may develop DSD-DH. Thus, the individual must be
monitored for leaking between CIC, and periodic urodynamic testing must
be performed for this alteration in detrusor behavior. During
urodynamics, intravesical instillation of cold saline may indicate
return of reflex activity or help better characterize the lesion.
Realizing that suprasacral lesions exhibit detrusor areflexia
at initial insult but progress to hyperreflexic state over time is
important. Conversely, sacral cord lesions are associated with areflexic
bladders that may become hypertonic overtime.
Spinal cord lesions (above the sixth thoracic vertebrae)
Individuals who sustain a complete cord transection above the
sixth thoracic vertebrae (T6) most often will have urodynamic findings
of detrusor hyperreflexia, striated sphincter dyssynergia, and smooth
sphincter dyssynergia. A unique complication of T6 injury is autonomic
dysreflexia.
Autonomic dysreflexia is an exaggerated sympathetic response
to any stimuli below the level of the lesion. This occurs most commonly
with lesions of the cervical cord. Often, the inciting event is
instrumentation of the urinary bladder or the rectum, causing visceral
distention.
Symptoms of autonomic dysreflexia include sweating, headache,
hypertension, and reflex bradycardia. Acute management of autonomic
dysreflexia is to decompress the rectum or bladder. Decompression
usually will reverse the effects of unopposed sympathetic outflow. If
additional measures are required, parenteral ganglionic or adrenergic
blocking agents, such as chlorpromazine, may be used.
Oral blocking agents, including terazosin, may be used for
prophylactically treating patients with autonomic dysreflexia.
Alternatively, spinal anesthetic may be used as a prophylactic measure
whenever bladder instrumentation is considered.
Spinal cord lesions (below T6)
Individuals who sustain spinal cord lesions below T6 level
will have urodynamic findings of detrusor hyperreflexia, striated
sphincter dyssynergia, and smooth sphincter dyssynergia but no autonomic
dysreflexia.
Neurologic evaluation will reveal skeletal muscle spasticity
with hyperreflexic deep tendon reflexes. Affected patients will
demonstrate extensor plantar response and positive Babinski sign.
These individuals will experience incomplete bladder emptying
secondary to detrusor sphincter dyssynergia, or loss of facilitatory
input from higher centers. Cornerstone of treatment involves CIC and
anticholinergic medications.
Multiple sclerosis
MS is caused by focal demyelinating lesions of the central
nervous system. It most commonly involves the posterior and lateral
columns of the cervical spinal cord. Usually, poor correlation exists
between the clinical symptoms and urodynamic findings. Thus, using
urodynamic studies to evaluate patients with MS is critical.
The most common urodynamic finding is detrusor hyperreflexia,
occurring in as many as 50-90% of patients with MS. As many as 50% of
patients will demonstrate DSD-DH. Detrusor areflexia occurs in 20-30% of
cases. The optimum therapy for a patient with MS and incontinence must
be individualized and based on the urodynamic findings.
Peripheral Nerve Lesions
Peripheral nerve lesions due to diabetes mellitus, tabes
dorsalis, herpes zoster, herniated lumbar disk disease, and radical
pelvic surgery result in detrusor areflexia.
Diabetic cystopathy
Usually, neurogenic bladder dysfunction occurs 10 or more
years after the onset of diabetes mellitus. Neurogenic bladder occurs
because of autonomic and peripheral neuropathy. A metabolic derangement
of the Schwann cell results in segmental demyelination and impaired
nerve conduction.
The first symptoms of diabetic cystopathy are loss of
sensation of bladder filling followed by loss of motor function. Classic
urodynamic findings associated with this condition are elevated
residual urine, decreased bladder sensation, impaired detrusor
contractility, and, eventually, detrusor areflexia. Paradoxically, DHIC
also has been observed. Treatment of diabetic cystopathy is CIC,
long-term indwelling catheterization, or urinary diversion.
Tabes dorsalis (neurosyphilis)
In tabes dorsalis, central and peripheral nerve conduction is
impaired. Affected patients experience decreased bladder sensation and
increased voiding intervals.
The most common urodynamic finding associated with neurosyphilis is detrusor areflexia with normal sphincteric function.
Herpes zoster
Herpes zoster is a neuropathy associated with painful
vesicular eruptions in the distribution of the affected nerve. The
herpes virus lies dormant in the dorsal root ganglia or the sacral
nerves.
Sacral nerve involvement leads to impairment of detrusor
function. The early stages of herpes infection are associated with lower
urinary tract symptoms of urinary frequency, urgency, and urge
incontinence. Later stages include decreased bladder sensation,
increased residual urine, and urinary retention. Urinary retention is
self-limited and will resolve spontaneously with clearing of the herpes
infection.
Herniated disc
Slow and progressive herniation of the lumbar disc may cause
irritation of the sacral nerves and cause detrusor hyperreflexia.
Conversely, acute compression of the sacral roots associated with
deceleration trauma will prevent nerve conduction and result in detrusor
areflexia.
A typical urodynamic finding of sacral nerve injury is
detrusor areflexia with intact bladder sensation. Associated internal
sphincter denervation may occur. If the peripheral sympathetic nerves
are damaged, the internal sphincter will be open and nonfunctional.
Peripheral sympathetic nerve damage often occurs in association with
detrusor denervation. The striated sphincter, however, is preserved.
Pelvic surgery
Patients undergoing major pelvic surgery, such as radical
hysterectomy, abdominoperineal resection, proctocolectomy, or total
exenteration will experience bladder dysfunction postoperatively.
Most commonly, postsurgical patients will manifest symptoms of
detrusor areflexia. However, as many as 80% of affected patients will
experience spontaneous recovery of function within 6 months after
surgery.
Workup
Laboratory Studies
Urinalysis and urine culture: Urinary tract infection can cause irritative voiding symptoms and urge incontinence.
Urine cytology
Carcinoma-in-situ of the urinary bladder causes symptoms of
urinary frequency and urgency. Irritative voiding symptoms out of
proportion to the overall clinical picture and/or hematuria warrant
urine cytology and cystoscopy.
Chem 7 profile
Blood urea nitrogen (BUN) and creatinine (Cr) are checked if compromised renal function is suspected.
Other Tests
Voiding diary
A voiding diary is a daily record of the patient's bladder
activity. It is an objective documentation of the patient's voiding
pattern, incontinent episodes, and inciting events associated with
urinary incontinence.
Pad test
This is an objective test that documents the urine loss.
Intravesical methylene blue test or oral phenazopyridine or Urised
(which contains methylene blue) may be used. Methylene blue turns the
urine color blue; phenazopyridine turns the urine color orange.
Patients should resume their usual physical activities while
wearing a perineal pad. If the pads turn to orange or blue, the patient
is experiencing urine loss. If the pads remain white, moisture most
likely is a normal vaginal fluid.
Diagnostic Procedures
Postvoid residual urine
The postvoid residual urine (PVR) measurement is a part of
basic evaluation for urinary incontinence. If the PVR is high, the
bladder may be contractile or the bladder outlet may be obstructed. Both
of these conditions will cause urinary retention with overflow
incontinence.
Uroflow rate
Uroflow rate is a useful screening test used mainly to
evaluate bladder outlet obstruction. Uroflow rate is volume of urine
voided per unit of time.
Low uroflow rate may reflect urethral obstruction, a weak
detrusor, or a combination of both. This test alone cannot distinguish
an obstruction from a contractile detrusor.
Filling cystometrogram
A filling cystometrogram (CMG) assesses the bladder capacity,
compliance, and the presence of phasic contractions (detrusor
instability). Most commonly, liquid filling medium is used.
An average adult bladder holds approximately 50-500 mL of
urine. During the test, provocative maneuvers help to unveil bladder
instability.
Voiding cystometrogram (pressure-flow study)
Pressure-flow study simultaneously records the voiding
detrusor pressure and the rate of urinary flow. This is the only test
able to assess bladder contractility and the extent of a bladder outlet
obstruction.
Pressure-flow studies can be combined with voiding cystogram and videourodynamic study for complicated cases of incontinence.
Cystogram
A static cystogram (anteroposterior and lateral) helps to
confirm the presence of stress incontinence, the degree of urethral
motion, and the presence of a cystocele. Intrinsic sphincter deficiency
will be evident by an open bladder neck. The presence of a vesicovaginal
fistula or bladder diverticulum also may be noted.
A voiding cystogram can assess bladder neck and urethral
function (internal and external sphincter) during filling and voiding
phases. A voiding cystogram can identify a urethral diverticulum,
urethral obstruction, and vesicoureteral reflux.
Electromyography
Electromyography (EMG) helps to ascertain the presence of
coordinated or uncoordinated voiding. Failure of urethral relaxation
during bladder contraction results in uncoordinated voiding (detrusor
sphincter dyssynergia). EMG allows accurate diagnosis of detrusor
sphincter dyssynergia common in spinal cord injuries.
Cystoscopy
The role of cystoscopy in the evaluation of neurogenic bladder is to allow discovery of bladder lesions (eg, bladder cancer, bladder stone) that would remain undiagnosed by urodynamics alone.
General agreement is that cystoscopy is indicated for patients
complaining of persistent irritative voiding symptoms or hematuria. The
physician can diagnose obvious causes of bladder overactivity, such as
cystitis, stone, and tumor, easily. This information is important in
determining the etiology of the incontinence and may influence treatment
decisions.
Videourodynamics
Videourodynamics is the criterion standard for evaluation of a
patient with incontinence. Videourodynamics combines the radiographic
findings of voiding cystourethrogram (VCUG) and multichannel
urodynamics.
Videourodynamics enables documentation of lower urinary tract
anatomy, such as vesicoureteral reflux and bladder diverticulum, as well
as the functional pressure-flow relationship between the bladder and
the urethra.
Treatment & Management
Medical Care
Treatment of urinary incontinence varies by type, as follows:
-
Stress incontinence may be treated with surgical and nonsurgical means
-
Urge incontinence may be treated with behavioral modification or with bladder-relaxing agents
-
Mixed incontinence may require medications as well as surgery
-
Overflow incontinence may be treated with some type of catheter regimen
-
Functional incontinence may be resolved by treating the
underlying cause (eg, urinary tract infection, constipation) or by
simply changing a few medications
Do not consider anti-incontinence products to be a cure-all
for urinary incontinence; however, judicious use of pads and devices to
contain urine loss and maintain skin integrity are extremely useful in
selected cases. Absorbent pads and internal and external collecting
devices have an important role in the management of chronic
incontinence. The criteria for use of these products are fairly
straightforward, and they are beneficial for women who meet the
following conditions:
-
Failure of all other treatments and persistent incontinence
-
Illness or disability that prevents participation in behavioral programs
-
Inability to benefit from medications
-
Incontinence disorders that cannot be corrected by surgery
-
Awaiting surgery
Absorbent products
Absorbent products are pads or garments designed to absorb
urine to protect the skin and clothing. Available in both disposable and
reusable forms, they are a temporary means of keeping the patient dry
until a more permanent solution becomes available. By reducing wetness
and odor, they help maintain the patient's comfort and allow her to
function in normal activities. They may be used temporarily until a
definitive treatment takes effect or if the treatment yields
less-than-perfect results. Absorbent products are helpful during the
initial assessment and workup of urinary incontinence. As an adjunct to
behavioral and pharmacologic therapies, they play an important role in
the care of persons with intractable incontinence.
Do not use absorbent products instead of definitive
interventions to decrease or eliminate urinary incontinence. Early
dependency on absorbent pads may be a deterrent to achieving continence,
providing the wearer a false sense of security. Chronic use of
absorbent products may lead to inevitable acceptance of the incontinence
condition, which removes the motivation to seek evaluation and
treatment. In addition, improper use of absorbent products may
contribute to skin breakdown and urinary tract infections. Thus,
appropriate use, meticulous care, and frequent pad or garment changes
are needed when absorbent products are used.
Absorbent products used include underpads, pant liners
(shields and guards), adult diapers (briefs), a variety of washable
pants and disposable pad systems, or combinations of these products.
More than 50% of members in Help for Incontinent People (HIP) use some
form of protective garment to remain dry. In addition, 47% of elderly
men and women use some type of absorbent product. In nursing homes,
disposable diapers or reusable pad and pant systems are used.
Unlike sanitary napkins, these absorbent products are
specially designed to trap urine, minimize odor, and keep the patient
dry. Different types of products with varying degrees of absorbency
exist. These products may absorb 20-300 mL, depending on the brand and
the absorbent material of the product. Absorbent pads and garments that
are available include panty shields, pant guards, undergarments,
combination pad-pant systems, adult diaper garments, and special bed
pads.
For occasional minimal urine loss, panty shields (small
absorbent inserts) may be used. For light incontinence, guards
(close-fitting pads) may be more appropriate. Absorbent guards are
attached to the underwear and can be worn under normal clothing.
Adult undergarments (full-length pads) are bulkier and more
absorbent than guards. They may be held in place by waist straps or snug
underwear. Adult briefs are the bulkiest type of protection, offering
the highest level of absorbency, and are secured in place with
self-adhesive tape.
Absorbent bed pads also are available to protect the bed
sheets and mattresses at night. They are available in different sizes
and absorbencies.
Urethral occlusive devices
Urethral occlusive devices are artificial devices that may be
inserted into the urethra or placed over the urethral meatus to prevent
urinary leakage. These devices are palliative measures to prevent
involuntary urine loss. Urethral occlusive devices are more attractive
than absorbent pads because they tend to keep the patient drier;
however, they may be more difficult and expensive to use than pads.
Urethral occlusive devices must be removed after several hours or after
each voiding.
Unlike pads, these devices may be more difficult to change.
With device manipulation, patients may soil their hands. The risk that a
urethral plug may fall into the bladder or fall off the urethra always
exists. Urethral occlusive devices, perhaps, are best suited for an
active woman with incontinence who does not desire surgery.
Catheters
Urinary diversion, using various catheters, has been one of
the mainstays of anti-incontinence therapy. The use of catheters for
bladder drainage has withstood the test of time. Bladder catheterization
may be a temporary measure or a permanent solution for urinary
incontinence. Different types of bladder catheterization include
indwelling urethral catheters, suprapubic tubes, and self-intermittent
catheterization.
Indwelling urethral catheters
Commonly known as Foley catheters, indwelling urethral
catheters historically have been the mainstay of treatment for bladder
dysfunction. If urethral catheters are used for a long-term condition,
they must be changed monthly. These catheters may be changed at an
office, a clinic, or at home by a visiting nurse. The standard catheter
size for treating urinary retention is 16F or 18F, with a 5-mL balloon
filled with 10 mL of sterile water. Larger catheters (eg, 22F, 24F) with
bigger balloons are used for treating grossly bloody urine found in
other urologic conditions or diseases. Proper management of indwelling
urethral catheters varies per individual.
The usual practice is to change indwelling catheters once
every month. The catheter and bag are replaced on a monthly basis;
however, catheters that develop encrustations and problems with urine
drainage must be changed more frequently. All indwelling catheters in
the urinary bladder for more than 2 weeks become colonized with
bacteria. Bacterial colonization does not mean the patient has clinical
bladder infection. Symptoms of bladder infection include foul odor,
purulent urine, and hematuria. Fever with flank pain often is present if
upper tracts are involved. If bladder infection occurs, change the
entire catheter and the drainage system. The urinary drainage bag does
not need to be disinfected to prevent infection.
Routine irrigation of catheters is not required. However, some
authors favor the use of 0.25% acetic acid irrigation because it is
bacteriostatic, minimizes catheter encrustation, and diminishes the
odor. When used, 30 mL is instilled into the bladder and allowed to
freely drain on a twice daily basis.
Patients do not have to take continuous antibiotics while
using the catheter. In fact, continuous antibiotic therapy is
contraindicated while a catheter is used. Prolonged use of antibiotics
to prevent infection actually may cause paradoxical generation of
bacteria that are resistant to common antibiotics. Indwelling use of a
Foley catheter in individuals who are homebound requires close
supervision by a visiting nurse and additional personal hygiene care.
In spite of its apparent advantages, the use of a Foley
catheter for a prolonged period of time (eg, months to years) is
strongly discouraged. Long-term use of urethral catheters poses
significant health hazards. Indwelling urethral catheters are a
significant cause of urinary tract infections that involve the urethra,
bladder, and kidneys. Within 2-4 weeks after catheter insertion,
bacteria will be present in the bladder of most women. Asymptomatic
bacterial colonization is common and does not pose a health hazard.
However, untreated symptomatic urinary tract infections may lead to
urosepsis and death. The death rate of nursing home residents with
urethral catheters has been found to be three times higher than that of
residents without catheters; this may be more a reflection of the
severity of comorbid conditions that lead to the clinical decision to
use chronic bladder drainage than causation from the use of chronic
bladder drainage.
The use of a urethral catheter is contraindicated in the
treatment of urge incontinence. Other problems associated with
indwelling urethral catheters include encrustation of the catheter,
bladder spasms resulting in urinary leakage, hematuria, and urethritis.
More severe complications include formation of bladder stones,
development of periurethral abscess, renal damage, and urethral erosion.
Another problem of long-term catheterization is bladder
contracture, which occurs with urethral catheters as well as suprapubic
tubes. Anticholinergic therapy and intermittent clamping of the catheter
in combination have been reported to be beneficial for preserving the
bladder integrity with long-term catheter use. Individuals who did not
use the medication and daily clamping regimen experienced a decrease in
bladder capacity and vesicoureteral reflux. For this reason, some
physicians recommend using anticholinergic medications with intermittent
clamping of the catheter if lower urinary tract reconstruction is
anticipated in the future.
Restrict the use of indwelling catheters to the following situations:
-
As comfort measures for the terminally ill
-
To avoid contamination or to promote healing of severe pressure sores
-
In cases of inoperable urethral obstruction that prevent bladder emptying
-
In individuals who are severely impaired and for whom alternative interventions are not an option
-
When an individual lives alone and a caregiver is unavailable to provide other supportive measures
-
For acutely ill patients who require accurate monitoring of fluid balance
-
For severely impaired persons for whom bed and clothing changes are painful or disruptive
However, when long-term use of a urethral catheter is anticipated, a suprapubic catheter is an attractive alternative.
Suprapubic catheters
A suprapubic tube is an attractive alternative to long-term
urethral catheter use. The most common use of a suprapubic catheter is
in individuals with spinal cord injuries and a malfunctioning bladder.
Both paraplegic and quadriplegic individuals have benefited from this
form of urinary diversion. When suprapubic tubes are needed, usually
smaller (eg, 14F, 16F) catheters are placed. Like the urethral catheter,
suprapubic tubes should be changed once a month on a regular basis.
Suprapubic catheters have many advantages. With a suprapubic
catheter, the risk of urethral damage is eliminated. Multiple voiding
trials may be performed without having to remove the catheter. Because
the catheter comes out of the lower abdomen rather than the vaginal
area, a suprapubic tube is more patient-friendly. Bladder spasms occur
less often because the suprapubic catheter does not irritate the trigone
as does the urethral catheter. In addition, suprapubic tubes are more
sanitary for the individual, and bladder infections are minimized
because the tube is away from the perineum.
Suprapubic catheters are changed easily by either a nurse or a
doctor. Unlike the urethral catheter, a suprapubic tube is less likely
to become dislodged because the exit site is so small. When the tube is
removed, the hole in the abdomen quickly seals itself within 1-2 days.
Indications for suprapubic catheters include short-term use
following gynecologic, urologic, and other types of surgery. Suprapubic
catheters may be used whenever the clinical situation requires the use
of a bladder drainage device; however, suprapubic catheters are
contraindicated in persons with chronic unstable bladders or intrinsic
sphincter deficiency because involuntary urine loss is not prevented. A
suprapubic tube does not prevent bladder spasms from occurring in
unstable bladders nor does it improve the urethral closure mechanism in
an incompetent urethra.
Potential complications with chronic suprapubic
catheterization are similar to those associated with indwelling urethral
catheters, including leakage around the catheter, bladder stone
formation, urinary tract infection, and catheter obstruction.
During the initial placement of a suprapubic tube, a potential
for bowel injury exists. Although uncommon, bowel perforation is known
to occur with first-time placement of suprapubic tubes. Other potential
complications include cellulitis around the tube site and hematoma.
If the suprapubic tube falls out inadvertently, the exit hole
of the tube will seal up and close quickly within 24 hours if the tube
is not replaced with a new one. If tube dislodgment is recognized
promptly, a new tube can be reinserted quickly and painlessly as long as
the tube site remains patent.
A suprapubic catheter is an alternative solution to an
indwelling urethral catheter in women who require chronic bladder
drainage. Potential problems unique to suprapubic catheters include skin
infection, hematoma, bowel injury, and problems with catheter
reinsertion. Long-term management of a suprapubic tube also may be
problematic if the health care provider lacks the knowledge and
expertise of suprapubic catheter management or if the homebound
individual lacks quick access to a medical center in case of an
emergency. In the appropriate situation, the suprapubic catheter affords
many advantages over long-term urethral catheters.
Intermittent catheterization
Intermittent catheterization or self-catheterization is a mode
of draining the bladder at timed intervals, as opposed to continuous
bladder drainage. A prerequisite for self-catheterization is the
patients' ability to use their hands and arms; however, in a situation
in which a patient is physically or mentally impaired, a caregiver or
health professional can perform intermittent catheterization for the
patient. Of all 3 possible options (ie, urethral catheter, suprapubic
tube, intermittent catheterization), intermittent catheterization is the
best solution for bladder decompression of a motivated individual who
is not physically handicapped or mentally impaired.
Many studies of young individuals with spinal cord injuries
have shown that intermittent catheterization is preferable to indwelling
catheters (ie, urethral catheter, suprapubic tube) for both men and
women. Intermittent catheterization has become a healthy alternative to
indwelling catheters for individuals with chronic urinary retention due
to an obstructed bladder, a weak bladder, or a nonfunctioning bladder.
Young children with myelomeningocele have benefited from the use of
intermittent catheterization.
For those children, antibiotic prophylaxis (low-dose
chemoprophylaxis) has commonly been prescribed for urinary tract
infections. A study by Zegers et al found that this practice can be
safely discontinued, especially in males, patients with low urinary
tract infection rates, and patients without vesicoureteral reflux.
In addition, self-catheterization is recommended by some
surgeons for women during the acute healing process after
anti-incontinence surgery.
Intermittent catheterization may be performed using a soft,
red, rubber catheter or a short, rigid, plastic catheter. The use of
plastic catheters is preferable to red rubber catheters because they are
easier to clean and last longer.
The bladder must be drained on a regular basis, either based
on a timed interval (eg, on awakening, every 3-6 hours during the day,
and before bed) or based on bladder volume. Remember that the average
adult bladder holds approximately 400-500 mL of urine. Ideally, the
amount drained each time should not exceed 400-500 mL. This drainage
limit may require decreasing the fluid intake or increasing the
frequency of catheterizations. If catheterization is performed every 6
hours and the amount drained is 700 mL, increase the frequency of
catheterization to, perhaps, every 4 hours to maintain the volume
drained at 400-500 mL.
Intermittent catheterization is designed to simulate normal
voiding. Usually, the average adult empties the bladder four to five
times a day. Thus, catheterization should occur four to five times a
day; however, individual catheterization schedules may vary, depending
on the amount of fluid taken in during the day.
Candidates for intermittent catheterization must have
motivation and intact physical and cognitive abilities. Anyone who has
good use of her hands and arms can perform self-catheterization. Young
children and the older population are able to do this every day without
problems. For individuals who are impaired, a home caregiver or a
visiting nurse can be instructed to perform intermittent
catheterization. Self-catheterization may be performed almost anywhere,
including at home and at work.
Intermittent catheterization may be performed using either a
sterile catheter or a nonsterile clean catheter. Intermittent
catheterization, using a clean technique, is recommended for young
individuals with a bladder that cannot empty and without any other
available options. Patients should wash their hands with soap and water.
Sterile gloves are not necessary. Clean intermittent catheterization
results in lower rates of infection than the rates noted with indwelling
catheters.
Studies show that in patients with spinal cord injuries, the
incidence of bacteria in the bladder is 1-3% per catheterization, and
one to four episodes of bacteriuria occur per 100 days of intermittent
catheterization performed four times a day. Furthermore, the infections
that do occur usually are managed without complications.
In general, routine use of long-term suppressive therapy with
antibiotics in patients with chronic clean intermittent catheterization
is not recommended. The use of chronic suppressive antibiotic therapy in
people regularly using clean intermittent catheterization is
undesirable because it may result in the emergence of resistant
bacterial strains.
A study of a patients with acute spinal cord injury at 15
North American centers revealed that using a hydrophilic-coated catheter
for intermittent catheterization delayed the onset of first
antibiotic-treated symptomatic urinary tract infections. In addition, a
reduction in incidence of symptomatic urinary tract infection was noted
during inpatient rehabilitation for these patients.
In high-risk populations, such as patients with an internal
prosthesis (eg, artificial heart valve, artificial hip) or patients who
are immunosuppressed because of age or disease, determine whether to use
antibiotic therapy for asymptomatic bacteriuria on individual merits.
For older individuals and those with a weak immune system, the
sterile technique of intermittent catheterization has been recommended.
Older persons are at higher risk than younger persons for developing
bacteriuria and other complications caused by intermittent
catheterization because they do not have a strong defense system against
infection. Although the incidence of infection and other complications
for older patients who are using sterile versus clean intermittent
catheterization is not well established, sterile intermittent
catheterization appears to be the safest method for this high-risk
population.
Potential advantages of performing intermittent
catheterization include patient autonomy, freedom from indwelling
catheter and bags, and unimpeded sexual relations. Potential
complications of intermittent catheterization include bladder infection,
urethral trauma,
urethral inflammation, and stricture. Concurrent use of anticholinergic
therapy will maintain acceptable intravesical pressures and prevent
bladder contracture. Studies have demonstrated that long-term use of
intermittent catheterization appears to be preferable to indwelling
catheterization (ie, urethral catheter, suprapubic tube) with respect to
urinary tract infections and the development of stones within the
bladder or kidneys.
Overall, the management of infections in the setting of
catheters and drainage tubes is challenging. Experimental use of
bacterial interference represents a novel and perhaps effective method
at the prevention of infections; however, at the present time, it is
difficult to do clinically outside of the research setting. Further
studies may prove this modality more clinically useful to practice
environments.
Surgical Care
Surgical care for stress incontinence involves procedures that increase urethral outlet resistance, which include the following:
Surgical care for urge incontinence involves procedures that
improve bladder compliance or bladder capacity, which include the
following:
A Cochrane review that included four randomized controlled
trials of botulinum A toxin injection as a treatment for
detrusor-sphincter dyssynergia (DSD) found that intraurethral injections
might improve some urodynamic measures after 30 days, but the studies
had a high risk of bias, the quality of the evidence was limited, and
the need for reinjection is a significant drawback. The authors advised
that more study of effectiveness needed; optimal dose and mode of
injection remain to be determined, and sphincterotomy might be a more
effective option for long-term treatment.
Diet
The fact that certain foods in a daily diet can worsen
symptoms of urinary frequency and urge incontinence is well known. If a
patient's diet contains dietary stimulants, changes in her diet may help
ameliorate incontinence symptoms. Dietary stimulants are substances
contained in the food or drink that either cause or exacerbate
irritative voiding symptoms. By eliminating or minimizing the intake of
dietary stimulants, unwanted bladder symptoms can be improved or
possibly cured. Avoidance of dietary stimulants begins with consumer
awareness through careful label reading and maintaining a daily diet
diary. Experimenting with dietary changes is not appropriate for
everyone, and dietary experimentation should be instituted on an
individual basis.
Foods
Foods that contain heavy or hot spices may contribute to urge
incontinence. A few medical reports have alluded to the fact that
avoiding spicy foods may have a beneficial effect on urinary
incontinence. Some examples of hot spices include curry, chili pepper,
cayenne pepper, and dry mustard.
A second food group that may worsen irritative voiding
symptoms is citrus fruit. Fruits and juices that have a high potassium
concentration may worsen preexisting urge incontinence. Examples of
fruits that have significant potassium include grapefruits and oranges.
A third food group that may worsen urinary bladder
incontinence is chocolate-containing sweets. Chocolate snacks and treats
contain caffeine. Caffeine is a bladder-unfriendly agent. Excessive
intake of chocolate confectioneries worsens irritative bladder symptoms.
Beverages
The quantity and quality of refreshments consumed will
influence urinary voiding symptoms. An average American adult requires a
daily allowance of approximately 6-8 glasses of fluids. Fluids refer to
all the beverages a person consumes in a day, including water, soda,
and milk. The human body receives water from beverages consumed, water
contained in the food ingested, and water metabolized from food eaten.
The recommended amount of fluids consumed (all types) in 24 hours totals
6-8 glasses. The benefits of adequate fluid intake include prevention
of dehydration, constipation, urinary tract infection, and kidney stone
formation.
Some patients tend to drink water excessively. Some women
drink water because they enjoy the taste. Others take medication that
makes their mouths dry, so they drink more water. Some women who are
trying to lose weight are on a diet that requires consuming abundant
amounts of water. Drinking water excessively actually worsens irritative
bladder symptoms. The exact amount of fluid needed per day is
calculated based on the patient's lean body mass. Thus, the amount of
fluid requirement will vary per individual.
Some older women do not drink enough fluids to keep themselves
well hydrated. They minimize their fluid intake to unacceptable levels,
thinking that if they drink less, they will experience less
incontinence. Trying to prevent incontinence by restricting fluids
excessively may lead to bladder irritation and actually worsen urge
incontinence. In addition, dehydration contributes to constipation. If a
patient has a problem with constipation, recommend eating a high-fiber
diet, receiving adequate hydration, and administering laxatives.
Many drinks contain caffeine. Caffeine is a natural diuretic,
and it has a direct excitatory effect on bladder smooth muscle. Thus,
caffeine-containing products produce excessive urine and exacerbate
symptoms of urinary frequency and urgency. Caffeine-containing products
include coffee, tea, hot chocolate, and sodas. Even chocolate milk and
many over-the-counter medications contain caffeine.
Of caffeine-containing products, coffee contains the most
caffeine. Drip coffee contains the most caffeine, followed by percolated
coffee and then instant coffee. Even decaffeinated coffee contains a
small amount of caffeine. Decaffeinated coffee contains an amount of
caffeine similar to the amount in chocolate milk. Persons who consume a
large amount of caffeine should slowly decrease the amount of caffeine
consumed to avoid significant withdrawal responses such as headache and
depression.
Studies have shown that drinking carbonated beverages, citrus
fruits drinks, and acidic juices may worsen irritative voiding or urge
symptoms. Consumption of artificial sweeteners also has been theorized
to contribute to urge incontinence.
Nighttime voiding and incontinence are major problems in the
older population. Women who have nocturia more than twice a night or
experience nighttime bed-wetting may benefit from fluid restriction and
the elimination of caffeine-containing beverages from their diet in the
evening. Patients should restrict fluids after dinnertime so they can
sleep uninterrupted through the night.
Management of lower-extremity edema
Individuals who develop edema of the lower extremities during
the day experience nighttime voiding because the excess fluid from the
lower extremities returns to the heart with recumbent positioning. This
problem may be treated with a behavior technique, support hose, and/or
medications.
Advise these individuals to elevate their lower extremities
several hours during the late afternoon or evening to stimulate a
natural diuresis and limit the amount of edema present at bedtime.
Support hose (Jobst) or intermittent, sequential compression devices
(SCDs) used briefly at the end of the day can reduce lower extremity
edema and minimize nighttime diuresis, thus improving sleep.
Judicious use of diuretics has been associated with a decrease
in lower-extremity edema and lower nighttime urine volumes. Depending
on other medical conditions, changing the time of administration of the
diuretic to the morning may prevent large nighttime volumes of voiding.
Pelvic floor exercise
Anti-incontinence exercises emphasize rehabilitating and
strengthening the pelvic floor muscles that are critical in maintaining
urinary continence. Pelvic floor muscles also are known as levator ani
muscles because they function to levitate or elevate the pelvic organs
into their proper place. When levator muscles weaken and fail, pelvic
prolapse and stress incontinence result. An anatomic defect of the
levator ani musculature requires physical rehabilitation. If aggressive
physical therapy does not work, surgery is warranted.
Pelvic muscle exercises may be used alone, augmented with
vaginal cones, or reinforced with biofeedback therapy or with electrical
stimulation. Behavioral treatment, including pelvic muscle exercises
and educated use, is a safe and effective intervention that should be a
first-line treatment for urge and mixed incontinence.
Pelvic floor exercises, sometimes called Kegel exercises, are a
rehabilitation technique used to tighten and tone the pelvic floor
muscles. These exercises empower the external urinary sphincter to
prevent stress incontinence and build up the pelvic floor muscles to
avert impending pelvic prolapse. In addition, Kegel exercises may be
performed to eliminate urge incontinence. Contraction of the external
urinary sphincter induces reflex bladder relaxation. Pelvic floor muscle
rehabilitation may be used to reprogram the urinary bladder to decrease
the frequency of incontinence episodes.
Individuals who benefit the most from pelvic floor exercises
tend to be young healthy women who can identify the levator muscles
accurately. Older adults with weak pelvic tone or women who have
difficulty recognizing the right muscles will need adjunct therapy such
as biofeedback or electrical stimulation. Pelvic floor exercises work
best in mild cases of stress incontinence associated with urethral
hypermobility but not intrinsic sphincter deficiency. These
rehabilitation exercises may be used for urge incontinence as well as
mixed incontinence. They also benefit men who develop urinary
incontinence following prostate surgery.
Pelvic floor muscle exercises are performed by drawing in or
lifting up the levator ani muscles as if to control urination or
defecation with minimal contraction of abdominal, buttock, or inner
thigh muscles.
For urge incontinence, pelvic floor muscle exercises are used
to retrain the bladder. When the patient contracts the external urethral
sphincter, the bladder automatically relaxes, so the urge to urinate
eventually subsides. Strong contractions of the pelvic floor muscles
will suppress bladder contractions. Whenever patients feel urinary
urgency, they may try to stop the feeling by contracting the pelvic
floor muscles. These steps will provide the patient more time to walk
slowly to the bathroom with urinary control.
By regularly training the external sphincter, patients can
gradually increase the time between urination from 1-3 hours. Patients
should begin to see improvement in 3-4 weeks. Thus, this technique may
be used for urge symptoms, urge incontinence, and mixed incontinence
(stress and urge incontinence).
When performing these drills, patients should not contract
their abdominal muscles. Contracting the abdominal muscles is
counterproductive and merely worsens urinary incontinence. In general,
tailor a regimented program of exercises and repetitions to each
individual so that the muscle strength increases progressively. Some
patients may need more intensive training than others.
Patients should practice contracting the levator ani muscles
immediately before and during situations when leakage may occur. This
will condition the external sphincter instinctively to contract with
increases in abdominal pressure or when the need to urinate is imminent.
This is known as the guarding reflex. When the patient tightens the
external urinary sphincter just as a sneeze is about to occur, the
involuntary urine loss is thwarted. By squeezing the levator ani muscles
when the patient feels the sense of urgency, the sensation of impending
bladder contraction will dissipate. By making this maneuver a habit,
patients will develop a protective mechanism against stress and urge
incontinence.
The beneficial effects of pelvic floor muscle exercises alone
have been well documented in medical literature. Successful reduction in
urinary incontinence has been reported to range from 56-95%. Pelvic
floor exercises are effective, even after multiple anti-incontinence
surgeries.
Vaginal weights
Vaginal weight training is an effective form of pelvic floor
muscle rehabilitation for stress incontinence in premenopausal women.
Vaginal weights are tamponlike special help aids used to enhance pelvic
floor muscle exercises. Shaped like a small cone, vaginal weights
(identical shape and volume) come in a set of 5, with increasing weights
(ie, 20, 32.5, 45, 60, and 75 g). As part of a progressive resistive
exercise program, a single weight is inserted into the vagina and held
in place by tightening the perivaginal muscles (levator ani muscles) for
as many as 15 minutes. As the levator ani muscles become stronger, the
exercise may be increased to 30 minutes.
This exercise is performed twice daily. The intravaginal
weight provides the sensory feedback for the desired pelvic muscle
contraction. The sustained contraction required to retain the weight
within the vagina increases the strength of the pelvic floor muscles.
The best results are achieved when standard pelvic muscle
exercises (Kegel exercises) are performed with intravaginal weights. In
premenopausal women with stress incontinence, the subjective cure or
improved continence status was approximately 70-80% after 4-6 weeks of
treatment. Vaginal weight training also may be useful for women who are
postmenopausal with stress incontinence; however, vaginal weights are
not effective in the treatment of pelvic organ prolapse.
Biofeedback
Biofeedback therapy is a form of pelvic floor muscle
rehabilitation using an electronic device for individuals having
difficulty identifying levator ani muscles. Biofeedback therapy is
recommended for treatment of stress incontinence, urge incontinence, and
mixed incontinence. Biofeedback therapy uses a computer and electronic
instruments to relay auditory or visual information to the patient about
the status of pelvic muscle activity. These devices allow the patient
to receive immediate visual feedback on the activity of the pelvic floor
muscles.
Biofeedback is an intensive therapy, with weekly sessions
performed in an office or a hospital by a trained professional, and it
often is followed by a regimen of pelvic floor muscle exercises at home.
During a biofeedback therapy, a special tampon-shaped sensor is
inserted in the patient's vagina or rectum and a second sensor is placed
on her abdomen. These sensors detect electrical signals from the pelvic
floor muscles. The patient is instructed to contract and relax the
pelvic floor muscles upon command. When the exercises are performed
properly, the electric signals from the pelvic floor muscles are
registered on a computer screen. Biofeedback, using multi-measurement
recording, displays the simultaneous measurement of pelvic and abdominal
muscle activity on the computer monitor.
Biofeedback allows the patient to correctly identify the
pelvic muscles that need rehabilitation. The benefit of biofeedback
therapy is that it provides the patient with minute-by-minute feedback
on the quality and intensity of her pelvic floor contraction. Combining
bladder and urinary sphincter biofeedback allows the patient to regulate
the pelvic muscle contraction in response to increasing bladder volumes
and to monitor the bladder activity. Biofeedback is best used in
conjunction with pelvic floor muscle exercises and bladder training.
Studies on biofeedback combined with pelvic floor exercises
show a 54-87% improvement with incontinence. The best biofeedback
protocol is one that reinforces levator ani muscle contraction with
inhibition of abdominal and bladder contraction. Reports using this
method show a 76-82% reduction in urinary incontinence. Biofeedback also
has been used successfully in treatment of men with urge incontinence
and intermittent stress incontinence after prostate surgery.
Medical studies have demonstrated significant improvement in
urinary incontinence in women with neurologic disease and in the frail
older population when a combination of biofeedback and bladder training
is used. Biofeedback provides a specific reinforcement for pelvic muscle
contraction that is isolated from the counterproductive abdominal
contraction. Therefore, awareness of levator ani muscle contraction can
be achieved more efficiently using biofeedback than vaginal palpation
alone.
Biofeedback produces a greater reduction in female urinary
incontinence compared to pelvic muscle exercises alone. Overall, the
medical literature indicates that pelvic muscle exercises and other
behavioral strategies, with or without biofeedback, can cure or reduce
incontinence. However, the maximum benefit is derived from any pelvic
muscle rehabilitation and education program when ongoing reinforcement
and guidance, such as biofeedback therapy, are provided.
Electrical stimulation
Electrical stimulation is a more sophisticated form of
biofeedback used for pelvic floor muscle rehabilitation. This treatment
involves stimulation of levator ani muscles using painless electric
shocks. Electrical stimulation of pelvic floor muscles produces a
contraction of the levator ani muscles and external urethral sphincter
while inhibiting bladder contraction. This therapy depends on a
preserved reflex arc through the intact sacral micturition center. Like
biofeedback, electrical stimulation can be performed at the office or at
home. Electrical stimulation can be used in conjunction with
biofeedback or pelvic floor muscle exercises.
Electrical stimulation therapy requires a similar type of
probe and equipment as those used for biofeedback. This form of muscle
rehabilitation is similar to the biofeedback therapy, except small
electric shocks are used. Nonimplantable pelvic floor electrical
stimulation uses vaginal sensors, anal sensors, or surface electrodes.
Adverse reactions are minimal.
Like biofeedback, pelvic floor muscle electrical stimulation
has been shown to be effective in treating female stress incontinence,
as well as urge and mixed incontinence. Electrical stimulation may be
most beneficial when stress incontinence and very weak or damaged pelvic
floor muscles coexist. A regimented program of electrical stimulation
will help these weakened pelvic muscles contract so they can become
stronger. For women with urge incontinence, electrical stimulation may
help the bladder relax and prevent it from contracting involuntarily.
Research indicates that pelvic floor electrical stimulation
can reduce urinary incontinence significantly in women with stress
incontinence and may be effective in men and women with urge and mixed
incontinence. Incidence of urge incontinence secondary to neurologic
diseases may be decreased with this therapy. Electrical stimulation
appears to be most effective when augmented with pelvic floor exercises.
Long-term data report that with electrical stimulation the rate of
cured or improved patients ranged from 54-77%; however, in order to
derive significant benefit, perform stimulation for a minimum of 4
weeks. Patients must continue pelvic floor exercises after the
treatment. Unfortunately, this treatment does not appear to benefit
cognitively impaired patients.
Bladder training
Bladder training involves relearning how to urinate. This
method of rehabilitation most often is used for active women with urge
incontinence and sensory urge symptoms. Often, patients find that when
they respond to symptoms of urge and return to the bathroom soon after
they have voided, they do not expel significant urine. In other words,
though the bladder is not full, it is signaling that it is time to void.
Bladder training generally consists of self-education,
scheduled voiding with conscious delay of voiding, and positive
reinforcement. Although bladder training is used primarily for urge
incontinence, this program may be used for simple stress incontinence
and mixed incontinence. Bladder training requires the patient to resist
or inhibit the sensation of urgency and postpone voiding. Patients
urinate according to a scheduled timetable rather than the symptoms of
urge.
Bladder training uses dietary tactics such as adjustment of
fluid intake and avoidance of dietary stimulants. In addition,
distraction and relaxation techniques allow delayed voiding to help
distend the urinary bladder. By using these strategies, patients can
induce the bladder to accommodate progressively larger voiding volumes.
Initially, the interval goal is determined by the patient's
current voiding habits and is not enforced at night. Regardless of the
initial voiding pattern, the first voiding interval may be increased by
15- to 30-minute increments. As the bladder becomes accustomed to this
delay in voiding, the interval between mandatory voids is increased
progressively, with simultaneous distraction or relaxation techniques
and dietary modification. The interval goal between each void usually is
set between 2 and 3 hours and may be set further apart if desired.
Another method of bladder training is to maintain the
prearranged schedule and disregard the unscheduled voids. However,
patients need to continue to maintain the prearranged voiding times.
They will need to continue this program for several months.
Alternatively, bladder ultrasound may be employed. If patients
need an objective demonstration that their bladder is relatively empty,
a portable bladder scanner may be used. A bladder scanner is a portable
ultrasound machine that measures the amount of urine present in a
patient's bladder. With this device, patients can void when their
bladder fills to a certain volume rather than responding to the
sensation of needing to go to the bathroom. When patients feel the need
to void, they can check the bladder using the scanner to see how much
urine is present. If the bladder is empty, patients should ignore the
sensation of needing to go to the bathroom.
Bladder training has been used primarily to manage urge
incontinence; however, it also may be used for stress and mixed
incontinence. This form of training is useful in young women but is
difficult to implement in cognitively impaired persons. Bladder training
may not be successful in frail women who are older. Medical reports
demonstrate that bladder training is effective in reducing urinary
incontinence. With bladder training, the rate of patients with mixed
incontinence that have been cured is reported to be 12%, while the
improvement rate was 75% after 6 months.
Medications Used to Treat Neurogenic Bladder
Stress incontinence results from a weak urinary sphincter. The
internal sphincter contains high concentrations of alpha-adrenergic
receptors. Activation of the alpha-receptors results in contraction of
the internal urethral sphincter and increases the urethral resistance to
urinary flow. Sympathomimetic drugs, estrogen, and tricyclic agents
increase bladder outlet resistance to improve symptoms of stress urinary
incontinence. Medical conditions that cause urge incontinence may be
neurologic or nonneurologic. The urethra is normal, but the bladder is
hyperactive or overactive. Pharmacologic therapy for stress incontinence
and an overactive bladder may be most effective when combined with a
pelvic exercise regimen. The 3 main categories of drugs used to treat
urge incontinence include anticholinergic drugs, antispasmodics, and
tricyclic antidepressant agents.
All drugs with anticholinergic adverse effects are
contraindicated if patients have documented narrow-angle glaucoma.
Wide-angle glaucoma is not a contraindication to their use. Urinary
retention, bowel obstruction, ulcerative colitis, myasthenia gravis, and
severe heart diseases are contraindications for anticholinergic use.
These agents may impair the patient's ability to perform hazardous
activities, such as driving or operating heavy machinery, because of the
potential for drowsiness. Anticholinergic drugs should not be taken in
combination with alcohol, sedatives, or hypnotic drugs.
When a single drug treatment does not work, combination
therapy, such as oxybutynin (Ditropan) and imipramine (Tofranil) may be
used. Although their mechanism of action differs, oxybutynin and
imipramine work together to improve urge incontinence. Oxybutynin causes
direct smooth muscle relaxation of the urinary bladder and has local
anesthetic properties. Imipramine has a direct inhibitory and local
anesthetic effect on the bladder smooth muscle, like oxybutynin;
however, imipramine also increases the bladder outlet resistance at the
level of the bladder neck. Thus, the combination of these drugs produces
a synergistic effect to relax the unstable bladder to hold in urine and
prevent urge incontinence. Potential anticholinergic adverse effects
may be additive because both drugs have similar adverse reactions.
Estrogen derivatives
Conjugated estrogen increases the tone of urethral muscle by
up-regulating the alpha-adrenergic receptors in the surrounding area and
enhances alpha-adrenergic contractile response to strengthen pelvic
muscles, which is important in urethral support (prevents urethral
hypermobility). Mucosal turgor of periurethral tissue from proper
nourishment enhances urethral mucosal coaptation. Result is an improved
mucosal seal effect, which is important in urethral function (prevents
intrinsic sphincter deficiency). Estrogen supplementation appears to be
the most effective in postmenopausal women with mild-to-moderate
incontinence. Both types of stress incontinence benefit from estrogen
fortification.
Pharmacologic therapy using estrogen derivatives results in
few cures (0-14%) but may cause subjective improvement in 29-66% of
women. Limited evidence suggests that oral or vaginal estrogen therapy
may benefit some women with stress and mixed urinary incontinence. Other
potential beneficial effects of estrogen use include decreased bone
loss and resolution of hot flashes during menopause.
When estrogen is used long-term, addition of progestin therapy
is recommended to prevent endometrial hyperplasia in women with an
intact uterus. Progestin (eg, medroxyprogesterone
2.5-10 mg/d) is needed for 10-13 d to provide maximum maturation of
endometrium and to eliminate any hyperplastic changes. Progestin may be
administered continuously or intermittently.
Conjugated estrogen (Premarin)
Conjugated estrogen
may be used as an adjunctive pharmacologic agent for women who are
postmenopausal with stress or mixed incontinence. The oral or vaginal
form of estrogen may be used. Premarin vaginal cream is available in a
package with a plastic applicator and a tube that contains 42.5 g of
conjugated estrogens. Each gram contains 0.625 mg of conjugated
estrogens. Estrogen cream is readily absorbed through the skin and
mucous membranes.
Routinely prescribing conjugated estrogens to premenopausal
women is not recommended. Use medication in women who are postmenopausal
and incontinent and who have had a hysterectomy. For postmenopausal
women with an intact uterus, cautiously recommend a short-term low-dose
regimen of Premarin with frequent monitoring.
Adult dosing is 0.625 mg PO qd for 21 consecutive days,
followed by 7 days without the drug (eg, 3 wk on and 1 wk off); repeat
the regimen prn and taper off or discontinue at 3- to 6-mo intervals.
Two to four grams (0.5-1 applicator) of cream may be administered
intravaginally qd in a usual cyclic regimen. Pediatric dosing has not
been established.
Conjugated estrogen is a pregnancy category X drug.
Anticholinergic drugs
Anticholinergic drugs are the first line medicinal therapy in
women with urge incontinence. They are effective in treating urge
incontinence because they inhibit involuntary bladder contractions. They
are also useful in treating urinary incontinence associated with
urinary frequency, urgency, and nocturnal enuresis. All anticholinergic
drugs have similar performance profiles and toxicity. Potential adverse
effects of all anticholinergic agents include blurred vision, dry mouth,
heart palpitations, drowsiness, and facial flushing. When
anticholinergic drugs are used in excess, acute urinary retention in the
bladder may occur.
Propantheline bromide (Pro Banthine)
Propantheline bromide
is the typical prototype for all anticholinergic agents. It blocks
action of acetylcholine at postganglionic parasympathetic receptor
sites. In a medical study, propantheline bromide was shown to decrease
incidence of urge incontinence by 13-17% when 30 mg was used qid. When
stronger doses were used (60 mg qid), the cure rate was reported to be
over 90%.
Adult dosing is 15 mg PO tid/qid. Pediatric dosing has not been established.
Propantheline bromide is a pregnancy category C drug.
Dicyclomine hydrochloride (Bentyl)
Dicyclomine hydrochloride
is an anticholinergic agent with smooth muscle relaxant properties. It
blocks the action of acetylcholine at parasympathetic sites in secretory
glands and smooth muscle. In a medical study, subjective improvement
was reported by 62% of the subjects while taking dicyclomine
hydrochloride 10 mg tid. The reported cure rate was 90%.
Adult dosing is 10-20 mg PO tid. Pediatric dosing has not been established.
Dicyclomine hydrochloride is a pregnancy category B drug.
Hyoscyamine sulfate (Levsin/SL, Levsin, Levsinex, Cystospaz M, Levbid)
Hyoscyamine sulfate
is an anticholinergic agent with antispasmodic properties used for the
treatment of urge incontinence. It blocks the action of acetylcholine at
parasympathetic sites in smooth muscle, secretory glands, and the CNS,
which in turn has antispasmodic effects. It is absorbed well by the GI
tract. Food does not affect absorption. Hyoscyamine sulfate is available
in sublingual form (Levsin SL), conventional tablets (Levsin),
extended-release capsules (Levsinex Timecaps, Cystospaz-M), and
extended-release tablets (Levbid).
Adult dosing is 0.125 mg PO q4h; alternatively, 0.375 mg PO
bid can be used. For severe symptoms, dosing is 0.375 mg PO tid.
Pediatric dosing has not been established.
Hyoscyamine sulfate is a pregnancy category C drug.
Antispasmodic drugs
These relax the smooth muscles of the urinary bladder. By
exerting a direct spasmolytic action on the smooth muscle of the
bladder, antispasmodic drugs have been reported to increase bladder
capacity and effectively decrease or eliminate urge incontinence. The
adverse-effect profile of antispasmodic drugs is similar to that of
anticholinergic agents. These drugs may impair the patient's ability to
perform activities requiring mental alertness and physical coordination.
Drinking alcohol and using sedatives in combination with these
antispasmodic drugs is contraindicated.
Solifenacin succinate (VESIcare)
Solifenacin succinate
elicits competitive muscarinic receptor antagonist activity, which
results in anticholinergic effect and inhibition of bladder smooth
muscle contraction. It is indicated for overactive bladder with symptoms
of urgency, frequency, and urge incontinence.
Adult dosing is 5 mg PO qd; if tolerated, it may be increased to 10 mg PO qd.
Pediatric dosing has not been established.
Solifenacin succinate is a pregnancy category C drug.
Darifenacin (Enablex)
Darifenacin
is an extended-release product that elicits competitive muscarinic
receptor antagonistic activity. It reduces bladder smooth muscle
contractions. It has a high affinity for M
3 receptors
involved in bladder and GI smooth muscle contraction, saliva production,
and iris sphincter function. Darifenacin is indicated for overactive
bladder with symptoms of urge incontinence, urgency, and frequency. The
product should be swallowed whole; do not chew, divide, or crush.
Adult dosing is 7.5 mg PO qd initially; after 2 wk, the dose
may be increased to 15 mg PO qd based on response. Do not exceed 7.5 mg
PO qd in patients with moderate hepatic impairment (Child-Pugh class B)
or who are receiving potent CYP-450 3A4 inhibitors. Pediatric dosing has
not been established.
Darifenacin is a pregnancy category C drug.
Oxybutynin chloride (Ditropan IR, Ditropan XL)
Oxybutynin chloride
has both anticholinergic and direct smooth muscle relaxant effects on
urinary bladder. It provides a local anesthetic effect on irritable
bladder. Urodynamic studies have shown oxybutynin increases bladder
size, decreases frequency of symptoms, and delays initial desire to
void.
Ditropan XL has an innovative drug delivery system—oral
osmotic delivery system (OROS). The Ditropan XL tablet has a bilayer
core that contains a drug layer and a push layer that contains osmotic
components. The outer tablet is composed of a semipermeable membrane
with a precision laser-drilled hole that allows the drug to be released
at a constant rate.
When the drug is ingested, the aqueous environment in the GI
tract causes water to enter the tablet via the semipermeable membrane at
constant rate. Introduction of water inside the tablet liquifies the
drug and causes the push layer to swell osmotically. As the push layer
swells, it forces the drug suspension out of the hole at a constant rate
over a 24-h period.
Ditropan XL achieves steady-state levels over a 24-h period.
It avoids first-pass metabolism of the liver and upper GI tract to avoid
cytochrome P450 enzymes. It has excellent efficacy with minimal adverse
effects.
Medical studies have shown that oxybutynin chloride reduces
incontinence episodes by 83-90%. The total continence rate has been
reported to be 41-50%. The mean reduction in urinary frequency was 23%.
In clinical trials, only 1% stopped taking Ditropan XL because of dry
mouth, and less than 1% stopped taking Ditropan XL due to CNS adverse
effects.
Adult dosing of Ditropan IR is 2.5 mg PO tid, titrate prn to 5
mg bid/tid/qid. Dosing of Ditropan XL is 5-15 mg PO qd. Pediatric
dosing has not been established.
Oxybutynin chloride is a pregnancy category B drug.
Tolterodine L-tartrate (Detrol and Detrol LA)
Tolterodine L-tartrate
is a competitive muscarinic receptor antagonist for overactive bladder.
It differs from other anticholinergic types in that it has selectivity
for urinary bladder over salivary glands. It exhibits high specificity
for muscarinic receptors and has minimal activity or affinity for other
neurotransmitter receptors and other potential targets such as calcium
channels. In clinical studies, the mean decrease in urge incontinence
episodes was 50% and the mean decrease in urinary frequency was 17%.
Adult dosing of Detrol is 2 mg PO bid. Dosing of Detrol LA is 4 mg PO qd. Pediatric dosing has not been established.
Tolterodine L-tartrate is a pregnancy category C drug.
Trospium (Sanctura)
Trospium
is a quaternary ammonium compound that elicits antispasmodic and
antimuscarinic effects. It antagonizes acetylcholine effect on
muscarinic receptors. Parasympathetic effect reduces smooth muscle tone
in the bladder. Trospium is indicated to treat symptoms of overactive
bladder (eg, urinary incontinence, urgency, frequency).
Adult dosing is 20 mg PO bid; it should be taken on an empty
stomach at least 1 h before meals. In patients with a CrCl < 30
mL/min, dosing is 20 mg PO hs. In patients >75 years, dosing may be
titrated downward to 20 mg PO qd based on tolerability. Pediatric dosing
has not been established.
Trospium is a pregnancy category C drug.
Fesoterodine (Toviaz)
Fesoterodine
is a competitive muscarinic receptor antagonist. The antagonistic
effect results in decreased bladder smooth muscle contractions. It is
indicated for symptoms of overactive bladder (eg, urinary urge
incontinence, urgency, and frequency). Fesoterodine is available as a 4-
or 8-mg extended-release tab.
Adult dosing is 4 mg PO qd; it may be increased to 8 mg/d.
Dosing is not to exceed 4 mg PO qd in severe renal dysfunction (ie, CrCl
< 30 mL/min) or with coadministration of drugs that decrease
fesoterodine’s metabolism (eg, ketoconazole, itraconazole,
clarithromycin). Pediatric dosing has not been established.
Fesoterodine is a pregnancy category C drug.
Tricyclic antidepressant drugs
Historically, these drugs were used to treat major depression;
however, they have an additional use that is not FDA approved—treatment
of bladder dysfunction. They function to increase norepinephrine and
serotonin levels. In addition, they exhibit anticholinergic and direct
muscle relaxant effects on the urinary bladder.
Imipramine hydrochloride (Tofranil)
Imipramine hydrochloride
is a typical tricyclic antidepressant. It facilitates urine storage by
decreasing bladder contractility and increasing outlet resistance. It
has alpha-adrenergic effect on the bladder neck and antispasmodic effect
on detrusor muscle. Imipramine hydrochloride has a local anesthetic
effect on bladder mucosa.
Adult dosing is 10-50 mg PO qd/tid; the range is 25-100 mg qd. Pediatric dosing has not been established.
Imipramine hydrochloride is a pregnancy category D drug.
Amitriptyline hydrochloride (Elavil)
Amitriptyline hydrochloride
is a tricyclic antidepressant with sedative properties. It increases
circulating levels of norepinephrine and serotonin by blocking their
reuptake at nerve endings and is ineffective for use in urge
incontinence. However, it is extremely effective in decreasing symptoms
of urinary frequency in women with pelvic floor muscle dysfunction.
Amitriptyline hydrochloride restores serotonin levels and helps break
the cycle of pelvic floor muscle spasms. It is well-tolerated and
effective in most women with urinary frequency.
Adult dosing is 10 mg/d PO; titrate prn by 10 mg/wk until
maximum dose of 150 mg is reached, urinary symptoms disappear, or
adverse effects become intolerable. Pediatric dosing has not been
established.
Amitriptyline hydrochloride is a pregnancy category D drug.
Follow-up
Complications
Prolonged contact of urine with unprotected skin causes
contact dermatitis and skin breakdown. If left untreated, these skin
disorders may lead to pressure sores and ulcers, possibly resulting in
secondary infections. For individuals with a decompensated bladder that
does not empty well, the postvoid residual urine can lead to overgrowth
of bacteria and subsequent urinary tract infection. Untreated urinary
tract infections may lead to urosepsis and death.
Complications of specific interventions include the following:
-
Long-term indwelling catheters may cause recurrent bladder
infection, bladder stones, ascending pyelonephritis, and urethral
erosion
-
Intermittent catheterization may result in bladder infections or urethral injury
-
Long-term suprapubic tubes may result in bladder spasms, bladder stone formation, and bladder infection
-
Potential problems unique to suprapubic catheters include skin
infection, hematoma, bowel injury, and problems with catheter
reinsertion
Prognosis
Prognosis of a patient with incontinence is excellent with
modern health care. With improvement in information technology,
well-trained medical staff, and advances in modern medical knowledge,
patients who are incontinent should not experience the morbidity and
mortality of the past. Although the ultimate well being of a patient who
is incontinent depends on the underlying condition that has
precipitated urinary incontinence, urinary incontinence itself is easily
treated and prevented by properly trained health care personnel.
Patient education
For patient education information, see Bladder Control Problems, Bladder Control Medications, Inability to Urinate, and Foley Catheter.
Medical/legal pitfalls
Failure to diagnose and treat urinary retention may result in adverse consequences.
Rule out narrow-angle glaucoma prior to prescribing an
anticholinergic agent. Narrow-angle glaucoma may be converted to
open-angle glaucoma by an experienced ophthalmologist.
When patients are taking anticholinergic agents, monitor these patients to prevent pharmacologically induced urinary retention.
