Neurogenic Bladder

Overview
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 phasesfilling 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 tractthe 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-Barr 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 retentiondetrusor 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 statedetrusor 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 5090% 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
Pyridium or Urised may be used. Methylene blue and Urised turns the urine color blue; Pyridium
turns the urine color orange.
Patients should resume their usual physical activities while wearing a Peri-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. 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 precise role of cystoscopy in the evaluation of neurogenic bladder allows discovery of
bladder lesions (eg, bladder cancer, bladder stone) that would remain undiagnosed by
urodynamics alone.
General agreement is that cystoscopy is indicated for people 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

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:
(1) women who fail all other treatments and remain incontinent, (2) women who are too ill or
disabled to participate in behavioral programs, (3) women who cannot be helped by medications,
(4) women with incontinence disorders that cannot be corrected by surgery, and (5) women who
are 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 lessthan-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.[1] c
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. Chronic dependence on these catheters is extremely
risky because 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
3 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: (1) as comfort measures for
the terminally ill, (2) to avoid contamination or to promote healing of severe pressure sores, (3)
in case of inoperable urethral obstruction that prevents bladder emptying, (4) in individuals who
are severely impaired and for whom alternative interventions are not an option, (5) when an
individual lives alone and a caregiver is unavailable to provide other supportive measures, (6) for
acutely ill persons in whom accurate fluid balance must be monitored, and (7) 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 people who are paraplegic and people who are quadriplegic 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, change the suprapubic tube 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 catheters 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.[2]
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 4-5 times a day. Thus, catheterization should occur 4-5 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 selfcatheterization. Young children and the older population are able to do this everyday 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 at
home, at workanywhere.

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 1-4 episodes of bacteriuria occur per 100 days of intermittent
catheterization performed 4 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.[3]
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 the older population and individuals with a weak immune system, the sterile technique of
intermittent catheterization has been recommended. Persons who are older 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.[4]

Surgical Care

Surgical care for stress incontinence involves procedures that increase urethral outlet resistance.
Operations that increase urethral resistance include bladder neck suspension, periurethral bulking
therapy, sling procedures, and artificial urinary sphincter.
Surgical care for urge incontinence involves procedures that improve bladder compliance or
bladder capacity; these include sacral neuromodulation, botulinum toxin injections,[5, 6] detrusor
myomectomy, and bladder augmentation.
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.
Certain food products exacerbate symptoms of urge incontinence.
Food

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.
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 in a recumbent
position. 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.
Activity

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. They are named levator 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 used as a first-line
treatment for urge and mixed incontinence. If the patient is using abdominal muscles or
contracting their buttocks, they are not doing these exercises properly. If patients have difficulty
identifying the levator muscles, biofeedback therapy may be instituted. For selected individuals,
electrical stimulation further enhances pelvic muscle rehabilitation therapy.
Pelvic floor exercise

Pelvic floor exercise refers to strengthening the levator muscles lining the floor of the bony
pelvis. The first step in pelvic muscle rehabilitation is to establish a better awareness of the
levator muscle function. Pelvic floor exercises, sometimes called Kegel exercises, are a
rehabilitation technique used to tighten and tone the pelvic floor muscles (ie, levator ani) that
have become weak over time. 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 multimeasurement 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 shortterm 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 M3
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 systemoral 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 4or 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 fesoterodines 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 approvedtreatment 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.
Chronic indwelling catheters may cause recurrent bladder infection, bladder stones, ascending
pyelonephritis, and urethral erosion.
The use of intermittent catheterization may result in bladder infections or urethral injury.
Chronic 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.

Untreated urinary tract infections may lead to urosepsis and death.

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 individuals.
Patient education

For excellent patient education resources, see eMedicineHealth's patient education articles
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.