Neurogenic Bladder
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Dr. R Medanki
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Neurogenic Bladder
Author: Raymond R Rackley, MD; Chief Editor: Edward David Kim, MD, FACS more...
Updated: Dec 6, 2013
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
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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.
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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, suprasacralinfrapontine spinal cord trauma can cause overstimulation of the pudendal nerve, resulting in urinary retention.
Physiology and Pathophysiology
Physiology
During the course of a day, an average person will void approximately 4-8 times. The urinary bladder is in
storage mode for most of the day, allowing an individual to engage in more important activities than urination.
Normal bladder function consists of 2 phases—filling and emptying. The normal micturition cycle requires that
the urinary bladder and the urethral sphincter work together as a coordinated unit to store and empty urine.
During urinary storage, the bladder acts as a low-pressure receptacle, while the urinary sphincter maintains
high resistance to urinary flow to keep the bladder outlet closed. During urine elimination, the bladder contracts
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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
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primitive voiding reflex may reappear in people with spinal cord injuries.
Delaying voiding or voluntary voiding
Bladder function is automatic but completely governed by the brain, which makes the final decision on whether
or not to void. The normal function of urination means that an individual has the ability to stop and start urination
on command. In addition, the individual has the ability to delay urination until a socially acceptable time and
place. The healthy adult is aware of bladder filling and can willfully initiate or delay voiding.
In a healthy adult, the PMC functions as an on-off switch that is activated by stretch receptors in the bladder
wall and is, in turn, modulated by inhibitory and excitatory neurologic influences from the brain. When the
bladder is full, the stretch receptors are activated. The individual perceives the activation of the stretch
receptors as the bladder being full, which signals a need to void.
When an individual cannot find a bathroom nearby, the brain bombards the PMC with a multitude of inhibitory
signals to prevent detrusor contractions. At the same time, an individual may actively contract the levator
muscles to keep the external sphincter closed or initiate distracting techniques to suppress urination.
Thus, the voiding process requires coordination of both the ANS and somatic nervous system, which are in turn
controlled by the PMC located in the brainstem.
Pathophysiology
If a problem occurs within the nervous system, the entire voiding cycle is affected. Any part of the nervous
system may be affected, including the brain, pons, spinal cord, sacral cord, and peripheral nerves. A
dysfunctional voiding condition results in different symptoms, ranging from acute urinary retention to an
overactive bladder or to a combination of both.
Urinary incontinence results from a dysfunction of the bladder, the sphincter, or both. Bladder overactivity
(spastic bladder) is associated with the symptoms of urge incontinence, while sphincter underactivity
(decreased resistance) results in symptomatic stress incontinence. A combination of detrusor overactivity and
sphincter underactivity may result in mixed symptoms.
Brain lesion
Lesions of the brain above the pons destroy the master control center, causing a complete loss of voiding
control. The voiding reflexes of the lower urinary tract—the primitive voiding reflex—remain intact. Affected
individuals show signs of urge incontinence, or spastic bladder (medically termed detrusor hyperreflexia or
overactivity). The bladder empties too quickly and too often, with relatively low quantities, and storing urine in
the bladder is difficult. Usually, people with this problem rush to the bathroom and even leak urine before
reaching their destination. They may wake up frequently at night to void.
Typical examples of a brain lesion are stroke, brain tumor, or Parkinson disease. Hydrocephalus, cerebral palsy,
and Shy-Drager syndrome also are brain lesions. Shy-Drager syndrome is a rare condition that also causes the
bladder neck to remain open.
Spinal cord lesion
Diseases or injuries of the spinal cord between the pons and the sacral spinal cord also result in spastic bladder
or overactive bladder. People who are paraplegic or quadriplegic have lower extremity spasticity. Initially, after
spinal cord trauma, the individual enters a spinal shock phase where the nervous system shuts down. After
6-12 weeks, the nervous system reactivates. When the nervous system becomes reactivated, it causes
hyperstimulation of the affected organs. For example, the legs become spastic.
These people experience urge incontinence. The bladder empties too quickly and too frequently. The voiding
disorder is similar to that of the brain lesion except that the external sphincter may have paradoxical
contractions as well. If both the bladder and external sphincter become spastic at the same time, the affected
individual will sense an overwhelming desire to urinate but only a small amount of urine may dribble out. The
medical term for this is detrusor-sphincter dyssynergia because the bladder and the external sphincter are not
in synergy. Even though the bladder is trying to force out urine, the external sphincter is tightening to prevent
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urine from leaving.
The causes of spinal cord injuries include motor vehicle and diving accidents. Multiple sclerosis (MS) is a
common cause of spinal cord disease in young women. Those with MS also may exhibit visual disturbances,
known as optic neuritis. Children born with myelomeningocele may have spastic bladders and/or an open
urethra. Conversely, some children with myelomeningocele may have a hypocontractile bladder instead of a
spastic bladder.
Sacral cord injury
Selected injuries of the sacral cord and the corresponding nerve roots arising from the sacral cord may prevent
the bladder from emptying. If a sensory neurogenic bladder is present, the affected individual may not be able
to sense when the bladder is full. In the case of a motor neurogenic bladder, the individual will sense the
bladder is full and the detrusor may not contract, a condition known as detrusor areflexia. These individuals
have difficulty eliminating urine and experience overflow incontinence; the bladder gradually overdistends until
the urine spills out. Typical causes are a sacral cord tumor, herniated disc, and injuries that crush the pelvis.
This condition also may occur after a lumbar laminectomy, radical hysterectomy, or abdominoperineal resection.
Some teenagers suddenly develop an abnormal voiding pattern and often are evaluated for tethered cord
syndrome, a neurologic condition in which the tip of the sacral cord is stuck near the sacrum and cannot stretch
as the child grows taller. Ischemic changes of the sacral cord associated with the tethering cause the
manifestation of dysfunctional voiding symptoms.
Peripheral nerve injury
Diabetes mellitus and AIDS are 2 of the conditions causing peripheral neuropathy resulting in urinary retention.
These diseases destroy the nerves to the bladder and may lead to silent, painless distention of the bladder.
Patients with chronic diabetes lose the sensation of bladder filling first, before the bladder decompensates.
Similar to injury to the sacral cord, affected individuals will have difficulty urinating. They also may have a
hypocontractile bladder.
Other diseases manifesting this condition are poliomyelitis, Guillain-Barré syndrome, severe herpes in the
genitoanal area, pernicious anemia, and neurosyphilis (tabes dorsalis).
Summary of definitions
Neurogenic bladder is a malfunctioning bladder due to any type of neurologic disorder.
Detrusor hyperreflexia refers to overactive bladder symptoms due to a suprapontine upper motor neuron
neurologic disorder. External sphincter functions normally. The detrusor muscle and the external sphincter
function in synergy (in coordination).
DSD-DH refers to overactive bladder symptoms due to neurologic upper motor neuron disorder of the
suprasacral spinal cord. Paradoxically, the patient is in urinary retention. Both the detrusor and the sphincter are
contracting at the same time; they are in dyssynergy (lack of coordination).
Detrusor hyperreflexia with impaired contractility (DHIC) refers to overactive bladder symptoms, but the detrusor
cannot generate enough pressure to allow complete emptying. The external sphincter is in synergy with
detrusor contraction. The detrusor is too weak to mount an adequate contraction for proper voiding to occur.
The condition is similar to urinary retention, but irritating voiding symptoms are prevalent.
Detrusor instability refers to overactive bladder symptoms without neurologic impairment. External sphincter
functions normally, in synergy.
Overactive bladder refers to symptoms of urinary urgency, with or without urge incontinence, usually associated
with frequency and nocturia. The cause may be neurologic or nonneurologic.
Detrusor areflexia is complete inability of the detrusor to empty due to a lower motor neuron lesion (eg, sacral
cord or peripheral nerves).
Urinary retention is the inability of the urinary bladder to empty. The cause may be neurologic or nonneurologic.
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Types of Neurogenic Bladders
Supraspinal Lesions
Supraspinal lesions refer to those lesions of the central nervous system involving the area above the pons.
They include cerebrovascular accident, brain tumor, Parkinson disease, and Shy-Drager syndrome.
Cerebrovascular accident
After a stroke, the brain may enter into a temporary acute cerebral shock phase. During this time, the urinary
bladder will be in retention—detrusor areflexia. Almost 25% of affected individuals develop acute urinary
retention after a stroke.
After the cerebral shock phase wears off, the bladder demonstrates detrusor hyperreflexia with coordinated
urethral sphincter activity. This occurs because the PMC is released from the cerebral inhibitory center. When
the patient manifests symptoms of detrusor hyperreflexia, the individual will complain of urinary frequency,
urgency, and urge incontinence.
The treatment for the cerebral shock phase is indwelling Foley catheter or clean intermittent catheterization
(CIC). When the bladder becomes hyperreflexic, institute therapies to facilitate bladder filling and storage with
anticholinergic medications.
Brain tumor
Detrusor hyperreflexia with coordinated urethral sphincter is the most common observed urodynamic pattern
associated with a brain tumor.
When the patient manifests symptoms of detrusor hyperreflexia, the individual complains of urinary frequency,
urgency, and urge incontinence. First-line treatment for detrusor hyperreflexia includes anticholinergic
medication.
Parkinson disease
This is a degenerative disorder of pigmented neurons of substantia nigra. It results in dopamine deficiency and
increased cholinergic activity in the corpus striatum.
Patients with Parkinson disease manifest symptoms of bradykinesia, skeletal muscle tremor, cogwheel rigidity,
and masked facies. Symptoms specific to the urinary bladder include urinary frequency, urgency, nocturia, and
urge incontinence.
Typical urodynamic findings for Parkinson disease are most consistent with detrusor hyperreflexia and urethral
sphincter bradykinesia. The striated urethral sphincter often demonstrates poorly sustained contraction.
Similar to other supraspinal lesions, the treatment for Parkinson disease is to facilitate bladder filling and
promote urinary storage with anticholinergic agents.
If patients with Parkinson disease exhibit symptoms of bladder outlet obstruction (BOO) due to benign prostatic
enlargement (BPE), the diagnosis of BOO should be confirmed by multichannel urodynamic studies. The most
common cause of postprostatectomy incontinence in the patient with Parkinson disease is detrusor
hyperreflexia.
If transurethral resection of the prostate (TURP) is performed without urodynamic confirmation of obstruction,
the patient may become totally incontinent after the TURP procedure.
Shy-Drager syndrome
Shy-Drager syndrome is a rare, progressive, and degenerative disease affecting the ANS with multisystem
organ atrophy. In addition to Parkinson-like symptoms, cerebellar ataxia and autonomic dysfunction are
common. Affected individuals demonstrate orthostatic hypotension, anhidrosis, and urinary incontinence.
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Degeneration of the nucleus of Onuf results in denervation of the external striated sphincter. Sympathetic nerve
atrophy causes nonfunctional bladder and an open bladder neck.
Urodynamic evaluation often reveals detrusor hyperreflexia, although a few individuals may have detrusor
areflexia or poorly sustained bladder contractions. Often, the bladder neck (internal sphincter) will be open at
rest, with striated sphincter denervation.
The treatment for Shy-Drager syndrome is to facilitate urinary storage with anticholinergic agents coupled with
CIC or indwelling catheter. Patients with Shy-Drager syndrome should avoid undergoing TURP because the risk
of total incontinence is high.
Spinal Cord Lesions
Spinal cord injury
When an individual sustains a spinal cord injury from a diving accident or motor vehicle injury, the initial
response from the nervous system is spinal shock. During this spinal shock phase, the affected individual
experiences flaccid paralysis below the level of injury, and the somatic reflex activity is either depressed or
absent.
The anal and bulbocavernosus reflex typically is absent. The autonomic activity is depressed, and the individual
experiences urinary retention and constipation. Urodynamic findings are consistent with areflexic detrusor and
rectum. The internal and external urethral sphincter activities, however, are normal.
The spinal shock phase typically lasts 6-12 weeks; it may be prolonged in some cases. During this time, the
urinary bladder must be drained with CIC or indwelling urethral catheter.
When the spinal shock phase wears off, bladder function returns but the detrusor activity increases in reflex
excitability to an overactive state—detrusor hyperreflexia. Depending on the level of the lesion, the individual
may develop DSD-DH. Thus, the individual must be monitored for leaking between CIC, and periodic
urodynamic testing must be performed for this alteration in detrusor behavior. During urodynamics, intravesical
instillation of cold saline may indicate return of reflex activity or help better characterize the lesion.
Realizing that suprasacral lesions exhibit detrusor areflexia at initial insult but progress to hyperreflexic state
over time is important. Conversely, sacral cord lesions are associated with areflexic bladders that may become
hypertonic overtime.
Spinal cord lesions (above the sixth thoracic vertebrae)
Individuals who sustain a complete cord transection above the sixth thoracic vertebrae (T6) most often will have
urodynamic findings of detrusor hyperreflexia, striated sphincter dyssynergia, and smooth sphincter
dyssynergia. A unique complication of T6 injury is autonomic dysreflexia.
Autonomic dysreflexia is an exaggerated sympathetic response to any stimuli below the level of the lesion. This
occurs most commonly with lesions of the cervical cord. Often, the inciting event is instrumentation of the
urinary bladder or the rectum, causing visceral distention.
Symptoms of autonomic dysreflexia include sweating, headache, hypertension, and reflex bradycardia. Acute
management of autonomic dysreflexia is to decompress the rectum or bladder. Decompression usually will
reverse the effects of unopposed sympathetic outflow. If additional measures are required, parenteral ganglionic
or adrenergic blocking agents, such as chlorpromazine, may be used.
Oral blocking agents, including terazosin, may be used for prophylactically treating patients with autonomic
dysreflexia. Alternatively, spinal anesthetic may be used as a prophylactic measure whenever bladder
instrumentation is considered.
Spinal cord lesions (below T6)
Individuals who sustain spinal cord lesions below T6 level will have urodynamic findings of detrusor
hyperreflexia, striated sphincter dyssynergia, and smooth sphincter dyssynergia but no autonomic dysreflexia.
Neurologic evaluation will reveal skeletal muscle spasticity with hyperreflexic deep tendon reflexes. Affected
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patients will demonstrate extensor plantar response and positive Babinski sign.
These individuals will experience incomplete bladder emptying secondary to detrusor sphincter dyssynergia, or
loss of facilitatory input from higher centers. Cornerstone of treatment involves CIC and anticholinergic
medications.
Multiple sclerosis
MS is caused by focal demyelinating lesions of the central nervous system. It most commonly involves the
posterior and lateral columns of the cervical spinal cord. Usually, poor correlation exists between the clinical
symptoms and urodynamic findings. Thus, using urodynamic studies to evaluate patients with MS is critical.
The most common urodynamic finding is detrusor hyperreflexia, occurring in as many as 50-90% of patients
with MS. As many as 50% of patients will demonstrate DSD-DH. Detrusor areflexia occurs in 20-30% of cases.
The optimum therapy for a patient with MS and incontinence must be individualized and based on the
urodynamic findings.
Peripheral Nerve Lesions
Peripheral nerve lesions due to diabetes mellitus, tabes dorsalis, herpes zoster, herniated lumbar disk disease,
and radical pelvic surgery result in detrusor areflexia.
Diabetic cystopathy
Usually, neurogenic bladder dysfunction occurs 10 or more years after the onset of diabetes mellitus.
Neurogenic bladder occurs because of autonomic and peripheral neuropathy. A metabolic derangement of the
Schwann cell results in segmental demyelination and impaired nerve conduction.
The first symptoms of diabetic cystopathy are loss of sensation of bladder filling followed by loss of motor
function. Classic urodynamic findings associated with this condition are elevated residual urine, decreased
bladder sensation, impaired detrusor contractility, and, eventually, detrusor areflexia. Paradoxically, DHIC also
has been observed. Treatment of diabetic cystopathy is CIC, long-term indwelling catheterization, or urinary
diversion.
Tabes dorsalis (neurosyphilis)
In tabes dorsalis, central and peripheral nerve conduction is impaired. Affected patients experience decreased
bladder sensation and increased voiding intervals.
The most common urodynamic finding associated with neurosyphilis is detrusor areflexia with normal
sphincteric function.
Herpes zoster
Herpes zoster is a neuropathy associated with painful vesicular eruptions in the distribution of the affected
nerve. The herpes virus lies dormant in the dorsal root ganglia or the sacral nerves.
Sacral nerve involvement leads to impairment of detrusor function. The early stages of herpes infection are
associated with lower urinary tract symptoms of urinary frequency, urgency, and urge incontinence. Later stages
include decreased bladder sensation, increased residual urine, and urinary retention. Urinary retention is
self-limited and will resolve spontaneously with clearing of the herpes infection.
Herniated disc
Slow and progressive herniation of the lumbar disc may cause irritation of the sacral nerves and cause detrusor
hyperreflexia. Conversely, acute compression of the sacral roots associated with deceleration trauma will
prevent nerve conduction and result in detrusor areflexia.
A typical urodynamic finding of sacral nerve injury is detrusor areflexia with intact bladder sensation. Associated
internal sphincter denervation may occur. If the peripheral sympathetic nerves are damaged, the internal
sphincter will be open and nonfunctional. Peripheral sympathetic nerve damage often occurs in association with
detrusor denervation. The striated sphincter, however, is preserved.
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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.
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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.
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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 less-than-perfect results. Absorbent products are helpful during the initial
assessment and workup of urinary incontinence. As an adjunct to behavioral and pharmacologic therapies, they
play an important role in the care of persons with intractable incontinence.
Do not use absorbent products instead of definitive interventions to decrease or eliminate urinary incontinence.
Early dependency on absorbent pads may be a deterrent to achieving continence, providing the wearer a false
sense of security. Chronic use of absorbent products may lead to inevitable acceptance of the incontinence
condition, which removes the motivation to seek evaluation and treatment. In addition, improper use of
absorbent products may contribute to skin breakdown and urinary tract infections. Thus, appropriate use,
meticulous care, and frequent pad or garment changes are needed when absorbent products are used.
Absorbent products used include underpads, pant liners (shields and guards), adult diapers (briefs), a variety of
washable pants and disposable pad systems, or combinations of these products. More than 50% of members in
Help for Incontinent People (HIP) use some form of protective garment to remain dry. In addition, 47% of elderly
men and women use some type of absorbent product. In nursing homes, disposable diapers or reusable pad
and pant systems are used.
Unlike sanitary napkins, these absorbent products are specially designed to trap urine, minimize odor, and keep
the patient dry. Different types of products with varying degrees of absorbency exist. These products may
absorb 20-300 mL, depending on the brand and the absorbent material of the product. Absorbent pads and
garments that are available include panty shields, pant guards, undergarments, combination pad-pant systems,
adult diaper garments, and special bed pads.
For occasional minimal urine loss, panty shields (small absorbent inserts) may be used. For light incontinence,
guards (close-fitting pads) may be more appropriate. Absorbent guards are attached to the underwear and can
be worn under normal clothing.
Adult undergarments (full-length pads) are bulkier and more absorbent than guards. They may be held in place
by waist straps or snug underwear. Adult briefs are the bulkiest type of protection, offering the highest level of
absorbency, and are secured in place with self-adhesive tape.
Absorbent bed pads also are available to protect the bed sheets and mattresses at night. They are available in
different sizes and absorbencies.
Urethral occlusive devices
Urethral occlusive devices are artificial devices that may be inserted into the urethra or placed over the urethral
meatus to prevent urinary leakage. These devices are palliative measures to prevent involuntary urine loss.
Urethral occlusive devices are more attractive than absorbent pads because they tend to keep the patient drier;
however, they may be more difficult and expensive to use than pads. Urethral occlusive devices must be
removed after several hours or after each voiding.
Unlike pads, these devices may be more difficult to change. With device manipulation, patients may soil their
hands. The risk that a urethral plug may fall into the bladder or fall off the urethra always exists. Urethral
occlusive devices, perhaps, are best suited for an active woman with incontinence who does not desire surgery.
Catheters
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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
[1]
indwelling urethral catheters, suprapubic tubes, and self-intermittent catheterization. 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.
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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 patientfriendly. 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
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urinary tract infections. A study by Zegers et al found that this practice can be safely discontinued, especially in
[2]
males, patients with low urinary tract infection rates, and patients without vesicoureteral reflux.
In addition, self-catheterization is recommended by some surgeons for women during the acute healing process
after anti-incontinence surgery.
Intermittent catheterization may be performed using a soft, red, rubber catheter or a short, rigid, plastic catheter.
The use of plastic catheters is preferable to red rubber catheters because they are easier to clean and last
longer.
The bladder must be drained on a regular basis, either based on a timed interval (eg, on awakening, every 3-6
hours during the day, and before bed) or based on bladder volume. Remember that the average adult bladder
holds approximately 400-500 mL of urine. Ideally, the amount drained each time should not exceed 400-500
mL. This drainage limit may require decreasing the fluid intake or increasing the frequency of catheterizations. If
catheterization is performed every 6 hours and the amount drained is 700 mL, increase the frequency of
catheterization to, perhaps, every 4 hours to maintain the volume drained at 400-500 mL.
Intermittent catheterization is designed to simulate normal voiding. Usually, the average adult empties the
bladder 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 self-catheterization. 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 work—anywhere.
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
[3]
was noted during inpatient rehabilitation for these patients.
In high-risk populations, such as patients with an internal prosthesis (eg, artificial heart valve, artificial hip) or
patients who are immunosuppressed because of age or disease, determine whether to use antibiotic therapy for
asymptomatic bacteriuria on individual merits.
For 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
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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
[4]
studies may prove this modality more clinically useful to practice environments.
Surgical Care
Surgical care for stress incontinence involves procedures that increase urethral outlet resistance. 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;
[5, 6]
these include sacral neuromodulation, botulinum toxin injections,
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
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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
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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
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Biofeedback therapy is a form of pelvic floor muscle rehabilitation using an electronic device for individuals
having difficulty identifying levator ani muscles. Biofeedback therapy is recommended for treatment of stress
incontinence, urge incontinence, and mixed incontinence. Biofeedback therapy uses a computer and electronic
instruments to relay auditory or visual information to the patient about the status of pelvic muscle activity. These
devices allow the patient to receive immediate visual feedback on the activity of the pelvic floor muscles.
Biofeedback is an intensive therapy, with weekly sessions performed in an office or a hospital by a trained
professional, and it often is followed by a regimen of pelvic floor muscle exercises at home. During a
biofeedback therapy, a special tampon-shaped sensor is inserted in the patient's vagina or rectum and a second
sensor is placed on her abdomen. These sensors detect electrical signals from the pelvic floor muscles. The
patient is instructed to contract and relax the pelvic floor muscles upon command. When the exercises are
performed properly, the electric signals from the pelvic floor muscles are registered on a computer screen.
Biofeedback, using multi-measurement recording, displays the simultaneous measurement of pelvic and
abdominal muscle activity on the computer monitor.
Biofeedback allows the patient to correctly identify the pelvic muscles that need rehabilitation. The benefit of
biofeedback therapy is that it provides the patient with minute-by-minute feedback on the quality and intensity of
her pelvic floor contraction. Combining bladder and urinary sphincter biofeedback allows the patient to regulate
the pelvic muscle contraction in response to increasing bladder volumes and to monitor the bladder activity.
Biofeedback is best used in conjunction with pelvic floor muscle exercises and bladder training.
Studies on biofeedback combined with pelvic floor exercises show a 54-87% improvement with incontinence.
The best biofeedback protocol is one that reinforces levator ani muscle contraction with inhibition of abdominal
and bladder contraction. Reports using this method show a 76-82% reduction in urinary incontinence.
Biofeedback also has been used successfully in treatment of men with urge incontinence and intermittent stress
incontinence after prostate surgery.
Medical studies have demonstrated significant improvement in urinary incontinence in women with neurologic
disease and in the frail older population when a combination of biofeedback and bladder training is used.
Biofeedback provides a specific reinforcement for pelvic muscle contraction that is isolated from the
counterproductive abdominal contraction. Therefore, awareness of levator ani muscle contraction can be
achieved more efficiently using biofeedback than vaginal palpation alone.
Biofeedback produces a greater reduction in female urinary incontinence compared to pelvic muscle exercises
alone. Overall, the medical literature indicates that pelvic muscle exercises and other behavioral strategies, with
or without biofeedback, can cure or reduce incontinence. However, the maximum benefit is derived from any
pelvic muscle rehabilitation and education program when ongoing reinforcement and guidance, such as
biofeedback therapy, are provided.
Electrical stimulation
Electrical stimulation is a more sophisticated form of biofeedback used for pelvic floor muscle rehabilitation. This
treatment involves stimulation of levator ani muscles using painless electric shocks. Electrical stimulation of
pelvic floor muscles produces a contraction of the levator ani muscles and external urethral sphincter while
inhibiting bladder contraction. This therapy depends on a preserved reflex arc through the intact sacral
micturition center. Like biofeedback, electrical stimulation can be performed at the office or at home. Electrical
stimulation can be used in conjunction with biofeedback or pelvic floor muscle exercises.
Electrical stimulation therapy requires a similar type of probe and equipment as those used for biofeedback.
This form of muscle rehabilitation is similar to the biofeedback therapy, except small electric shocks are used.
Nonimplantable pelvic floor electrical stimulation uses vaginal sensors, anal sensors, or surface electrodes.
Adverse reactions are minimal.
Like biofeedback, pelvic floor muscle electrical stimulation has been shown to be effective in treating female
stress incontinence, as well as urge and mixed incontinence. Electrical stimulation may be most beneficial when
stress incontinence and very weak or damaged pelvic floor muscles coexist. A regimented program of electrical
stimulation will help these weakened pelvic muscles contract so they can become stronger. For women with
urge incontinence, electrical stimulation may help the bladder relax and prevent it from contracting involuntarily.
Research indicates that pelvic floor electrical stimulation can reduce urinary incontinence significantly in women
with stress incontinence and may be effective in men and women with urge and mixed incontinence. Incidence
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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,
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ulcerative colitis, myasthenia gravis, and severe heart diseases are contraindications for anticholinergic use.
These agents may impair the patient's ability to perform hazardous activities, such as driving or operating heavy
machinery, because of the potential for drowsiness. Anticholinergic drugs should not be taken in combination
with alcohol, sedatives, or hypnotic drugs.
When a single drug treatment does not work, combination therapy, such as oxybutynin (Ditropan) and
imipramine (Tofranil) may be used. Although their mechanism of action differs, oxybutynin and imipramine work
together to improve urge incontinence. Oxybutynin causes direct smooth muscle relaxation of the urinary
bladder and has local anesthetic properties. Imipramine has a direct inhibitory and local anesthetic effect on the
bladder smooth muscle, like oxybutynin; however, imipramine also increases the bladder outlet resistance at the
level of the bladder neck. Thus, the combination of these drugs produces a synergistic effect to relax the
unstable bladder to hold in urine and prevent urge incontinence. Potential anticholinergic adverse effects may
be additive because both drugs have similar adverse reactions.
Estrogen derivatives
Conjugated estrogen increases the tone of urethral muscle by up-regulating the alpha-adrenergic receptors in
the surrounding area and enhances alpha-adrenergic contractile response to strengthen pelvic muscles, which
is important in urethral support (prevents urethral hypermobility). Mucosal turgor of periurethral tissue from
proper nourishment enhances urethral mucosal coaptation. Result is an improved mucosal seal effect, which is
important in urethral function (prevents intrinsic sphincter deficiency). Estrogen supplementation appears to be
the most effective in postmenopausal women with mild-to-moderate incontinence. Both types of stress
incontinence benefit from estrogen fortification.
Pharmacologic therapy using estrogen derivatives results in few cures (0-14%) but may cause subjective
improvement in 29-66% of women. Limited evidence suggests that oral or vaginal estrogen therapy may benefit
some women with stress and mixed urinary incontinence. Other potential beneficial effects of estrogen use
include decreased bone loss and resolution of hot flashes during menopause.
When estrogen is used long-term, addition of progestin therapy is recommended to prevent endometrial
hyperplasia in women with an intact uterus. Progestin (eg, medroxyprogesterone 2.5-10 mg/d) is needed for
10-13 d to provide maximum maturation of endometrium and to eliminate any hyperplastic changes. Progestin
may be administered continuously or intermittently.
Conjugated estrogen (Premarin)
Conjugated estrogen may be used as an adjunctive pharmacologic agent for women who are postmenopausal
with stress or mixed incontinence. The oral or vaginal form of estrogen may be used. Premarin vaginal cream is
available in a package with a plastic applicator and a tube that contains 42.5 g of conjugated estrogens. Each
gram contains 0.625 mg of conjugated estrogens. Estrogen cream is readily absorbed through the skin and
mucous membranes.
Routinely prescribing conjugated estrogens to premenopausal women is not recommended. Use medication in
women who are postmenopausal and incontinent and who have had a hysterectomy. For postmenopausal
women with an intact uterus, cautiously recommend a short-term low-dose regimen of Premarin with frequent
monitoring.
Adult dosing is 0.625 mg PO qd for 21 consecutive days, followed by 7 days without the drug (eg, 3 wk on and
1 wk off); repeat the regimen prn and taper off or discontinue at 3- to 6-mo intervals. Two to four grams (0.5-1
applicator) of cream may be administered intravaginally qd in a usual cyclic regimen. Pediatric dosing has not
been established.
Conjugated estrogen is a pregnancy category X drug.
Anticholinergic drugs
Anticholinergic drugs are the first line medicinal therapy in women with urge incontinence. They are effective in
treating urge incontinence because they inhibit involuntary bladder contractions. They are also useful in treating
urinary incontinence associated with urinary frequency, urgency, and nocturnal enuresis. All anticholinergic
drugs have similar performance profiles and toxicity. Potential adverse effects of all anticholinergic agents
include blurred vision, dry mouth, heart palpitations, drowsiness, and facial flushing. When anticholinergic drugs
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are used in excess, acute urinary retention in the bladder may occur.
Propantheline bromide (Pro Banthine)
Propantheline bromide is the typical prototype for all anticholinergic agents. It blocks action of acetylcholine at
postganglionic parasympathetic receptor sites. In a medical study, propantheline bromide was shown to
decrease incidence of urge incontinence by 13-17% when 30 mg was used qid. When stronger doses were
used (60 mg qid), the cure rate was reported to be over 90%.
Adult dosing is 15 mg PO tid/qid. Pediatric dosing has not been established.
Propantheline bromide is a pregnancy category C drug.
Dicyclomine hydrochloride (Bentyl)
Dicyclomine hydrochloride is an anticholinergic agent with smooth muscle relaxant properties. It blocks the
action of acetylcholine at parasympathetic sites in secretory glands and smooth muscle. In a medical study,
subjective improvement was reported by 62% of the subjects while taking dicyclomine hydrochloride 10 mg tid.
The reported cure rate was 90%.
Adult dosing is 10-20 mg PO tid. Pediatric dosing has not been established.
Dicyclomine hydrochloride is a pregnancy category B drug.
Hyoscyamine sulfate (Levsin/SL, Levsin, Levsinex, Cystospaz M, Levbid)
Hyoscyamine sulfate is an anticholinergic agent with antispasmodic properties used for the treatment of urge
incontinence. It blocks the action of acetylcholine at parasympathetic sites in smooth muscle, secretory glands,
and the CNS, which in turn has antispasmodic effects. It is absorbed well by the GI tract. Food does not affect
absorption. Hyoscyamine sulfate is available in sublingual form (Levsin SL), conventional tablets (Levsin),
extended-release capsules (Levsinex Timecaps, Cystospaz-M), and extended-release tablets (Levbid).
Adult dosing is 0.125 mg PO q4h; alternatively, 0.375 mg PO bid can be used. For severe symptoms, dosing is
0.375 mg PO tid. Pediatric dosing has not been established.
Hyoscyamine sulfate is a pregnancy category C drug.
Antispasmodic drugs
These relax the smooth muscles of the urinary bladder. By exerting a direct spasmolytic action on the smooth
muscle of the bladder, antispasmodic drugs have been reported to increase bladder capacity and effectively
decrease or eliminate urge incontinence. The adverse-effect profile of antispasmodic drugs is similar to that of
anticholinergic agents. These drugs may impair the patient's ability to perform activities requiring mental
alertness and physical coordination. Drinking alcohol and using sedatives in combination with these
antispasmodic drugs is contraindicated.
Solifenacin succinate (VESIcare)
Solifenacin succinate elicits competitive muscarinic receptor antagonist activity, which results in anticholinergic
effect and inhibition of bladder smooth muscle contraction. It is indicated for overactive bladder with symptoms
of urgency, frequency, and urge incontinence.
Adult dosing is 5 mg PO qd; if tolerated, it may be increased to 10 mg PO qd.
Pediatric dosing has not been established.
Solifenacin succinate is a pregnancy category C drug.
Darifenacin (Enablex)
Darifenacin is an extended-release product that elicits competitive muscarinic receptor antagonistic activity. It
reduces bladder smooth muscle contractions. It has a high affinity for M 3 receptors involved in bladder and GI
smooth muscle contraction, saliva production, and iris sphincter function. Darifenacin is indicated for overactive
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bladder with symptoms of urge incontinence, urgency, and frequency. The product should be swallowed whole;
do not chew, divide, or crush.
Adult dosing is 7.5 mg PO qd initially; after 2 wk, the dose may be increased to 15 mg PO qd based on
response. Do not exceed 7.5 mg PO qd in patients with moderate hepatic impairment (Child-Pugh class B) or
who are receiving potent CYP-450 3A4 inhibitors. Pediatric dosing has not been established.
Darifenacin is a pregnancy category C drug.
Oxybutynin chloride (Ditropan IR, Ditropan XL)
Oxybutynin chloride has both anticholinergic and direct smooth muscle relaxant effects on urinary bladder. It
provides a local anesthetic effect on irritable bladder. Urodynamic studies have shown oxybutynin increases
bladder size, decreases frequency of symptoms, and delays initial desire to void.
Ditropan XL has an innovative drug delivery system—oral osmotic delivery system (OROS). The Ditropan XL
tablet has a bilayer core that contains a drug layer and a push layer that contains osmotic components. The
outer tablet is composed of a semipermeable membrane with a precision laser-drilled hole that allows the drug
to be released at a constant rate.
When the drug is ingested, the aqueous environment in the GI tract causes water to enter the tablet via the
semipermeable membrane at constant rate. Introduction of water inside the tablet liquifies the drug and causes
the push layer to swell osmotically. As the push layer swells, it forces the drug suspension out of the hole at a
constant rate over a 24-h period.
Ditropan XL achieves steady-state levels over a 24-h period. It avoids first-pass metabolism of the liver and
upper GI tract to avoid cytochrome P450 enzymes. It has excellent efficacy with minimal adverse effects.
Medical studies have shown that oxybutynin chloride reduces incontinence episodes by 83-90%. The total
continence rate has been reported to be 41-50%. The mean reduction in urinary frequency was 23%. In clinical
trials, only 1% stopped taking Ditropan XL because of dry mouth, and less than 1% stopped taking Ditropan XL
due to CNS adverse effects.
Adult dosing of Ditropan IR is 2.5 mg PO tid, titrate prn to 5 mg bid/tid/qid. Dosing of Ditropan XL is 5-15 mg PO
qd. Pediatric dosing has not been established.
Oxybutynin chloride is a pregnancy category B drug.
Tolterodine L-tartrate (Detrol and Detrol LA)
Tolterodine L-tartrate is a competitive muscarinic receptor antagonist for overactive bladder. It differs from other
anticholinergic types in that it has selectivity for urinary bladder over salivary glands. It exhibits high specificity
for muscarinic receptors and has minimal activity or affinity for other neurotransmitter receptors and other
potential targets such as calcium channels. In clinical studies, the mean decrease in urge incontinence
episodes was 50% and the mean decrease in urinary frequency was 17%.
Adult dosing of Detrol is 2 mg PO bid. Dosing of Detrol LA is 4 mg PO qd. Pediatric dosing has not been
established.
Tolterodine L-tartrate is a pregnancy category C drug.
Trospium (Sanctura)
Trospium is a quaternary ammonium compound that elicits antispasmodic and antimuscarinic effects. It
antagonizes acetylcholine effect on muscarinic receptors. Parasympathetic effect reduces smooth muscle tone
in the bladder. Trospium is indicated to treat symptoms of overactive bladder (eg, urinary incontinence, urgency,
frequency).
Adult dosing is 20 mg PO bid; it should be taken on an empty stomach at least 1 h before meals. In patients
with a CrCl < 30 mL/min, dosing is 20 mg PO hs. In patients >75 years, dosing may be titrated downward to 20
mg PO qd based on tolerability. Pediatric dosing has not been established.
Trospium is a pregnancy category C drug.
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Fesoterodine (Toviaz)
Fesoterodine is a competitive muscarinic receptor antagonist. The antagonistic effect results in decreased
bladder smooth muscle contractions. It is indicated for symptoms of overactive bladder (eg, urinary urge
incontinence, urgency, and frequency). Fesoterodine is available as a 4- or 8-mg extended-release tab.
Adult dosing is 4 mg PO qd; it may be increased to 8 mg/d. Dosing is not to exceed 4 mg PO qd in severe renal
dysfunction (ie, CrCl < 30 mL/min) or with coadministration of drugs that decrease fesoterodine’s metabolism
(eg, ketoconazole, itraconazole, clarithromycin). Pediatric dosing has not been established.
Fesoterodine is a pregnancy category C drug.
Tricyclic antidepressant drugs
Historically, these drugs were used to treat major depression; however, they have an additional use that is not
FDA approved—treatment of bladder dysfunction. They function to increase norepinephrine and serotonin
levels. In addition, they exhibit anticholinergic and direct muscle relaxant effects on the urinary bladder.
Imipramine hydrochloride (Tofranil)
Imipramine hydrochloride is a typical tricyclic antidepressant. It facilitates urine storage by decreasing bladder
contractility and increasing outlet resistance. It has alpha-adrenergic effect on the bladder neck and
antispasmodic effect on detrusor muscle. Imipramine hydrochloride has a local anesthetic effect on bladder
mucosa.
Adult dosing is 10-50 mg PO qd/tid; the range is 25-100 mg qd. Pediatric dosing has not been established.
Imipramine hydrochloride is a pregnancy category D drug.
Amitriptyline hydrochloride (Elavil)
Amitriptyline hydrochloride is a tricyclic antidepressant with sedative properties. It increases circulating levels of
norepinephrine and serotonin by blocking their reuptake at nerve endings and is ineffective for use in urge
incontinence. However, it is extremely effective in decreasing symptoms of urinary frequency in women with
pelvic floor muscle dysfunction. Amitriptyline hydrochloride restores serotonin levels and helps break the cycle
of pelvic floor muscle spasms. It is well-tolerated and effective in most women with urinary frequency.
Adult dosing is 10 mg/d PO; titrate prn by 10 mg/wk until maximum dose of 150 mg is reached, urinary
symptoms disappear, or adverse effects become intolerable. Pediatric dosing has not been established.
Amitriptyline hydrochloride is a pregnancy category D drug.
Follow-up
Complications
Prolonged contact of urine with unprotected skin causes contact dermatitis and skin breakdown. If left
untreated, these skin disorders may lead to pressure sores and ulcers, possibly resulting in secondary
infections. For individuals with a decompensated bladder that does not empty well, the postvoid residual urine
can lead to overgrowth of bacteria and subsequent urinary tract infection.
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.
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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.
Contributor Information and Disclosures
Author
Raymond R Rackley, MD Professor of Surgery, Cleveland Clinic Lerner College of Medicine; Staff
Physician, Center for Neurourology, Female Pelvic Health and Female Reconstructive Surgery, Glickman
Urological Institute, Cleveland Clinic, Beachwood Family Health Center, and Willoughby Hills Family Health
Center; Director, The Urothelial Biology Laboratory, Lerner Research Institute, Cleveland Clinic
Raymond R Rackley, MD is a member of the following medical societies: American Urological Association
Disclosure: Pfizer, Novartis, Proctor & Gamble, Allergan Honoraria None; Pfizer, Novartis, Proctor & Gamble,
Allergan Consulting fee Other
Coauthor(s)
Sandip P Vasavada, MD Physician, Associate Professor of Surgery, Cleveland Clinic Lerner College of
Medicine, Center for Female Urology and Genitourinary Reconstructive Surgery, The Glickman Urological
and Kidney Institute; Joint Appointment with Women's Institute, Cleveland Clinic
Sandip P Vasavada, MD is a member of the following medical societies: American Urogynecologic Society,
American Urological Association, International Continence Society, Society for Urology and Engineering, and
Society of Urodynamics and Female Urology
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Disclosure: NDI Medical, LLC Ownership interest Review panel membership; allergan Consulting fee
Speaking and teaching; medtronic Consulting fee Speaking and teaching
Farzeen Firoozi, MD Clinical Fellow, Center for Female Urology and Pelvic Reconstructive Surgery,
Glickman Urological Institute, Cleveland Clinic Foundation
Farzeen Firoozi, MD is a member of the following medical societies: American Medical Association and
American Urological Association
Disclosure: Nothing to disclose.
Michael S Ingber, MD Clinical Fellow, Glickman Urological and Kidney Institute of the Cleveland Clinic
Disclosure: Nothing to disclose.
Specialty Editor Board
Raymond R Rackley, MD Professor of Surgery, Cleveland Clinic Lerner College of Medicine; Staff
Physician, Center for Neurourology, Female Pelvic Health and Female Reconstructive Surgery, Glickman
Urological Institute, Cleveland Clinic, Beachwood Family Health Center, and Willoughby Hills Family Health
Center; Director, The Urothelial Biology Laboratory, Lerner Research Institute, Cleveland Clinic
Raymond R Rackley, MD is a member of the following medical societies: American Urological Association
Disclosure: Pfizer, Novartis, Proctor & Gamble, Allergan Honoraria None; Pfizer, Novartis, Proctor & Gamble,
Allergan Consulting fee Other
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center
College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment
Shlomo Raz, MD Professor, Department of Surgery, Division of Urology, University of California at Los
Angeles School of Medicine
Shlomo Raz, MD is a member of the following medical societies: American College of Surgeons, American
Medical Association, American Urological Association, and California Medical Association
Disclosure: Nothing to disclose.
J Stuart Wolf Jr, MD, FACS David A Bloom Professor of Urology, Associate Chair for Clinical Operations,
Director, Division of Endourology and Stone Disease, Department of Urology, University of Michigan Medical
School
J Stuart Wolf Jr, MD, FACS is a member of the following medical societies: American College of Surgeons,
American Urological Association, Catholic Medical Association, Endourological Society, Society for Urology
and Engineering, Society of Laparoendoscopic Surgeons, Society of University Urologists, and Society of
Urologic Oncology
Disclosure: Nothing to disclose.
Chief Editor
Edward David Kim, MD, FACS Professor of Surgery, Division of Urology, University of Tennessee Graduate
School of Medicine; Consulting Staff, University of Tennessee Medical Center
Edward David Kim, MD, FACS is a member of the following medical societies: American College of
Surgeons, American Society for Reproductive Medicine, American Society of Andrology, American Urological
Association, Sexual Medicine Society of North America, and Tennessee Medical Association
Disclosure: Lilly None Advisor; Astellas Honoraria Speaking and teaching; Watson Honoraria Speaking and
teaching; Warner Chilcott Honoraria Speaking and teaching; Auxilium Honoraria Speaking and teaching; Eli
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Lilly Honoraria Speaking and teaching
References
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