199027507 neurogenic bladder

8/19/2019 199027507 Neurogenic Bladder

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Neurogenic Bladder

Overview

The normal function of the urinary bladder is to store and expel urine in a coordinated, controlledfashion. 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 onthe 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 carefulmedical 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 sets of peripheral nerves arising from the autonomic nervoussystem (!NS) 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.

"ertain lesions or diseases of the brain, including stro#e, cancer, or dementia, result in loss ofvoluntary control of the normal micturition reflex.

The signal transmitted by the brain is routed through $ intermediate stops (the brainstem and the

sacral spinal cord) prior to reaching the bladder.

Brainstem

The brainstem is located at the base of the s#ull. %ithin the brainstem is a speciali&ed area

#nown 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 theywor# in synergy. The mechanical process of urination is coordinated by the pons in the area


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#nown as the pontine micturition center ('"). The '" coordinates the urethral sphincter

relaxation and detrusor contraction to facilitate urination. See the image below.

The pons is a major relay center between the brain and

the bladder. The mechanical process of urination is coordinated by the pons in the

area known as the pontine micturition center (PMC).

The conscious sensations associated with bladder activity are transmitted to the pons from the

cerebral cortex. The interaction of a variety of excitatory and inhibitory neuronal systems is the

function of the '", which is characteri&ed by its inborn excitatory nature. The '" functionsas a relay switch in the voiding pathway. Stimulation of the '" causes the urethral sphincters

to open while facilitating the detrusor to contract and expel the urine.

The '" 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 '" is part of the socialtraining that children experience during growth and development. sually the brain ta#es over

the control of the pons at age *+ years, which is why most children undergo toilet training at this

age.

%hen the bladder becomes full, the stretch receptors of the detrusor muscle send a signal to the pons, which in turn notifies the brain. 'eople perceive this signal (bladder fullness) as a sudden

desire to go to the bathroom. nder normal situations, the brain sends an inhibitory signal to the

pons to inhibit the bladder from contracting until a bathroom is found.

%hen the '" is deactivated, the urge to urinate disappears, allowing the patient to delayurination until finding a socially acceptable time and place. %hen 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. t is located in the

spinal canal and is protected by the cerebrospinal fluid, meninges, and a vertebral column. t isapproximately -+ inches long in an adult. !long its course, the spinal cord sprouts off many

nerve branches to different parts of the body.

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The spinal cord functions as a long communication pathway between the brainstem and the

sacral spinal cord. %hen 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 interpretsthis signal and sends a reply via the pons that travels down the spinal cord to the sacral cord and,

subseuently, to the bladder.

n the normal cycle of bladder filling and emptying, the spinal cord acts as an important

intermediary between the pons and the sacral cord. !n intact spinal cord is critical for normalmicturition.

f spinal cord injury has occurred, the patient will demonstrate symptoms of urinary freuency,

urgency, and urge incontinence but will be unable to empty his or her bladder completely. Thisoccurs because the urinary bladder and the sphincter are both overactive, a condition termed

detrusor sphincter dyssynergia with detrusor hyperreflexia (/S/*/0).

The sacral spinal cord is the terminal portion of the spinal cord situated at the lower bac# in the

lumbar area. This is a speciali&ed area of the spinal cord #nown as the sacral reflex center. t isresponsible for bladder contractions. The sacral reflex center is the primitive voiding center.

n 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. %hen urine fills the infant bladder, an excitatory signal is sent to the sacralcord. %hen 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.

! continuous cycle of bladder filling and emptying occurs, which is why infants and young

children are dependent on diapers until they are toilet trained. !s the child1s brain matures anddevelops, it gradually dominates the control of the bladder and the urinary sphincters to inhibit

involuntary voiding until complete control is attained. 2oluntary continence usually is attained by age *+ years. 3y this time, control of the voiding process has been relinuished by the sacral

reflex center of the sacral cord to the higher center in the brain.

f the sacral cord becomes severely injured (eg, spinal tumor, herniated disc), the bladder may

not function. !ffected patients may develop urinary retention, termed detrusor areflexia. Thedetrusor will be unable to contract, so the patient will not be able to urinate and urinary retention

will occur.

Peripheral nerves

'eripheral nerves form an intricate networ# of pathways for sending and receiving information

throughout the body. The nerves originate from the main trun# 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 oneof the ordinary senses (ie, hearing, sight, smell, touch, taste, euilibrium). The bladder and the

urethral sphincters are under the influence of their corresponding nerves.


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The !NS lies outside of the central nervous system. t regulates the actions of the internal organs

(eg, intestines, heart, bladder) under involuntary control. The !NS is divided into the

sympathetic and the parasympathetic nervous system.

nder normal conditions, the bladder and the internal urethral sphincter primarily are under

sympathetic nervous system control. %hen the sympathetic nervous system is active, it causesthe bladder to increase its capacity without increasing detrusor resting pressure (accommodation)

and stimulates the internal urinary sphincter to remain tightly closed. The sympathetic activityalso inhibits parasympathetic stimulation. %hen 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 sympatheticnervous system. n terms of urinary function, the parasympathetic nerves stimulate the detrusor

to contract. mmediately preceding parasympathetic stimulation, the sympathetic influence on

the internal urethral sphincter becomes suppressed so that the internal sphincter relaxes and

opens. n addition, the activity of the pudendal nerve is inhibited to cause the external sphincter

to open. The result is facilitation of voluntary urination.

4i#e the !NS, 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. 5xamples of these muscles are the external urinary sphincter and the pelvicdiaphragm. The pudendal nerve originates from the nucleus of 6nuf and regulates the voluntary

actions of the external urinary sphincter and the pelvic diaphragm. !ctivation of the pudendal

nerve causes contraction of the external sphincter and the pelvic floor muscles, which occurswith activities such as 7egel exercises. /ifficult or prolonged vaginal delivery may cause

temporary neurapraxia of the pudendal nerve and cause stress urinary incontinence. "onversely,

suprasacral*infrapontine spinal cord trauma can cause overstimulation of the pudendal nerve,

resulting in urinary retention.

Physiology and Pathophysiology

Physiology

/uring the course of a day, an average person will void approximately +*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 $ phases9filling and emptying. The normal micturition

cycle reuires that the urinary bladder and the urethral sphincter wor# together as a coordinatedunit to store and empty urine. /uring urinary storage, the bladder acts as a low*pressure

receptacle, while the urinary sphincter maintains high resistance to urinary flow to #eep the

bladder outlet closed. /uring urine elimination, the bladder contracts to expel urine while theurinary sphincter opens (low resistance) to allow unobstructed urinary flow and bladder

emptying.


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Filling phase

/uring the filling phase, the bladder accumulates increasing volumes of urine while the pressureinside the bladder remains low. The pressure within the bladder must be lower than the urethral

pressure during the filling phase. f the bladder pressure is greater than the urethral pressure

(resistance), urine will lea# out.

The filling of the urinary bladder depends on the intrinsic viscoelastic properties of the bladderand 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 trierinbladder contractions.

• Sympathetic nerves directly cause rela!ation and e!pansion of the detrusormuscle.

• Sympathetic nerves close the bladder neck by constrictin the internalurethral sphincter. This sympathetic input to the lower urinary tract isconstantly active durin bladder "llin.

!s the bladder fills, the pudendal nerve becomes excited. Stimulation of the pudendal nerve

results in contraction of the external urethral sphincter. "ontraction 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 #nown as the continence

mechanism.

The pressure gradients within the bladder and urethra play an important functional role in normalmicturition. !s long as the urethral pressure is higher than that of the bladder, patients will

remain continent. f the urethral pressure is abnormally low or if the intravesical pressure is

abnormally high, urinary incontinence will result.

!s the bladder initially fills, a small rise in pressure occurs within the bladder (intravesical pressure). %hen the urethral sphincter is closed, the pressure inside the urethra (intraurethral

pressure) is higher than the pressure within the bladder. %hile the intraurethral pressure is higher

than the intravesical pressure, urinary continence is maintained.

/uring some physical activities and with coughing, snee&ing, or laughing, the pressure within the

abdomen rises sharply. This rise is transmitted to both the bladder and urethra. !s long as the pressure is evenly transmitted to both the bladder and urethra, urine will not lea#. %hen the

pressure transmitted to the bladder is greater than urethra, urine will lea# out, resulting in stressincontinence.


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Emptying phase

The storage phase of the urinary bladder can be switched to the voiding phase eitherinvoluntarily (reflexively) or voluntarily. nvoluntary reflex voiding occurs in an infant when the

volume of urine exceeds the voiding threshold. %hen 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 bac# to the bladder indicating that it is time to empty the bladder.

!t 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 urethralresistance.

%hen the urethral sphincters relax and open, the parasympathetic nerves trigger contraction of

the detrusor. %hen 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.

! 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. 3ecause urination is unregulated by the infant1s brain, predicting when the infantwill urinate is difficult.

!s the infant brain develops, the '" also matures and gradually assumes voiding control.

%hen the infant enters childhood (usually at age *+ years), this primitive voiding reflex

becomes suppressed and the brain dominates bladder function, which is why toilet trainingusually is successful at age *+ years. 0owever, this primitive voiding reflex may reappear in

people with spinal cord injuries.

Delaying voiding or voluntary voiding

3ladder function is automatic but completely governed by the brain, which ma#es 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. n addition, the individual has the ability todelay urination until a socially acceptable time and place. The healthy adult is aware of bladder

filling and can willfully initiate or delay voiding.

n a healthy adult, the '" 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 influencesfrom the brain. %hen 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.

%hen an individual cannot find a bathroom nearby, the brain bombards the '" with amultitude of inhibitory signals to prevent detrusor contractions. !t the same time, an individual


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may actively contract the levator muscles to #eep the external sphincter closed or initiate

distracting techniues to suppress urination.

Thus, the voiding process reuires coordination of both the !NS and somatic nervous system,which are in turn controlled by the '" located in the brainstem.

Pathophysiology

f a problem occurs within the nervous system, the entire voiding cycle is affected. !ny part ofthe nervous system may be affected, including the brain, pons, spinal cord, sacral cord, and

peripheral nerves. ! dysfunctional voiding condition results in different symptoms, ranging from

acute urinary retention to an overactive bladder or to a combination of both.

rinary incontinence results from a dysfunction of the bladder, the sphincter, or both. 3ladderoveractivity (spastic bladder) is associated with the symptoms of urge incontinence, while

sphincter underactivity (decreased resistance) results in symptomatic stress incontinence. !

combination of detrusor overactivity and sphincter underactivity may result in mixed symptoms.

Brain lesion

4esions 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 tract9the primitive voiding reflex9

remain intact. !ffected individuals show signs of urge incontinence, or spastic bladder(medically termed detrusor hyperreflexia or overactivity). The bladder empties too uic#ly and

too often, with relatively low uantities, and storing urine in the bladder is difficult. sually,

people with this problem rush to the bathroom and even lea# urine before reaching theirdestination. They may wa#e up freuently at night to void.

Typical examples of a brain lesion are stro#e, brain tumor, or 'ar#inson disease. 0ydrocephalus,

cerebral palsy, and Shy*/rager syndrome also are brain lesions. Shy*/rager syndrome is a rare

condition that also causes the bladder nec# to remain open.

Spinal cord lesion

/iseases or injuries of the spinal cord between the pons and the sacral spinal cord also result in

spastic bladder or overactive bladder. 'eople who are paraplegic or uadriplegic have lowerextremity spasticity. nitially, after spinal cord trauma, the individual enters a spinal shoc# phase

where the nervous system shuts down. !fter ;*-$ wee#s, the nervous system reactivates. %hen

the nervous system becomes reactivated, it causes hyperstimulation of the affected organs.


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dyssynergia because the bladder and the external sphincter are not in synergy. 5ven though the

bladder is trying to force out urine, the external sphincter is tightening to prevent urine from

leaving.

The causes of spinal cord injuries include motor vehicle and diving accidents. ultiple sclerosis

(S) is a common cause of spinal cord disease in young women. Those with S also mayexhibit visual disturbances, #nown as optic neuritis. "hildren born with myelomeningocele may

have spastic bladders and=or an open urethra. "onversely, some children with myelomeningocelemay 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 cordmay prevent the bladder from emptying. f a sensory neurogenic bladder is present, the affected

individual may not be able to sense when the bladder is full. n the case of a motor neurogenic

bladder, the individual will sense the bladder is full and the detrusor may not contract, a

condition #nown as detrusor areflexia. These individuals have difficulty eliminating urine andexperience 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. Thiscondition 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 stuc# nearthe sacrum and cannot stretch as the child grows taller. schemic changes of the sacral cord

associated with the tethering cause the manifestation of dysfunctional voiding symptoms.

Peripheral nerve injury

/iabetes mellitus and !/S are $ 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. 'atients with chronic diabetes lose the sensation of bladder

filling first, before the bladder decompensates. Similar to injury to the sacral cord, affectedindividuals will have difficulty urinating. They also may have a hypocontractile bladder.

6ther diseases manifesting this condition are poliomyelitis, ?uillain*3arr@ syndrome, severe

herpes in the genitoanal area, pernicious anemia, and neurosyphilis (tabes dorsalis).

Summary of denitions

Neurogenic bladder is a malfunctioning bladder due to any type of neurologic disorder.

/etrusor hyperreflexia refers to overactive bladder symptoms due to a suprapontine upper motor

neuron neurologic disorder. 5xternal sphincter functions normally. The detrusor muscle and theexternal sphincter function in synergy (in coordination).

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/S/*/0 refers to overactive bladder symptoms due to neurologic upper motor neuron disorder

of the suprasacral spinal cord. 'aradoxically, the patient is in urinary retention. 3oth the detrusor

and the sphincter are contracting at the same time> they are in dyssynergy (lac# of coordination).

/etrusor hyperreflexia with impaired contractility (/0") refers to overactive bladder

symptoms, but the detrusor cannot generate enough pressure to allow complete emptying. Theexternal sphincter is in synergy with detrusor contraction. The detrusor is too wea# to mount an

adeuate contraction for proper voiding to occur. The condition is similar to urinary retention, but irritating voiding symptoms are prevalent.

/etrusor instability refers to overactive bladder symptoms without neurologic impairment.

5xternal sphincter functions normally, in synergy.

6veractive bladder refers to symptoms of urinary urgency, with or without urge incontinence,usually associated with freuency and nocturia. The cause may be neurologic or nonneurologic.

/etrusor areflexia is complete inability of the detrusor to empty due to a lower motor neuronlesion (eg, sacral cord or peripheral nerves).

rinary retention is the inability of the urinary bladder to empty. The cause may be neurologic or nonneurologic.

ypes of Neurogenic Bladders

Supraspinal !esions

Supraspinal lesions refer to those lesions of the central nervous system involving the area above

the pons. They include cerebrovascular accident, brain tumor, 'ar#inson disease, and Shy*/rager syndrome.

"ere#rovascular accident

!fter a stro#e, the brain may enter into a temporary acute cerebral shoc# phase. /uring this time,the urinary bladder will be in retention9detrusor areflexia. !lmost $AB of affected individuals

develop acute urinary retention after a stro#e.

!fter the cerebral shoc# phase wears off, the bladder demonstrates detrusor hyperreflexia withcoordinated urethral sphincter activity. This occurs because the '" is released from the

cerebral inhibitory center. %hen the patient manifests symptoms of detrusor hyperreflexia, theindividual will complain of urinary freuency, urgency, and urge incontinence.

The treatment for the cerebral shoc# phase is indwelling


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Brain tumor

/etrusor hyperreflexia with coordinated urethral sphincter is the most common observedurodynamic pattern associated with a brain tumor.

%hen the patient manifests symptoms of detrusor hyperreflexia, the individual complains ofurinary freuency, urgency, and urge incontinence.


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The treatment for Shy*/rager syndrome is to facilitate urinary storage with anticholinergic

agents coupled with "" or indwelling catheter. 'atients with Shy*/rager syndrome should

avoid undergoing TC' because the ris# of total incontinence is high.

Spinal "ord !esions

Spinal cord injury

%hen an individual sustains a spinal cord injury from a diving accident or motor vehicle injury,the initial response from the nervous system is spinal shoc#. /uring this spinal shoc# 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, andthe individual experiences urinary retention and constipation. rodynamic findings are

consistent with areflexic detrusor and rectum. The internal and external urethral sphincter

activities, however, are normal.

The spinal shoc# phase typically lasts ;*-$ wee#s> it may be prolonged in some cases. /uringthis time, the urinary bladder must be drained with "" or indwelling urethral catheter.

%hen the spinal shoc# phase wears off, bladder function returns but the detrusor activity

increases in reflex excitability to an overactive state9detrusor hyperreflexia. /epending on the

level of the lesion, the individual may develop /S/*/0. Thus, the individual must be monitoredfor lea#ing between "", and periodic urodynamic testing must be performed for this alteration

in detrusor behavior. /uring urodynamics, intravesical instillation of cold saline may indicate

return of reflex activity or help better characteri&e the lesion.

Ceali&ing that suprasacral lesions exhibit detrusor areflexia at initial insult but progress tohyperreflexic state over time is important. "onversely, sacral cord lesions are associated with

areflexic bladders that may become hypertonic overtime.

Spinal cord lesions (above the sixth thoracic vertebrae)

ndividuals who sustain a complete cord transection above the sixth thoracic vertebrae (T;) mostoften will have urodynamic findings of detrusor hyperreflexia, striated sphincter dyssynergia,

and smooth sphincter dyssynergia. ! uniue complication of T; injury is autonomic dysreflexia.

!utonomic dysreflexia is an exaggerated sympathetic response to any stimuli below the level ofthe lesion. This occurs most commonly with lesions of the cervical cord. 6ften, the inciting eventis instrumentation of the urinary bladder or the rectum, causing visceral distention.

Symptoms of autonomic dysreflexia include sweating, headache, hypertension, and reflex

bradycardia. !cute management of autonomic dysreflexia is to decompress the rectum or

bladder. /ecompression usually will reverse the effects of unopposed sympathetic outflow. f


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additional measures are reuired, parenteral ganglionic or adrenergic bloc#ing agents, such as

chlorproma&ine, may be used.

6ral bloc#ing agents, including tera&osin, may be used for prophylactically treating patients withautonomic dysreflexia. !lternatively, spinal anesthetic may be used as a prophylactic measure

whenever bladder instrumentation is considered.

Spinal cord lesions (below T6)

ndividuals who sustain spinal cord lesions below T; level will have urodynamic findings of

detrusor hyperreflexia, striated sphincter dyssynergia, and smooth sphincter dyssynergia but noautonomic dysreflexia.

Neurologic evaluation will reveal s#eletal muscle spasticity with hyperreflexic deep tendon

reflexes. !ffected patients will demonstrate extensor plantar response and positive 3abins#i sign.

These individuals will experience incomplete bladder emptying secondary to detrusor sphincterdyssynergia, or loss of facilitatory input from higher centers. "ornerstone of treatment involves

"" and anticholinergic medications.

Multiple sclerosis

S is caused by focal demyelinating lesions of the central nervous system. t most commonly

involves the posterior and lateral columns of the cervical spinal cord. sually, poor correlationexists between the clinical symptoms and urodynamic findings. Thus, using urodynamic studies

to evaluate patients with S is critical.

The most common urodynamic finding is detrusor hyperreflexia, occurring in as many as AD*EDB of patients with S. !s many as ADB of patients will demonstrate /S/*/0. /etrusor

areflexia occurs in $D*DB of cases. The optimum therapy for a patient with S and

incontinence must be individuali&ed and based on the urodynamic findings.

Peripheral Nerve Lesions

'eripheral nerve lesions due to diabetes mellitus, tabes dorsalis, herpes &oster, herniated lumbardis# disease, and radical pelvic surgery result in detrusor areflexia.

Diabetic cystopathy

sually, neurogenic bladder dysfunction occurs -D or more years after the onset of diabetes

mellitus. Neurogenic bladder occurs because of autonomic and peripheral neuropathy. !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. "lassic urodynamic findings associated with this condition are elevated


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residual urine, decreased bladder sensation, impaired detrusor contractility, and, eventually,

detrusor areflexia. 'aradoxically, /0" also has been observed. Treatment of diabetic cystopathy

is "", long*term indwelling catheteri&ation, or urinary diversion.

Tabes dorsalis (neurosyphilis)

n tabes dorsalis, central and peripheral nerve conduction is impaired. !ffected patients

experience decreased bladder sensation and increased voiding intervals.

The most common urodynamic finding associated with neurosyphilis is detrusor areflexia with

normal sphincteric function.

erpes !oster

0erpes &oster 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 freuency, urgency, andurge incontinence. 4ater stages include decreased bladder sensation, increased residual urine, and

urinary retention. rinary retention is self*limited and will resolve spontaneously with clearing

of the herpes infection.

erniated disc

Slow and progressive herniation of the lumbar disc may cause irritation of the sacral nerves and

cause detrusor hyperreflexia. "onversely, acute compression of the sacral roots associated with

deceleration trauma will prevent nerve conduction and result in detrusor areflexia.

! typical urodynamic finding of sacral nerve injury is detrusor areflexia with intact bladdersensation. !ssociated internal sphincter denervation may occur. f the peripheral sympathetic

nerves are damaged, the internal sphincter will be open and nonfunctional. 'eripheral

sympathetic nerve damage often occurs in association with detrusor denervation. The striatedsphincter, however, is preserved.

Pelvic sur"ery

'atients undergoing major pelvic surgery, such as radical hysterectomy, abdominoperineal

resection, proctocolectomy, or total exenteration will experience bladder dysfunction postoperatively.

ost commonly, postsurgical patients will manifest symptoms of detrusor areflexia. 0owever, as

many as 8DB of affected patients will experience spontaneous recovery of function within ;

months after surgery.


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&or$up

!a#oratory Studies

rinalysis and urine culture: rinary tract infection can cause irritative voiding symptoms and

urge incontinence.

#rine cytolo"y

"arcinoma*in*situ of the urinary bladder causes symptoms of urinary freuency and urgency.

rritative voiding symptoms out of proportion to the overall clinical picture and=or hematuriawarrant urine cytology and cystoscopy.

$he% & pro'ile

3lood urea nitrogen (3N) and creatinine ("r) are chec#ed if compromised renal function is

suspected.

Other ests

oidin" diary

! voiding diary is a daily record of the patient1s bladder activity. t is an objective documentation

of the patient1s voiding pattern, incontinent episodes, and inciting events associated with urinaryincontinence.

Pad test

This is an objective test that documents the urine loss. ntravesical methylene blue test or oral

'yridium or rised may be used. ethylene blue and rised turns the urine color blue> 'yridium

turns the urine color orange.

'atients should resume their usual physical activities while wearing a 'eri*pad. f the pads turn to

orange or blue, the patient is experiencing urine loss. f the pads remain white, moisture most

li#ely is a normal vaginal fluid.

Diagnostic Procedures

Postvoid residual urine

The postvoid residual urine ('2C) measurement is a part of basic evaluation for urinary

incontinence.

f the '2C is high, the bladder may be contractile or the bladder outlet may be obstructed. 3othof these conditions will cause urinary retention with overflow incontinence.


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#ro'low rate

roflow rate is a useful screening test used mainly to evaluate bladder outlet obstruction.

roflow rate is volume of urine voided per unit of time.

4ow uroflow rate may reflect urethral obstruction, a wea# detrusor, or a combination of both.This test alone cannot distinguish an obstruction from a contractile detrusor.

illin" cysto%etro"ra%

! filling cystometrogram ("?) assesses the bladder capacity, compliance, and the presence of

phasic contractions (detrusor instability). ost commonly, liuid filling medium is used.

!n average adult bladder holds approximately AD*ADD m4 of urine. /uring the test, provocativemaneuvers help to unveil bladder instability.

oidin" cysto%etro"ra% (pressure*'low study)

'ressure*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 outletobstruction.

'ressure*flow studies can be combined with voiding cystogram and videourodynamic study for

complicated cases of incontinence.

$ysto"ra%

! static cystogram (anteroposterior and lateral) helps to confirm the presence of stressincontinence, the degree of urethral motion, and the presence of a cystocele. ntrinsic sphincter

deficiency will be evident by an open bladder nec#. 'resence of a vesicovaginal fistula or

bladder diverticulum also may be noted.

! voiding cystogram can assess bladder nec# and urethral function (internal and externalsphincter) during filling and voiding phases. ! voiding cystogram can identify a urethral

diverticulum, urethral obstruction, and vesicoureteral reflux.

+lectro%yo"raphy

5lectromyography (5?) helps to ascertain the presence of coordinated or uncoordinatedvoiding.


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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.

?eneral agreement is that cystoscopy is indicated for people complaining of persistent irritative

voiding symptoms or hematuria. The physician can diagnose obvious causes of bladderoveractivity, such as cystitis, stone, and tumor, easily. This information is important in

determining the etiology of the incontinence and may influence treatment decisions.

ideourodyna%ics

2ideourodynamics is the criterion standard for evaluation of a patient with incontinence.

2ideourodynamics combines the radiographic findings of voiding cystourethrogram (2"?)

and multichannel urodynamics.

2ideourodynamics 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.

reatment ' (anagement

(edical "are

Stress incontinence may be treated with surgical and nonsurgical means.

rge incontinence may be treated with behavioral modification or with bladder*relaxing agents.

ixed incontinence may reuire medications as well as surgery.

6verflow incontinence may be treated with some type of catheter regimen.

however,

judicious use of pads and devices to contain urine loss and maintain s#in integrity are extremely

useful in selected cases. !bsorbent pads and internal and external collecting devices have animportant 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:(-) women who fail all other treatments and remain incontinent, ($) women who are too ill ordisabled to participate in behavioral programs, () women who cannot be helped by medications,

(+) women with incontinence disorders that cannot be corrected by surgery, and (A) women who

are awaiting surgery.

http://emedicine.medscape.com/article/438262-overviewhttp://emedicine.medscape.com/article/453539-overview#showallhttp://emedicine.medscape.com/article/438262-overviewhttp://emedicine.medscape.com/article/453539-overview#showall


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)#sor#ent products

!bsorbent products are pads or garments designed to absorb urine to protect the s#in andclothing. !vailable in both disposable and reusable forms, they are a temporary means of #eeping

the patient dry until a more permanent solution becomes available. 3y reducing wetness and

odor, they help maintain the patient1s comfort and allow her to function in normal activities. Theymay be used temporarily until a definitive treatment ta#es effect or if the treatment yields less*

than*perfect results. !bsorbent products are helpful during the initial assessment and wor#up of

urinary incontinence. !s an adjunct to behavioral and pharmacologic therapies, they play an

important role in the care of persons with intractable incontinence.

/o not use absorbent products instead of definitive interventions to decrease or eliminate urinary

incontinence. 5arly dependency on absorbent pads may be a deterrent to achieving continence,

providing the wearer a false sense of security. "hronic use of absorbent products may lead to

inevitable acceptance of the incontinence condition, which removes the motivation to see#evaluation and treatment. n addition, improper use of absorbent products may contribute to s#in

brea#down and urinary tract infections. Thus, appropriate use, meticulous care, and freuent pador garment changes are needed when absorbent products are used.

!bsorbent 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. ore than ADB of members in 0elp for ncontinent 'eople (0') use some form of

protective garment to remain dry. n addition, +FB of elderly men and women use some type ofabsorbent product. n nursing homes, disposable diapers or reusable pad and pant systems are

used.

nli#e sanitary nap#ins, these absorbent products are specially designed to trap urine, minimi&e

odor, and #eep the patient dry. /ifferent types of products with varying degrees of absorbencyexist. These products may absorb $D*DD m4, depending on the brand and the absorbent material

of the product. !bsorbent pads and garments that are available include panty shields, pant

guards, undergarments, combination pad*pant systems, adult diaper garments, and special bed pads.


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*rethral occlusive devices

rethral occlusive devices are artificial devices that may be inserted into the urethra or placedover the urethral meatus to prevent urinary lea#age. These devices are palliative measures to

prevent involuntary urine loss. rethral occlusive devices are more attractive than absorbent

pads because they tend to #eep the patient drier> however, they may be more difficult andexpensive to use than pads. rethral occlusive devices must be removed after several hours or

after each voiding.

nli#e pads, these devices may be more difficult to change. %ith device manipulation, patients

may soil their hands. The ris# that a urethral plug may fall into the bladder or fall off the urethraalways exists. rethral occlusive devices, perhaps, are best suited for an active woman with

incontinence who does not desire surgery.

"atheters

rinary diversion, using various catheters, has been one of the mainstays of anti*incontinencetherapy. The use of catheters for bladder drainage has withstood the test of time. 3ladder

catheteri&ation may be a temporary measure or a permanent solution for urinary incontinence.

/ifferent types of bladder catheteri&ation include indwelling urethral catheters, suprapubic tubes,and self*intermittent catheteri&ation.G-H c

+ndwelling urethral catheters

"ommonly #nown as


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'atients do not have to ta#e continuous antibiotics while using the catheter. n fact, continuous

antibiotic therapy is contraindicated while a catheter is used. 'rolonged use of antibiotics to

prevent infection actually may cause paradoxical generation of bacteria that are resistant tocommon antibiotics. ndwelling use of a


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malfunctioning bladder. 3oth people who are paraplegic and people who are uadriplegic have

benefited from this form of urinary diversion. %hen suprapubic tubes are needed, usually smaller

(eg, -+


21/36

patients1 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

catheteri&ation for the patient. 6f all possible options (ie, urethral catheter, suprapubic tube,intermittent catheteri&ation), intermittent catheteri&ation is the best solution for bladder

decompression of a motivated individual who is not physically handicapped or mentally

impaired.

any studies of young individuals with spinal cord injuries have shown that intermittentcatheteri&ation is preferable to indwelling catheters (ie, urethral catheter, suprapubic tube) for

both men and women. ntermittent catheteri&ation has become a healthy alternative to indwelling

catheters for individuals with chronic urinary retention due to an obstructed bladder, a wea# bladder, or a nonfunctioning bladder. Ioung children with myelomeningocele have benefited

from the use of intermittent catheteri&ation.

however,

individual catheteri&ation schedules may vary, depending on the amount of fluid ta#en in during

the day.

"andidates for intermittent catheteri&ation must have motivation and intact physical andcognitive abilities. !nyone who has good use of her hands and arms can perform self*

catheteri&ation. Ioung children and the older population are able to do this everyday without

problems.


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ntermittent catheteri&ation may be performed using either a sterile catheter or a nonsterile clean

catheter. ntermittent catheteri&ation, using a clean techniue, is recommended for young

individuals with a bladder that cannot empty and without any other available options. 'atientsshould wash their hands with soap and water. Sterile gloves are not necessary. "lean intermittent

catheteri&ation 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

-*B per catheteri&ation and -*+ episodes of bacteriuria occur per -DD days of intermittentcatheteri&ation performed + times a day.


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Surgical "are

Surgical care for stress incontinence involves procedures that increase urethral outlet resistance.6perations that increase urethral resistance include bladder nec# suspension, periurethral bul#ing

therapy, sling procedures, and artificial urinary sphincter .

Surgical care for urge incontinence involves procedures that improve bladder compliance or

bladder capacity> these include sacral neuromodulation, botulinum toxin injections,GA, ;H detrusormyomectomy, and bladder augmentation.

Diet

The fact that certain foods in a daily diet can worsen symptoms of urinary freuency and urgeincontinence is well #nown. f a patient1s diet contains dietary stimulants, changes in her diet

may help ameliorate incontinence symptoms. /ietary stimulants are substances contained in the

food or drin# that either cause or exacerbate irritative voiding symptoms. 3y eliminating or

minimi&ing the inta#e of dietary stimulants, unwanted bladder symptoms can be improved or possibly cured. !voidance of dietary stimulants begins with consumer awareness through careful

label reading and maintaining a daily diet diary. 5xperimenting with dietary changes is not

appropriate for everyone, and dietary experimentation should be instituted on an individual basis."ertain food products exacerbate symptoms of urge incontinence.

Food


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Some patients tend to drin# water excessively. Some women drin# water because they enjoy the

taste. 6thers ta#e medication that ma#es their mouths dry, so they drin# more water. Some

women who are trying to lose weight are on a diet that reuires consuming abundant amounts ofwater. /rin#ing water excessively actually worsens irritative bladder symptoms. The exact

amount of fluid needed per day is calculated based on the patient1s lean body mass. Thus, the

amount of fluid reuirement will vary per individual.

Some older women do not drin# enough fluids to #eep themselves well hydrated. They minimi&etheir fluid inta#e to unacceptable levels, thin#ing that if they drin# less, they will experience less

incontinence. Trying to prevent incontinence by restricting fluids excessively may lead to

bladder irritation and actually worsen urge incontinence. n addition, dehydration contributes toconstipation. f a patient has a problem with constipation, recommend eating a high*fiber diet,

receiving adeuate hydration, and administering laxatives.

any drin#s contain caffeine. "affeine 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 freuency and urgency. "affeine*containing products includecoffee, tea, hot chocolate, and sodas. 5ven chocolate mil# and many over*the*counter

medications contain caffeine. 6f caffeine*containing products, coffee contains the most caffeine./rip coffee contains the most caffeine, followed by percolated coffee and then instant coffee.

5ven decaffeinated coffee contains a small amount of caffeine. /ecaffeinated coffee contains an

amount of caffeine similar to the amount in chocolate mil#. 'ersons who consume a largeamount of caffeine should slowly decrease the amount of caffeine consumed to avoid significant

withdrawal responses such as headache and depression.

Studies have shown that drin#ing carbonated beverages, citrus fruits drin#s, and acidic juices

may worsen irritative voiding or urge symptoms. "onsumption of artificial sweeteners also has

been theori&ed to contribute to urge incontinence.

Nighttime voiding and incontinence are major problems in the older population. %omen 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 theevening. 'atients should restrict fluids after dinnertime so they can sleep uninterrupted through

the night.

ndividuals 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 techniue, support hose, and=or

medications. !dvise 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 (Kobst) or intermittent, seuential compression devices (S"/s) used

briefly at the end of the day can reduce lower extremity edema and minimi&e nighttime diuresis,

thus improving sleep.


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Kudicious use of diuretics has been associated with a decrease in lower*extremity edema and

lower nighttime urine volumes. /epending on other medical conditions, changing the time of

administration of the diuretic to the morning may prevent large nighttime volumes of voiding.

)ctivity

!nti*incontinence exercises emphasi&e rehabilitating and strengthening the pelvic floor muscles

that are critical in maintaining urinary continence. 'elvic floor muscles also are #nown as levator ani muscles. They are named levator muscles because they function to levitate or elevate the

pelvic organs into their proper place. %hen levator muscles wea#en and fail, pelvic prolapse and

stress incontinence result. !n anatomic defect of the levator ani musculature reuires physicalrehabilitation. f aggressive physical therapy does not wor#, surgery is warranted.

'elvic muscle exercises may be used alone, augmented with vaginal cones, or reinforced with

biofeedbac# therapy or with electrical stimulation. 3ehavioral 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. f the patient is using abdominal muscles orcontracting their buttoc#s, they are not doing these exercises properly. f patients have difficulty

identifying the levator muscles, biofeedbac# therapy may be instituted.


26/36


27/36

The best results are achieved when standard pelvic muscle exercises (7egel exercises) are

performed with intravaginal weights. n premenopausal women with stress incontinence, the

subjective cure or improved continence status was approximately FD*8DB after +*; wee#s oftreatment. 2aginal 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.

Biofeed#ac$

3iofeedbac# therapy is a form of pelvic floor muscle rehabilitation using an electronic device for

individuals having difficulty identifying levator ani muscles. 3iofeedbac# therapy isrecommended for treatment of stress incontinence, urge incontinence, and mixed incontinence.

3iofeedbac# 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 feedbac# on the activity of the pelvic floor muscles.

3iofeedbac# is an intensive therapy, with wee#ly sessions performed in an office or a hospital bya trained professional, and it often is followed by a regimen of pelvic floor muscle exercises at

home. /uring a biofeedbac# therapy, a special tampon*shaped sensor is inserted in the patient1svagina 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. %hen the exercises are performed properly, the electric signals

from the pelvic floor muscles are registered on a computer screen. 3iofeedbac#, using multi*measurement recording, displays the simultaneous measurement of pelvic and abdominal muscle

activity on the computer monitor.

3iofeedbac# allows the patient to correctly identify the pelvic muscles that need rehabilitation.

The benefit of biofeedbac# therapy is that it provides the patient with minute*by*minutefeedbac# on the uality and intensity of her pelvic floor contraction. "ombining bladder and

urinary sphincter biofeedbac# allows the patient to regulate the pelvic muscle contraction in

response to increasing bladder volumes and to monitor the bladder activity. 3iofeedbac# is bestused in conjunction with pelvic floor muscle exercises and bladder training.

Studies on biofeedbac# combined with pelvic floor exercises show a A+*8FB improvement with

incontinence. The best biofeedbac# protocol is one that reinforces levator ani muscle contraction

with inhibition of abdominal and bladder contraction. Ceports using this method show a F;*8$Breduction in urinary incontinence. 3iofeedbac# also has been used successfully in treatment of

men with urge incontinence and intermittent stress incontinence after prostate surgery.

edical studies have demonstrated significant improvement in urinary incontinence in womenwith neurologic disease and in the frail older population when a combination of biofeedbac# and

bladder training is used. 3iofeedbac# 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 biofeedbac#than vaginal palpation alone.


28/36

3iofeedbac# produces a greater reduction in female urinary incontinence compared to pelvic

muscle exercises alone. 6verall, the medical literature indicates that pelvic muscle exercises and

other behavioral strategies, with or without biofeedbac#, can cure or reduce incontinence.0owever, the maximum benefit is derived from any pelvic muscle rehabilitation and education

program when ongoing reinforcement and guidance, such as biofeedbac# therapy, are provided.

Electrical stimulation

5lectrical stimulation is a more sophisticated form of biofeedbac# used for pelvic floor muscle

rehabilitation. This treatment involves stimulation of levator ani muscles using painless electric

shoc#s. 5lectrical stimulation of pelvic floor muscles produces a contraction of the levator animuscles and external urethral sphincter while inhibiting bladder contraction. This therapy

depends on a preserved reflex arc through the intact sacral micturition center. 4i#e biofeedbac#,

electrical stimulation can be performed at the office or at home. 5lectrical stimulation can be

used in conjunction with biofeedbac# or pelvic floor muscle exercises.

5lectrical stimulation therapy reuires a similar type of probe and euipment as those used for biofeedbac#. This form of muscle rehabilitation is similar to the biofeedbac# therapy, except

small electric shoc#s are used. Nonimplantable pelvic floor electrical stimulation uses vaginalsensors, anal sensors, or surface electrodes. !dverse reactions are minimal.

4i#e biofeedbac#, pelvic floor muscle electrical stimulation has been shown to be effective in

treating female stress incontinence, as well as urge and mixed incontinence. 5lectrical

stimulation may be most beneficial when stress incontinence and very wea# or damaged pelvicfloor muscles coexist. ! regimented program of electrical stimulation will help these wea#ened

pelvic muscles contract so they can become stronger. however, in order to derive significant

benefit, perform stimulation for a minimum of + wee#s. 'atients must continue pelvic floor

exercises after the treatment. nfortunately, this treatment does not appear to benefit cognitivelyimpaired patients.

Bladder training

3ladder training involves relearning how to urinate. This method of rehabilitation most often isused for active women with urge incontinence and sensory urge symptoms. 6ften, 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. n other words, though the bladder is not full, it issignaling that it is time to void.


29/36

3ladder training generally consists of self*education, scheduled voiding with conscious delay of

voiding, and positive reinforcement. !lthough bladder training is used primarily for urge

incontinence, this program may be used for simple stress incontinence and mixed incontinence.3ladder training reuires the patient to resist or inhibit the sensation of urgency and postpone

voiding. 'atients urinate according to a scheduled timetable rather than the symptoms of urge.

3ladder training uses dietary tactics such as adjustment of fluid inta#e and avoidance of dietary

stimulants. n addition, distraction and relaxation techniues allow delayed voiding to helpdistend the urinary bladder. 3y using these strategies, patients can induce the bladder to

accommodate progressively larger voiding volumes. nitially, the interval goal is determined by

the patient1s current voiding habits and is not enforced at night. Cegardless of the initial voiding pattern, the first voiding interval may be increased by -A* to D*minute increments. !s the

bladder becomes accustomed to this delay in voiding, the interval between mandatory voids is

increased progressively, with simultaneous distraction or relaxation techniues and dietarymodification. The interval goal between each void usually is set between $ and hours and may

be set further apart if desired.

!nother method of bladder training is to maintain the prearranged schedule and disregard the

unscheduled voids. 0owever, patients need to continue to maintain the prearranged voidingtimes. They will need to continue this program for several months.

!lternatively, bladder ultrasound may be employed. f patients need an objective demonstration

that their bladder is relatively empty, a portable bladder scanner may be used. ! bladder scanner

is a portable ultrasound machine that measures the amount of urine present in a patient1s bladder.%ith 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. %hen patients feel the need to

void, they can chec# the bladder using the scanner to see how much urine is present. f the

bladder is empty, patients should ignore the sensation of needing to go to the bathroom.

3ladder 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. 3ladder training may not be successful infrail women who are older. edical reports demonstrate that bladder training is effective in

reducing urinary incontinence. %ith bladder training, the rate of patients with mixed

incontinence that have been cured is reported to be -$B, while the improvement rate was FABafter ; months.

(edications *sed to reat Neurogenic Bladder

Stress incontinence results from a wea# urinary sphincter. The internal sphincter contains highconcentrations of alpha*adrenergic receptors. !ctivation 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 toimprove symptoms of stress urinary incontinence. edical conditions that cause urge

incontinence may be neurologic or nonneurologic. The urethra is normal, but the bladder is

hyperactive or overactive. 'harmacologic therapy for stress incontinence and an overactive


30/36

bladder may be most effective when combined with a pelvic exercise regimen. The main

categories of drugs used to treat urge incontinence include anticholinergic drugs, antispasmodics,

and tricyclic antidepressant agents.

!ll drugs with anticholinergic adverse effects are contraindicated if patients have documented

narrow*angle glaucoma. %ide*angle glaucoma is not a contraindication to their use. rinaryretention, bowel obstruction, ulcerative colitis, myasthenia gravis, and severe heart diseases are

contraindications for anticholinergic use. These agents may impair the patient1s ability to performha&ardous activities, such as driving or operating heavy machinery, because of the potential for

drowsiness. !nticholinergic drugs should not be ta#en in combination with alcohol, sedatives, or

hypnotic drugs.

%hen a single drug treatment does not wor#, combination therapy, such as oxybutynin

(/itropan) and imipramine (Tofranil) may be used. !lthough their mechanism of action differs,

oxybutynin and imipramine wor# together to improve urge incontinence. 6xybutynin causes

direct smooth muscle relaxation of the urinary bladder and has local anesthetic properties.

mipramine has a direct inhibitory and local anesthetic effect on the bladder smooth muscle, li#eoxybutynin> however, imipramine also increases the bladder outlet resistance at the level of the

bladder nec#. Thus, the combination of these drugs produces a synergistic effect to relax theunstable bladder to hold in urine and prevent urge incontinence. 'otential anticholinergic adverse

effects may be additive because both drugs have similar adverse reactions.

Estrogen derivatives

"onjugated 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). ucosal turgor of periurethral tissue from proper nourishment enhances urethralmucosal coaptation. Cesult is an improved mucosal seal effect, which is important in urethral

function (prevents intrinsic sphincter deficiency). 5strogen supplementation appears to be the

most effective in postmenopausal women with mild*to*moderate incontinence. 3oth types ofstress incontinence benefit from estrogen fortification.

'harmacologic therapy using estrogen derivatives results in few cures (D*-+B) but may cause

subjective improvement in $E*;;B of women. 4imited evidence suggests that oral or vaginal

estrogen therapy may benefit some women with stress and mixed urinary incontinence. 6ther potential beneficial effects of estrogen use include decreased bone loss and resolution of hot

flashes during menopause.

%hen estrogen is used long*term, addition of progestin therapy is recommended to preventendometrial hyperplasia in women with an intact uterus. 'rogestin (eg, medroxyprogesterone

$.A*-D mg=d) is needed for -D*- d to provide maximum maturation of endometrium and to

eliminate any hyperplastic changes. 'rogestin may be administered continuously or

intermittently.

$onju"ated estro"en (Pre%arin)

http://reference.medscape.com/drug/depo-provera-depo-subq-provera-104-medroxyprogesterone-342782http://reference.medscape.com/drug/depo-provera-depo-subq-provera-104-medroxyprogesterone-342782http://reference.medscape.com/drug/depo-provera-depo-subq-provera-104-medroxyprogesterone-342782http://reference.medscape.com/drug/depo-provera-depo-subq-provera-104-medroxyprogesterone-342782


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"onjugated 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. 'remarin vaginal cream is available in a pac#age with a plastic applicator and a tube thatcontains +$.A g of conjugated estrogens. 5ach gram contains D.;$A mg of conjugated estrogens.

5strogen cream is readily absorbed through the s#in and mucous membranes.

Coutinely prescribing conjugated estrogens to premenopausal women is not recommended. se

medication in women who are postmenopausal and incontinent and who have had ahysterectomy. repeat the regimen prn and taper off or discontinue at * to ;*mo

intervals. Two to four grams (D.A*- applicator) of cream may be administered intravaginally d

in a usual cyclic regimen. 'ediatric dosing has not been established.

"onjugated estrogen is a pregnancy category L drug.

)nticholinergic drugs

!nticholinergic 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 freuency, urgency,

and nocturnal enuresis. !ll anticholinergic drugs have similar performance profiles and toxicity.

'otential adverse effects of all anticholinergic agents include blurred vision, dry mouth, heart

palpitations, drowsiness, and facial flushing. %hen anticholinergic drugs are used in excess,acute urinary retention in the bladder may occur.

Propantheline bro%ide (Pro ,anthine)

'ropantheline bromide is the typical prototype for all anticholinergic agents. t bloc#s action of

acetylcholine at postganglionic parasympathetic receptor sites. n a medical study, propantheline bromide was shown to decrease incidence of urge incontinence by -*-FB when D mg was used

id. %hen stronger doses were used (;D mg id), the cure rate was reported to be over EDB.

!dult dosing is -A mg '6 tid=id. 'ediatric dosing has not been established.

'ropantheline bromide is a pregnancy category " drug.

Dicyclo%ine hydrochloride (,entyl)

/icyclomine hydrochloride is an anticholinergic agent with smooth muscle relaxant properties. t bloc#s the action of acetylcholine at parasympathetic sites in secretory glands and smooth

muscle. n a medical study, subjective improvement was reported by ;$B of the subjects while

ta#ing dicyclomine hydrochloride -D mg tid. The reported cure rate was EDB.

http://reference.medscape.com/drug/premarin-estrogens-conjugated-342771http://reference.medscape.com/drug/pro-banthine-propantheline-342000http://reference.medscape.com/drug/bentyl-dicyclomine-341987http://reference.medscape.com/drug/bentyl-dicyclomine-341987http://reference.medscape.com/drug/premarin-estrogens-conjugated-342771http://reference.medscape.com/drug/pro-banthine-propantheline-342000http://reference.medscape.com/drug/bentyl-dicyclomine-341987


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!dult dosing is -D*$D mg '6 tid. 'ediatric dosing has not been established.

/icyclomine hydrochloride is a pregnancy category 3 drug.

yoscya%ine sul'ate (Levsin-SL. Levsin. Levsinex. $ystospa! M. Levbid)

0yoscyamine sulfate is an anticholinergic agent with antispasmodic properties used for thetreatment of urge incontinence. t bloc#s the action of acetylcholine at parasympathetic sites in

smooth muscle, secretory glands, and the "NS, which in turn has antispasmodic effects. t is

absorbed well by the ? tract. if tolerated, it may be increased to -D mg '6 d.

'ediatric dosing has not been established.

Solifenacin succinate is a pregnancy category " drug.

Dari'enacin (+nablex)

/arifenacin is an extended*release product that elicits competitive muscarinic receptorantagonistic activity. t reduces bladder smooth muscle contractions. t has a high affinity for

receptors involved in bladder and ? smooth muscle contraction, saliva production, and iris

sphincter function. /arifenacin is indicated for overactive bladder with symptoms of urge

http://reference.medscape.com/drug/levbid-levsin-hyoscyamine-341990http://reference.medscape.com/drug/vesicare-solifenacin-342848http://reference.medscape.com/drug/vesicare-solifenacin-342848http://reference.medscape.com/drug/enablex-darifenacin-342850http://reference.medscape.com/drug/levbid-levsin-hyoscyamine-341990http://reference.medscape.com/drug/vesicare-solifenacin-342848http://reference.medscape.com/drug/enablex-darifenacin-342850


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incontinence, urgency, and freuency. The product should be swallowed whole> do not chew,

divide, or crush.

!dult dosing is F.A mg '6 d initially> after $ w#, the dose may be increased to -A mg '6 d based on response. /o not exceed F.A mg '6 d in patients with moderate hepatic impairment

("hild*'ugh class 3) or who are receiving potent "I'*+AD !+ inhibitors. 'ediatric dosing hasnot been established.

/arifenacin is a pregnancy category " drug.

0xybutynin chloride (Ditropan /1. Ditropan 2L)

6xybutynin chloride has both anticholinergic and direct smooth muscle relaxant effects on

urinary bladder. t provides a local anesthetic effect on irritable bladder. rodynamic studies

have shown oxybutynin increases bladder si&e, decreases freuency of symptoms, and delays

initial desire to void.

/itropan L4 has an innovative drug delivery system9oral osmotic delivery system (6C6S).

The /itropan L4 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 witha precision laser*drilled hole that allows the drug to be released at a constant rate.

%hen the drug is ingested, the aueous environment in the ? tract causes water to enter the

tablet via the semipermeable membrane at constant rate. ntroduction of water inside the tablet

liuifies the drug and causes the push layer to swell osmotically. !s the push layer swells, itforces the drug suspension out of the hole at a constant rate over a $+*h period.

/itropan L4 achieves steady*state levels over a $+*h period. t avoids first*pass metabolism ofthe liver and upper ? tract to avoid cytochrome '+AD en&ymes. t has excellent efficacy with

minimal adverse effects.

edical studies have shown that oxybutynin chloride reduces incontinence episodes by 8*EDB.The total continence rate has been reported to be +-*ADB. The mean reduction in urinary

freuency was $B. n clinical trials, only -B stopped ta#ing /itropan L4 because of dry

mouth, and less than -B stopped ta#ing /itropan L4 due to "NS adverse effects.

!dult dosing of /itropan C is $.A mg '6 tid, titrate prn to A mg bid=tid=id. /osing of /itropanL4 is A*-A mg '6 d. 'ediatric dosing has not been established.

6xybutynin chloride is a pregnancy category 3 drug.

Tolterodine L*tartrate (Detrol and Detrol L3)

Tolterodine 4*tartrate is a competitive muscarinic receptor antagonist for overactive bladder. tdiffers from other anticholinergic types in that it has selectivity for urinary bladder over salivary

glands. t exhibits high specificity for muscarinic receptors and has minimal activity or affinity

http://reference.medscape.com/drug/ditropan-xl-oxybutynin-343066http://reference.medscape.com/drug/detrol-la-tolterodine-342841http://reference.medscape.com/drug/ditropan-xl-oxybutynin-343066http://reference.medscape.com/drug/detrol-la-tolterodine-342841


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for other neurotransmitter receptors and other potential targets such as calcium channels. n

clinical studies, the mean decrease in urge incontinence episodes was ADB and the mean

decrease in urinary freuency was -FB.

!dult dosing of /etrol is $ mg '6 bid. /osing of /etrol 4! is + mg '6 d. 'ediatric dosing has

not been established.

Tolterodine 4*tartrate is a pregnancy category " drug.

Trospiu% (Sanctura)

Trospium is a uaternary ammonium compound that elicits antispasmodic and antimuscariniceffects. t antagoni&es acetylcholine effect on muscarinic receptors. 'arasympathetic effect

reduces smooth muscle tone in the bladder. Trospium is indicated to treat symptoms of

overactive bladder (eg, urinary incontinence, urgency, freuency).

!dult dosing is $D mg '6 bid> it should be ta#en on an empty stomach at least - h before meals.n patients with a "r"l M D m4=min, dosing is $D mg '6 hs. n patients FA years, dosing may

be titrated downward to $D mg '6 d based on tolerability. 'ediatric dosing has not been

established.

Trospium is a pregnancy category " drug.

esoterodine (Tovia!)


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mipramine hydrochloride is a typical tricyclic antidepressant. t facilitates urine storage by

decreasing bladder contractility and increasing outlet resistance. t has alpha*adrenergic effect on

the bladder nec# and antispasmodic effect on detrusor muscle. mipramine hydrochloride has alocal anesthetic effect on bladder mucosa.

!dult dosing is -D*AD mg '6 d=tid> the range is $A*-DD mg d. 'ediatric dosing has not beenestablished.

mipramine hydrochloride is a pregnancy category / drug.

3%itriptyline hydrochloride (+lavil)

!mitriptyline hydrochloride is a tricyclic antidepressant with sedative properties. t increases

circulating levels of norepinephrine and serotonin by bloc#ing their reupta#e at nerve endings

and is ineffective for use in urge incontinence. 0owever, it is extremely effective in decreasing

symptoms of urinary freuency in women with pelvic floor muscle dysfunction. !mitriptyline

hydrochloride restores serotonin levels and helps brea# the cycle of pelvic floor muscle spasms.t is well*tolerated and effective in most women with urinary freuency.

!dult dosing is -D mg=d '6> titrate prn by -D mg=w# until maximum dose of -AD mg is reached,urinary symptoms disappear, or adverse effects become intolerable. 'ediatric dosing has not been

established.

!mitriptyline hydrochloride is a pregnancy category / drug.

Follow%up

"omplications

'rolonged contact of urine with unprotected s#in causes contact dermatitis and s#in brea#down.

f left untreated, these s#in disorders may lead to pressure sores and ulcers, possibly resulting in

secondary infections.


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ntreated urinary tract infections may lead to urosepsis and death.

Prognosis

'rognosis of a patient with incontinence is excellent with modern health care. %ith improvement

in information technology, well*trained medical staff, and advances in modern medical#nowledge, patients who are incontinent should not experience the morbidity and mortality of

the past. !lthough the ultimate well being of a patient who is incontinent depends on theunderlying condition that has precipitated urinary incontinence, urinary incontinence itself is

easily treated and prevented by properly trained health care individuals.

Patient education

199027507 neurogenic bladder

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