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Neurogenic Bladder

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.

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 nervous system (!NS) and somatic nervous system. The central nervous system is composed of the brain, brain stem, and the spinal cord.

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 of voluntary 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.

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 they wor# in synergy. The mechanical process of urination is coordinated by the pons in the area

#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 '(" functions as 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 social training 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 delay urination 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 is approximately -+ inches long in an adult. !long 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. %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 interprets this signal and sends a reply via the pons that travels down the spinal cord to the sacral cord and, subse.uently, 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 normal micturition. ,f spinal cord injury has occurred, the patient will demonstrate symptoms of urinary fre.uency, 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 (/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 is responsible 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 sacral cord. %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 and develops, 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 relin.uished 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. The detrusor 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 one of the ordinary senses (ie, hearing, sight, smell, touch, taste, e.uilibrium). The bladder and the urethral sphincters are under the influence of their corresponding nerves.

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 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. %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 sympathetic nervous 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 pelvic diaphragm. 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 occurs with 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


/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 re.uires that the urinary bladder and the urethral sphincter wor# together as a coordinated unit 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 the urinary sphincter opens (low resistance) to allow unobstructed urinary flow and bladder emptying.

Filling phase

/uring 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. ,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 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 tri erin bladder contractions. Sympathetic nerves directly cause rela!ation and e!pansion of the detrusor muscle. Sympathetic nerves close the bladder neck by constrictin the internal urethral sphincter. This sympathetic input to the lower urinary tract is constantly active durin bladder fillin .

!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 normal micturition. !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 stress incontinence.
Emptying phase

The storage phase of the urinary bladder can be switched to the voiding phase either involuntarily (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 urethral resistance. %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 infant will 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 training usually 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 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. ,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 influences from 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 a multitude of inhibitory signals to prevent detrusor contractions. !t the same time, an individual may actively contract the levator muscles to #eep the external sphincter closed or initiate distracting techni.ues to suppress urination. Thus, the voiding process re.uires coordination of both the !NS and somatic nervous system, which are in turn controlled by the '(" located in the brainstem.


,f a problem occurs within the nervous system, the entire voiding cycle is affected. !ny part of the 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. 3ladder overactivity (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 their destination. They may wa#e up fre.uently 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 lower extremity 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. <or example, the legs become spastic. These people experience urge incontinence. The bladder empties too .uic#ly and too fre.uently. The voiding disorder is similar to that of the brain lesion except that the external sphincter may have paradoxical contractions as well. ,f 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. 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 may

exhibit visual disturbances, #nown as optic neuritis. "hildren born with myelomeningocele may have spastic bladders and=or an open urethra. "onversely, 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. ,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 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 stuc# near the 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, affected individuals 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 definitions

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 the external sphincter function in synergy (in coordination). /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. The

external sphincter is in synergy with detrusor contraction. The detrusor is too wea# to mount an ade.uate 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 fre.uency and nocturia. The cause may be neurologic or nonneurologic. /etrusor areflexia is complete inability of the detrusor to empty due to a lower motor neuron lesion (eg, sacral cord or peripheral nerves). )rinary retention is the inability of the urinary bladder to empty. The cause may be neurologic or nonneurologic.

Types 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 with coordinated urethral sphincter activity. This occurs because the '(" is released from the cerebral inhibitory center. %hen the patient manifests symptoms of detrusor hyperreflexia, the individual will complain of urinary fre.uency, urgency, and urge incontinence. The treatment for the cerebral shoc# phase is indwelling <oley catheter or clean intermittent catheteri&ation (","). %hen the bladder becomes hyperreflexic, institute therapies to facilitate bladder filling and storage with anticholinergic medications.
Brain tumor

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

%hen the patient manifests symptoms of detrusor hyperreflexia, the individual complains of urinary fre.uency, urgency, and urge incontinence. <irst*line treatment for detrusor hyperreflexia includes anticholinergic medication.
Par#inson disease

This is a degenerative disorder of pigmented neurons of substantia nigra. ,t results in dopamine deficiency and increased cholinergic activity in the corpus striatum. 'atients with 'ar#inson disease manifest symptoms of brady#inesia, s#eletal muscle tremor, cogwheel rigidity, and mas#ed facies. Symptoms specific to the urinary bladder include urinary fre.uency, urgency, nocturia, and urge incontinence. Typical urodynamic findings for 'ar#inson disease are most consistent with detrusor hyperreflexia and urethral sphincter brady#inesia. The striated urethral sphincter often demonstrates poorly sustained contraction. Similar to other supraspinal lesions, the treatment for 'ar#inson disease is to facilitate bladder filling and promote urinary storage with anticholinergic agents. ,f patients with 'ar#inson disease exhibit symptoms of bladder outlet obstruction (366) due to benign prostatic enlargement (3'5), the diagnosis of 366 should be confirmed by multichannel urodynamic studies. The most common cause of postprostatectomy incontinence in the patient with 'ar#inson disease is detrusor hyperreflexia. ,f transurethral resection of the prostate (T)C') is performed without urodynamic confirmation of obstruction, the patient may become totally incontinent after the T)C' procedure.
Shy$Drager syndrome

Shy*/rager syndrome is a rare, progressive, and degenerative disease affecting the !NS with multisystem organ atrophy. ,n addition to 'ar#inson*li#e symptoms, cerebellar ataxia and autonomic dysfunction are common. !ffected individuals demonstrate orthostatic hypotension, anhidrosis, and urinary incontinence. /egeneration of the nucleus of 6nuf results in denervation of the external striated sphincter. Sympathetic nerve atrophy causes nonfunctional bladder and an open bladder nec#. )rodynamic evaluation often reveals detrusor hyperreflexia, although a few individuals may have detrusor areflexia or poorly sustained bladder contractions. 6ften, the bladder nec# (internal sphincter) will be open at rest, with striated sphincter denervation. 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 T)C' 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, and the 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. /uring this 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 monitored for 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 to hyperreflexic 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;) most often will have urodynamic findings of detrusor hyperreflexia, striated sphincter dyssynergia, and smooth sphincter dyssynergia. ! uni.ue complication of T; injury is autonomic dysreflexia. !utonomic 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. 6ften, 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. !cute management of autonomic dysreflexia is to decompress the rectum or bladder. /ecompression usually will reverse the effects of unopposed sympathetic outflow. ,f additional measures are re.uired, 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 with autonomic 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 no autonomic 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 sphincter dyssynergia, 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 correlation exists 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 lumbar dis# 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 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 fre.uency, urgency, and urge 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 bladder sensation. !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 striated sphincter, 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.

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 fre.uency and urgency. ,rritative voiding symptoms out of proportion to the overall clinical picture and=or hematuria warrant urine cytology and cystoscopy. $he% & pro'ile 3lood urea nitrogen (3)N) and creatinine ("r) are chec#ed if compromised renal function is suspected.
Other Tests

(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 urinary incontinence. 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. 3oth of these conditions will cause urinary retention with overflow incontinence.

#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, li.uid filling medium is used. !n average adult bladder holds approximately AD*ADD m4 of urine. /uring the test, provocative maneuvers 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 outlet obstruction. '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 stress incontinence, 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 external sphincter) 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 uncoordinated voiding. <ailure of urethral relaxation during bladder contraction results in uncoordinated voiding (detrusor sphincter dyssynergia). 5(? allows accurate diagnosis of detrusor sphincter dyssynergia common in spinal cord injuries. $ystoscopy

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 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. (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.

Treatment & '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 re.uire medications as well as surgery. 6verflow incontinence may be treated with some type of catheter regimen. <unctional incontinence may be resolved by treating the underlying cause (eg, urinary tract infection, constipation) or by simply changing a few medications. /o 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 s#in integrity are extremely useful in selected cases. !bsorbent 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: (-) women who fail all other treatments and remain incontinent, ($) women who are too ill or disabled 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.

("sor"ent products

!bsorbent products are pads or garments designed to absorb urine to protect the s#in and clothing. !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. They may 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 fre.uent pad or 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 of absorbent 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 absorbency exist. 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. <or occasional minimal urine loss, panty shields (small absorbent inserts) may be used. <or light incontinence, guards (close*fitting pads) may be more appropriate. !bsorbent guards are attached to the underwear and can be worn under normal clothing. !dult undergarments (full*length pads) are bul#ier and more absorbent than guards. They may be held in place by waist straps or snug underwear. !dult briefs are the bul#iest type of protection, offering the highest level of absorbency, and are secured in place with self*adhesive tape. !bsorbent bed pads also are available to protect the bed sheets and mattresses at night. They are available in different si&es and absorbencies.

)rethral occlusive devices

)rethral occlusive devices are artificial devices that may be inserted into the urethra or placed over 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 and expensive 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 urethra always exists. )rethral occlusive devices, perhaps, are best suited for an active woman with incontinence who does not desire surgery.

)rinary 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. 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 <oley catheters, indwelling urethral catheters historically have been the mainstay of treatment for bladder dysfunction. ,f 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 si&e for treating urinary retention is -;< or -8<, with a A*m4 balloon filled with -D m4 of sterile water. 4arger catheters (eg, $$<, $+<) with bigger balloons are used for treating grossly bloody urine found in other urologic conditions or diseases. 'roper 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 fre.uently. !ll indwelling catheters in the urinary bladder for more than $ wee#s become coloni&ed with bacteria. 3acterial coloni&ation does not mean the patient has clinical bladder infection. Symptoms of bladder infection include foul odor, purulent urine, and hematuria. <ever with flan# pain often is present if upper tracts are involved. ,f bladder infection occurs, change the entire catheter and the drainage system. The urinary drainage bag does not need to be disinfected to prevent infection. Coutine irrigation of catheters is not re.uired. 0owever, some authors favor the use of D.$AB acetic acid irrigation because it is bacteriostatic, minimi&es catheter encrustation, and diminishes the odor. %hen used, D m4 is instilled into the bladder and allowed to freely drain on a twice daily basis.

'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 to common antibiotics. ,ndwelling use of a <oley catheter in individuals who are homebound re.uires close supervision by a visiting nurse and additional personal hygiene care. ,n spite of its apparent advantages, the use of a <oley catheter for a prolonged period of time (eg, months to years) is strongly discouraged. "hronic dependence on these catheters is extremely ris#y because long*term use of urethral catheters poses significant health ha&ards. ,ndwelling urethral catheters are a significant cause of urinary tract infections that involve the urethra, bladder, and #idneys. %ithin $*+ wee#s after catheter insertion, bacteria will be present in the bladder of most women. !symptomatic bacterial coloni&ation is common and does not pose a health ha&ard. 0owever, untreated symptomatic urinary tract infections may lead to urosepsis and death. The death rate of nursing home residents with urethral catheters has been found to be times higher than that of residents without catheters> this may be more a reflection of the severity of comorbid conditions that lead to the clinical decision to use chronic bladder drainage than causation from the use of chronic bladder drainage. The use of a urethral catheter is contraindicated in the treatment of urge incontinence. 6ther problems associated with indwelling urethral catheters include encrustation of the catheter, bladder spasms resulting in urinary lea#age, hematuria, and urethritis. (ore severe complications include formation of bladder stones, development of periurethral abscess, renal damage, and urethral erosion. !nother problem of long*term catheteri&ation is bladder contracture, which occurs with urethral catheters as well as suprapubic tubes. !nticholinergic therapy and intermittent clamping of the catheter in combination have been reported to be beneficial for preserving the bladder integrity with long*term catheter use. ,ndividuals who did not use the medication and daily clamping regimen experienced a decrease in bladder capacity and vesicoureteral reflux. <or this reason, some physicians recommend using anticholinergic medications with intermittent clamping of the catheter if lower urinary tract reconstruction is anticipated in the future. Cestrict the use of indwelling catheters to the following situations: (-) as comfort measures for the terminally ill, ($) to avoid contamination or to promote healing of severe pressure sores, ( ) in case of inoperable urethral obstruction that prevents bladder emptying, (+) in individuals who are severely impaired and for whom alternative interventions are not an option, (A) when an individual lives alone and a caregiver is unavailable to provide other supportive measures, (;) for acutely ill persons in whom accurate fluid balance must be monitored, and (F) for severely impaired persons for whom bed and clothing changes are painful or disruptive. 0owever, when long*term use of a urethral catheter is anticipated, a suprapubic catheter is an attractive alternative.
Suprapu"ic catheters

! 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. 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, -+<, -;<) catheters are placed. 4i#e the urethral catheter, change the suprapubic tube once a month on a regular basis. Suprapubic catheters have many advantages. %ith a suprapubic catheter, the ris# of urethral damage is eliminated. (ultiple voiding trials may be performed without having to remove the catheter. 3ecause the catheter comes out of the lower abdomen rather than the vaginal area, a suprapubic tube is more patient*friendly. 3ladder spasms occur less often because the suprapubic catheter does not irritate the trigone as does the urethral catheter. ,n addition, suprapubic tubes are more sanitary for the individual, and bladder infections are minimi&ed because the tube is away from the perineum. Suprapubic catheters are changed easily by either a nurse or a doctor. )nli#e the urethral catheter, a suprapubic tube is less li#ely to become dislodged because the exit site is so small. %hen the tube is removed, the hole in the abdomen .uic#ly seals itself within -*$ days. ,ndications for suprapubic catheters include short*term use following gynecologic, urologic, and other types of surgery. Suprapubic catheters may be used whenever the clinical situation re.uires 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. ! suprapubic tube does not prevent bladder spasms from occurring in unstable bladders nor does it improve the urethral closure mechanism in an incompetent urethra. 'otential complications with chronic suprapubic catheteri&ation are similar to those associated with indwelling urethral catheters, including lea#age around the catheter, bladder stone formation, urinary tract infection, and catheter obstruction. /uring the initial placement of a suprapubic tube, a potential for bowel injury exists. !lthough uncommon, bowel perforation is #nown to occur with first*time placement of suprapubic tubes. 6ther potential complications include cellulitis around the tube site and hematoma. ,f the suprapubic tube falls out inadvertently, the exit hole of the tube will seal up and close .uic#ly within $+ hours if the tube is not replaced with a new one. ,f tube dislodgment is recogni&ed promptly, a new tube can be reinserted .uic#ly and painlessly as long as the tube site remains patent. ! suprapubic catheter is an alternative solution to an indwelling urethral catheter in women who re.uire chronic bladder drainage. 'otential problems uni.ue to suprapubic catheters include s#in infection, hematoma, bowel injury, and problems with catheter reinsertion. 4ong*term management of a suprapubic tube also may be problematic if the health care provider lac#s the #nowledge and expertise of suprapubic catheters or if the homebound individual lac#s .uic# access to a medical center in case of an emergency. ,n the appropriate situation, the suprapubic catheter affords many advantages over long*term urethral catheters.
*ntermittent catheteri+ation

,ntermittent catheteri&ation or self*catheteri&ation is a mode of draining the bladder at timed intervals, as opposed to continuous bladder drainage. ! prere.uisite for self*catheteri&ation is the

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 intermittent catheteri&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. <or those children, antibiotic prophylaxis (low*dose chemoprophylaxis) has commonly been prescribed for urinary tract infections. ! study by Jegers et al found that this practice can be safely discontinued, especially in males, patients with low urinary tract infection rates, and patients without vesicoureteral reflux.G$H ,n addition, self*catheteri&ation is recommended by some surgeons for women during the acute healing process after anti*incontinence surgery. ,ntermittent catheteri&ation 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 awa#ening, every *; hours during the day, and before bed) or based on bladder volume. Cemember that the average adult bladder holds approximately +DD*ADD m4 of urine. ,deally, the amount drained each time should not exceed +DD*ADD m4. This drainage limit may re.uire decreasing the fluid inta#e or increasing the fre.uency of catheteri&ations. ,f catheteri&ation is performed every ; hours and the amount drained is FDD m4, increase the fre.uency of catheteri&ation to, perhaps, every + hours to maintain the volume drained at +DD*ADD m4. ,ntermittent catheteri&ation is designed to simulate normal voiding. )sually, the average adult empties the bladder +*A times a day. Thus, catheteri&ation should occur +*A times a day> 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 and cognitive 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. <or individuals who are impaired, a home caregiver or a visiting nurse can be instructed to perform intermittent catheteri&ation. Self*catheteri&ation may be performed at home, at wor#9anywhere.

,ntermittent catheteri&ation may be performed using either a sterile catheter or a nonsterile clean catheter. ,ntermittent catheteri&ation, using a clean techni.ue, is recommended for young individuals with a bladder that cannot empty and without any other available options. 'atients should 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 intermittent catheteri&ation performed + times a day. <urthermore, the infections that do occur usually are managed without complications. ,n general, routine use of long*term suppressive therapy with antibiotics in patients with chronic clean intermittent catheteri&ation is not recommended. The use of chronic suppressive antibiotic therapy in people regularly using clean intermittent catheteri&ation is undesirable because it may result in the emergence of resistant bacterial strains. ! study of a patients with acute spinal cord injury at -A North !merican centers revealed that using a hydrophilic*coated catheter for intermittent catheteri&ation delayed the onset of first antibiotic*treated symptomatic urinary tract infections. ,n addition, a reduction in incidence of symptomatic urinary tract infection was noted during inpatient rehabilitation for these patients.G H ,n high*ris# 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. <or the older population and individuals with a wea# immune system, the sterile techni.ue of intermittent catheteri&ation has been recommended. 'ersons who are older are at higher ris# than younger persons for developing bacteriuria and other complications caused by intermittent catheteri&ation because they do not have a strong defense system against infection. !lthough the incidence of infection and other complications for older patients who are using sterile versus clean intermittent catheteri&ation is not well established, sterile intermittent catheteri&ation appears to be the safest method for this high*ris# population. 'otential advantages of performing intermittent catheteri&ation include patient autonomy, freedom from indwelling catheter and bags, and unimpeded sexual relations. 'otential complications of intermittent catheteri&ation include bladder infection, urethral trauma, urethral inflammation, and stricture. "oncurrent use of anticholinergic therapy will maintain acceptable intravesical pressures and prevent bladder contracture. Studies have demonstrated that long*term use of intermittent catheteri&ation appears to be preferable to indwelling catheteri&ation (ie, urethral catheter, suprapubic tube) with respect to urinary tract infections and the development of stones within the bladder or #idneys. 6verall, the management of infections in the setting of catheters and drainage tubes is challenging. 5xperimental 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. <urther studies may prove this modality more clinically useful to practice environments.G+H

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 detrusor myomectomy, and bladder augmentation.

The fact that certain foods in a daily diet can worsen symptoms of urinary fre.uency and urge incontinence 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.

<oods that contain heavy or hot spices may contribute to urge incontinence. ! 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. ! second food group that may worsen irritative voiding symptoms is citrus fruit. <ruits and juices that have a high potassium concentration may worsen preexisting urge incontinence. 5xamples of fruits that have significant potassium include grapefruits and oranges. ! third food group that may worsen urinary bladder incontinence is chocolate*containing sweets. "hocolate snac#s and treats contain caffeine. "affeine is a bladder*unfriendly agent. 5xcessive inta#e of chocolate confectioneries worsens irritative bladder symptoms.

The .uantity and .uality of refreshments consumed will influence urinary voiding symptoms. !n average !merican adult re.uires a daily allowance of approximately ;*8 glasses of fluids. <luids refer to all the beverages a person consumes in a day, including water, soda, and mil#. The human body receives water from beverages consumed, water contained in the food ingested, and water metaboli&ed from food eaten. The recommended amount of fluids consumed (all types) in $+ hours totals ;*8 glasses. The benefits of ade.uate fluid inta#e include prevention of dehydration, constipation, urinary tract infection, and #idney stone formation.

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 re.uires consuming abundant amounts of water. /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 re.uirement will vary per individual. Some older women do not drin# enough fluids to #eep themselves well hydrated. They minimi&e their 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 to constipation. ,f a patient has a problem with constipation, recommend eating a high*fiber diet, receiving ade.uate 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 fre.uency and urgency. "affeine*containing products include coffee, 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 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 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 the evening. '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 techni.ue, 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, se.uential 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.

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.

!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 re.uires physical rehabilitation. ,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 or contracting their buttoc#s, they are not doing these exercises properly. ,f patients have difficulty identifying the levator muscles, biofeedbac# therapy may be instituted. <or selected individuals, electrical stimulation further enhances pelvic muscle rehabilitation therapy.
Pelvic floor e,ercise

'elvic 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. 'elvic floor exercises, sometimes called 7egel exercises, are a rehabilitation techni.ue used to tighten and tone the pelvic floor muscles (ie, levator ani) that have become wea# 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. ,n addition, 7egel exercises may be performed to eliminate urge incontinence. "ontraction of the external urinary sphincter induces reflex bladder relaxation. 'elvic floor muscle rehabilitation may be used to reprogram the urinary bladder to decrease the fre.uency of incontinence episodes. ,ndividuals who benefit the most from pelvic floor exercises tend to be young healthy women who can identify the levator muscles accurately. 6lder adults with wea# pelvic tone or women who have difficulty recogni&ing the right muscles will need adjunct therapy such as biofeedbac# or electrical stimulation. 'elvic floor exercises wor# 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. 'elvic 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, buttoc#, or inner thigh muscles.

<or urge incontinence, pelvic floor muscle exercises are used to retrain the bladder. %hen 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. %henever 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 wal# slowly to the bathroom with urinary control. 3y regularly training the external sphincter, patients can gradually increase the time between urination from -* hours. 'atients should begin to see improvement in *+ wee#s. Thus, this techni.ue may be used for urge symptoms, urge incontinence, and mixed incontinence (stress and urge incontinence). %hen performing these drills, patients should not contract their abdominal muscles. "ontracting the abdominal muscles is counterproductive and merely worsens urinary incontinence. ,n 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. 'atients should practice contracting the levator ani muscles immediately before and during situations when lea#age 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 #nown as the guarding reflex. %hen the patient tightens the external urinary sphincter just as a snee&e is about to occur, the involuntary urine loss is thwarted. 3y s.uee&ing the levator ani muscles when the patient feels the sense of urgency, the sensation of impending bladder contraction will dissipate. 3y ma#ing 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 A;*EAB. 'elvic floor exercises are effective, even after multiple anti*incontinence surgeries.
-aginal weights

2aginal weight training is an effective form of pelvic floor muscle rehabilitation for stress incontinence in premenopausal women. 2aginal weights are tamponli#e special help aids used to enhance pelvic floor muscle exercises. Shaped li#e a small cone, vaginal weights (identical shape and volume) come in a set of A, with increasing weights (ie, $D, $.A, +A, ;D, and FA g). !s 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 -A minutes. !s the levator ani muscles become stronger, the exercise may be increased to D minutes. This exercise is performed twice daily. The intravaginal weight provides the sensory feedbac# for the desired pelvic muscle contraction. The sustained contraction re.uired 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 (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 of treatment. 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.

3iofeedbac# therapy is a form of pelvic floor muscle rehabilitation using an electronic device for individuals having difficulty identifying levator ani muscles. 3iofeedbac# therapy is recommended 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 by a 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 patient1s 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. %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*minute feedbac# 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 best used 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$B reduction 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 women with 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.

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 ani muscles 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 re.uires a similar type of probe and e.uipment 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 vaginal sensors, 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 pelvic floor muscles coexist. ! regimented program of electrical stimulation will help these wea#ened pelvic muscles contract so they can become stronger. <or women with urge incontinence, electrical stimulation may help the bladder relax and prevent it from contracting involuntarily. Cesearch 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. ,ncidence of urge incontinence secondary to neurologic diseases may be decreased with this therapy. 5lectrical stimulation appears to be most effective when augmented with pelvic floor exercises. 4ong*term data report that with electrical stimulation the rate of cured or improved patients ranged from A+*FFB> 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 cognitively impaired patients.
Bladder training

3ladder training involves relearning how to urinate. This method of rehabilitation most often is used 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 is signaling that it is time to void.

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 re.uires 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 techni.ues allow delayed voiding to help distend 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 techni.ues and dietary modification. 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 voiding times. 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 in frail 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 FAB after ; months.

'edications )sed to Treat Neurogenic Bladder

Stress incontinence results from a wea# urinary sphincter. The internal sphincter contains high concentrations 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 to improve 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

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. )rinary retention, bowel obstruction, ulcerative colitis, myasthenia gravis, and severe heart diseases are contraindications for anticholinergic use. These agents may impair the patient1s ability to perform ha&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#e oxybutynin> 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 the unstable 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 urethral mucosal 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 of stress 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 prevent endometrial 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)

"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 that contains +$.A g of conjugated estrogens. 5ach gram contains D.;$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 a hysterectomy. <or postmenopausal women with an intact uterus, cautiously recommend a short* term low*dose regimen of 'remarin with fre.uent monitoring. !dult dosing is D.;$A mg '6 .d for $- consecutive days, followed by F days without the drug (eg, w# on and - w# off)> 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 fre.uency, 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 '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.

!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. $ystospa! M. Levbid) 0yoscyamine sulfate is an anticholinergic agent with antispasmodic properties used for the treatment of urge incontinence. ,t bloc#s the action of acetylcholine at parasympathetic sites in smooth muscle, secretory glands, and the "NS, which in turn has antispasmodic effects. ,t is absorbed well by the ?, tract. <ood does not affect absorption. 0yoscyamine sulfate is available in sublingual form (4evsin S4), conventional tablets (4evsin), extended*release capsules (4evsinex Timecaps, "ystospa&*(), and extended*release tablets (4evbid). !dult dosing is D.-$A mg '6 .+h> alternatively, D. FA mg '6 bid can be used. <or severe symptoms, dosing is D. FA mg '6 tid. 'ediatric dosing has not been established. 0yoscyamine sulfate is a pregnancy category " drug.
(ntispasmodic drugs

These relax the smooth muscles of the urinary bladder. 3y 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 patient1s ability to perform activities re.uiring mental alertness and physical coordination. /rin#ing alcohol and using sedatives in combination with these antispasmodic drugs is contraindicated. Soli'enacin succinate ((+S/care) Solifenacin succinate elicits competitive muscarinic receptor antagonist activity, which results in anticholinergic effect and inhibition of bladder smooth muscle contraction. ,t is indicated for overactive bladder with symptoms of urgency, fre.uency, and urge incontinence. !dult dosing is A mg '6 .d> 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 receptor antagonistic 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

incontinence, urgency, and fre.uency. 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 has not 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 fre.uency 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 with a precision laser*drilled hole that allows the drug to be released at a constant rate. %hen the drug is ingested, the a.ueous environment in the ?, tract causes water to enter the tablet via the semipermeable membrane at constant rate. ,ntroduction of water inside the tablet li.uifies the drug and causes the push layer to swell osmotically. !s the push layer swells, it forces 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 of the 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 fre.uency 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 /osing of /itropan L4 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. ,t differs 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

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 fre.uency 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 antimuscarinic effects. ,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, fre.uency). !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 NFA 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!) <esoterodine is a competitive muscarinic receptor antagonist. The antagonistic effect results in decreased bladder smooth muscle contractions. ,t is indicated for symptoms of overactive bladder (eg, urinary urge incontinence, urgency, and fre.uency). <esoterodine is available as a +* or 8*mg extended*release tab. !dult dosing is + mg '6 .d> it may be increased to 8 mg=d. /osing is not to exceed + mg '6 .d in severe renal dysfunction (ie, "r"l M D m4=min) or with coadministration of drugs that decrease fesoterodineOs metabolism (eg, #etocona&ole, itracona&ole, clarithromycin). 'ediatric dosing has not been established. <esoterodine is a pregnancy category " drug.
Tricyclic antidepressant drugs

0istorically, these drugs were used to treat major depression> however, they have an additional use that is not </! approved9treatment of bladder dysfunction. They function to increase norepinephrine and serotonin levels. ,n addition, they exhibit anticholinergic and direct muscle relaxant effects on the urinary bladder. /%ipra%ine hydrochloride (To'ranil)

,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 a local 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 been established. ,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 fre.uency 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 fre.uency. !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.


'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. <or individuals with a decompensated bladder that does not empty well, the postvoid residual urine can lead to overgrowth of bacteria and subse.uent urinary tract infection. "hronic indwelling catheters may cause recurrent bladder infection, bladder stones, ascending pyelonephritis, and urethral erosion. The use of intermittent catheteri&ation may result in bladder infections or urethral injury. "hronic suprapubic tubes may result in bladder spasms, bladder stone formation, and bladder infection. 'otential problems uni.ue to suprapubic catheters include s#in infection, hematoma, bowel injury, and problems with catheter reinsertion.

)ntreated urinary tract infections may lead to urosepsis and death.


'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 the underlying condition that has precipitated urinary incontinence, urinary incontinence itself is easily treated and prevented by properly trained health care individuals.
Patient education

<or excellent patient education resources, see e(edicine0ealth1s patient education articles 3ladder "ontrol 'roblems, 3ladder "ontrol (edications, ,nability to )rinate, and <oley "atheter.
' pitfalls

<ailure to diagnose and treat urinary retention may result in adverse conse.uences. Cule out narrow*angle glaucoma prior to prescribing an anticholinergic agent. Narrow*angle glaucoma may be converted to open*angle glaucoma by an experienced ophthalmologist. %hen patients are ta#ing anticholinergic agents, monitor these patients to prevent pharmacologically induced urinary retention.