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Neurogenic Bladder

  • Author: Bradley C Gill, MD, MS; Chief Editor: Edward David Kim, MD, FACS  more...
 
Updated: Dec 11, 2015
 

Overview

The normal function of the urinary bladder is to store and expel urine in a coordinated, controlled fashion. This coordinated activity is regulated by the central and peripheral nervous systems. Neurogenic bladder is a term applied to a malfunctioning urinary bladder due to neurologic dysfunction or insult emanating from internal or external trauma, disease, or injury.

Symptoms of neurogenic bladder range from detrusor underactivity to overactivity, depending on the site of neurologic insult. The urinary sphincter also may be affected, resulting in sphincter underactivity or overactivity and loss of coordination with bladder function. The appropriate therapy and a successful outcome are predicated upon accurate diagnosis through a careful medical and voiding history together with a variety of clinical examinations, including urodynamics and selective radiographic imaging studies.

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Neuroanatomy

Normal voiding essentially is a spinal reflex that is modulated by the central nervous system (brain and spinal cord), which coordinates the functions of the bladder and urethra. The bladder and urethra are innervated by 3 sets of peripheral nerves arising from the autonomic nervous system (ANS) and somatic nervous system. The central nervous system is composed of the brain, brain stem, and the spinal cord.

Brain

The brain is the master control of the entire urinary system.

The micturition control center is located in the frontal lobe of the brain. The primary activity of this area is to send tonically inhibitory signals to the detrusor muscle to prevent the bladder from emptying (contracting) until a socially acceptable time and place to urinate is available.

Certain lesions or diseases of the brain, including stroke, cancer, or dementia, result in loss of voluntary control of the normal micturition reflex.

The signal transmitted by the brain is routed through 2 intermediate stops (the brainstem and the sacral spinal cord) prior to reaching the bladder.

Brainstem

The brainstem is located at the base of the skull. Within the brainstem is a specialized area known as the pons, a major relay center between the brain and the bladder. The pons is responsible for coordinating the activities of the urinary sphincters and the bladder so that they work in synergy. The mechanical process of urination is coordinated by the pons in the area known as the pontine micturition center (PMC). The PMC coordinates the urethral sphincter relaxation and detrusor contraction to facilitate urination. See the image below.

The pons is a major relay center between the brain The pons is a major relay center between the brain and the bladder. The mechanical process of urination is coordinated by the pons in the area known as the pontine micturition center (PMC).

The conscious sensations associated with bladder activity are transmitted to the pons from the cerebral cortex. The interaction of a variety of excitatory and inhibitory neuronal systems is the function of the PMC, which is characterized by its inborn excitatory nature. The PMC functions as a relay switch in the voiding pathway. Stimulation of the PMC causes the urethral sphincters to open while facilitating the detrusor to contract and expel the urine.

The PMC is affected by emotions, which is why some people may experience incontinence when they are excited or scared. The ability of the brain to control the PMC is part of the social training that children experience during growth and development. Usually the brain takes over the control of the pons at age 3-4 years, which is why most children undergo toilet training at this age.

When the bladder becomes full, the stretch receptors of the detrusor muscle send a signal to the pons, which in turn notifies the brain. People perceive this signal (bladder fullness) as a sudden desire to go to the bathroom. Under normal situations, the brain sends an inhibitory signal to the pons to inhibit the bladder from contracting until a bathroom is found.

When the PMC is deactivated, the urge to urinate disappears, allowing the patient to delay urination until finding a socially acceptable time and place. When urination is appropriate, the brain sends excitatory signals to the pons, allowing the urinary sphincters to open and the detrusor to empty.

Spinal cord

The spinal cord extends from the brainstem down to the lumbosacral spine. It is located in the spinal canal and is protected by the cerebrospinal fluid, meninges, and a vertebral column. It is approximately 14 inches long in an adult. Along its course, the spinal cord sprouts off many nerve branches to different parts of the body.

The spinal cord functions as a long communication pathway between the brainstem and the sacral spinal cord. When the sacral cord receives the sensory information from the bladder, this signal travels up the spinal cord to the pons and then ultimately to the brain. The brain interprets this signal and sends a reply via the pons that travels down the spinal cord to the sacral cord and, subsequently, to the bladder.

In the normal cycle of bladder filling and emptying, the spinal cord acts as an important intermediary between the pons and the sacral cord. An intact spinal cord is critical for normal micturition.

If spinal cord injury has occurred, the patient will demonstrate symptoms of urinary frequency, urgency, and urge incontinence but will be unable to empty his or her bladder completely. This occurs because the urinary bladder and the sphincter are both overactive, a condition termed detrusor sphincter dyssynergia with detrusor hyperreflexia (DSD-DH).

The sacral spinal cord is the terminal portion of the spinal cord situated at the lower back in the lumbar area. This is a specialized area of the spinal cord known as the sacral reflex center. It is responsible for bladder contractions. The sacral reflex center is the primitive voiding center.

In infants, the higher center of voiding control (the brain) is not mature enough to command the bladder, which is why control of urination in infants and young children comes from signals sent from the sacral cord. When urine fills the infant bladder, an excitatory signal is sent to the sacral cord. When this signal is received by the sacral cord, the spinal reflex center automatically triggers the detrusor to contract. The result is involuntary detrusor contractions with coordinated voiding.

A continuous cycle of bladder filling and emptying occurs, which is why infants and young children are dependent on diapers until they are toilet trained. As the child's brain matures and develops, it gradually dominates the control of the bladder and the urinary sphincters to inhibit involuntary voiding until complete control is attained. Voluntary continence usually is attained by age 3-4 years. By this time, control of the voiding process has been relinquished by the sacral reflex center of the sacral cord to the higher center in the brain.

If the sacral cord becomes severely injured (eg, spinal tumor, herniated disc), the bladder may not function. Affected patients may develop urinary retention, termed detrusor areflexia. The detrusor will be unable to contract, so the patient will not be able to urinate and urinary retention will occur.

Peripheral nerves

Peripheral nerves form an intricate network of pathways for sending and receiving information throughout the body. The nerves originate from the main trunk of the spinal cord and branch out in different directions to cover the entire body. Nerves convert the internal and external environmental stimuli to electrical signals so that the human body can understand stimuli as one of the ordinary senses (ie, hearing, sight, smell, touch, taste, equilibrium). The bladder and the urethral sphincters are under the influence of their corresponding nerves.

The ANS lies outside of the central nervous system. It regulates the actions of the internal organs (eg, intestines, heart, bladder) under involuntary control. The ANS is divided into the sympathetic and the parasympathetic nervous system.

Under normal conditions, the bladder and the internal urethral sphincter primarily are under sympathetic nervous system control. When the sympathetic nervous system is active, it causes the bladder to increase its capacity without increasing detrusor resting pressure (accommodation) and stimulates the internal urinary sphincter to remain tightly closed. The sympathetic activity also inhibits parasympathetic stimulation. When the sympathetic nervous system is active, urinary accommodation occurs and the micturition reflex is inhibited.

The parasympathetic nervous system functions in a manner opposite to that of the sympathetic nervous system. In terms of urinary function, the parasympathetic nerves stimulate the detrusor to contract. Immediately preceding parasympathetic stimulation, the sympathetic influence on the internal urethral sphincter becomes suppressed so that the internal sphincter relaxes and opens. In addition, the activity of the pudendal nerve is inhibited to cause the external sphincter to open. The result is facilitation of voluntary urination.

Like the ANS, the somatic nervous system is a part of the nervous system that lies outside of the central spinal cord. The somatic nervous system regulates the actions of the muscles under voluntary control. Examples of these muscles are the external urinary sphincter and the pelvic diaphragm. The pudendal nerve originates from the nucleus of Onuf and regulates the voluntary actions of the external urinary sphincter and the pelvic diaphragm. Activation of the pudendal nerve causes contraction of the external sphincter and the pelvic floor muscles, which occurs with activities such as Kegel exercises. Difficult or prolonged vaginal delivery may cause temporary neurapraxia of the pudendal nerve and cause stress urinary incontinence. Conversely, suprasacral-infrapontine spinal cord trauma can cause overstimulation of the pudendal nerve, resulting in urinary retention.

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Physiology and Pathophysiology

Physiology

During the course of a day, an average person will void approximately 4-8 times. The urinary bladder is in storage mode for most of the day, allowing an individual to engage in more important activities than urination.

Normal bladder function consists of 2 phases—filling and emptying. The normal micturition cycle requires that the urinary bladder and the urethral sphincter work together as a coordinated unit to store and empty urine. During urinary storage, the bladder acts as a low-pressure receptacle, while the urinary sphincter maintains high resistance to urinary flow to keep the bladder outlet closed. During urine elimination, the bladder contracts to expel urine while the urinary sphincter opens (low resistance) to allow unobstructed urinary flow and bladder emptying.

Filling phase

During the filling phase, the bladder accumulates increasing volumes of urine while the pressure inside the bladder remains low. The pressure within the bladder must be lower than the urethral pressure during the filling phase. If the bladder pressure is greater than the urethral pressure (resistance), urine will leak out.

The filling of the urinary bladder depends on the intrinsic viscoelastic properties of the bladder and the inhibition of the parasympathetic nerves. Thus, bladder filling primarily is a passive event.

Sympathetic nerves also facilitate urine storage in the following ways:

  • Sympathetic nerves inhibit the parasympathetic nerves from triggering bladder contractions.
  • Sympathetic nerves directly cause relaxation and expansion of the detrusor muscle.
  • Sympathetic nerves close the bladder neck by constricting the internal urethral sphincter. This sympathetic input to the lower urinary tract is constantly active during bladder filling.

As the bladder fills, the pudendal nerve becomes excited. Stimulation of the pudendal nerve results in contraction of the external urethral sphincter. Contraction of the external sphincter, coupled with that of the internal sphincter, maintains urethral pressure (resistance) higher than normal bladder pressure. The combination of both urinary sphincters is known as the continence mechanism.

The pressure gradients within the bladder and urethra play an important functional role in normal micturition. As long as the urethral pressure is higher than that of the bladder, patients will remain continent. If the urethral pressure is abnormally low or if the intravesical pressure is abnormally high, urinary incontinence will result.

As the bladder initially fills, a small rise in pressure occurs within the bladder (intravesical pressure). When the urethral sphincter is closed, the pressure inside the urethra (intraurethral pressure) is higher than the pressure within the bladder. While the intraurethral pressure is higher than the intravesical pressure, urinary continence is maintained.

During some physical activities and with coughing, sneezing, or laughing, the pressure within the abdomen rises sharply. This rise is transmitted to both the bladder and urethra. As long as the pressure is evenly transmitted to both the bladder and urethra, urine will not leak. When the pressure transmitted to the bladder is greater than urethra, urine will leak out, resulting in stress incontinence.

Emptying phase

The storage phase of the urinary bladder can be switched to the voiding phase either involuntarily (reflexively) or voluntarily. Involuntary reflex voiding occurs in an infant when the volume of urine exceeds the voiding threshold. When the bladder is filled to capacity, the stretch receptors within the bladder wall signal the sacral cord. The sacral cord, in turn, sends a message back to the bladder indicating that it is time to empty the bladder.

At this point, the pudendal nerve causes relaxation of the levator ani so that the pelvic floor muscle relaxes. The pudendal nerve also signals the external sphincter to open. The sympathetic nerves send a message to the internal sphincter to relax and open, resulting in a lower urethral resistance.

When the urethral sphincters relax and open, the parasympathetic nerves trigger contraction of the detrusor. When the bladder contracts, the pressure generated by the bladder overcomes the urethral pressure, resulting in urinary flow. These coordinated series of events allow unimpeded, automatic emptying of the urine.

A repetitious cycle of bladder filling and emptying occurs in newborn infants. The bladder empties as soon as it fills because the brain of an infant has not matured enough to regulate the urinary system. Because urination is unregulated by the infant's brain, predicting when the infant will urinate is difficult.

As the infant brain develops, the PMC also matures and gradually assumes voiding control. When the infant enters childhood (usually at age 3-4 years), this primitive voiding reflex becomes suppressed and the brain dominates bladder function, which is why toilet training usually is successful at age 3-4 years. However, this primitive voiding reflex may reappear in people with spinal cord injuries.

Delaying voiding or voluntary voiding

Bladder function is automatic but completely governed by the brain, which makes the final decision on whether or not to void. The normal function of urination means that an individual has the ability to stop and start urination on command. In addition, the individual has the ability to delay urination until a socially acceptable time and place. The healthy adult is aware of bladder filling and can willfully initiate or delay voiding.

In a healthy adult, the PMC functions as an on-off switch that is activated by stretch receptors in the bladder wall and is, in turn, modulated by inhibitory and excitatory neurologic influences from the brain. When the bladder is full, the stretch receptors are activated. The individual perceives the activation of the stretch receptors as the bladder being full, which signals a need to void.

When an individual cannot find a bathroom nearby, the brain bombards the PMC with a multitude of inhibitory signals to prevent detrusor contractions. At the same time, an individual may actively contract the levator muscles to keep the external sphincter closed or initiate distracting techniques to suppress urination.

Thus, the voiding process requires coordination of both the ANS and somatic nervous system, which are in turn controlled by the PMC located in the brainstem.

Pathophysiology

If a problem occurs within the nervous system, the entire voiding cycle is affected. Any part of the nervous system may be affected, including the brain, pons, spinal cord, sacral cord, and peripheral nerves. A dysfunctional voiding condition results in different symptoms, ranging from acute urinary retention to an overactive bladder or to a combination of both.

Urinary incontinence results from a dysfunction of the bladder, the sphincter, or both. Bladder overactivity (spastic bladder) is associated with the symptoms of urge incontinence, while sphincter underactivity (decreased resistance) results in symptomatic stress incontinence. A combination of detrusor overactivity and sphincter underactivity may result in mixed symptoms.

Brain lesion

Lesions of the brain above the pons destroy the master control center, causing a complete loss of voiding control. The voiding reflexes of the lower urinary tract—the primitive voiding reflex—remain intact. Affected individuals show signs of urge incontinence, or spastic bladder (medically termed detrusor hyperreflexia or overactivity). The bladder empties too quickly and too often, with relatively low quantities, and storing urine in the bladder is difficult. Usually, people with this problem rush to the bathroom and even leak urine before reaching their destination. They may wake up frequently at night to void.

Typical examples of a brain lesion are stroke, brain tumor, or Parkinson disease. Hydrocephalus, cerebral palsy, and Shy-Drager syndrome also are brain lesions. Shy-Drager syndrome is a rare condition that also causes the bladder neck to remain open.

Spinal cord lesion

Diseases or injuries of the spinal cord between the pons and the sacral spinal cord also result in spastic bladder or overactive bladder. People who are paraplegic or quadriplegic have lower extremity spasticity. Initially, after spinal cord trauma, the individual enters a spinal shock phase where the nervous system shuts down. After 6-12 weeks, the nervous system reactivates. When the nervous system becomes reactivated, it causes hyperstimulation of the affected organs. For example, the legs become spastic.

These people experience urge incontinence. The bladder empties too quickly and too frequently. The voiding disorder is similar to that of the brain lesion except that the external sphincter may have paradoxical contractions as well. If both the bladder and external sphincter become spastic at the same time, the affected individual will sense an overwhelming desire to urinate but only a small amount of urine may dribble out. The medical term for this is detrusor-sphincter dyssynergia because the bladder and the external sphincter are not in synergy. Even though the bladder is trying to force out urine, the external sphincter is tightening to prevent urine from leaving.

The causes of spinal cord injuries include motor vehicle and diving accidents. Multiple sclerosis (MS) is a common cause of spinal cord disease in young women. Those with MS also may exhibit visual disturbances, known as optic neuritis. Children born with myelomeningocele may have spastic bladders and/or an open urethra. Conversely, some children with myelomeningocele may have a hypocontractile bladder instead of a spastic bladder.

Sacral cord injury

Selected injuries of the sacral cord and the corresponding nerve roots arising from the sacral cord may prevent the bladder from emptying. If a sensory neurogenic bladder is present, the affected individual may not be able to sense when the bladder is full. In the case of a motor neurogenic bladder, the individual will sense the bladder is full and the detrusor may not contract, a condition known as detrusor areflexia. These individuals have difficulty eliminating urine and experience overflow incontinence; the bladder gradually overdistends until the urine spills out. Typical causes are a sacral cord tumor, herniated disc, and injuries that crush the pelvis. This condition also may occur after a lumbar laminectomy, radical hysterectomy, or abdominoperineal resection.

Some teenagers suddenly develop an abnormal voiding pattern and often are evaluated for tethered cord syndrome, a neurologic condition in which the tip of the sacral cord is stuck near the sacrum and cannot stretch as the child grows taller. Ischemic changes of the sacral cord associated with the tethering cause the manifestation of dysfunctional voiding symptoms.

Peripheral nerve injury

Diabetes mellitus and AIDS are 2 of the conditions causing peripheral neuropathy resulting in urinary retention. These diseases destroy the nerves to the bladder and may lead to silent, painless distention of the bladder. Patients with chronic diabetes lose the sensation of bladder filling first, before the bladder decompensates. Similar to injury to the sacral cord, affected individuals will have difficulty urinating. They also may have a hypocontractile bladder.

Other diseases manifesting this condition are poliomyelitis, Guillain-Barré syndrome, severe herpes in the genitoanal area, pernicious anemia, and neurosyphilis (tabes dorsalis).

Summary of definitions

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

Detrusor hyperreflexia refers to overactive bladder symptoms due to a suprapontine upper motor neuron neurologic disorder. External sphincter functions normally. The detrusor muscle and the external sphincter function in synergy (in coordination).

DSD-DH refers to overactive bladder symptoms due to neurologic upper motor neuron disorder of the suprasacral spinal cord. Paradoxically, the patient is in urinary retention. Both the detrusor and the sphincter are contracting at the same time; they are in dyssynergy (lack of coordination).

Detrusor hyperreflexia with impaired contractility (DHIC) refers to overactive bladder symptoms, but the detrusor cannot generate enough pressure to allow complete emptying. The external sphincter is in synergy with detrusor contraction. The detrusor is too weak to mount an adequate contraction for proper voiding to occur. The condition is similar to urinary retention, but irritating voiding symptoms are prevalent.

Detrusor instability refers to overactive bladder symptoms without neurologic impairment. External sphincter functions normally, in synergy.

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

Detrusor areflexia is complete inability of the detrusor to empty due to a lower motor neuron lesion (eg, sacral cord or peripheral nerves).

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

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Types of Neurogenic Bladders

Supraspinal Lesions

Supraspinal lesions refer to those lesions of the central nervous system involving the area above the pons. They include cerebrovascular accident, brain tumor, Parkinson disease, and Shy-Drager syndrome.

Cerebrovascular accident

After a stroke, the brain may enter into a temporary acute cerebral shock phase. During this time, the urinary bladder will be in retention—detrusor areflexia. Almost 25% of affected individuals develop acute urinary retention after a stroke.

After the cerebral shock phase wears off, the bladder demonstrates detrusor hyperreflexia with coordinated urethral sphincter activity. This occurs because the PMC is released from the cerebral inhibitory center. When the patient manifests symptoms of detrusor hyperreflexia, the individual will complain of urinary frequency, urgency, and urge incontinence.

The treatment for the cerebral shock phase is indwelling Foley catheter or clean intermittent catheterization (CIC). When the bladder becomes hyperreflexic, institute therapies to facilitate bladder filling and storage with anticholinergic medications.

Brain tumor

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

When the patient manifests symptoms of detrusor hyperreflexia, the individual complains of urinary frequency, urgency, and urge incontinence. First-line treatment for detrusor hyperreflexia includes anticholinergic medication.

Parkinson disease

This is a degenerative disorder of pigmented neurons of substantia nigra. It results in dopamine deficiency and increased cholinergic activity in the corpus striatum.

Patients with Parkinson disease manifest symptoms of bradykinesia, skeletal muscle tremor, cogwheel rigidity, and masked facies. Symptoms specific to the urinary bladder include urinary frequency, urgency, nocturia, and urge incontinence.

Typical urodynamic findings for Parkinson disease are most consistent with detrusor hyperreflexia and urethral sphincter bradykinesia. The striated urethral sphincter often demonstrates poorly sustained contraction.

Similar to other supraspinal lesions, the treatment for Parkinson disease is to facilitate bladder filling and promote urinary storage with anticholinergic agents.

If patients with Parkinson disease exhibit symptoms of bladder outlet obstruction (BOO) due to benign prostatic enlargement (BPE), the diagnosis of BOO should be confirmed by multichannel urodynamic studies. The most common cause of postprostatectomy incontinence in the patient with Parkinson disease is detrusor hyperreflexia.

If transurethral resection of the prostate (TURP) is performed without urodynamic confirmation of obstruction, the patient may become totally incontinent after the TURP procedure.

Shy-Drager syndrome

Shy-Drager syndrome is a rare, progressive, and degenerative disease affecting the ANS with multisystem organ atrophy. In addition to Parkinson-like symptoms, cerebellar ataxia and autonomic dysfunction are common. Affected individuals demonstrate orthostatic hypotension, anhidrosis, and urinary incontinence.

Degeneration of the nucleus of Onuf results in denervation of the external striated sphincter. Sympathetic nerve atrophy causes nonfunctional bladder and an open bladder neck.

Urodynamic evaluation often reveals detrusor hyperreflexia, although a few individuals may have detrusor areflexia or poorly sustained bladder contractions. Often, the bladder neck (internal sphincter) will be open at rest, with striated sphincter denervation.

The treatment for Shy-Drager syndrome is to facilitate urinary storage with anticholinergic agents coupled with CIC or indwelling catheter. Patients with Shy-Drager syndrome should avoid undergoing TURP because the risk of total incontinence is high.

Spinal Cord Lesions

Spinal cord injury

When an individual sustains a spinal cord injury from a diving accident or motor vehicle injury, the initial response from the nervous system is spinal shock. During this spinal shock phase, the affected individual experiences flaccid paralysis below the level of injury, and the somatic reflex activity is either depressed or absent.

The anal and bulbocavernosus reflex typically is absent. The autonomic activity is depressed, and the individual experiences urinary retention and constipation. Urodynamic findings are consistent with areflexic detrusor and rectum. The internal and external urethral sphincter activities, however, are normal.

The spinal shock phase typically lasts 6-12 weeks; it may be prolonged in some cases. During this time, the urinary bladder must be drained with CIC or indwelling urethral catheter.

When the spinal shock phase wears off, bladder function returns but the detrusor activity increases in reflex excitability to an overactive state—detrusor hyperreflexia. Depending on the level of the lesion, the individual may develop DSD-DH. Thus, the individual must be monitored for leaking between CIC, and periodic urodynamic testing must be performed for this alteration in detrusor behavior. During urodynamics, intravesical instillation of cold saline may indicate return of reflex activity or help better characterize the lesion.

Realizing that suprasacral lesions exhibit detrusor areflexia at initial insult but progress to hyperreflexic state over time is important. Conversely, sacral cord lesions are associated with areflexic bladders that may become hypertonic overtime.

Spinal cord lesions (above the sixth thoracic vertebrae)

Individuals who sustain a complete cord transection above the sixth thoracic vertebrae (T6) most often will have urodynamic findings of detrusor hyperreflexia, striated sphincter dyssynergia, and smooth sphincter dyssynergia. A unique complication of T6 injury is autonomic dysreflexia.

Autonomic dysreflexia is an exaggerated sympathetic response to any stimuli below the level of the lesion. This occurs most commonly with lesions of the cervical cord. Often, the inciting event is instrumentation of the urinary bladder or the rectum, causing visceral distention.

Symptoms of autonomic dysreflexia include sweating, headache, hypertension, and reflex bradycardia. Acute management of autonomic dysreflexia is to decompress the rectum or bladder. Decompression usually will reverse the effects of unopposed sympathetic outflow. If additional measures are required, parenteral ganglionic or adrenergic blocking agents, such as chlorpromazine, may be used.

Oral blocking agents, including terazosin, may be used for prophylactically treating patients with autonomic dysreflexia. Alternatively, spinal anesthetic may be used as a prophylactic measure whenever bladder instrumentation is considered.

Spinal cord lesions (below T6)

Individuals who sustain spinal cord lesions below T6 level will have urodynamic findings of detrusor hyperreflexia, striated sphincter dyssynergia, and smooth sphincter dyssynergia but no autonomic dysreflexia.

Neurologic evaluation will reveal skeletal muscle spasticity with hyperreflexic deep tendon reflexes. Affected patients will demonstrate extensor plantar response and positive Babinski sign.

These individuals will experience incomplete bladder emptying secondary to detrusor sphincter dyssynergia, or loss of facilitatory input from higher centers. Cornerstone of treatment involves CIC and anticholinergic medications.

Multiple sclerosis

MS is caused by focal demyelinating lesions of the central nervous system. It most commonly involves the posterior and lateral columns of the cervical spinal cord. Usually, poor correlation exists between the clinical symptoms and urodynamic findings. Thus, using urodynamic studies to evaluate patients with MS is critical.

The most common urodynamic finding is detrusor hyperreflexia, occurring in as many as 50-90% of patients with MS. As many as 50% of patients will demonstrate DSD-DH. Detrusor areflexia occurs in 20-30% of cases. The optimum therapy for a patient with MS and incontinence must be individualized and based on the urodynamic findings.

Peripheral Nerve Lesions

Peripheral nerve lesions due to diabetes mellitus, tabes dorsalis, herpes zoster, herniated lumbar disk disease, and radical pelvic surgery result in detrusor areflexia.

Diabetic cystopathy

Usually, neurogenic bladder dysfunction occurs 10 or more years after the onset of diabetes mellitus. Neurogenic bladder occurs because of autonomic and peripheral neuropathy. A metabolic derangement of the Schwann cell results in segmental demyelination and impaired nerve conduction.

The first symptoms of diabetic cystopathy are loss of sensation of bladder filling followed by loss of motor function. Classic urodynamic findings associated with this condition are elevated residual urine, decreased bladder sensation, impaired detrusor contractility, and, eventually, detrusor areflexia. Paradoxically, DHIC also has been observed. Treatment of diabetic cystopathy is CIC, long-term indwelling catheterization, or urinary diversion.

Tabes dorsalis (neurosyphilis)

In tabes dorsalis, central and peripheral nerve conduction is impaired. Affected patients experience decreased bladder sensation and increased voiding intervals.

The most common urodynamic finding associated with neurosyphilis is detrusor areflexia with normal sphincteric function.

Herpes zoster

Herpes zoster is a neuropathy associated with painful vesicular eruptions in the distribution of the affected nerve. The herpes virus lies dormant in the dorsal root ganglia or the sacral nerves.

Sacral nerve involvement leads to impairment of detrusor function. The early stages of herpes infection are associated with lower urinary tract symptoms of urinary frequency, urgency, and urge incontinence. Later stages include decreased bladder sensation, increased residual urine, and urinary retention. Urinary retention is self-limited and will resolve spontaneously with clearing of the herpes infection.

Herniated disc

Slow and progressive herniation of the lumbar disc may cause irritation of the sacral nerves and cause detrusor hyperreflexia. Conversely, acute compression of the sacral roots associated with deceleration trauma will prevent nerve conduction and result in detrusor areflexia.

A typical urodynamic finding of sacral nerve injury is detrusor areflexia with intact bladder sensation. Associated internal sphincter denervation may occur. If the peripheral sympathetic nerves are damaged, the internal sphincter will be open and nonfunctional. Peripheral sympathetic nerve damage often occurs in association with detrusor denervation. The striated sphincter, however, is preserved.

Pelvic surgery

Patients undergoing major pelvic surgery, such as radical hysterectomy, abdominoperineal resection, proctocolectomy, or total exenteration will experience bladder dysfunction postoperatively.

Most commonly, postsurgical patients will manifest symptoms of detrusor areflexia. However, as many as 80% of affected patients will experience spontaneous recovery of function within 6 months after surgery.

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Workup

Laboratory Studies

Urinalysis and urine culture: Urinary tract infection can cause irritative voiding symptoms and urge incontinence.

Urine cytology

Carcinoma-in-situ of the urinary bladder causes symptoms of urinary frequency and urgency. Irritative voiding symptoms out of proportion to the overall clinical picture and/or hematuria warrant urine cytology and cystoscopy.

Chem 7 profile

Blood urea nitrogen (BUN) and creatinine (Cr) are checked if compromised renal function is suspected.

Other Tests

Voiding diary

A voiding diary is a daily record of the patient's bladder activity. It is an objective documentation of the patient's voiding pattern, incontinent episodes, and inciting events associated with urinary incontinence.

Pad test

This is an objective test that documents the urine loss. Intravesical methylene blue test or oral phenazopyridine or Urised (which contains methylene blue) may be used. Methylene blue turns the urine color blue; phenazopyridine turns the urine color orange.

Patients should resume their usual physical activities while wearing a perineal pad. If the pads turn to orange or blue, the patient is experiencing urine loss. If the pads remain white, moisture most likely is a normal vaginal fluid.

Diagnostic Procedures

Postvoid residual urine

The postvoid residual urine (PVR) measurement is a part of basic evaluation for urinary incontinence. If the PVR is high, the bladder may be contractile or the bladder outlet may be obstructed. Both of these conditions will cause urinary retention with overflow incontinence.

Uroflow rate

Uroflow rate is a useful screening test used mainly to evaluate bladder outlet obstruction. Uroflow rate is volume of urine voided per unit of time.

Low uroflow rate may reflect urethral obstruction, a weak detrusor, or a combination of both. This test alone cannot distinguish an obstruction from a contractile detrusor.

Filling cystometrogram

A filling cystometrogram (CMG) assesses the bladder capacity, compliance, and the presence of phasic contractions (detrusor instability). Most commonly, liquid filling medium is used.

An average adult bladder holds approximately 50-500 mL of urine. During the test, provocative maneuvers help to unveil bladder instability.

Voiding cystometrogram (pressure-flow study)

Pressure-flow study simultaneously records the voiding detrusor pressure and the rate of urinary flow. This is the only test able to assess bladder contractility and the extent of a bladder outlet obstruction.

Pressure-flow studies can be combined with voiding cystogram and videourodynamic study for complicated cases of incontinence.

Cystogram

A static cystogram (anteroposterior and lateral) helps to confirm the presence of stress incontinence, the degree of urethral motion, and the presence of a cystocele. Intrinsic sphincter deficiency will be evident by an open bladder neck. The presence of a vesicovaginal fistula or bladder diverticulum also may be noted.

A voiding cystogram can assess bladder neck and urethral function (internal and external sphincter) during filling and voiding phases. A voiding cystogram can identify a urethral diverticulum, urethral obstruction, and vesicoureteral reflux.

Electromyography

Electromyography (EMG) helps to ascertain the presence of coordinated or uncoordinated voiding. Failure of urethral relaxation during bladder contraction results in uncoordinated voiding (detrusor sphincter dyssynergia). EMG allows accurate diagnosis of detrusor sphincter dyssynergia common in spinal cord injuries.

Cystoscopy

The role of cystoscopy in the evaluation of neurogenic bladder is to allow discovery of bladder lesions (eg, bladder cancer, bladder stone) that would remain undiagnosed by urodynamics alone.

General agreement is that cystoscopy is indicated for patients complaining of persistent irritative voiding symptoms or hematuria. The physician can diagnose obvious causes of bladder overactivity, such as cystitis, stone, and tumor, easily. This information is important in determining the etiology of the incontinence and may influence treatment decisions.

Videourodynamics

Videourodynamics is the criterion standard for evaluation of a patient with incontinence. Videourodynamics combines the radiographic findings of voiding cystourethrogram (VCUG) and multichannel urodynamics.

Videourodynamics enables documentation of lower urinary tract anatomy, such as vesicoureteral reflux and bladder diverticulum, as well as the functional pressure-flow relationship between the bladder and the urethra.

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Treatment & Management

Medical Care

Treatment of urinary incontinence varies by type, as follows:

  • Stress incontinence may be treated with surgical and nonsurgical means
  • Urge incontinence may be treated with behavioral modification or with bladder-relaxing agents
  • Mixed incontinence may require medications as well as surgery
  • Overflow incontinence may be treated with some type of catheter regimen
  • Functional incontinence may be resolved by treating the underlying cause (eg, urinary tract infection, constipation) or by simply changing a few medications

Do not consider anti-incontinence products to be a cure-all for urinary incontinence; however, judicious use of pads and devices to contain urine loss and maintain skin integrity are extremely useful in selected cases. Absorbent pads and internal and external collecting devices have an important role in the management of chronic incontinence. The criteria for use of these products are fairly straightforward, and they are beneficial for women who meet the following conditions:

  • Failure of all other treatments and persistent incontinence
  • Illness or disability that prevents participation in behavioral programs
  • Inability to benefit from medications
  • Incontinence disorders that cannot be corrected by surgery
  • Awaiting surgery

Absorbent products

Absorbent products are pads or garments designed to absorb urine to protect the skin and clothing. Available in both disposable and reusable forms, they are a temporary means of keeping the patient dry until a more permanent solution becomes available. By reducing wetness and odor, they help maintain the patient's comfort and allow her to function in normal activities. They may be used temporarily until a definitive treatment takes effect or if the treatment yields less-than-perfect results. Absorbent products are helpful during the initial assessment and workup of urinary incontinence. As an adjunct to behavioral and pharmacologic therapies, they play an important role in the care of persons with intractable incontinence.

Do not use absorbent products instead of definitive interventions to decrease or eliminate urinary incontinence. Early dependency on absorbent pads may be a deterrent to achieving continence, providing the wearer a false sense of security. Chronic use of absorbent products may lead to inevitable acceptance of the incontinence condition, which removes the motivation to seek evaluation and treatment. In addition, improper use of absorbent products may contribute to skin breakdown and urinary tract infections. Thus, appropriate use, meticulous care, and frequent pad or garment changes are needed when absorbent products are used.

Absorbent products used include underpads, pant liners (shields and guards), adult diapers (briefs), a variety of washable pants and disposable pad systems, or combinations of these products. More than 50% of members in Help for Incontinent People (HIP) use some form of protective garment to remain dry. In addition, 47% of elderly men and women use some type of absorbent product. In nursing homes, disposable diapers or reusable pad and pant systems are used.

Unlike sanitary napkins, these absorbent products are specially designed to trap urine, minimize odor, and keep the patient dry. Different types of products with varying degrees of absorbency exist. These products may absorb 20-300 mL, depending on the brand and the absorbent material of the product. Absorbent pads and garments that are available include panty shields, pant guards, undergarments, combination pad-pant systems, adult diaper garments, and special bed pads.

For occasional minimal urine loss, panty shields (small absorbent inserts) may be used. For light incontinence, guards (close-fitting pads) may be more appropriate. Absorbent guards are attached to the underwear and can be worn under normal clothing.

Adult undergarments (full-length pads) are bulkier and more absorbent than guards. They may be held in place by waist straps or snug underwear. Adult briefs are the bulkiest type of protection, offering the highest level of absorbency, and are secured in place with self-adhesive tape.

Absorbent bed pads also are available to protect the bed sheets and mattresses at night. They are available in different sizes and absorbencies.

Urethral occlusive devices

Urethral occlusive devices are artificial devices that may be inserted into the urethra or placed over the urethral meatus to prevent urinary leakage. These devices are palliative measures to prevent involuntary urine loss. Urethral occlusive devices are more attractive than absorbent pads because they tend to keep the patient drier; however, they may be more difficult and expensive to use than pads. Urethral occlusive devices must be removed after several hours or after each voiding.

Unlike pads, these devices may be more difficult to change. With device manipulation, patients may soil their hands. The risk that a urethral plug may fall into the bladder or fall off the urethra always exists. Urethral occlusive devices, perhaps, are best suited for an active woman with incontinence who does not desire surgery.

Catheters

Urinary diversion, using various catheters, has been one of the mainstays of anti-incontinence therapy. The use of catheters for bladder drainage has withstood the test of time. Bladder catheterization may be a temporary measure or a permanent solution for urinary incontinence. Different types of bladder catheterization include indwelling urethral catheters, suprapubic tubes, and self-intermittent catheterization.[1] c

Indwelling urethral catheters

Commonly known as Foley catheters, indwelling urethral catheters historically have been the mainstay of treatment for bladder dysfunction. If urethral catheters are used for a long-term condition, they must be changed monthly. These catheters may be changed at an office, a clinic, or at home by a visiting nurse. The standard catheter size for treating urinary retention is 16F or 18F, with a 5-mL balloon filled with 10 mL of sterile water. Larger catheters (eg, 22F, 24F) with bigger balloons are used for treating grossly bloody urine found in other urologic conditions or diseases. Proper management of indwelling urethral catheters varies per individual.

The usual practice is to change indwelling catheters once every month. The catheter and bag are replaced on a monthly basis; however, catheters that develop encrustations and problems with urine drainage must be changed more frequently. All indwelling catheters in the urinary bladder for more than 2 weeks become colonized with bacteria. Bacterial colonization does not mean the patient has clinical bladder infection. Symptoms of bladder infection include foul odor, purulent urine, and hematuria. Fever with flank pain often is present if upper tracts are involved. If bladder infection occurs, change the entire catheter and the drainage system. The urinary drainage bag does not need to be disinfected to prevent infection.

Routine irrigation of catheters is not required. However, some authors favor the use of 0.25% acetic acid irrigation because it is bacteriostatic, minimizes catheter encrustation, and diminishes the odor. When used, 30 mL is instilled into the bladder and allowed to freely drain on a twice daily basis.

Patients do not have to take continuous antibiotics while using the catheter. In fact, continuous antibiotic therapy is contraindicated while a catheter is used. Prolonged use of antibiotics to prevent infection actually may cause paradoxical generation of bacteria that are resistant to common antibiotics. Indwelling use of a Foley catheter in individuals who are homebound requires close supervision by a visiting nurse and additional personal hygiene care.

In spite of its apparent advantages, the use of a Foley catheter for a prolonged period of time (eg, months to years) is strongly discouraged. Long-term use of urethral catheters poses significant health hazards. Indwelling urethral catheters are a significant cause of urinary tract infections that involve the urethra, bladder, and kidneys. Within 2-4 weeks after catheter insertion, bacteria will be present in the bladder of most women. Asymptomatic bacterial colonization is common and does not pose a health hazard. However, untreated symptomatic urinary tract infections may lead to urosepsis and death. The death rate of nursing home residents with urethral catheters has been found to be three times higher than that of residents without catheters; this may be more a reflection of the severity of comorbid conditions that lead to the clinical decision to use chronic bladder drainage than causation from the use of chronic bladder drainage.

The use of a urethral catheter is contraindicated in the treatment of urge incontinence. Other problems associated with indwelling urethral catheters include encrustation of the catheter, bladder spasms resulting in urinary leakage, hematuria, and urethritis. More severe complications include formation of bladder stones, development of periurethral abscess, renal damage, and urethral erosion.

Another problem of long-term catheterization is bladder contracture, which occurs with urethral catheters as well as suprapubic tubes. Anticholinergic therapy and intermittent clamping of the catheter in combination have been reported to be beneficial for preserving the bladder integrity with long-term catheter use. Individuals who did not use the medication and daily clamping regimen experienced a decrease in bladder capacity and vesicoureteral reflux. For this reason, some physicians recommend using anticholinergic medications with intermittent clamping of the catheter if lower urinary tract reconstruction is anticipated in the future.

Restrict the use of indwelling catheters to the following situations:

  • As comfort measures for the terminally ill
  • To avoid contamination or to promote healing of severe pressure sores
  • In cases of inoperable urethral obstruction that prevent bladder emptying
  • In individuals who are severely impaired and for whom alternative interventions are not an option
  • When an individual lives alone and a caregiver is unavailable to provide other supportive measures
  • For acutely ill patients who require accurate monitoring of fluid balance
  • For severely impaired persons for whom bed and clothing changes are painful or disruptive

However, when long-term use of a urethral catheter is anticipated, a suprapubic catheter is an attractive alternative.

Suprapubic catheters

A suprapubic tube is an attractive alternative to long-term urethral catheter use. The most common use of a suprapubic catheter is in individuals with spinal cord injuries and a malfunctioning bladder. Both paraplegic and quadriplegic individuals have benefited from this form of urinary diversion. When suprapubic tubes are needed, usually smaller (eg, 14F, 16F) catheters are placed. Like the urethral catheter, suprapubic tubes should be changed once a month on a regular basis.

Suprapubic catheters have many advantages. With a suprapubic catheter, the risk of urethral damage is eliminated. Multiple voiding trials may be performed without having to remove the catheter. Because the catheter comes out of the lower abdomen rather than the vaginal area, a suprapubic tube is more patient-friendly. Bladder spasms occur less often because the suprapubic catheter does not irritate the trigone as does the urethral catheter. In addition, suprapubic tubes are more sanitary for the individual, and bladder infections are minimized because the tube is away from the perineum.

Suprapubic catheters are changed easily by either a nurse or a doctor. Unlike the urethral catheter, a suprapubic tube is less likely to become dislodged because the exit site is so small. When the tube is removed, the hole in the abdomen quickly seals itself within 1-2 days.

Indications for suprapubic catheters include short-term use following gynecologic, urologic, and other types of surgery. Suprapubic catheters may be used whenever the clinical situation requires the use of a bladder drainage device; however, suprapubic catheters are contraindicated in persons with chronic unstable bladders or intrinsic sphincter deficiency because involuntary urine loss is not prevented. A suprapubic tube does not prevent bladder spasms from occurring in unstable bladders nor does it improve the urethral closure mechanism in an incompetent urethra.

Potential complications with chronic suprapubic catheterization are similar to those associated with indwelling urethral catheters, including leakage around the catheter, bladder stone formation, urinary tract infection, and catheter obstruction.

During the initial placement of a suprapubic tube, a potential for bowel injury exists. Although uncommon, bowel perforation is known to occur with first-time placement of suprapubic tubes. Other potential complications include cellulitis around the tube site and hematoma.

If the suprapubic tube falls out inadvertently, the exit hole of the tube will seal up and close quickly within 24 hours if the tube is not replaced with a new one. If tube dislodgment is recognized promptly, a new tube can be reinserted quickly and painlessly as long as the tube site remains patent.

A suprapubic catheter is an alternative solution to an indwelling urethral catheter in women who require chronic bladder drainage. Potential problems unique to suprapubic catheters include skin infection, hematoma, bowel injury, and problems with catheter reinsertion. Long-term management of a suprapubic tube also may be problematic if the health care provider lacks the knowledge and expertise of suprapubic catheter management or if the homebound individual lacks quick access to a medical center in case of an emergency. In the appropriate situation, the suprapubic catheter affords many advantages over long-term urethral catheters.

Intermittent catheterization

Intermittent catheterization or self-catheterization is a mode of draining the bladder at timed intervals, as opposed to continuous bladder drainage. A prerequisite for self-catheterization is the patients' ability to use their hands and arms; however, in a situation in which a patient is physically or mentally impaired, a caregiver or health professional can perform intermittent catheterization for the patient. Of all 3 possible options (ie, urethral catheter, suprapubic tube, intermittent catheterization), intermittent catheterization is the best solution for bladder decompression of a motivated individual who is not physically handicapped or mentally impaired.

Many studies of young individuals with spinal cord injuries have shown that intermittent catheterization is preferable to indwelling catheters (ie, urethral catheter, suprapubic tube) for both men and women. Intermittent catheterization has become a healthy alternative to indwelling catheters for individuals with chronic urinary retention due to an obstructed bladder, a weak bladder, or a nonfunctioning bladder. Young children with myelomeningocele have benefited from the use of intermittent catheterization.

For those children, antibiotic prophylaxis (low-dose chemoprophylaxis) has commonly been prescribed for urinary tract infections. A study by Zegers et al found that this practice can be safely discontinued, especially in males, patients with low urinary tract infection rates, and patients without vesicoureteral reflux.[2]

In addition, self-catheterization is recommended by some surgeons for women during the acute healing process after anti-incontinence surgery.

Intermittent catheterization may be performed using a soft, red, rubber catheter or a short, rigid, plastic catheter. The use of plastic catheters is preferable to red rubber catheters because they are easier to clean and last longer.

The bladder must be drained on a regular basis, either based on a timed interval (eg, on awakening, every 3-6 hours during the day, and before bed) or based on bladder volume. Remember that the average adult bladder holds approximately 400-500 mL of urine. Ideally, the amount drained each time should not exceed 400-500 mL. This drainage limit may require decreasing the fluid intake or increasing the frequency of catheterizations. If catheterization is performed every 6 hours and the amount drained is 700 mL, increase the frequency of catheterization to, perhaps, every 4 hours to maintain the volume drained at 400-500 mL.

Intermittent catheterization is designed to simulate normal voiding. Usually, the average adult empties the bladder four to five times a day. Thus, catheterization should occur four to five times a day; however, individual catheterization schedules may vary, depending on the amount of fluid taken in during the day.

Candidates for intermittent catheterization must have motivation and intact physical and cognitive abilities. Anyone who has good use of her hands and arms can perform self-catheterization. Young children and the older population are able to do this every day without problems. For individuals who are impaired, a home caregiver or a visiting nurse can be instructed to perform intermittent catheterization. Self-catheterization may be performed almost anywhere, including at home and at work.

Intermittent catheterization may be performed using either a sterile catheter or a nonsterile clean catheter. Intermittent catheterization, using a clean technique, is recommended for young individuals with a bladder that cannot empty and without any other available options. Patients should wash their hands with soap and water. Sterile gloves are not necessary. Clean intermittent catheterization results in lower rates of infection than the rates noted with indwelling catheters.

Studies show that in patients with spinal cord injuries, the incidence of bacteria in the bladder is 1-3% per catheterization, and one to four episodes of bacteriuria occur per 100 days of intermittent catheterization performed four times a day. Furthermore, the infections that do occur usually are managed without complications.

In general, routine use of long-term suppressive therapy with antibiotics in patients with chronic clean intermittent catheterization is not recommended. The use of chronic suppressive antibiotic therapy in people regularly using clean intermittent catheterization is undesirable because it may result in the emergence of resistant bacterial strains.

A study of a patients with acute spinal cord injury at 15 North American centers revealed that using a hydrophilic-coated catheter for intermittent catheterization delayed the onset of first antibiotic-treated symptomatic urinary tract infections. In addition, a reduction in incidence of symptomatic urinary tract infection was noted during inpatient rehabilitation for these patients.[3]

In high-risk populations, such as patients with an internal prosthesis (eg, artificial heart valve, artificial hip) or patients who are immunosuppressed because of age or disease, determine whether to use antibiotic therapy for asymptomatic bacteriuria on individual merits.

For older individuals and those with a weak immune system, the sterile technique of intermittent catheterization has been recommended. Older persons are at higher risk than younger persons for developing bacteriuria and other complications caused by intermittent catheterization because they do not have a strong defense system against infection. Although the incidence of infection and other complications for older patients who are using sterile versus clean intermittent catheterization is not well established, sterile intermittent catheterization appears to be the safest method for this high-risk population.

Potential advantages of performing intermittent catheterization include patient autonomy, freedom from indwelling catheter and bags, and unimpeded sexual relations. Potential complications of intermittent catheterization include bladder infection, urethral trauma, urethral inflammation, and stricture. Concurrent use of anticholinergic therapy will maintain acceptable intravesical pressures and prevent bladder contracture. Studies have demonstrated that long-term use of intermittent catheterization appears to be preferable to indwelling catheterization (ie, urethral catheter, suprapubic tube) with respect to urinary tract infections and the development of stones within the bladder or kidneys.

Overall, the management of infections in the setting of catheters and drainage tubes is challenging. Experimental use of bacterial interference represents a novel and perhaps effective method at the prevention of infections; however, at the present time, it is difficult to do clinically outside of the research setting. Further studies may prove this modality more clinically useful to practice environments.[4]

Surgical Care

Surgical care for stress incontinence involves procedures that increase urethral outlet resistance, which include the following:

Surgical care for urge incontinence involves procedures that improve bladder compliance or bladder capacity, which include the following:

A Cochrane review that included four randomized controlled trials of botulinum A toxin injection as a treatment for detrusor-sphincter dyssynergia (DSD) found that intraurethral injections might improve some urodynamic measures after 30 days, but the studies had a high risk of bias, the quality of the evidence was limited, and the need for reinjection is a significant drawback. The authors advised that more study of effectiveness needed; optimal dose and mode of injection remain to be determined, and sphincterotomy might be a more effective option for long-term treatment.[7]

Diet

The fact that certain foods in a daily diet can worsen symptoms of urinary frequency and urge incontinence is well known. If a patient's diet contains dietary stimulants, changes in her diet may help ameliorate incontinence symptoms. Dietary stimulants are substances contained in the food or drink that either cause or exacerbate irritative voiding symptoms. By eliminating or minimizing the intake of dietary stimulants, unwanted bladder symptoms can be improved or possibly cured. Avoidance of dietary stimulants begins with consumer awareness through careful label reading and maintaining a daily diet diary. Experimenting with dietary changes is not appropriate for everyone, and dietary experimentation should be instituted on an individual basis.

Foods

Foods that contain heavy or hot spices may contribute to urge incontinence. A few medical reports have alluded to the fact that avoiding spicy foods may have a beneficial effect on urinary incontinence. Some examples of hot spices include curry, chili pepper, cayenne pepper, and dry mustard.

A second food group that may worsen irritative voiding symptoms is citrus fruit. Fruits and juices that have a high potassium concentration may worsen preexisting urge incontinence. Examples of fruits that have significant potassium include grapefruits and oranges.

A third food group that may worsen urinary bladder incontinence is chocolate-containing sweets. Chocolate snacks and treats contain caffeine. Caffeine is a bladder-unfriendly agent. Excessive intake of chocolate confectioneries worsens irritative bladder symptoms.

Beverages

The quantity and quality of refreshments consumed will influence urinary voiding symptoms. An average American adult requires a daily allowance of approximately 6-8 glasses of fluids. Fluids refer to all the beverages a person consumes in a day, including water, soda, and milk. The human body receives water from beverages consumed, water contained in the food ingested, and water metabolized from food eaten. The recommended amount of fluids consumed (all types) in 24 hours totals 6-8 glasses. The benefits of adequate fluid intake include prevention of dehydration, constipation, urinary tract infection, and kidney stone formation.

Some patients tend to drink water excessively. Some women drink water because they enjoy the taste. Others take medication that makes their mouths dry, so they drink more water. Some women who are trying to lose weight are on a diet that requires consuming abundant amounts of water. Drinking water excessively actually worsens irritative bladder symptoms. The exact amount of fluid needed per day is calculated based on the patient's lean body mass. Thus, the amount of fluid requirement will vary per individual.

Some older women do not drink enough fluids to keep themselves well hydrated. They minimize their fluid intake to unacceptable levels, thinking that if they drink less, they will experience less incontinence. Trying to prevent incontinence by restricting fluids excessively may lead to bladder irritation and actually worsen urge incontinence. In addition, dehydration contributes to constipation. If a patient has a problem with constipation, recommend eating a high-fiber diet, receiving adequate hydration, and administering laxatives.

Many drinks contain caffeine. Caffeine is a natural diuretic, and it has a direct excitatory effect on bladder smooth muscle. Thus, caffeine-containing products produce excessive urine and exacerbate symptoms of urinary frequency and urgency. Caffeine-containing products include coffee, tea, hot chocolate, and sodas. Even chocolate milk and many over-the-counter medications contain caffeine.

Of caffeine-containing products, coffee contains the most caffeine. Drip coffee contains the most caffeine, followed by percolated coffee and then instant coffee. Even decaffeinated coffee contains a small amount of caffeine. Decaffeinated coffee contains an amount of caffeine similar to the amount in chocolate milk. Persons who consume a large amount of caffeine should slowly decrease the amount of caffeine consumed to avoid significant withdrawal responses such as headache and depression.

Studies have shown that drinking carbonated beverages, citrus fruits drinks, and acidic juices may worsen irritative voiding or urge symptoms. Consumption of artificial sweeteners also has been theorized to contribute to urge incontinence.

Nighttime voiding and incontinence are major problems in the older population. Women who have nocturia more than twice a night or experience nighttime bed-wetting may benefit from fluid restriction and the elimination of caffeine-containing beverages from their diet in the evening. Patients should restrict fluids after dinnertime so they can sleep uninterrupted through the night.

Management of lower-extremity edema

Individuals who develop edema of the lower extremities during the day experience nighttime voiding because the excess fluid from the lower extremities returns to the heart with recumbent positioning. This problem may be treated with a behavior technique, support hose, and/or medications.

Advise these individuals to elevate their lower extremities several hours during the late afternoon or evening to stimulate a natural diuresis and limit the amount of edema present at bedtime. Support hose (Jobst) or intermittent, sequential compression devices (SCDs) used briefly at the end of the day can reduce lower extremity edema and minimize nighttime diuresis, thus improving sleep.

Judicious use of diuretics has been associated with a decrease in lower-extremity edema and lower nighttime urine volumes. Depending on other medical conditions, changing the time of administration of the diuretic to the morning may prevent large nighttime volumes of voiding.

Pelvic floor exercise

Anti-incontinence exercises emphasize rehabilitating and strengthening the pelvic floor muscles that are critical in maintaining urinary continence. Pelvic floor muscles also are known as levator ani muscles because they function to levitate or elevate the pelvic organs into their proper place. When levator muscles weaken and fail, pelvic prolapse and stress incontinence result. An anatomic defect of the levator ani musculature requires physical rehabilitation. If aggressive physical therapy does not work, surgery is warranted.

Pelvic muscle exercises may be used alone, augmented with vaginal cones, or reinforced with biofeedback therapy or with electrical stimulation. Behavioral treatment, including pelvic muscle exercises and educated use, is a safe and effective intervention that should be a first-line treatment for urge and mixed incontinence.

Pelvic floor exercises, sometimes called Kegel exercises, are a rehabilitation technique used to tighten and tone the pelvic floor muscles. These exercises empower the external urinary sphincter to prevent stress incontinence and build up the pelvic floor muscles to avert impending pelvic prolapse. In addition, Kegel exercises may be performed to eliminate urge incontinence. Contraction of the external urinary sphincter induces reflex bladder relaxation. Pelvic floor muscle rehabilitation may be used to reprogram the urinary bladder to decrease the frequency of incontinence episodes.

Individuals who benefit the most from pelvic floor exercises tend to be young healthy women who can identify the levator muscles accurately. Older adults with weak pelvic tone or women who have difficulty recognizing the right muscles will need adjunct therapy such as biofeedback or electrical stimulation. Pelvic floor exercises work best in mild cases of stress incontinence associated with urethral hypermobility but not intrinsic sphincter deficiency. These rehabilitation exercises may be used for urge incontinence as well as mixed incontinence. They also benefit men who develop urinary incontinence following prostate surgery.

Pelvic floor muscle exercises are performed by drawing in or lifting up the levator ani muscles as if to control urination or defecation with minimal contraction of abdominal, buttock, or inner thigh muscles.

For urge incontinence, pelvic floor muscle exercises are used to retrain the bladder. When the patient contracts the external urethral sphincter, the bladder automatically relaxes, so the urge to urinate eventually subsides. Strong contractions of the pelvic floor muscles will suppress bladder contractions. Whenever patients feel urinary urgency, they may try to stop the feeling by contracting the pelvic floor muscles. These steps will provide the patient more time to walk slowly to the bathroom with urinary control.

By regularly training the external sphincter, patients can gradually increase the time between urination from 1-3 hours. Patients should begin to see improvement in 3-4 weeks. Thus, this technique may be used for urge symptoms, urge incontinence, and mixed incontinence (stress and urge incontinence).

When performing these drills, patients should not contract their abdominal muscles. Contracting the abdominal muscles is counterproductive and merely worsens urinary incontinence. In general, tailor a regimented program of exercises and repetitions to each individual so that the muscle strength increases progressively. Some patients may need more intensive training than others.

Patients should practice contracting the levator ani muscles immediately before and during situations when leakage may occur. This will condition the external sphincter instinctively to contract with increases in abdominal pressure or when the need to urinate is imminent. This is known as the guarding reflex. When the patient tightens the external urinary sphincter just as a sneeze is about to occur, the involuntary urine loss is thwarted. By squeezing the levator ani muscles when the patient feels the sense of urgency, the sensation of impending bladder contraction will dissipate. By making this maneuver a habit, patients will develop a protective mechanism against stress and urge incontinence.

The beneficial effects of pelvic floor muscle exercises alone have been well documented in medical literature. Successful reduction in urinary incontinence has been reported to range from 56-95%. Pelvic floor exercises are effective, even after multiple anti-incontinence surgeries.

Vaginal weights

Vaginal weight training is an effective form of pelvic floor muscle rehabilitation for stress incontinence in premenopausal women. Vaginal weights are tamponlike special help aids used to enhance pelvic floor muscle exercises. Shaped like a small cone, vaginal weights (identical shape and volume) come in a set of 5, with increasing weights (ie, 20, 32.5, 45, 60, and 75 g). As part of a progressive resistive exercise program, a single weight is inserted into the vagina and held in place by tightening the perivaginal muscles (levator ani muscles) for as many as 15 minutes. As the levator ani muscles become stronger, the exercise may be increased to 30 minutes.

This exercise is performed twice daily. The intravaginal weight provides the sensory feedback for the desired pelvic muscle contraction. The sustained contraction required to retain the weight within the vagina increases the strength of the pelvic floor muscles.

The best results are achieved when standard pelvic muscle exercises (Kegel exercises) are performed with intravaginal weights. In premenopausal women with stress incontinence, the subjective cure or improved continence status was approximately 70-80% after 4-6 weeks of treatment. Vaginal weight training also may be useful for women who are postmenopausal with stress incontinence; however, vaginal weights are not effective in the treatment of pelvic organ prolapse.

Biofeedback

Biofeedback therapy is a form of pelvic floor muscle rehabilitation using an electronic device for individuals having difficulty identifying levator ani muscles. Biofeedback therapy is recommended for treatment of stress incontinence, urge incontinence, and mixed incontinence. Biofeedback therapy uses a computer and electronic instruments to relay auditory or visual information to the patient about the status of pelvic muscle activity. These devices allow the patient to receive immediate visual feedback on the activity of the pelvic floor muscles.

Biofeedback is an intensive therapy, with weekly sessions performed in an office or a hospital by a trained professional, and it often is followed by a regimen of pelvic floor muscle exercises at home. During a biofeedback therapy, a special tampon-shaped sensor is inserted in the patient's vagina or rectum and a second sensor is placed on her abdomen. These sensors detect electrical signals from the pelvic floor muscles. The patient is instructed to contract and relax the pelvic floor muscles upon command. When the exercises are performed properly, the electric signals from the pelvic floor muscles are registered on a computer screen. Biofeedback, using multi-measurement recording, displays the simultaneous measurement of pelvic and abdominal muscle activity on the computer monitor.

Biofeedback allows the patient to correctly identify the pelvic muscles that need rehabilitation. The benefit of biofeedback therapy is that it provides the patient with minute-by-minute feedback on the quality and intensity of her pelvic floor contraction. Combining bladder and urinary sphincter biofeedback allows the patient to regulate the pelvic muscle contraction in response to increasing bladder volumes and to monitor the bladder activity. Biofeedback is best used in conjunction with pelvic floor muscle exercises and bladder training.

Studies on biofeedback combined with pelvic floor exercises show a 54-87% improvement with incontinence. The best biofeedback protocol is one that reinforces levator ani muscle contraction with inhibition of abdominal and bladder contraction. Reports using this method show a 76-82% reduction in urinary incontinence. Biofeedback also has been used successfully in treatment of men with urge incontinence and intermittent stress incontinence after prostate surgery.

Medical studies have demonstrated significant improvement in urinary incontinence in women with neurologic disease and in the frail older population when a combination of biofeedback and bladder training is used. Biofeedback provides a specific reinforcement for pelvic muscle contraction that is isolated from the counterproductive abdominal contraction. Therefore, awareness of levator ani muscle contraction can be achieved more efficiently using biofeedback than vaginal palpation alone.

Biofeedback produces a greater reduction in female urinary incontinence compared to pelvic muscle exercises alone. Overall, the medical literature indicates that pelvic muscle exercises and other behavioral strategies, with or without biofeedback, can cure or reduce incontinence. However, the maximum benefit is derived from any pelvic muscle rehabilitation and education program when ongoing reinforcement and guidance, such as biofeedback therapy, are provided.

Electrical stimulation

Electrical stimulation is a more sophisticated form of biofeedback used for pelvic floor muscle rehabilitation. This treatment involves stimulation of levator ani muscles using painless electric shocks. Electrical stimulation of pelvic floor muscles produces a contraction of the levator ani muscles and external urethral sphincter while inhibiting bladder contraction. This therapy depends on a preserved reflex arc through the intact sacral micturition center. Like biofeedback, electrical stimulation can be performed at the office or at home. Electrical stimulation can be used in conjunction with biofeedback or pelvic floor muscle exercises.

Electrical stimulation therapy requires a similar type of probe and equipment as those used for biofeedback. This form of muscle rehabilitation is similar to the biofeedback therapy, except small electric shocks are used. Nonimplantable pelvic floor electrical stimulation uses vaginal sensors, anal sensors, or surface electrodes. Adverse reactions are minimal.

Like biofeedback, pelvic floor muscle electrical stimulation has been shown to be effective in treating female stress incontinence, as well as urge and mixed incontinence. Electrical stimulation may be most beneficial when stress incontinence and very weak or damaged pelvic floor muscles coexist. A regimented program of electrical stimulation will help these weakened pelvic muscles contract so they can become stronger. For women with urge incontinence, electrical stimulation may help the bladder relax and prevent it from contracting involuntarily.

Research indicates that pelvic floor electrical stimulation can reduce urinary incontinence significantly in women with stress incontinence and may be effective in men and women with urge and mixed incontinence. Incidence of urge incontinence secondary to neurologic diseases may be decreased with this therapy. Electrical stimulation appears to be most effective when augmented with pelvic floor exercises. Long-term data report that with electrical stimulation the rate of cured or improved patients ranged from 54-77%; however, in order to derive significant benefit, perform stimulation for a minimum of 4 weeks. Patients must continue pelvic floor exercises after the treatment. Unfortunately, this treatment does not appear to benefit cognitively impaired patients.

Bladder training

Bladder training involves relearning how to urinate. This method of rehabilitation most often is used for active women with urge incontinence and sensory urge symptoms. Often, patients find that when they respond to symptoms of urge and return to the bathroom soon after they have voided, they do not expel significant urine. In other words, though the bladder is not full, it is signaling that it is time to void.

Bladder training generally consists of self-education, scheduled voiding with conscious delay of voiding, and positive reinforcement. Although bladder training is used primarily for urge incontinence, this program may be used for simple stress incontinence and mixed incontinence. Bladder training requires the patient to resist or inhibit the sensation of urgency and postpone voiding. Patients urinate according to a scheduled timetable rather than the symptoms of urge.

Bladder training uses dietary tactics such as adjustment of fluid intake and avoidance of dietary stimulants. In addition, distraction and relaxation techniques allow delayed voiding to help distend the urinary bladder. By using these strategies, patients can induce the bladder to accommodate progressively larger voiding volumes.

Initially, the interval goal is determined by the patient's current voiding habits and is not enforced at night. Regardless of the initial voiding pattern, the first voiding interval may be increased by 15- to 30-minute increments. As the bladder becomes accustomed to this delay in voiding, the interval between mandatory voids is increased progressively, with simultaneous distraction or relaxation techniques and dietary modification. The interval goal between each void usually is set between 2 and 3 hours and may be set further apart if desired.

Another method of bladder training is to maintain the prearranged schedule and disregard the unscheduled voids. However, patients need to continue to maintain the prearranged voiding times. They will need to continue this program for several months.

Alternatively, bladder ultrasound may be employed. If patients need an objective demonstration that their bladder is relatively empty, a portable bladder scanner may be used. A bladder scanner is a portable ultrasound machine that measures the amount of urine present in a patient's bladder. With this device, patients can void when their bladder fills to a certain volume rather than responding to the sensation of needing to go to the bathroom. When patients feel the need to void, they can check the bladder using the scanner to see how much urine is present. If the bladder is empty, patients should ignore the sensation of needing to go to the bathroom.

Bladder training has been used primarily to manage urge incontinence; however, it also may be used for stress and mixed incontinence. This form of training is useful in young women but is difficult to implement in cognitively impaired persons. Bladder training may not be successful in frail women who are older. Medical reports demonstrate that bladder training is effective in reducing urinary incontinence. With bladder training, the rate of patients with mixed incontinence that have been cured is reported to be 12%, while the improvement rate was 75% after 6 months.

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Medications Used to Treat Neurogenic Bladder

Stress incontinence results from a weak urinary sphincter. The internal sphincter contains high concentrations of alpha-adrenergic receptors. Activation of the alpha-receptors results in contraction of the internal urethral sphincter and increases the urethral resistance to urinary flow. Sympathomimetic drugs, estrogen, and tricyclic agents increase bladder outlet resistance to improve symptoms of stress urinary incontinence. Medical conditions that cause urge incontinence may be neurologic or nonneurologic. The urethra is normal, but the bladder is hyperactive or overactive. Pharmacologic therapy for stress incontinence and an overactive bladder may be most effective when combined with a pelvic exercise regimen. The 3 main categories of drugs used to treat urge incontinence include anticholinergic drugs, antispasmodics, and tricyclic antidepressant agents.

All drugs with anticholinergic adverse effects are contraindicated if patients have documented narrow-angle glaucoma. Wide-angle glaucoma is not a contraindication to their use. Urinary retention, bowel obstruction, ulcerative colitis, myasthenia gravis, and severe heart diseases are contraindications for anticholinergic use. These agents may impair the patient's ability to perform hazardous activities, such as driving or operating heavy machinery, because of the potential for drowsiness. Anticholinergic drugs should not be taken in combination with alcohol, sedatives, or hypnotic drugs.

When a single drug treatment does not work, combination therapy, such as oxybutynin (Ditropan) and imipramine (Tofranil) may be used. Although their mechanism of action differs, oxybutynin and imipramine work together to improve urge incontinence. Oxybutynin causes direct smooth muscle relaxation of the urinary bladder and has local anesthetic properties. Imipramine has a direct inhibitory and local anesthetic effect on the bladder smooth muscle, like oxybutynin; however, imipramine also increases the bladder outlet resistance at the level of the bladder neck. Thus, the combination of these drugs produces a synergistic effect to relax the unstable bladder to hold in urine and prevent urge incontinence. Potential anticholinergic adverse effects may be additive because both drugs have similar adverse reactions.

Estrogen derivatives

Conjugated estrogen increases the tone of urethral muscle by up-regulating the alpha-adrenergic receptors in the surrounding area and enhances alpha-adrenergic contractile response to strengthen pelvic muscles, which is important in urethral support (prevents urethral hypermobility). Mucosal turgor of periurethral tissue from proper nourishment enhances urethral mucosal coaptation. Result is an improved mucosal seal effect, which is important in urethral function (prevents intrinsic sphincter deficiency). Estrogen supplementation appears to be the most effective in postmenopausal women with mild-to-moderate incontinence. Both types of stress incontinence benefit from estrogen fortification.

Pharmacologic therapy using estrogen derivatives results in few cures (0-14%) but may cause subjective improvement in 29-66% of women. Limited evidence suggests that oral or vaginal estrogen therapy may benefit some women with stress and mixed urinary incontinence. Other potential beneficial effects of estrogen use include decreased bone loss and resolution of hot flashes during menopause.

When estrogen is used long-term, addition of progestin therapy is recommended to prevent endometrial hyperplasia in women with an intact uterus. Progestin (eg, medroxyprogesterone 2.5-10 mg/d) is needed for 10-13 d to provide maximum maturation of endometrium and to eliminate any hyperplastic changes. Progestin may be administered continuously or intermittently.

Conjugated estrogen (Premarin)

Conjugated estrogen may be used as an adjunctive pharmacologic agent for women who are postmenopausal with stress or mixed incontinence. The oral or vaginal form of estrogen may be used. Premarin vaginal cream is available in a package with a plastic applicator and a tube that contains 42.5 g of conjugated estrogens. Each gram contains 0.625 mg of conjugated estrogens. Estrogen cream is readily absorbed through the skin and mucous membranes.

Routinely prescribing conjugated estrogens to premenopausal women is not recommended. Use medication in women who are postmenopausal and incontinent and who have had a hysterectomy. For postmenopausal women with an intact uterus, cautiously recommend a short-term low-dose regimen of Premarin with frequent monitoring.

Adult dosing is 0.625 mg PO qd for 21 consecutive days, followed by 7 days without the drug (eg, 3 wk on and 1 wk off); repeat the regimen prn and taper off or discontinue at 3- to 6-mo intervals. Two to four grams (0.5-1 applicator) of cream may be administered intravaginally qd in a usual cyclic regimen. Pediatric dosing has not been established.

Conjugated estrogen is a pregnancy category X drug.

Anticholinergic drugs

Anticholinergic drugs are the first line medicinal therapy in women with urge incontinence. They are effective in treating urge incontinence because they inhibit involuntary bladder contractions. They are also useful in treating urinary incontinence associated with urinary frequency, urgency, and nocturnal enuresis. All anticholinergic drugs have similar performance profiles and toxicity. Potential adverse effects of all anticholinergic agents include blurred vision, dry mouth, heart palpitations, drowsiness, and facial flushing. When anticholinergic drugs are used in excess, acute urinary retention in the bladder may occur.

Propantheline bromide (Pro Banthine)

Propantheline bromide is the typical prototype for all anticholinergic agents. It blocks action of acetylcholine at postganglionic parasympathetic receptor sites. In a medical study, propantheline bromide was shown to decrease incidence of urge incontinence by 13-17% when 30 mg was used qid. When stronger doses were used (60 mg qid), the cure rate was reported to be over 90%.

Adult dosing is 15 mg PO tid/qid. Pediatric dosing has not been established.

Propantheline bromide is a pregnancy category C drug.

Dicyclomine hydrochloride (Bentyl)

Dicyclomine hydrochloride is an anticholinergic agent with smooth muscle relaxant properties. It blocks the action of acetylcholine at parasympathetic sites in secretory glands and smooth muscle. In a medical study, subjective improvement was reported by 62% of the subjects while taking dicyclomine hydrochloride 10 mg tid. The reported cure rate was 90%.

Adult dosing is 10-20 mg PO tid. Pediatric dosing has not been established.

Dicyclomine hydrochloride is a pregnancy category B drug.

Hyoscyamine sulfate (Levsin/SL, Levsin, Levsinex, Cystospaz M, Levbid)

Hyoscyamine sulfate is an anticholinergic agent with antispasmodic properties used for the treatment of urge incontinence. It blocks the action of acetylcholine at parasympathetic sites in smooth muscle, secretory glands, and the CNS, which in turn has antispasmodic effects. It is absorbed well by the GI tract. Food does not affect absorption. Hyoscyamine sulfate is available in sublingual form (Levsin SL), conventional tablets (Levsin), extended-release capsules (Levsinex Timecaps, Cystospaz-M), and extended-release tablets (Levbid).

Adult dosing is 0.125 mg PO q4h; alternatively, 0.375 mg PO bid can be used. For severe symptoms, dosing is 0.375 mg PO tid. Pediatric dosing has not been established.

Hyoscyamine sulfate is a pregnancy category C drug.

Antispasmodic drugs

These relax the smooth muscles of the urinary bladder. By exerting a direct spasmolytic action on the smooth muscle of the bladder, antispasmodic drugs have been reported to increase bladder capacity and effectively decrease or eliminate urge incontinence. The adverse-effect profile of antispasmodic drugs is similar to that of anticholinergic agents. These drugs may impair the patient's ability to perform activities requiring mental alertness and physical coordination. Drinking alcohol and using sedatives in combination with these antispasmodic drugs is contraindicated.

Solifenacin succinate (VESIcare)

Solifenacin succinate elicits competitive muscarinic receptor antagonist activity, which results in anticholinergic effect and inhibition of bladder smooth muscle contraction. It is indicated for overactive bladder with symptoms of urgency, frequency, and urge incontinence.

Adult dosing is 5 mg PO qd; if tolerated, it may be increased to 10 mg PO qd.

Pediatric dosing has not been established.

Solifenacin succinate is a pregnancy category C drug.

Darifenacin (Enablex)

Darifenacin is an extended-release product that elicits competitive muscarinic receptor antagonistic activity. It reduces bladder smooth muscle contractions. It has a high affinity for M3 receptors involved in bladder and GI smooth muscle contraction, saliva production, and iris sphincter function. Darifenacin is indicated for overactive bladder with symptoms of urge incontinence, urgency, and frequency. The product should be swallowed whole; do not chew, divide, or crush.

Adult dosing is 7.5 mg PO qd initially; after 2 wk, the dose may be increased to 15 mg PO qd based on response. Do not exceed 7.5 mg PO qd in patients with moderate hepatic impairment (Child-Pugh class B) or who are receiving potent CYP-450 3A4 inhibitors. Pediatric dosing has not been established.

Darifenacin is a pregnancy category C drug.

Oxybutynin chloride (Ditropan IR, Ditropan XL)

Oxybutynin chloride has both anticholinergic and direct smooth muscle relaxant effects on urinary bladder. It provides a local anesthetic effect on irritable bladder. Urodynamic studies have shown oxybutynin increases bladder size, decreases frequency of symptoms, and delays initial desire to void.

Ditropan XL has an innovative drug delivery system—oral osmotic delivery system (OROS). The Ditropan XL tablet has a bilayer core that contains a drug layer and a push layer that contains osmotic components. The outer tablet is composed of a semipermeable membrane with a precision laser-drilled hole that allows the drug to be released at a constant rate.

When the drug is ingested, the aqueous environment in the GI tract causes water to enter the tablet via the semipermeable membrane at constant rate. Introduction of water inside the tablet liquifies the drug and causes the push layer to swell osmotically. As the push layer swells, it forces the drug suspension out of the hole at a constant rate over a 24-h period.

Ditropan XL achieves steady-state levels over a 24-h period. It avoids first-pass metabolism of the liver and upper GI tract to avoid cytochrome P450 enzymes. It has excellent efficacy with minimal adverse effects.

Medical studies have shown that oxybutynin chloride reduces incontinence episodes by 83-90%. The total continence rate has been reported to be 41-50%. The mean reduction in urinary frequency was 23%. In clinical trials, only 1% stopped taking Ditropan XL because of dry mouth, and less than 1% stopped taking Ditropan XL due to CNS adverse effects.

Adult dosing of Ditropan IR is 2.5 mg PO tid, titrate prn to 5 mg bid/tid/qid. Dosing of Ditropan XL is 5-15 mg PO qd. Pediatric dosing has not been established.

Oxybutynin chloride is a pregnancy category B drug.

Tolterodine L-tartrate (Detrol and Detrol LA)

Tolterodine L-tartrate is a competitive muscarinic receptor antagonist for overactive bladder. It differs from other anticholinergic types in that it has selectivity for urinary bladder over salivary glands. It exhibits high specificity for muscarinic receptors and has minimal activity or affinity for other neurotransmitter receptors and other potential targets such as calcium channels. In clinical studies, the mean decrease in urge incontinence episodes was 50% and the mean decrease in urinary frequency was 17%.

Adult dosing of Detrol is 2 mg PO bid. Dosing of Detrol LA is 4 mg PO qd. Pediatric dosing has not been established.

Tolterodine L-tartrate is a pregnancy category C drug.

Trospium (Sanctura)

Trospium is a quaternary ammonium compound that elicits antispasmodic and antimuscarinic effects. It antagonizes acetylcholine effect on muscarinic receptors. Parasympathetic effect reduces smooth muscle tone in the bladder. Trospium is indicated to treat symptoms of overactive bladder (eg, urinary incontinence, urgency, frequency).

Adult dosing is 20 mg PO bid; it should be taken on an empty stomach at least 1 h before meals. In patients with a CrCl < 30 mL/min, dosing is 20 mg PO hs. In patients >75 years, dosing may be titrated downward to 20 mg PO qd based on tolerability. Pediatric dosing has not been established.

Trospium is a pregnancy category C drug.

Fesoterodine (Toviaz)

Fesoterodine is a competitive muscarinic receptor antagonist. The antagonistic effect results in decreased bladder smooth muscle contractions. It is indicated for symptoms of overactive bladder (eg, urinary urge incontinence, urgency, and frequency). Fesoterodine is available as a 4- or 8-mg extended-release tab.

Adult dosing is 4 mg PO qd; it may be increased to 8 mg/d. Dosing is not to exceed 4 mg PO qd in severe renal dysfunction (ie, CrCl < 30 mL/min) or with coadministration of drugs that decrease fesoterodine’s metabolism (eg, ketoconazole, itraconazole, clarithromycin). Pediatric dosing has not been established.

Fesoterodine is a pregnancy category C drug.

Tricyclic antidepressant drugs

Historically, these drugs were used to treat major depression; however, they have an additional use that is not FDA approved—treatment of bladder dysfunction. They function to increase norepinephrine and serotonin levels. In addition, they exhibit anticholinergic and direct muscle relaxant effects on the urinary bladder.

Imipramine hydrochloride (Tofranil)

Imipramine hydrochloride is a typical tricyclic antidepressant. It facilitates urine storage by decreasing bladder contractility and increasing outlet resistance. It has alpha-adrenergic effect on the bladder neck and antispasmodic effect on detrusor muscle. Imipramine hydrochloride has a local anesthetic effect on bladder mucosa.

Adult dosing is 10-50 mg PO qd/tid; the range is 25-100 mg qd. Pediatric dosing has not been established.

Imipramine hydrochloride is a pregnancy category D drug.

Amitriptyline hydrochloride (Elavil)

Amitriptyline hydrochloride is a tricyclic antidepressant with sedative properties. It increases circulating levels of norepinephrine and serotonin by blocking their reuptake at nerve endings and is ineffective for use in urge incontinence. However, it is extremely effective in decreasing symptoms of urinary frequency in women with pelvic floor muscle dysfunction. Amitriptyline hydrochloride restores serotonin levels and helps break the cycle of pelvic floor muscle spasms. It is well-tolerated and effective in most women with urinary frequency.

Adult dosing is 10 mg/d PO; titrate prn by 10 mg/wk until maximum dose of 150 mg is reached, urinary symptoms disappear, or adverse effects become intolerable. Pediatric dosing has not been established.

Amitriptyline hydrochloride is a pregnancy category D drug.

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Follow-up

Complications

Prolonged contact of urine with unprotected skin causes contact dermatitis and skin breakdown. If left untreated, these skin disorders may lead to pressure sores and ulcers, possibly resulting in secondary infections.

For individuals with a decompensated bladder that does not empty well, the postvoid residual urine can lead to overgrowth of bacteria and subsequent urinary tract infection (UTI). In patients with neurogenic bladder, UTIs often do not produce classic symptoms; instead, these patients may present with abdominal or back pain, increased spasticity, and urinary incontinence. Untreated UTIs can quickly lead to life-threatening autonomic dysreflexia or sepsis, whereas overtreatment promotes antibiotic resistance. However, there are few evidence-based practices for preventing UTI in this population.[8]

Complications of specific interventions include the following:

  • Long-term indwelling catheters may cause recurrent bladder infection, bladder stones, ascending pyelonephritis, and urethral erosion
  • Intermittent catheterization may result in bladder infections or urethral injury
  • Long-term suprapubic tubes may result in bladder spasms, bladder stone formation, and bladder infection
  • Potential problems unique to suprapubic catheters include skin infection, hematoma, bowel injury, and problems with catheter reinsertion

Prognosis

Prognosis of a patient with incontinence is excellent with modern health care. With improvement in information technology, well-trained medical staff, and advances in modern medical knowledge, patients who are incontinent should not experience the morbidity and mortality of the past. Although the ultimate well being of a patient who is incontinent depends on the underlying condition that has precipitated urinary incontinence, urinary incontinence itself is easily treated and prevented by properly trained health care personnel.

Patient education

For patient education information, see Bladder Control Problems, Bladder Control Medications, Inability to Urinate, and Foley Catheter.

Patients may well conduct Internet searches for information on their condition. Using  the search terms "neurogenic bladder intermittent catheter" and "spinal cord injury intermittent catheter", Ho et al found 71 videos online  that covered these topics. However, most of the videos provided poor-quality information, and some offered information contradictory to European Urological Association guidelines for intermittent catheterization. Videos that the authors deemed of good quality were not prominently ranked by the YouTube search algorithm, suggesting that users would be less likely to access those.[9]

 

Medical/legal pitfalls

Failure to diagnose and treat urinary retention may result in adverse consequences.

Rule out narrow-angle glaucoma prior to prescribing an anticholinergic agent. Narrow-angle glaucoma may be converted to open-angle glaucoma by an experienced ophthalmologist.

When patients are taking anticholinergic agents, monitor these patients to prevent pharmacologically induced urinary retention.

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Contributor Information and Disclosures
Author

Bradley C Gill, MD, MS Resident Physician, Department of Urology, Glickman Urological and Kidney Institute; Clinical Instructor of Surgery, Cleveland Clinic Lerner College of Medicine, Education Institute; Department of Biomedical Engineering, Lerner Research Institute, Cleveland Clinic

Bradley C Gill, MD, MS is a member of the following medical societies: American College of Surgeons, American Urological Association, Societe Internationale d'Urologie (International Society of Urology)

Disclosure: Nothing to disclose.

Coauthor(s)

Raymond R Rackley, MD Professor of Surgery, Cleveland Clinic Lerner College of Medicine; Staff Physician, Center for Neurourology, Female Pelvic Health and Female Reconstructive Surgery, Glickman Urological Institute, Cleveland Clinic, Beachwood Family Health Center, and Willoughby Hills Family Health Center; Director, The Urothelial Biology Laboratory, Lerner Research Institute, Cleveland Clinic

Raymond R Rackley, MD is a member of the following medical societies: American Urological Association

Disclosure: Nothing to disclose.

Sandip P Vasavada, MD Physician, Associate Professor of Surgery, Cleveland Clinic Lerner College of Medicine, Center for Female Urology and Genitourinary Reconstructive Surgery, The Glickman Urological and Kidney Institute; Joint Appointment with Women's Institute, Cleveland Clinic

Sandip P Vasavada, MD is a member of the following medical societies: American Urological Association, Engineering and Urology Society, American Urogynecologic Society, International Continence Society, Society of Urodynamics, Female Pelvic Medicine and Urogenital Reconstruction

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Medtronic, Allergan and Axonics<br/>Received ownership interest from NDI Medical, LLC for review panel membership; Received consulting fee from allergan for speaking and teaching; Received consulting fee from medtronic for speaking and teaching; Received consulting fee from boston scientific for consulting.

Farzeen Firoozi, MD Clinical Fellow, Center for Female Urology and Pelvic Reconstructive Surgery, Glickman Urological Institute, Cleveland Clinic Foundation

Farzeen Firoozi, MD is a member of the following medical societies: American Medical Association, American Urological Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Shlomo Raz, MD Professor, Department of Surgery, Division of Urology, University of California, Los Angeles, David Geffen School of Medicine

Shlomo Raz, MD is a member of the following medical societies: American College of Surgeons, American Medical Association, American Urological Association, California Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Edward David Kim, MD, FACS Professor of Surgery, Division of Urology, University of Tennessee Graduate School of Medicine; Consulting Staff, University of Tennessee Medical Center

Edward David Kim, MD, FACS is a member of the following medical societies: American College of Surgeons, Tennessee Medical Association, Sexual Medicine Society of North America, American Society for Reproductive Medicine, American Society of Andrology, American Urological Association

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Repros.

Additional Contributors

Raymond R Rackley, MD Professor of Surgery, Cleveland Clinic Lerner College of Medicine; Staff Physician, Center for Neurourology, Female Pelvic Health and Female Reconstructive Surgery, Glickman Urological Institute, Cleveland Clinic, Beachwood Family Health Center, and Willoughby Hills Family Health Center; Director, The Urothelial Biology Laboratory, Lerner Research Institute, Cleveland Clinic

Raymond R Rackley, MD is a member of the following medical societies: American Urological Association

Disclosure: Nothing to disclose.

Acknowledgements

Michael S Ingber, MD Clinical Fellow, Glickman Urological and Kidney Institute of the Cleveland Clinic

Disclosure: Nothing to disclose.

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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).
 
 
 
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