PATIENT STATUS I. IDENTITY Name : Tn. S Sex : male Age : 61 years Religion : Islam Address : Jl.

Mawar III RT 05 RW 05 Date of admission : 28/06/2012 II. ANAMNESIS Anamnesis was taken on mei 29 June 2012 by autoanamnesa. Chief complain Patient came with cannot urinating Present Illness history Patient came to Arjawinangung hospital complaint couldnt urinating since a week before admitted into Arjawinangun Hospital. This urinating distraction already felt since 7 months ago. At the begining patient felt not smooth when urinating, urinating frequency became more often but it felt like un-finished, low stream, faltering, and patient have to put extra energry when urinating. Patient said he/she often urinating in the night. 6 days before admitted into Arjawinangun Hospital, urinating felt more not smooth and pain, until a day before went to hospital patient cannot urinating at all and he/she felt pain in the lower abdomen part. Patient sid he/she never take any medicine for this complain. Sign of fever, urinating emission is brancing, driping, stone out when urinating, red color urinating or incontinence are denied. There no malignancy in family history III. PHYSICAL EXAMINATION Physical examination was done on mei 22, 2012 Status Generalis 1

Consciousness: compos mentis Vital Sign Blood Pressure 140/80 mmHg Temperature : 36,5 C Pulse : 88/ mnt Respiratory Rate : 19/ mnt Head : normochepali, black hair Eye : pupil round and isochor. SI (-/-) . CA (-/-). DRL (+/+). Thoraks : Torax symmetric. Lung resonant. Breath sound vesicular with no added sound. Cardiovascular : good S1,S2, no murmur, no gallop. Abdomen : Inspection : the stomach does not bulge, darm contour (-), darm steifung(-), venectation (-), mass(-) Auscultation : bowel sound (+) Palpation : tenderness (-), liver and spleen not palpable,

muscular defans (-), abdominal mass (-), pain abdominal (-) Percussion : timpani in the whole field abdomen

Ekstremities : warm, edema (-), sianosis(-) Status Lokalis Rectal Examination : Sphingter ani tone normal Mucosa : smooth Ampula : not collapsed Prostat : Prominent, rubbery consistency, flat surface, symmetrical right and left, nodules (-), tenderness (-), the upper limit was not palpable Gloves : blood (-), feces (+), mucous (+)

IV. SUPPORTING EXAMINATION Laboratory studies : Hematocrite Hemoglobin Leukocyte count Trombocyte count GDS Ureum Kreatinin SGOT SGPT 44,2 % 10,4 gr/dL 12,6 /L 398 /l 94 mg/dl 30,8 0,99 17 23

V. WORKING DIAGNOSIS Benign prostatic hyperplasia (BPH) with susp. Neurogenic bladder VI. MANAGEMENT Operation open prostat IVFD RL 20 TPM CEFOTAXIME 2*1 gr KETOROLAC 2*1 AMP RANITIDIN 2*1 AMP Bladder training (bladder drill)

REFERENCE NEUROGENIC BLADDER

The normal function of the urinary bladder is to store and expel urine in a coordinated, controlled fashion. This coordinated activity is regulated by the central and peripheral nervous systems. Neurogenic bladder is a term applied to a malfunctioning urinary bladder due to neurologic dysfunction or insult emanating from internal or external trauma, disease, or injury. Symptoms of neurogenic bladder range from detrusor underactivity to overactivity, depending on the site of neurologic insult. The urinary sphincter also may be affected, resulting in sphincter underactivity or overactivity and loss of coordination with bladder function. The appropriate therapy and a successful outcome are predicated upon accurate diagnosis through a careful medical and voiding history together with a variety of clinical examinations, including urodynamics and selective radiographic imaging studies.

Physiology During the course of a day, an average person will void approximately 4-8 times. The urinary bladder is in storage mode for most of the day, allowing an individual to engage in more important activities than urination. Normal bladder function consists of 2 phasesfilling and emptying. The normal micturition cycle requires that the urinary bladder and the urethral sphincter work together as a coordinated unit to store and empty urine. During urinary storage, the bladder acts as a low-pressure receptacle, while the urinary sphincter maintains high resistance to urinary flow to keep the bladder outlet closed. During urine elimination, the bladder contracts to expel urine while the urinary sphincter opens (low resistance) to allow unobstructed urinary flow and bladder emptying.

Filling phase

During the filling phase, the bladder accumulates increasing volumes of urine while the pressure inside the bladder remains low. The pressure within the bladder must be lower than the urethral pressure during the filling phase. If the bladder pressure is greater than the urethral pressure (resistance), urine will leak out. The filling of the urinary bladder depends on the intrinsic viscoelastic properties of the bladder and the inhibition of the parasympathetic nerves. Thus, bladder filling primarily is a passive event. Sympathetic nerves also facilitate urine storage in the following ways:

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

As the bladder fills, the pudendal nerve becomes excited. Stimulation of the pudendal nerve results in contraction of the external urethral sphincter. Contraction of the external sphincter, coupled with that of the internal sphincter, maintains urethral pressure (resistance) higher than normal bladder pressure. The combination of both urinary sphincters is known as the continence mechanism. The pressure gradients within the bladder and urethra play an important functional role in normal micturition. As long as the urethral pressure is higher than that of the bladder, patients will remain continent. If the urethral pressure is abnormally low or if the intravesical pressure is abnormally high, urinary incontinence will result. As the bladder initially fills, a small rise in pressure occurs within the bladder (intravesical pressure). When the urethral sphincter is closed, the pressure inside the urethra (intraurethral pressure) is higher than the pressure within the bladder. While the intraurethral pressure is higher than the intravesical pressure, urinary continence is maintained. During some physical activities and with coughing, sneezing, or laughing, the pressure within the abdomen rises sharply. This rise is transmitted to both the bladder and urethra. As long as the pressure is evenly transmitted to both the bladder and

urethra, urine will not leak. When the pressure transmitted to the bladder is greater than urethra, urine will leak out, resulting in stress incontinence. Emptying phase The storage phase of the urinary bladder can be switched to the voiding phase either involuntarily (reflexively) or voluntarily. Involuntary reflex voiding occurs in an infant when the volume of urine exceeds the voiding threshold. When the bladder is filled to capacity, the stretch receptors within the bladder wall signal the sacral cord. The sacral cord, in turn, sends a message back to the bladder indicating that it is time to empty the bladder. At this point, the pudendal nerve causes relaxation of the levator ani so that the pelvic floor muscle relaxes. The pudendal nerve also signals the external sphincter to open. The sympathetic nerves send a message to the internal sphincter to relax and open, resulting in a lower urethral resistance. When the urethral sphincters relax and open, the parasympathetic nerves trigger contraction of the detrusor. When the bladder contracts, the pressure generated by the bladder overcomes the urethral pressure, resulting in urinary flow. These coordinated series of events allow unimpeded, automatic emptying of the urine. A repetitious cycle of bladder filling and emptying occurs in newborn infants. The bladder empties as soon as it fills because the brain of an infant has not matured enough to regulate the urinary system. Because urination is unregulated by the infant's brain, predicting when the infant will urinate is difficult. As the infant brain develops, the PMC also matures and gradually assumes voiding control. When the infant enters childhood (usually at age 3-4 years), this primitive voiding reflex becomes suppressed and the brain dominates bladder function, which is why toilet training usually is successful at age 3-4 years. However, this primitive voiding reflex may reappear in people with spinal cord injuries. Delaying voiding or voluntary voiding Bladder function is automatic but completely governed by the brain, which makes the final decision on whether or not to void. The normal function of urination means that an individual has the ability to stop and start urination on command. In addition, the individual has the ability to delay urination until a socially acceptable

time and place. The healthy adult is aware of bladder filling and can willfully initiate or delay voiding. In a healthy adult, the PMC functions as an on-off switch that is activated by stretch receptors in the bladder wall and is, in turn, modulated by inhibitory and excitatory neurologic influences from the brain. When the bladder is full, the stretch receptors are activated. The individual perceives the activation of the stretch receptors as the bladder being full, which signals a need to void. When an individual cannot find a bathroom nearby, the brain bombards the PMC with a multitude of inhibitory signals to prevent detrusor contractions. At the same time, an individual may actively contract the levator muscles to keep the external sphincter closed or initiate distracting techniques to suppress urination. Thus, the voiding process requires coordination of both the ANS and somatic nervous system, which are in turn controlled by the PMC located in the brainstem. Pathophysiology If a problem occurs within the nervous system, the entire voiding cycle is affected. Any part of the nervous system may be affected, including the brain, pons, spinal cord, sacral cord, and peripheral nerves. A dysfunctional voiding condition results in different symptoms, ranging from acute urinary retention to an overactive bladder or to a combination of both. Urinary incontinence results from a dysfunction of the bladder, the sphincter, or both. Bladder overactivity (spastic bladder) is associated with the symptoms of urge incontinence, while sphincter underactivity (decreased resistance) results in symptomatic stress incontinence. A combination of detrusor overactivity and sphincter underactivity may result in mixed symptoms. Brain lesion Lesions of the brain above the pons destroy the master control center, causing a complete loss of voiding control. The voiding reflexes of the lower urinary tract the primitive voiding reflexremain 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 612 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 8

present, the affected individual may not be able to sense when the bladder is full. In the case of a motor neurogenic bladder, the individual will sense the bladder is full and the detrusor may not contract, a condition known as detrusor areflexia. These individuals have difficulty eliminating urine and experience overflow incontinence; the bladder gradually overdistends until the urine spills out. Typical causes are a sacral cord tumor, herniated disc, and injuries that crush the pelvis. This condition also may occur after a lumbar laminectomy, radical hysterectomy, or abdominoperineal resection. Some teenagers suddenly develop an abnormal voiding pattern and often are evaluated for tethered cord syndrome, a neurologic condition in which the tip of the sacral cord is stuck near the sacrum and cannot stretch as the child grows taller. Ischemic changes of the sacral cord associated with the tethering cause the manifestation of dysfunctional voiding symptoms. Peripheral nerve injury Diabetes mellitus and AIDS are 2 of the conditions causing peripheral neuropathy resulting in urinary retention. These diseases destroy the nerves to the bladder and may lead to silent, painless distention of the bladder. Patients with chronic diabetes lose the sensation of bladder filling first, before the bladder decompensates. Similar to injury to the sacral cord, affected individuals will have difficulty urinating. They also may have a hypocontractile bladder. Other diseases manifesting this condition are poliomyelitis, Guillain-Barr syndrome, severe herpes in the genitoanal area, pernicious anemia, and neurosyphilis (tabes dorsalis).

Workup Laboratory Studies Urinalysis and urine culture: Urinary tract infection can cause irritative voiding symptoms and urge incontinence. Urine cytology

Carcinoma-in-situ of the urinary bladder causes symptoms of urinary frequency and urgency. Irritative voiding symptoms out of proportion to the overall clinical picture and/or hematuria warrant urine cytology and cystoscopy. Chem 7 profile Blood urea nitrogen (BUN) and creatinine (Cr) are checked if compromised renal function is suspected. Other Tests Voiding diary A voiding diary is a daily record of the patient's bladder activity. It is an objective documentation of the patient's voiding pattern, incontinent episodes, and inciting events associated with urinary incontinence. Pad test This is an objective test that documents the urine loss. Intravesical methylene blue test or oral Pyridium or Urised may be used. Methylene blue and Urised turns the urine color blue; Pyridium turns the urine color orange. Patients should resume their usual physical activities while wearing a Peri-pad. If the pads turn to orange or blue, the patient is experiencing urine loss. If the pads remain white, moisture most likely is a normal vaginal fluid. Diagnostic Procedures Postvoid residual urine The postvoid residual urine (PVR) measurement is a part of basic evaluation for urinary incontinence. If the PVR is high, the bladder may be contractile or the bladder outlet may be obstructed. Both of these conditions will cause urinary retention with overflow incontinence. Uroflow rate Uroflow rate is a useful screening test used mainly to evaluate bladder outlet obstruction. Uroflow rate is volume of urine voided per unit of time.

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Low uroflow rate may reflect urethral obstruction, a weak detrusor, or a combination of both. This test alone cannot distinguish an obstruction from a contractile detrusor. Filling cystometrogram A filling cystometrogram (CMG) assesses the bladder capacity, compliance, and the presence of phasic contractions (detrusor instability). Most commonly, liquid filling medium is used. An average adult bladder holds approximately 50-500 mL of urine. During the test, provocative maneuvers help to unveil bladder instability. Voiding cystometrogram (pressure-flow study) Pressure-flow study simultaneously records the voiding detrusor pressure and the rate of urinary flow. This is the only test able to assess bladder contractility and the extent of a bladder outlet obstruction. Pressure-flow studies can be combined with voiding cystogram and videourodynamic study for complicated cases of incontinence. Cystogram A static cystogram (anteroposterior and lateral) helps to confirm the presence of stress incontinence, the degree of urethral motion, and the presence of a cystocele. Intrinsic sphincter deficiency will be evident by an open bladder neck. Presence of a vesicovaginal fistula or bladder diverticulum also may be noted. A voiding cystogram can assess bladder neck and urethral function (internal and external sphincter) during filling and voiding phases. A voiding cystogram can identify a urethral diverticulum, urethral obstruction, and vesicoureteral reflux. Electromyography Electromyography (EMG) helps to ascertain the presence of coordinated or uncoordinated voiding. Failure of urethral relaxation during bladder contraction results in uncoordinated voiding (detrusor sphincter dyssynergia). EMG allows accurate diagnosis of detrusor sphincter dyssynergia common in spinal cord injuries.

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Cystoscopy The precise role of cystoscopy in the evaluation of neurogenic bladder allows discovery of bladder lesions (eg, bladder cancer, bladder stone) that would remain undiagnosed by urodynamics alone. General agreement is that cystoscopy is indicated for people complaining of persistent irritative voiding symptoms or hematuria. The physician can diagnose obvious causes of bladder overactivity, such as cystitis, stone, and tumor, easily. This information is important in determining the etiology of the incontinence and may influence treatment decisions. Videourodynamics Videourodynamics is the criterion standard for evaluation of a patient with incontinence. Videourodynamics combines the radiographic findings of voiding cystourethrogram (VCUG) and multichannel urodynamics. Videourodynamics enables documentation of lower urinary tract anatomy, such as vesicoureteral reflux and bladder diverticulum, as well as the functional pressure-flow relationship between the bladder and the urethra. Treatment & Management Medical Care Stress incontinence may be treated with surgical and nonsurgical means. Urge incontinence may be treated with behavioral modification or with bladderrelaxing 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

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external collecting devices have an important role in the management of chronic incontinence. The criteria for use of these products are fairly straightforward, and they are beneficial for women who meet the following conditions: (1) women who fail all other treatments and remain incontinent, (2) women who are too ill or disabled to participate in behavioral programs, (3) women who cannot be helped by medications, (4) women with incontinence disorders that cannot be corrected by surgery, and (5) women who are awaiting surgery. Absorbent products Absorbent products are pads or garments designed to absorb urine to protect the skin and clothing. Available in both disposable and reusable forms, they are a temporary means of keeping the patient dry until a more permanent solution becomes available. By reducing wetness and odor, they help maintain the patient's comfort and allow her to function in normal activities. They may be used temporarily until a definitive treatment takes effect or if the treatment yields less-than-perfect results. Absorbent products are helpful during the initial assessment and workup of urinary incontinence. As an adjunct to behavioral and pharmacologic therapies, they play an important role in the care of persons with intractable incontinence. 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.

Catheters Urinary diversion, using various catheters, has been one of the mainstays of antiincontinence 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.

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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. 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 selfcatheterization 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. Surgical Care Surgical care for stress incontinence involves procedures that increase urethral outlet resistance. Operations that increase urethral resistance include bladder neck suspension, periurethral bulking therapy, sling procedures, and artificial urinary sphincter. Surgical care for urge incontinence involves procedures that improve bladder compliance or bladder capacity; these include sacral neuromodulation, botulinum toxin injections,[4, 5] detrusor myomectomy, and bladder augmentation. Diet The fact that certain foods in a daily diet can worsen symptoms of urinary frequency and urge incontinence is well known. If a patient's diet contains dietary stimulants,

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changes in her diet may help ameliorate incontinence symptoms. Dietary stimulants are substances contained in the food or drink that either cause or exacerbate irritative voiding symptoms. By eliminating or minimizing the intake of dietary stimulants, unwanted bladder symptoms can be improved or possibly cured. Avoidance of dietary stimulants begins with consumer awareness through careful label reading and maintaining a daily diet diary. Experimenting with dietary changes is not appropriate for everyone, and dietary experimentation should be instituted on an individual basis. Certain food products exacerbate symptoms of urge incontinence. Food Foods that contain heavy or hot spices may contribute to urge incontinence. A few medical reports have alluded to the fact that avoiding spicy foods may have a beneficial effect on urinary incontinence. Some examples of hot spices include curry, chili pepper, cayenne pepper, and dry mustard. A second food group that may worsen irritative voiding symptoms is citrus fruit. Fruits and juices that have a high potassium concentration may worsen preexisting urge incontinence. Examples of fruits that have significant potassium include grapefruits and oranges. A third food group that may worsen urinary bladder incontinence is chocolatecontaining sweets. Chocolate snacks and treats contain caffeine. Caffeine is a bladderunfriendly 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 68 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. Activity 15

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

Pelvic floor exercise Pelvic floor exercise refers to strengthening the levator muscles lining the floor of the bony pelvis. The first step in pelvic muscle rehabilitation is to establish a better awareness of the levator muscle function. Pelvic floor exercises, sometimes called Kegel exercises, are a rehabilitation technique used to tighten and tone the pelvic floor muscles (ie, levator ani) that have become weak over time. These exercises empower the external urinary sphincter to prevent stress incontinence and build up the pelvic floor muscles to avert impending pelvic prolapse. In addition, Kegel exercises may be performed to eliminate urge incontinence. Contraction of the external urinary sphincter induces reflex bladder relaxation. Pelvic floor muscle rehabilitation may be used to reprogram the urinary bladder to decrease the frequency of incontinence episodes.

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.

Biofeedback

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

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.

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.

Medications Used to Treat Neurogenic Bladder

Estrogen derivatives Conjugated estrogen increases the tone of urethral muscle by up-regulating the alphaadrenergic receptors in the surrounding area and enhances alpha-adrenergic contractile response to strengthen pelvic muscles, which is important in urethral

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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.

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.

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.

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

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Complications Prolonged contact of urine with unprotected skin causes contact dermatitis and skin breakdown. If left untreated, these skin disorders may lead to pressure sores and ulcers, possibly resulting in secondary infections. For individuals with a decompensated bladder that does not empty well, the postvoid residual urine can lead to overgrowth of bacteria and subsequent urinary tract infection. Chronic indwelling catheters may cause recurrent bladder infection, bladder stones, ascending pyelonephritis, and urethral erosion. The use of intermittent catheterization may result in bladder infections or urethral injury. Chronic suprapubic tubes may result in bladder spasms, bladder stone formation, and bladder infection. Potential problems unique to suprapubic catheters include skin infection, hematoma, bowel injury, and problems with catheter reinsertion. Untreated urinary tract infections may lead to urosepsis and death.

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

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Daftar Pustaka Benevento B.T. and Marca L. Sipski. 2002.Neurogenic Bladder, Nuer ogenic Bowel, and Sexual Dysfunction in People With Spinal Cord Injury. Phys Ther. 82 (6): 601-612. Faiz and Moffat. 2004. At a Glance ANATOMI. Jakarta : Erlangga Fowler CJ. 1993. Neurogenic bladder dysfunction and its management , In Greenwood R et al.Neurological rehabilitation. New Tork : Churc hil Livingstone Guyton and Hall. 2007. Buku Ajar Fisiologi Kedokteran Edisi 11. Jaka rta : EGC Greenfield, et al. 1997. Essentials of Surgery : Scientific Principles an d Practice 2nd Edition.McGraw-Hill Companies, Inc Kottke FJ. 1990. Krusens handbook of physical medicine and rehabili taion. 4th ed.Philadelphia: WB Sounders Lindsay KW. 1997. Neurology and neurosurgery illustrated. 3rd ed. N ew York: Churcill Livingstone Perkash I. Management of neurogenic bladder dysfunction of the bladd er and bowel, In Rackley R. 2009. Neurogenic Bladder. Medscape

reference. In : http://emedicine.medscape.com/article/453539overview#a7 (Diakses 1 0 Juli 2012)

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Ropper, Allan H and Brown Robert H. 2005. Adams and Victor s Principles of Neurology Eighth Edition. McGrawHill Companies, Inc. Sheerwood, L. 2001. Fisiologi Manusia dari Sel ke Sistem Edisi 2. Jak arta : EGC

Snell, RS. 2006. Neuroanatomi Klinik untuk Mahasiswa Kedokteran E disi 6. Jakarta : EGC Waxman, Stephan G. 2010. A Lange Medical Book Clinical Neur oanatomi Twenty-Sixth Edition. McGraw-Hill Companies, Inc. www.Herryyudha.com

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