Urinary incontinence (UI) is a very common health problem in women, especially in the elderly. This can be disruptive and embarrassing, with the potential of being disabling. There are many definitions recognized, but the most basic, yet complete is the involuntary loss of urine that is sufficient to be a problem.⁷ UI affects more than 13 million Americans in community and institutional settings. Most affected individuals do not seek help for incontinence, primarily because of embarrassment or because they are not aware that help is available.

Various studies have estimated the prevalence of UI for different age groups. One survey suggested that as many as 51% of the 17 to 25 age group of healthy, young, nulliparous females experience stress incontinence at least once.⁵³ In another, 26% of females 30 to 59 years of age experience UI at some time in adult life.²⁰ Non-institutionalized patients older than 60 via the mesa survey(medical, epidemiology, social aspects of aging) showed 38% experiencing UI, where institutionalized patients were upwards of 50%.⁵²

Risk factors evaluated include advanced age, smoking,²² obesity,²³ as well as prior childbirth, urogyn surgeries and radiation. High impact exercises did not seem to be a risk factor in one study of female olympic athletes.²¹ Ethnic variation suggest Indian and Caucasians have greater increase risk secondary to shorter urethral length (Avg. 3.5cm vs. 4.1cm) compared to African American women.⁵⁴ As the body ages, the bladder’s contractility, capacity, and ability to postpone voiding declines, while the prevalence of involuntary detrusor contractions increases. The maximal urethral closing pressure and length decline in women as they age and the post void residual increases to no more than 50-100ml.¹⁶

Costs of UI can be broken down into physical direct and indirect costs, psychosocial costs, and economic costs. Direct costs include skin irritations and infections, pressure ulcers, falls, urinary sepsis and physical activity restrictions. Indirect costs include drug side effects, adverse drug effects, and allergic reactions to drugs and materials. Psychosocial costs include embarrassment, depression, guilt, etc. and economic costs include supplies, labor, laundry, diagnosis and treatment.²⁰ A recent estimate of the direct costs of caring for persons of all ages with UI is $11.2 billion annually in the community and $5.2 billion in nursing homes (based on 1994 dollars). ³¹These costs will only increase in America as its population is living longer, with projections for the year 2040 of 20 to 25 % of the population being over the age of 65.

Anatomy and Physiology In discussing urinary incontinence, a good understanding of the anatomy and physiology must be had if one wants to understand the pathology and appropriate interventions available. The bladder serves as a reservoir for storage and periodic release of urine. Urine release is dependent on voluntary neural mechanisms that involve the brain and spinal cord. The bladder has been divided into two components: a body lying above the ureteral orifices, and a base consisting of the posterior trigone, deep detrusor, and anterior bladder wall. The bladder outlet is composed of the bladder base, urethra, and external sphincter. The muscularis of the bladder(detrusor) continues directly and inseparably into that of the urethra at the vesicourethral junction(bladder neck). The body detrusor (fundus or dome) is the muscular unit largely responsible for both reservoir and pump functions of the bladder during the micturition cycle. Being distensible, it allows the bladder to accommodate increasing amounts of urine during the filling ( storage) phase of micturition. Consisting of an interwoven meshwork without arrangement as discrete layers, the body can contract in unison, compressing bladder urine tridimensionally to pump it out during the voiding phase. Bundles of body detrusor become reorganized as they continue into the base detrusor becoming more indistensible. It is relatively fixed as a flat horizontal plate during the storage phase of micturition but is transformed vertically into a funnel cone by the contracting detrusor at the beginning of the voiding phase. This dynamic configuration entails that a flat base maintains continent closure of the vesical outlet during bladder filling and that the vertically funneled base pulls open the outlet to establish a conduit for urine during voiding. Traditionally, the bladder neck itself , or related circular ring had been considered as a smooth internal sphincter. In reality there is no discrete smooth muscle sphincter in the true anatomic sense, but rather a smooth sphincteric mechanism that comprises a complexly arranged musculature of the bladder base, vesicourethral junction(bladder neck) and subvesical (proximal) urethra. This is complemented in the female by other factors in organ structure, anatomic support by extrinsic pelvic relationships and attachments, and inherent biomechanical properties of the urethra. The urethral muscularis represents caudal extensions of the base detrusor into the urethral wall to form somewhat distinct layers of longitudinally and circularly oriented bundles. ¹⁸

At the most basic level, a reflex centered in the sacral micturition center governs urination. Afferent pathways (via somatic and autonomic nerves) carry information on bladder volume to the spinal cord as the bladder fills. Motor output is adjusted accordingly. Thus as the bladder fills, sympathetic tone closes the bladder neck, relaxes the dome of the bladder, and inhibits parasympathetic tone while somatic innervation maintains tone in the pelvic floor musculature (including striated muscle around the urethra). When urination occurs, sympathetic and somatic tones diminish, and parasympathetic cholinergically mediated impulses cause the bladder to contract. All of these processes are under the influence of higher centers in the brainstem, cerebral cortex, and the cerebellum. It appears that the cerebral cortex exerts a predominantly inhibitory influence while the brainstem facilitates urination. The loss of central cortical inhibiting influences over the sacral micturition center from diseases such as dementia, stroke, and Parkinsonism can produce incontinence in elderly patients. Disorders of the brainstem and suprasacral spinal cord can interfere with the coordination of bladder contractions and lowering of urethral resistance, as well as interruptions of the sacral innervation causing impaired bladder contraction and problems with compliance. Normal urination is a dynamic process, requiring the coordination of several physiological processes. Under normal circumstances, as the bladder fills, pressure remains low (<15cmH20). The first urge to void is variable but generally occurs between 150 and 350ml, and normal bladder capacity is 300-600ml. When normal urination is initiated, true detrusor pressure (bladder pressure minus intra-abdominal pressure) increases until it exceeds urethral resistance, and urine flow occurs. If at anytime during bladder filling total intravesical pressure exceed outlet resistance, urinary leakage will occur. This will happen if intra-abdominal pressure rises without a rise in true detrusor pressure by coughing or sneezing in someone with outlet or urethral sphincter weakness. This is termed genuine stress incontinence. Alternatively, the bladder can contract involuntarily and cause urinary leakage. This is detrusor over-activity, and is divided into detrusor hyper-reflexia with neuro disorders, and detrusor instability without a neuro disorder. So in summary, cholinergic innervation, specifically muscarinic, causes detrusor contraction and urethral relaxation, where as adrenergic innervation causes detrusor relaxation and urethral contraction. The involuntary smooth muscle of the bladder, and the voluntary skeletal muscle of the external sphincter maintain continence¹⁹.

So the three common types of UI involve one or a combination of two basic abnormalities in the lower genitourinary tract function: 1) failure to store urine secondary to hyperactive or poorly compliant bladder or by decreased outflow resistance; 2) failure to empty the bladder, caused by a poorly contractible bladder or by an increased outflow resistance.

Types of urinary incontinence are as follows:

• Transient
• Total
• Stress
• Urge
• Mixed
• Overflow
• Functional
• Transient involves reversible incontinence. This is usually worked up with a couple of mnemonic devices that are DIAPPERS and DRIP.

D for delirium-confusional state(drugs/acute illness)

I for infection (symptomatic urinary)

A for atrophic urethritis, vaginitis- 80%female elderly experiences this

P for pharmaceutical-side effects-sedatives, anticholinergic, hypnotics, alcohol,

antipsychotic, antidepressants, narcotics

P for psychological, especially severely depressed

E for excess urine output (chf, hyperglycemia)

R for restricted mobility (arthritis, hip defects, deconditioning, and claudication, spinal

stenosis, chf, poor eyesight, restraints, disequilibrium

S for stool impaction (10% of older patients-narcotic) with theory that a reflex bladder contraction is induced by rectal distention or that there is bladder outlet obstruction with an overflow type incontinence.¹⁶

D for delirium

R for restricted mobility, retention

I for infection, inflammation, impaction

P for polyuria, and pharmaceuticals¹⁹

• Total incontinence describes the patient who is incontinent all the time, in all positions. This is secondary to sphincter deficiency lost to previous surgery, nerve damage, cancer, or and abnormal tract (extra ureter). Urine loss may occur without any warning or sensory awaredness such as in paraplegics and some patients without overt neurologic dysfunction. ^{1,2,3,4,8,7,11,13,16,19,30}

• Stress incontinence involves the loss of urine associated with activities that result in an increase in intra-abdominal pressure (coughing, sneezing, lifting, and exercising). Genuine stress Incontinence is involuntary loss of urine in the absence of detrusor contraction or an over-distended bladder, where intravesical pressure exceeds the maximum closure pressure. Patients don’t leak in the supine position. This is related to the laxity of the pelvic floor musculature. This is more common in multiparous women, with previous pelvic surgery, or estrogen deficiency. This is more commonly from urethral hypermobility or significant displacement of the urethra and bladder neck during exertion when intra-abdominal pressure is raised. Stress incontinence is less commonly from intrinsic sphincter deficiency (ISD) where urethral closing pressure<20cm H₂0 which may be due to congenital sphincter weakness in patients with myelomeningocele, or pelvic denervation, or acquired after trauma, radiation therapy, or a sacral cord lesion. In women, ISD is commonly associated with multiple incontinence surgical procedures, as well as with hypoestrogenism, aging, or both. In this condition, the urethral sphincter is unable to generate enough resistance to retain urine in the bladder. Stress incontinence is the most common type of UI in younger women and the second most common in older women. Volume is normally small to moderate. ^{1,2,3,4,8,7,11,13,16,19,30}

• Urge incontinence describes the uncontrolled loss of urine that is preceded by a strong, unexpected urge to void unrelated to position or activity and is usually indicative of detrusor instability or sphincter dysfunction. Detrusor instability involves involuntary detrusor contractions that can cause UI with and without symptoms of urgency. It can also cause symptoms of urgency without concomitant incontinence. This can be related to the abnormal process of dysjunctional banding pattern of the muscle in the bladder that forms as it ages, causing increased spontaneous activity and asynchronous contractions. When a causative neurologic lesion is established, the DI is called detrusor hyper-reflexia. (i.e. stroke) In patients with suprasacral spinal cord lesions and multiple sclerosis,DH is commonly accompanied by detrusor sphincter dyssynergia(inappropriate contraction of the external sphincter with detrusor contraction). Side effects include urinary retention, vesicoureteral reflux, and subsequent renal damage. Another urodynamic diagnosis associated with the symptoms of UI in frail, elderly patients is detrusor hyperactivity with impaired bladder contractility (DHIC). This is the most common form in the elderly. They have involuntary detrusor contractions, yet must strain to empty their bladder either incompletely or completely. Patients with DHIC generally have symptoms of UI and an elevated pvr, but may also have symptoms of obstruction, stress incontinence, or overflow incontinence. Inflammatory conditions or neurogenic disorders are commonly associated with this type. Leakage of urine (often large volume, but variable) because of inability to delay voiding after sensation of bladder fullness is perceived secondary to detrusor motor and/or sensory instability, isolated or associated with one or more of the following: local (cystitis, urethritis, tumors, stones, divertic) cns disorders-stroke, dementia, Parkinson’s, suprasacral spinal cord injury, or disease. This is most often in the geriatric population in either sex. ^{1,2,3,4,8,7,11,13,16,19,30}

• Mixed usually involves stress and urge incontinence. This is usually idiopathic, but bacterial cystitis, bladder tumor, bladder outlet, neurogenic bladder must be excluded. This is common in women, especially older women. Often, however, one symptom (urge or stress) is more bothersome to the patient than the other. Identifying the most bothersome symptom is important in targeting diagnostic and therapeutic interventions. ^{1,2,3,4,8,7,11,13,16,19,30}

• Overflow incontinence describes chronic urinary retention that could result in overflow. This can be when a chronically distended bladder receives an additional increment of urine. The intravesical pressure just exceeds the outlet resistance, allowing a small amount of urine to dribble out. So there is leakage of urine (usually small amounts) resulting from the mechanical forces on an over distended bladder or from other effects of urinary retention on bladder and sphincter function secondary to a stricture, cystocele, acontractile bladder with diabetes, spinal injury, ms, drugs versus idiopathic causes. Outlet obstruction is rare in otherwise healthy older and younger women, and is usually secondary kinking associated with large cystocele or to obstruction to a previous bladder neck suspension. Detrusor underactivity is idiopathic with overflow incontinence. This may be due to an underactive detrusor, acontractile detrusor, or there is bladder outlet or urethral obstruction leading to overdistension and overflow. ^{1,2,3,4,8,7,11,13,16,19,30}

• Functional incontinence is leakage associated with the inability to toilet because of impairment of cognitive and or physical functioning, psychological unwillingness, or environmental barriers (i.e. severe dementia, depression, anger, and hostility.) There is a distinct geriatric deficit of cognition and mobility, implying urinary function is normal, but really after studies, normal urine fxn is the exception. This is not inevitable with dementia or immobility. ^{1,2,3,4,8,7,11,13,16,19,30} (17% of most severely demented institutional patients were continent and 50% would be if they could transfer.)⁷

The primary care physician should question their patients regularly to identify UI. Open-ended questions like "Do you ever lose your water when you don’t want to?" and "How long does it take to get to the bathroom when your bladder is full?" Then if a response is had one must pursue. But even pure symptoms of urine incontinence identify fewer than half of patients with pure genuine stress incontinence or detrusor instability: historic and clinical parameters do not improve the sensitivity of these symptoms.⁵ Standardized questionnaires have been established to help identify certain subsets of detrusor instability and stress incontinence and studies have shown a low sensitivity and specificity do not justify its use as a diagnostic tool in UI. This should not be the only determinant of diagnosis, nor should strategies be based on history alone^{. 24}

ALL Patients with UI should undergo a basic evaluation that include a history, physical exam, measure of pvr, and UA as AHCPR guidelines with goals to:

1) confirm the presence of UI.

2) identify condition, including potentially reversible ones, that may be contributing to the UI.

3) identify patients who require further evaluation before and therapeutic interventions are attempted and the patients who may receive initial treatment without further testing.

4.) identify a presumptive diagnosis if possible.³⁰

Focused medical, neurologic, GU history including an assessment of risk factors and a review of medications (prescription and nonprescription) and a detailed exploration of the symptoms of the UI and associated symptoms and factors, including

• Duration and characteristics
• Most bothersome sx
• Frequency, timing, amount of continent and incontinent episodes
• Precipitants of incontinence (cough, exertion, surgery, new medications)
• Other lower urinary tract symptoms
• Fluid intake pattern (caffeine, alcohol) and times
• Alterations in bowel habit or sexual function
• Previous treatment and their effects on UI
• Amount and types of pads, briefs, and protective devices
• Expectations
• Bladder record-very helpful-includes the freq., timing, amount per pt or caregiver
• MSE and assessment of mobility, living environment, social factors, toilet access³⁰

Physical Examination

• General-detect edema which can cause nocturia and nocturnal UI; detect neurologic abnormalities suggestive of MS, stroke, spinal cord compression, or other neurologic conditions and assess mobility, cognition, and manual dexterity to toileting.

• Abd.exam- to check for diastases rectii, organomegaly, masses, peritonitis, fluid collection etc. This could reflect influences on intraabdominal pressure and detrusor contractions. The bladder can’t be palpated unless it its distended, and is not evident on percussion unless it has a volume greater than 150cc.

• Rectal exam to test for perineal sensation, sphincter tone at rest and active, fecal impaction, or rectal mass,

• Pelvic exam in women to assess perineal skin condition, genital atrophy, prolapsed (cyst, rect, uterine) pelvic mass, paravaginal tone, or other abnormality. Palpation of the anterior vaginal wall and urethra may elicit a urethral discharge or tenderness that suggests a urethral diverticulum, cancer , or inflammatory condition of the urethra. Optimally, testing should be done when the bladder is full, but before urge to void. If an instantaneous leakage occurs with cough, then SUI is likely; if leakage is delayed or persists after the cough, DI should be suspected. If the test is initially performed in the lithotomy position and no leakage is observed, the test should be repeated in the upright position. Q tip test can infer urethral hypermobility, and is performed by sticking a Q tip into the urethra to the bladder neck and asking the patient to cough. If there is greater than 30 degree movement, then this could be suggestive of urethral hypermobility.

• Neurological Reflexes- bulbocavernosis reflex( S2-S3), cremasteric reflex(L1-L2), anal reflex (S2-S5) ³⁰

Neither history nor physical exam is sensitive or specific enough for inferring which type of UI is occurring, especially in the elderly. The post void residual can help in some instances. Accurate measurements of PVR can be accomplished either by catheter or by pelvic ultrasound. Before PVR is measured, the patient should void in the most comfortable and private environment possible. Observation is optional to observe signs of hesitancy, strain, slow or intermittent stream. The measurement is generally done within a few minutes of voiding by catheter or US. There really is not any literature for normal or minimal for abnormal PVRs. In general, PVRs of less than 50ml are considered adequate bladder emptying. Repetitive PVRs ranging from 100 to 200 or higher are considered inadequate. It becomes difficult with urine PVRs of 50-199 and clinical judgement becomes key. PVR may be influenced by whether the patient is ready to void, strains to void, really makes the effort to drain the bladder completely, and the environment or clinical settings the patient is in . Since the PVR may vary, repeated measure may be warranted in some patients. Alternative to catheterization is the use of pelvic US which is pretty accurate if you have access to one. ⁶

This is performed to detect conditions associated. with or contributing to UI such as hematuria (ca, stone, infxn) , glucosuria, pyuria, bacteriuria, and proteinuria. The use of the chemical strips varies considerably among methods and different patient populations. Therefore urine culture should be obtained when the chemical strips suggests infection or when symptoms suggests infection. With chronic UI in nursing home patients, eradication of bacteriuria with or without pyuria has no effect on morbidity, mortality, or the severity of UI. Thus, unless UI is of recent onset, has recently worsened, or is accompanied by other symptoms of infection, bacteriuria does not need be treated. Among noninstitutionalized patients, the relationship of bacteriuria (with or without pyuria) to UI is unclear. With research pending, infections should be treated when the UI patient is initially evaluated.³⁰

This relies on clinical suspicion so one should obtain a BUN, creatinine, glucose, calcium if compromised renal fxn is suspected or if the patient is experiencing polyuria (no diuretics involved). Urine cytology is not recommended in the routine evaluation of the incontinent patient. If concerned about bladder cancer secondary to hematuria or the acute onset of irritative voiding symptoms in the absence of UTI, then the patient requires cystoscopy and cytology to exclude bladder neoplasm.

After the above basic evaluation, all incontinent patients in whom transient causes of UI are discovered should be TX appropriately. If UI persists after transient cause are treated, further evaluation may be helpful before other therapy. If there are no transient causes and the patient evaluation suggests a particular type of UI then a therapeutic trial for that type of UI may be instigated. After basic evaluation and treatment, patients who fail or those who are not appropriate for TX based on presumptive Dx should undergo further evaluation.

Urodynamic, endoscopic, imaging

These tests are designed to determine the anatomic and functional status of the urinary bladder and urethra via a specialist.

Simple cystometry is appropriate for detection of abnormal detrusor compliance and contractility, measuring PVR, and determining capacity. This is a test of detrusor function and can assess bladder sensation, capacity, and compliance, and determine the presence and magnitude of both voluntary and involuntary detrusor contractions. The patient’s symptoms should be reproduced at the time of the contractions. This could be falsely negative with a genuinely overactive bladder. One could see involuntary contractions in symptomatic patients and in asymptomatic patients.

Other specialists like multi-channel or subtracted cystometrogram (CMG) and a voiding CMG or pressure flow study which is up to the urologist.

Uroflowmetry measures urine flow rate visually, electronically, or with a disposal unit. A flow curve is generated, but is not helpful in diagnosing the types of incontinence found in women. This may be helpful with patients who have difficulty with bladder emptying. You really can’t distinguish obstruction and detrusor weakness without a simultaneous measurement of detrusor function.

Urethral pressure profilometry is a urethral function test measuring resting and dynamic pressures in the urethra.

EMG of the striated urethral sphincter measures the integrity and function of its innervation. ³⁰

Cystoscopy is not recommended in the basic evaluation of UI but maybe indicated in the following: 1) a patient with sterile hematuria or pyuria 2) when urodynamics fail to duplicate symptoms 3) new onset of irritative voiding symptoms, bladder pain, recurrent cystitis, or potential foreign body. The role of cystoscopy is controversial. ³⁰

Videourodynamics is a technique that combines various urodynamic tests with simultaneous fluoroscopy and can be helpful in sorting out cases of complex incontinence problems. ³⁰

Treatment of Urinary Incontinence

• Behavioral
• Pharmacological
• Surgical

Treatment options including risks, benefits and outcomes should be discussed with the patient so that informed choices can be made. Generally, the least invasive treatment with the fewest potential adverse complications that is appropriate for the patient should be chosen first. For many forms of UI, behavioral techniques meet these criteria. However, an informed patient’s preference must be respected. A study of 150 patients, after being evaluated for UI and given options according to AHCPR guidelines, were studied on the decisions they made and the compliance with their decisions. When given options, patients choose nonoperative measures first, but compliance is poorer among patients who choose behavioral modification.¹⁷

This normally decreases the frequency of UI in most individuals when provided by knowledgeable health care providers, has no reported side effects, and does not limit future treatment options. Divided into caregiver dependent techniques for patients with cognitive and motor deficits and those requiring active rehabilitation and education techniques. This can be arbitrary. Any individual’s ability to actively participate varies on a continuum from complete dependence to full participation in the most complex behavioral therapies. For example, physically impaired patients who are cognitively intact may benefit from bladder training; pelvic muscle exercises (PME), and biofeedback therapy, but may depend on caregivers for assistance .

Behavioral techniques are listed below in the order of those requiring passive involvement to those requiring active participation:

• Toileting assistance—routine/scheduled toileting, habit training, prompted voiding
• Bladder retraining
• Pelvic muscle rehabilitation-PMEs, PMEs and bladder inhibition augmented by biofeedback therapy, PMEs augmented with vaginal weight training, and pelvic floor electrical stimulation.

All behavioral techniques involve educating the patient, the caregiver, or both and provide positive reinforcement for effort and progress. This should be offered to motivated individuals wishing to avoid more invasive procedures or dependence on protective garments, external devices, and medications. This can increase patient understanding of lower urinary tract function and the environmental factors affecting symptoms. These techniques can improve control of detrusor and pelvic muscle function. They generally require patient or caregiver involvement and continued practice. Before implementing behavioral therapy, patients should undergo basic evaluation, and must be tailored to the patient’s underlying problem, such as bladder training or habit training for urge UI and PMR for SUI. Patients with overflow UI are not primary candidates for behavioral intervention. Improved bladder control can occur, even in the cognitively impaired^.32

• Toileting Assistance

Include routine or scheduled toileting, habit training, and prompted voiding.

Routine or scheduled toileting is provided by the caregiver on a fixed schedule at regular intervals. The caregiver takes the patient to void every 2-4 hours including at night, with the goal to keep the patient dry. There is no effort to motivate the patient to delay voiding and resist urge, unlike in bladder retraining. A controlled study of 20 female’s aged 24 to 94 were instructed to void every 2 hours, regardless of urge for 2 weeks. Reports of 79% success rate for incontinence. ³³

Habit training is toileting scheduled to match the patient’s voiding habits. In a controlled study of habit training voiding patterns were identified in 51 NH residents with an electronic monitoring device ³² The nursing home staff were taught to toilet residents during the periods of greatest voiding frequency based on individual patterns per monitoring. A significant reduction in UI occurred over a 3-month period in 86%, with 1/3 showing 25% or greater improvement over baseline compared with an increase in UI observed in the control group. In addition, the volume of urine loss decreased significantly in the experimental group only. Nursing staff compliance was the only major issue, with resistance to changes in care routines. This is an excellent technique for patients in the home living with a caregiver.

Prompted voiding is recommended in patients who can learn to recognize some degree of bladder fullness or the need to void, or who can ask for assistance or respond when prompted to toilet. This population may not have sufficient cognitive ability to participate in other more complex behavioral therapies. The three major elements of prompted voiding are as follows: Monitoring (pt checked by caregivers on a regular basis and asked to report verbally if wet or dry.)Prompting (the pt is asked-prompted- to use the toilet.) Praising (the pt is praised for maintaining continence and for trying to toilet).

Three controlled trials ^34,35,36evaluated prompted voiding in nursing homes. The combined trials used prompted voiding for 251 residents and demonstrated significant reductions with no reported side effects. An average reduction of 0.8-1.8 episodes per patient per day reported was in contrast to the control group of 4.5 times per 12-hour period which remained unchanged. Residents with lower voiding frequencies (less than 4 in a 12 hour period) and those who toileted appropriately > 75% of the time during a brief 2 to 6 day prompted voiding trial were the most likely to show long term benefits with prompted voiding. Because nursing home staff administer the protocols, success relies on training, compliance, and incentives for active staff participation.

• Bladder Training

Is strongly recommended for management of urge (DI) and mixed incontinence, as well as for SUI. It is difficult to implement in cognitively impaired persons and frail, elderly patients.

Bladder Training (or retraining) has many variations but generally consists of 3 primary components: Education, Scheduled voiding with systematic delay of voiding, and positive reinforcement. This requires written, visual, and verbal instruction that addresses the physiology and the pathophysiology of the lower urinary tract, and the resistance or inhibition of the sensation of urgency, to postpone voiding, and to urinate according to a timetable rather than according to urinary urge. Initially, the interval goal is set between 2-3 hours, or determined by the patient’s present interval, and is not enforced during sleep hours. The voiding schedule progressively increases the interval between mandatory voids with concomitant distraction or relaxation techniques. The patient is thus taught to delay voiding when the urge to void occurs. If unable to delay voiding between scheduled toileting times, the schedule is adjusted and the interval time is reset from the time of the last void. Another method is to keep the prearranged schedule and disregard the unscheduled void between schedules. The training may continue for several months during which time the therapist provides positive reinforcement and instruction.

A controlled randomized study ³⁷ conducted of 131 women with sphincteric incompetence and unstable detrusor function using bladder retraining. Of the 60 women in the treatment group receiving bladder training with behavioral strategies to decrease urge, patient education, and a schedule of voiding, 12% became dry, and 75% had at least a 50% reduction in the number of incontinent episodes. This was maintained after 6 months with control subjects showing no changes.

• Pelvic muscle rehabilitation (exercises)

May be used alone or augmented with bladder inhibition biofeedback therapy or with vaginal weight training. Pelvic floor stimulation is another method of pelvic muscle rehabilitation. Health care providers must teach patients the correct method of distinguishing and contracting the pelvic muscles through digital vaginal exam, to verify appropriate muscle use, verbal feedback, or use of vaginal weights and biofeedback therapy to ensure accurate performance.

Teaching women PMEs may prevent UI, decrease the incidence of UI, and is strongly recommended for SUI, in conjunction with bladder training for urge incontinence.

PMEs, also known as Kegel exercises and pelvic floor exercises are performed to strengthen the voluntary periurethral and perivaginal muscles that contribute to the closing force of the urethra and to support of the pelvic visceral structures. First, sustain a contraction for at least 10 seconds, followed by an equal period of relaxation. Performed about 30-80 times a day for at least 8 weeks and this may need to be continued indefinitely. Elderly patients may require a longer time to train. This is indicated for women with stress incontinence and can reduce urgency and prevent urge UI. Several studies support the efficacy of PME’s. A controlled study ³⁸of 65 women ages 35 to 75, had a 62% reduction in UI episodes. But the most effective was uncontrolled in Italy with 95% reduction.³⁹ Also a study⁴⁰ in randomized control with PME vs. phenylpropanolamine hcl (PPA) where PME was found to be an effective alternative treatment for SUI comparable to PPA. Adherence to drug treatment was greater than to the exercise protocol. Evidence demonstrates that patients require repeated guidance over an extended period of time to derive optimal benefit from PME.

Pelvic muscle rehabilitation and bladder inhibition using biofeedback therapy are recommended for patients with stress UI, urge UI, and mixed UI. The aim of biofeedback therapy, which uses electronic or mechanical instruments to relay information to patients about their physiologic activity, is to improve bladder dysfunction by teaching people to change physiologic responses that mediate bladder control. The auditory or visual display of this information forms the core of biofeedback procedures. Biofeedback typically uses single measurements from surface, needle, vaginal, or anal probe, EMG or manometric methods. Biofeedback using multimeasurement feedback methods involves simultaneous measurements of pelvic and abdominal/detrusor muscle activity. The biofeedback protocol that has been associated with the largest and most consistent symptom reduction is one that reinforces pelvic muscle contraction concurrently with inhibition of abdominal and detrusor contraction. Reports using this multimeasurement method show a 75.9 to 82 percent reduction in UI across 6 studies involving 166 subjects ³⁰. The presumed benefit of the multimeasurement procedure is that it reinforces pelvic floor contraction directly with moment to moment feedback, which characterizes for the patient the quality and intensity of the contraction. Other studies have showed benefit in-patients with neurologic disease and in the frail elderly experiencing UI using a combination of multimeasurement biofeedback and other behavioral techniques such as bladder training.

Vaginal weight training is recommended for SUI in premenopausal women. Specially designed weights can augment PME. Weights 20 to 100gms are inserted intravaginally, with the tapered portion resting on the superior surface of the perineal muscle with the patient attempting to retain it by contracting the pelvic muscles up to 15 minutes. Studies revealed cure or greatly improved status 68-80% after 4-6 weeks.⁴¹

Pelvic Floor Electrical Stimulation has been shown to decrease incontinence in women with SUI, urge and mixed incontinence. This is performed via nonimplantable stimulation producing contraction of the levator ani, external urethral and anal sphincters, accompanied by a reflex inhibition of the detrusor. This activity depends on a preserved reflex arc through the sacral micturition center. Sensors or surface electrodes are perivaginally or perianally placed. Studies of 2 randomized control trials using active and placebo perianal surface patch neurostimulation for SUI in patients, along with PME instruction, reported cure or improvement rate of 86% and 33% in the placebo group.⁴² Using active and inactive vaginal plug devices in 52 women with SUI, a study reported objective cure or improvement in 48% and 13% of placebo group. Other studies used similar vaginal or anal plug devices from 20minutes to 20hours/day over 4weeks to 3.5months with cure or improvement rates ranging from 48 to 94% in 842 patients with SUI, urge, or mixed.⁴³

Only oxybutynin (Ditropan),flavoxate (Urispas), and hyoscyamine(Levsin) have FDA approval for UI. Imipramine (Tofranil) has FDA approval for enuresis in children but not adults

• Urge Incontinence: Detrusor Instability

The following agents are reported to be useful in DI as observed in clinical practice.

Anticholinergics are first line pharmacologic therapy for patients with DI. They block contraction of the normal bladder and probably the unstable bladder as well. All anticholinergics are contraindicated in-patients with documented narrow-angle, but not wide-angle, glaucoma.

Oxybutynin(Ditropan)2.5-5mg 3-4x day First Choice

Propantheline (Pro-Banthine)7.5 –30mg 3-5xday with higher doses(15-60mgqid) may be required Second Choice

Dicyclomine hcl (Bentyl) 10-20mgtid

Tricyclic antidepressants:

Imipramine (Tofranil)10-50mg tid, or qhs.

Doxepin (Sinequan)

Desipramine (Norpramin)

Nortriptyline (Aventyl, Pamelor)

Others:

Flavoxate( Urispas)100-200mg tid/qid

Hyoscyamine(Levsin) 0.375-0.75mg q 12 hr.

Calcium Channel Blockers

NSAIDS

Oxybutynin(Ditropan) has both anticholinergic and direct smooth muscle relaxant properties. In a review of 7 RCT evaluating the use of this agent for UI, 6/7 proved superior to placebo, with a reduction in UI in 15 to 58% over placebo. In the 1 study where no improvement was seen , a dose of 5mg bid used. There is some benefit with instillation into neuropathic bladders as well. ³⁰ Side effects include dry mouth, dry skin, blurred vision, MS changes, nausea, constipation, with severity increasing with dosage. Severe xerostomia occurred in 84% of subjects receiving 5mg of oxybutynin qid.⁴⁴

Propantheline(Pro-Banthine) is the prototype for anticholinergic agents in urologic conditions . No agent better approximates atropine’s effect on the bladder in vitro, although its CNS system side effects are less marked. It is inexpensive and has been used widely over time. Despite propantheline’s success in uncontrolled case series, review of controlled trials showed improvement over placebo, but a higher dropout rate with side effects. Experts agree that at least for less impaired patients who can tolerate full dosages, propantheline is effective. ³⁰ Side effects , in addition to urinary retention, are similar to all other anticholinergic agents with the most common being xerostomia.

Dicyclomine hcl(Bentyl) is an anticholinergic with smooth muscle relaxant properties. There are limited studies, with small populations. They suggest improvement vs. placebo. There are no studies comparing it against other anticholinergic agents, but it may be used as an alternative for UI, pending further research. ³⁰

Flavoxate(Urispas) is a tertiary amine with smooth muscle relaxant properties in vitro. 4 RCT did not demonstrate a significant benefit. At this time, this drug is not recommended for the treatment of DI. (Per AHCPR)

Hyoscyamine (Levsin) and other oral anticholinergic agents are known to be used in clinical practice in the treatment of DI; however no controlled studies are available for use in DI.

Calcium Channel Blockers theoretically should work since the influx of extracellular calcium causes detrusor contraction, but limited studies and side effects keep it from being recommended at this time.

NSAIDS should theoretically work because of their inhibition of prostaglandin "synthetase," which interferes with prostaglandin mediated bladder contractions , but limited research and side effects keep this from being recommended at this time.

Tricyclic Agents should be reserved for carefully evaluated patients. The usual oral dosages are 10-25 mg 1-3x day. They are widely used, but produce many adverse effects(cardiac and anticholinergic) with more risk in elderly patients. Limited research is available. 3 RCT with one in psychiatric inpatients in whom the type of UI was not established showed that imipramine, desipramine, and nortriptyline each resulted in statistically significant reduction in the number of wet nights.⁴⁵ The other 2 studies, one with doxepin,⁴⁶ the other with imipramine,⁴⁷ documented decreases in incontinence and overall patient preference for doxepin. Side effects in these studies included fatigue, xerostomia, dizziness, and blurred vision in the doxepin group and nausea and insomnia in the imipramine group.

Pharmacotherapy, at least in short-term trial, appears to benefit some patients with UI due to detrusor instability. However, regardless of the agent chosen, involuntary bladder contraction are usually not abolished; the warning time between appreciation of the need to void and the onset of bladder contraction is not affected; the degree of improvement is modest; and the cure is uncommon. These drugs should be used only in conjunction with a voiding schedule or behavioral intervention and only after other factors contributing to incontinence is addressed. Oxybutynin possesses the most favorable efficacy,safety, and pharmacokinetics profile of the agents for DI. Selection must be individualized(i.e. patient selection and cost.) Start low, and go slow while watching for side effects.

• Stress Incontinence: Urethral Sphincter Insufficiency

Agents that affect the high concentration of alpha-adrenergic receptors in the bladder neck, base , and proximal urethra are the drugs of choice. Sympathomimetic drugs with alpha adrenergic agonist activity presumably cause muscle contraction in these areas and thereby increase bladder outlet resistance. Drugs which increase resistance include direct alpha adrenergic agonist, estrogen supplementation both for direct effect on urethral mucosal and periurethral tissues and for enhancement of alpha adrenergic response, and beta adrenergic blocking agents that may allow unopposed stimulation of alpha receptor mediated contractile muscle responses.

Phenylpropanolamine(PPA) or pseudoephedrine is the first line pharmacologic therapy for women with SUI who have no contraindications for its use(HTN). PPA dose 25-100mg in sustained release form bid. Pseudoephedrine is 15-30mg tid.

PPA in sustained release form is the major alpha adrenergic agonist drug studied in women with stress incontinence. Pharmacologic therapy of incontinence caused by sphincter insufficiency using PPA appears to result in few cures UI, but may cause improvement in 20 to 60% of patients over placebo response from 7 prospective RCT of middle aged normotensive women with SI. ³⁰ Side-effects include anxiety, insomnia, agitation, respiratory difficulty, headache, sweating, hypertension and cardiac arrhythmias, all of which occur more commonly in elderly patients.

Oral or vaginal may be considered as an adjunctive pharmacologic agent for postmenopausal women with SUI or mixed incontinence. Conjugated estrogen is usually administered orally(0.3-1.25mg/day) or vaginally(2gm or fraction/day). Progestin may be given continuously or intermittently.

Because the vagina and urethra are similar in embryologic origin, estrogen supplementation in postmenopausal women may restore urethral mucosal coaptation and increase vascularity, tone, and the alpha-adrenergic responsiveness of urethral muscle. This effect is still completely not understood, but lots of studies support this, along with benefit in cardiac, bone, lipids. Transdermal, oral, and vaginal delivery of estrogen (plus progestin in non-hysterectomy patients) all work. This was evaluated in a meta-analysis of 6 RCT and 17 uncontrolled clinical series ^27,28 which demonstrated the favorable effects on incontinence in postmenopausal women treated with estrogen therapy(p<0.01 for all, and subjects with SUI p< 0.05).

Alpha adrenergic therapy plus estrogen supplementation

Combination is recommended of SUI in postmenopausal when initial single drug therapy has proven inadequate.

This is based on an estrogen-induced increased number , sensitivity of alpha-adrenergic receptors in the urethra, or both, so it potentiates the alpha-adrenergic contractile response to drug stimulation. 4 controlled studies combined ³⁰, suggests that this may be more effective than alpha-adrenergic agonist therapy alone. The possible risks of alpha-adrenergic drugs and estrogen do not appear to be increased when used together. This should be considered when initial therapy fails.

Tricyclic antidepressants are alternatives for SUI when first-line agents have proven unsatisfactory.

Imipramine, which possesses both alpha-adrenergic agonist activity(presumably mediated by blocking reuptake of norepinephrine ) and anticholinergic properties, has been reported to benefit women with stress incontinence.⁴⁸ Side effects include nausea, insomnia, weakness, fatigue, and postural hypotension.

Other drugs including beta-blockers(propanolol) have been investigated with mixed results. One study showed an improvement, but not all studies are consistent.⁴⁹

The decision to perform surgery for the treatment of UI should be made only after a precise focused assessment that includes: a comprehensive clinical evaluation with an objective confirmation of the pathophysiologic diagnosis and severity of urinary loss, a correlation of the anatomic and physiologic findings with the surgical plan, an estimation of surgical risk, and an estimation of the impact of the proposed surgery on the patient’s quality of life.

1)Surgeries that increase outlet resistance and relieve SUI and ISD:

2) Procedures that decrease detrusor instability and correct urge incontinence

3)Operations that remove outlet obstruction, thereby correcting overflow incontinence or reversing detrusor instability that is secondary to the outlet obstruction. ³⁰

1) Retropubic suspension- elevation of the lower urinary tract, particularly the urethrovesical junction, within the retropubic space.

2) Needle bladder neck suspension

3) Anterior vaginal repair. (inferior to above 2)

Procedures for Intrinsic Sphincter Deficiency

1. Sling procedures-recommended for ISD with coexisting hypermobility, or first line ISD. Involve placing a sling of either autologous or heterologous material, under the urethrovesical junction and anchoring it to retropubic or abdominal structures or both.
2. Periurethral bulking injections- first line for ISD, without hypermobility. Use of polytetrafluoroethylene(PTFE), collagen, or autologous fat under cystoscopic guidance into an incompetent periurethral area. Require skin test for sensitivity to the material.
3. Placement of an artificial sphincter is indicated in severe unresponsiveness to other surgical treatments and is rarely used as first line secondary to the high complication rate.

Only in highly symptomatic patients in whom nonoperative management has failed.

Urinary diversion-augmentation cystoplasty with a patch of detubularized intestine is the procedure of choice. Diversion with a urostomy or continent urinary diversion may be last resort.

Bladder denervation procedures (sub trigonal or subvesical phenol injection) ineffective in men and possibly effective in women.

Surgery, or intermittent catheterization or an indwelling catheter if nonsurgical candidates. Secondary to prior incontinent surgeries or severe pelvic prolapse.

Intermittent catheterization (IC) may be used secondary for supportive measures with spinal cord injury, persistent UI, or chronic urinary retention secondary to partially obstructed bladder. Long-term use of IC appears preferable to indwelling catheter in regard to complications such as infections, bladder stones and renal stones.⁵⁰ No studies of comparison have been performed. Other complications include urethral inflammation, stricture, false passage, hydronephrosis, and epididymitis.

Indwelling catheters are recommended for selected incontinent patients who are terminally ill or for patients with stage 3 or 4 pressure ulcers as short-term treatment. Changes usually every 30 days, but no evidence for this. Increase risk of complications as IC.

Supra-pubic catheters are for short-term use following gyn, uro, and other surgery, or as an alternative to long term catheter use. It is contraindicated as a long-term management option in persons with a chronic unstable bladder. (DI, DH) and ISD.

Female systems are available, but little research is available, but side effects are minimal including erythema and vaginal irritation. Comparison with indwelling catheters has not been performed yet..

Pessaries are recommended for symptomatic pelvic organ prolapse, as a temporary measure for surgical correction, and for nonsurgical or nonwilling patients. They should not be used with vaginal prolapse, or vaginitis, or in those who cannot remove or insert the device without routine access to a health care provider.

Recommended during evaluation, as an adjunct to other therapy or long term care for patients with chronic intractable urinary incontinence.

Types include shields(small absorbent perineal inserts), guards(close fitting products for light incontinence), undergarments(full-length pads with waist straps), combination pad-pant systems, adult diaper garments, and bed pads. These should not be used in place of therapeutic interventions to decrease or eliminate UI. In 1987, over $496 million was spent on absorbent products, which is half of the direct costs for incontinence in nursing homes.⁵¹

Urinary incontinence has a multifactorial etiology that must be individualized with each patient. It is a symptom rather than a disease. There is no magic question, nor is there one criteria that can be inferred as diagnostic of which type of UI the patient has. When approaching the patient with urinary incontinence, you must be systematic in your evaluation. From that evaluation, your decision on a therapeutic behavioral and/or pharmacologic trial- or referral to a specialist- will need to be addressed. Once again, it is not an inevitable outcome of growing older. Education is going to continue to be essential in both the patient and caregiver’s role in treating urinary incontinence. This is going to be an ever growing symptom as the population is growing older and living longer.

1. Rosenthal AJ, et al. Urinary incontinence in the elderly. Post Graduate Medicine, 1995 ; 97(5): 109-121.
2. Houston KA. Incontinence and the older woman. Clinics in Geriatric Medicine 1993; 9(1):156-171.
3. Consensus Conference, Urinary Incontinence in Adults. JAMA,1989;261(18): 2685-2690.
4. Pannill FC. Urinary Incontinence for the primary care physician. Connecticut Medicine, 1993; 57(5): 299-308.
5. Cundiff GW. Clinical predictors of urinary incontinence. Am J Obstet Gyn 1997; 177: 262-267.
6. Ouslander JG. Incontinence. In Hazzard WR, et al eds. Principles of Geriatric Medicine and Gerontology,3^rd ed. New York: McGraw Hill, 1994: 1229-1249.
7. Ouslander JG. Approach to the elderly patient with urinary incontinence. In: Kelly, WN. Textbook of Internal Medicine, Philadelphia: Lippincot-Raven Publisher, 1997: 2506-2511.
8. Harrison’s Principles of Internal Medicine, 14^th ed. New York: McGraw-Hill, 1998: 57-59.
9. Goodson JD. Approach to incontinence and other forms of lower urinary tract dysfunction. In: Gorol, AH, et al. Primary Care Medicine: Office Evaluation and Management of Adult Patients, 3^rd ed. Philadelphia: JB Lippincott, 1995: 687-694.
10. Resnick NM. Urinary Incontinence. The Lancet, 1995; 346: 94-99.
11. Rackly R, Kursh ED. Evaluation and medical management of female urinary incontinence. Comprehensive Therapy, 1996;22(9):547-553.
12. Clinical Practice Guideline: Managing acute and chronic urinary incontinence, AHCPR, Urinary Incontinence in Adults Guideline Updated Panel. American Family Physician, 1996; 54(5): 1661-1672.
13. McIntosh LJ, Richardson DA. 30-minute evaluation of incontinence in the older woman. Geriatrics, 1994;49(2):35-44.
14. Du Beau CE. Interpreting the effect of common medical conditions on voiding dysfunction in the elderly. Geriatric Urology, 1996; 23(1):11-18.
15. Fulty NH, Herzog AR. Epidemiology of urinary symptoms in the geriatric population. Geriatric Urology, 1996; 23(1):1-10.
16. Resnick NM. Geriatric Incontinence. Geriatric Urology, 1996;23(1): 55-74.
17. Diokno A, Yuhico M. Preference, compliance, initial outcomes of therapeutic options chosen by female patients with urinary incontinence. J. Urology, 1995; 154: 1727-1731.
18. Elbadaw A. Functional Anatomy of the organs of micturition. Uro Clinics of N America, 1996;23(2): 177-210.
19. Kane RL, et al. Essential of Clinical Geriatrics, 3^rd ed. New York: Mcgraw Hill, 1994:145-197.
20. Wyman JF. The ‘Costs’ of urinary incontinence. Euro Urology, 1997; 32(supp 2):13-19.
21. Ny Gaard IF. Does Prolonged, high impact activity contribute to later urinary incontinence? A retrospective cohort study of female olympians. Obstetrics and Gynecology, 1997;90(5):718-726.
22. Tampakoudi P, et al. Cigarette smoking and urinary incontinence in women- a new calculative method of estimating the exposure to smoke. Euro J Obst Gyn Repro Bio, 1995;63:27-30.
23. Mommsen, S, Foldspang A. Body mass index and adult female urinary incontinence. World J Urol, 1994; 12: 319-322.
24. Jensen JK, et al. The role of the patient history in diagnosis of urinary incontinence. Obst. Gyn, 1994;83(5): 904-910.
25. Andersen KE. Current concepts in treatment of disorders of micturition. Drugs, 1988; 35: 477-494.
26. Beizer JC. Urinary Incontinence in women: A review for the pharmacist. J Am Pharm Assoc, 1996;NS36(3): 196-202.
27. Marsh T. Estrogens for treating urinary incontinence in women. Am Pharm, 1993; NS33(11): 47-48,90.
28. Fantl JA, et al. Estrogen therapy in the management of urinary incontinence in post menopausal women: A meta- analysis first report of the hormones and urogenital therapy committee. Obstet Gyn, 1994;83(1): 12-18.
29. Brubaker L, et al. Transvaginal electrical stimulation for female urinary incontinence. Am J Obst Gyn, 1997;177(3): 536-540.
30. Fantl JA, Newman DK, Colling J, et al. Managing Acute and Chronic Urinary Incontinence. Clinical Practice Guidelines. AHCPR Pub. No. 96-0686. March 1996.
31. Hu T, et al. Clinical guidelines and cost implications—the case of urinary incontinence. Geriatr Nephrol Urol 1994;4:85-91.
32. Colling J, et al. The effects of patterned urge response toileting on urinary incontinence among nursing home residents. J AM Geriatr Soc 1992; 40: 135-41.
33. Godec CJ. Timed voiding: a useful tool in the treatment of urinary incontinence. Urology 1994;23(1):97-100.
34. Creason NS, et al. Prompted voiding therapy for urinary incontinence in aged female nursing home residents J Adv Nurs 1989;14: 120-6.
35. Hu TW, et al. A clinical trial of a behavioral therapy to reduce urinary incontinence in nursing homes. JAMA 1989:2 61(18):2656-62.
36. Shnelle JF. Treatment of urinary incontinence in nursing home patients by prompted voiding. J Am Geriatr Soc 1990;38:356-60.
37. Fantl JA, et al. Efficacy of bladder training in older women with urinary incontinence. JAMA 1991;265(5):609-13.
38. Dougherty M, et al. Graded pelvic muscle exercise. Effect on stress urinary incontinence. J Reprod Med 1993 Sep; 39(3): 684-91.
39. Benvenuti F, et al. Re-educative treatment of female genuine stress incontinence. AM J Phys Ther 1987; 66:155-68.
40. Wells T, et al. Pelvic muscle exercise for stress urinary incontinence in elderly women. J Am Geriatr Soc 1991; 39: 785-91.
41. Bridges N, et al. A prospective trial comparing interferential therapy and treatment using cones in patients with symptoms of stress incontinence. Neurourol Urodyn. 1988; 7(3): 267-8.
42. Blowman C, et al. Prospective double blind controlled trial of intensive physiotherapy with and without stimulation of the pelvic floor in treatment of genuine stress incontinence. Physiotherapy 1991; 77(10); 661-4.
43. Sand PK, et al. Pelvic floor electrical stimulation in the treatment of genuine stress incontinence: a multicenter, placebo-controlled trial. Am J Obstet Gynecol 1995;173:72-9.
44. Tapp AJ, et al. The treatment of detrusor instability in postmenopausal women with oxybutynin chloride: a double blind placebo controlled study. Br J Obstet Gynaecol. 1990 Jun;97(6):521-6.
45. Milner G, et al. A double blind assessment of antidepressants in the treatment of 212 enuretic patients. Med J Aust 1968 Jun;1(22):943-7.
46. Lose G, et al. Doxepin in the treatment of female detrusor over-activity: a randomized double-blind crossover study. J Urol 1989 Oct;142(4):1024-6.
47. Castleden CM, et al. Double blind study of imipramine and placebo for incontinence due to bladder instability. Age Ageing 1986;15(5):299-303.
48. Gilja I, et al. Conservative treatment of female stress incontinence with imipramine. J Urol 1984;132(5):909-11.
49. Gleason DM, et al. The urethral continence zone and its relation to stress incontinence. J Urol 1974:112(1):81-8.
50. Webb RJ, et al. Clean intermittent self catheterization in 172 adults. Br J Urol 1990;65:2023.
51. Sowell VA, et al. A cost comparison of five methods of managing urinary incontinence. Q Rev Biol 1987 Dec; 411-4.
52. Diokno AC, et al. Prevalence of urinary incontinence and other urologic urological symptoms in the non-institutionalized elderly. J Urol 1986;136:1022-5.
53. Wolin LH. Stress incontinence in young, healthy female subjects. J Urol 1969;101:545-549.
54. Burgio KL, et al. Prevalence, incidence , and correlates of urinary incontinence in healthy, middle aged women. J Urol 1991;146:1255-59.