Urinary Incontinence

The involuntary leakage of urine.

Eight to 34% of community-dwelling elderly persons suffer from urinary incontinence; rates are higher in women than in men, and urinary incontinence affects > 50% of elderly patients in hospitals and in nursing homes. Yet, urinary incontinence is abnormal regardless of age, mobility, mental status, or frailty. Moreover, incontinence often causes the affected person to feel embarrassed, isolated, stigmatized, depressed, and regressed; incontinent elderly persons are often institutionalized, because incontinence is a substantial burden to caregivers. Incontinence remains largely a neglected problem despite the fact that it is highly treatable and often curable.

Continence requires input from the central nervous system (CNS) and integrity of lower urinary tract function, as well as adequate mentation, mobility, motivation, and manual dexterity. The role of the CNS is complex and not fully understood. Overall, the CNS integrates control of the urinary tract. The pontine micturition center mediates synchronous detrusor contraction and sphincter relaxation, while higher centers in the frontal lobe, basal ganglia, and cerebellum exert inhibitory and facilitatory effects. Because lower urinary tract function involves so many CNS centers, the impact of diseases such as stroke and dementia, which rarely involve just one center, is often difficult to predict. For example, detrusor overactivity is no more common in demented patients than in those who are cognitively intact.

With age, bladder capacity, contractility, and the ability to postpone voiding decline, and uninhibited bladder contractions become more prevalent. The postvoiding residual volume increases, but probably to <= 50 to 100 mL. Urethral length and sphincter strength decline in women, and prostate size increases in most men. Daily ingested fluid is excreted later in the day and into the night. These changes enhance the likelihood of incontinence in an elderly person but alone do not cause it.

Etiology

Incontinence can be categorized by duration of symptoms, by clinical presentation, or by physiologic abnormality. Clinically, however, it is easier to divide the causes into those that are transient and those that reflect intrinsic urinary tract dysfunction (resulting in established urinary incontinence). The former usually reflect problems outside the urinary tract.

Transient incontinence: Transient incontinence is uncommon in younger persons but common in the elderly, in whom it should always be considered. The reversible causes can be recalled using the mnemonic DIAPPERS (misspelled with an extra P): Delirium, Infection (symptomatic urinary tract), Atrophic urethritis and vaginitis, Pharmaceuticals, Psychiatric disorders (especially depression), Excessive urine output (eg, from hyperglycemia), Restricted mobility, and Stool impaction. Diagnosis and treatment of the underlying cause are necessary. Untreated transient incontinence may become persistent but should not be considered established merely because it is long-standing.

In patients with delirium, incontinence abates once the underlying cause of delirium is identified and treated.

Symptomatic urinary tract infection (UTI) is a cause of transient incontinence, even in young women if dysuria and urgency are so severe that they cannot reach the toilet before voiding. Asymptomatic UTI, which is much more common in the elderly, does not cause incontinence.

Atrophic urethritis and vaginitis in postmenopausal women often cause lower urinary tract symptoms. Atrophic urethritis leads to epithelial and submucosal thinning of the urethral lining, which predisposes to local irritation and loss of the mucosal seal. Incontinence associated with atrophic urethritis is often characterized by urgency and dysuria. Treatment is with topical or systemic estrogen.

Alcohol and drug use (see Table 99-1) are common causes of transient incontinence in elderly persons.

Other psychiatric disorders that cause incontinence have not been well studied; however, they are probably less common in elderly than in younger persons. Initial intervention is directed at the psychiatric disorder, usually severe depression or lifelong neurosis.

Excessive urine output is caused by high fluid intake, diuretic use (including caffeine and alcohol), and metabolic abnormalities (eg, hyperglycemia, hypercalcemia). Nighttime incontinence can be caused or exacerbated by disorders associated with peripheral edema and excess nocturnal excretion, such as heart failure, peripheral venous insufficiency, hypoalbuminemia, and drug use (eg, nonsteroidal anti-inflammatory drugs, dihydropyridine calcium channel blockers).

Restricted mobility can prevent a patient from reaching the toilet and may result from physical limitations, restraint (eg, in a bed or a chair), or more subtle but correctable factors (eg, orthostatic or postprandial hypotension, foot lesions, poorly fitted shoes, impaired vision, fear of falling). If mobility cannot be improved, a urinal or bedside commode may ameliorate or resolve the incontinence.

Impacted stool causes urinary incontinence, especially in elderly patients. The mechanism may involve stimulation of opioid receptors or mechanical disturbance of the bladder or urethra. Patients with impacted stool usually present with symptoms of urge or overflow incontinence and typically have associated fecal incontinence. Removing the impacted stool restores continence.

Established incontinence: If leakage persists after transient causes of incontinence have been addressed, established incontinence due to lower urinary tract causes must be considered (see Table 99-2). Lower urinary tract malfunction generally is similar in elderly and younger persons, although the incidence of specific disorders varies by age.

Detrusor overactivity (involuntary bladder contractions) is the leading urinary tract cause of incontinence in elderly persons regardless of mental status and is also common in younger persons. Frequent and precipitant voiding is characteristic. The urge to void comes on abruptly. The volume of leakage is usually moderate to large, nocturia and nocturnal incontinence are common, sacral sensation and reflexes are preserved, and voluntary control of the anal sphincter is intact. The postvoiding residual volume is generally low; a residual volume of > 50 to 100 mL suggests outlet obstruction (although the residual volume may be nil in early obstruction), a large bladder diverticulum, pooling of urine in a cystocele (in women), or detrusor hyperactivity with impaired contractility (DHIC). A large residual volume is often found in patients with Parkinson's disease, spinal cord injury, or diabetic neuropathy.

Detrusor overactivity in the elderly may coexist with impaired contractility, resulting in DHIC. DHIC is associated with urgency, frequency, a weak flow rate, significant residual urine, and bladder trabeculation and may mimic prostatism in men or stress incontinence in women. Because the bladder contraction is weak in DHIC, urinary retention is common and may interfere with bladder relaxant therapy.

Outlet incompetence is the most common cause of incontinence in younger women and the second most common cause in elderly women. Outlet incompetence manifests as stress incontinence: instantaneous leakage (without bladder contraction) during stress maneuvers such as coughing, laughing, bending, or lifting. It is usually due to pelvic muscle or ligament laxity. A less common cause is intrinsic sphincter deficiency, which is usually due to operative trauma but can result from urethral atrophy; leakage may occur even when standing or sitting quietly. Stress-associated leakage can occur with urinary retention but not as a result of outlet incompetence. Stress incontinence in men is usually due to sphincter damage after radical prostatectomy.

Outlet obstruction is the second most common cause of incontinence in men, but most men with obstruction are not incontinent. Common causes include benign prostatic hyperplasia, prostate cancer, and urethral stricture. In women, outlet obstruction is rare but can occur in those who have had previous surgery for incontinence or who have a large cystocele that prolapses and kinks the urethra when straining to void. In either sex, if secondary detrusor overactivity develops, urge incontinence may result, and if detrusor decompensation supervenes, overflow incontinence may ensue.

Obstruction due to neurologic disease is invariably associated with a spinal cord lesion. Interruptions in pathways to the pontine micturition center (see Figure 99-1), where outlet relaxation is coordinated with bladder contraction, cause detrusor-sphincter dyssynergia. Rather than relaxing when the bladder contracts, the outlet contracts, leading to severe outlet obstruction with severe trabeculation, diverticula, and a "Christmas tree" deformation of the bladder; hydronephrosis; and renal failure.

Detrusor underactivity sufficient to cause urinary retention and overflow incontinence occurs in about 5% of incontinent persons. Causes include injury to the nerves supplying the bladder (eg, by disk compression or tumor involvement) or the autonomic neuropathy of diabetes, Parkinson's disease, alcoholism, and tabes dorsalis. In men with chronic outlet obstruction, the detrusor may be replaced by fibrosis, so the bladder fails to empty even when the obstruction is removed. In women, detrusor underactivity is usually idiopathic.

Symptoms of severe detrusor underactivity (eg, urgency, frequency, nocturia) may mimic those of detrusor overactivity, and urinary retention must be excluded before initiating treatment for detrusor overactivity. Less severe degrees of bladder weakness are common in elderly women. Although mild weakness does not cause incontinence, it can complicate treatment if other causes of incontinence also exist.

Functional problems in elderly persons (eg, environment, mentation, mobility, manual dexterity, medical factors, motivation) are often superimposed on lower urinary tract dysfunction. These factors may contribute to established incontinence but rarely cause it.

Symptoms and Signs

Many of the symptoms and signs are specific to the cause of incontinence.

Precipitancy (the abrupt sensation that urination is imminent regardless of the interval and amount of leakage that follows) is a reliable sign of detrusor overactivity. Whether and how much a patient with precipitancy leaks depends on bladder volume, the amount of warning, the accessibility of a toilet, the patient's mobility, and whether the accompanying sphincter relaxation can be overcome. For patients with no warning of imminent urination (often called reflex or unconscious incontinence), an abrupt gush of urine in the absence of a stress maneuver is also almost invariably due to detrusor overactivity.

Urinary frequency (> 7 voids/day) is a nonspecific symptom. Although it may be due to detrusor overactivity, it may instead reflect preemptive voiding habits, overflow incontinence, sensory urgency, a stable but poorly compliant bladder, depression, anxiety, or excessive urine production (eg, due to diabetes, hypercalcemia, or high fluid intake). Conversely, if persons with detrusor overactivity severely restrict fluid intake, they may void infrequently.

Nocturia (urination >= 2 times/night) must be placed in context; for example, two episodes may be normal for a person who sleeps 10 hours but not for one who sleeps 4 hours. In general, younger persons excrete most of their daily ingested fluid before bedtime, whereas many healthy elderly persons excrete most of theirs at night. The three major causes of nocturia are excessive urine output, sleep-related difficulties, and bladder and lower urinary tract dysfunction (see Table 99-3). The functional bladder capacity, which is defined by the largest single voided volume recorded in the voiding diary (see Table 99-4), can provide an important clue: if the volume of most nightly voids is much smaller than functional capacity, the patient has either a sleep-related problem (the patient voids because he is awake anyway) or a bladder problem. Whatever the cause, nocturia is usually treatable.

Obstructive and irritative symptoms are not specific for benign prostatic hyperplasia or bladder outlet obstruction, especially in elderly men. About one third of men referred for prostatectomy because of obstructive symptoms do not have obstruction; instead, they have an overactive detrusor, which will not be improved or may be exacerbated by surgery. Prostatism symptom scores may be used to assess symptom severity but should not be used to screen for or diagnose benign prostatic hyperplasia. All patients or their caregivers should be asked to identify which voiding symptoms are the most bothersome. For example, although a woman may have mixed stress and urge incontinence, the urge component may be more bothersome and should be the focus of the evaluation and treatment. A man with prostatism may be most bothered by nocturia, which may be remedied without treating the enlarged prostate.

Diagnosis

A voiding diary, kept by the patient or caregiver for 48 to 72 hours, is a record of the volume and time of each void and incontinent episode (see Table 99-4). The voiding diary is one of the most important components of the evaluation. It provides important clues to the cause of incontinence and helps in devising a therapeutic plan.

Physical examination is important for excluding causes of transient incontinence, detecting serious underlying conditions and causes of established incontinence, and evaluating comorbid disease and functional ability. Neurologic examination helps identify delirium, dementia, stroke, Parkinson's disease, spinal cord compression, and neuropathy (autonomic or peripheral). Additionally, spinal column deformities or dimples suggestive of dysraphism, bladder distention (indicative of bladder weakness or outlet obstruction), and stress incontinence should be explored.

Rectal examination should check for fecal impaction, masses, prostate nodules, sacral reflexes, and symmetry of the gluteal creases. Prostate size, as determined by palpation, correlates poorly with outlet obstruction. The rest of the rectal examination is actually a detailed neurourologic examination because the same sacral roots (S2-4) innervate the external urethral sphincter and the anal sphincter. Placing a finger in the patient's rectum, the examiner assesses motor innervation while the patient volitionally contracts and relaxes the anal sphincter. The other hand is placed on the patient's abdomen to check for abdominal straining, which can mimic sphincter contraction. Many neurologically intact elderly patients cannot volitionally contract the sphincter. However, successful sphincter contraction is evidence against a cord lesion. Innervation can be assessed further by testing the anal wink (S4-5) and bulbocavernosus (S2-4) reflexes. However, the absence of these reflexes (especially the anal wink) is not necessarily pathologic, nor does their presence exclude an underactive detrusor (eg, due to diabetic neuropathy). Finally, afferent nerve supply is assessed by testing perineal sensation.

Pelvic examination should be performed for all incontinent women. Pelvic muscle laxity may cause a cystocele, enterocele, rectocele, or uterine prolapse. Bulging of the anterior wall when the posterior wall is stabilized indicates a cystocele, whereas bulging of the posterior wall indicates a rectocele or enterocele. Unless severe (in which prolapse can kink the urethra and cause obstruction), pelvic floor muscle laxity indicates little about the cause of incontinence. Detrusor overactivity may exist in addition to a cystocele, and stress incontinence may exist without a cystocele.

The vagina should be inspected for signs of atrophic vaginitis, characterized by mucosal erythema, tenderness, friability, petechiae, telangiectasia, or vaginal erosions. Vaginal atrophy (not associated with incontinence) is characterized by loss of rugal folds and a thin, shiny mucosa. A cytologic maturation index showing 100% parabasal cells indicates atrophy but not necessarily atrophic vaginitis.

Stress testing, when performed properly, has a sensitivity and specificity of > 90%. With a full bladder, the patient assumes a position as close to upright as possible, spreads the legs, relaxes the perineal area, and provides a single, vigorous cough. Immediate leakage that starts and stops with the cough constitutes a positive result. A false-negative result may occur if the patient does not relax, the bladder is not full, the cough is not strong, or the test is conducted in the upright position in a woman with a large cystocele. In the last case, the test should be repeated with the patient in the supine position and the cystocele reduced, if possible. Delayed or persistent leakage suggests detrusor overactivity (triggered by coughing) rather than outlet incompetence. Performing the test when the patient has an abrupt urge (possibly reflecting detrusor overactivity) may cause false-positive results.

Observation of voiding provides much information about bladder and urethral function. If observation is not possible, flow rate can be assessed by a uroflow machine (uroflometer) or by a portable audio monitor (such as that used to monitor a baby's room at home). The patient should place a hand on the abdomen to check for straining during urination, especially if stress incontinence is suspected and surgery is contemplated, because straining suggests detrusor weakness that may predispose the patient to postoperative retention.

Postvoiding residual volume can be determined by catheterization or ultrasound. The postvoiding residual volume plus the voided volume provides an estimate of total bladder capacity and a crude assessment of bladder proprioception. Postvoiding residual volume > 50 to 100 mL suggests bladder weakness or outlet obstruction, but smaller amounts do not exclude either diagnosis, especially if the patient strained to void or double voided.

Laboratory Findings

Urinalysis should be performed and blood urea nitrogen and creatinine levels checked. Electrolytes should be measured if the patient is confused, urine culture should be obtained if dysuria is present, and serum concentrations of glucose and calcium (and albumin, to allow calculation of free calcium levels in sick, malnourished patients) should be measured if the voiding record suggests polyuria.

Urine cytology or cystoscopy should be performed if a patient has sterile hematuria, suprapubic or perineal discomfort, or a high risk of bladder cancer (eg, unexplained recent onset of urgency or urge incontinence, exposure to industrial dyes).

If the cause of incontinence cannot be determined, urodynamic evaluation should be considered. Urodynamic evaluation includes various tests (eg, cystometry, uroflowmetry, urethral profilometry) as well as x-ray imaging during bladder filling and emptying. The tests required depend on the clinical question. Although its precise role is debated, multichannel urodynamic evaluation is probably warranted when diagnostic uncertainty may affect therapy, when empiric therapy has failed and other approaches may be tried, or when surgery is being contemplated.

Treatment

Detrusor overactivity treatment begins with simple measures, such as treating peripheral edema, adjusting the timing or amount of fluid ingested, or providing a bedside commode or urinal. However, the cornerstone of treatment is behavior therapy.

Bladder retraining regimens, including techniques to suppress precipitancy, can extend the voiding interval. For example, in a patient who is incontinent every 3 hours, the regimen involves voiding every 2 hours during the daytime and suppressing urgency in between. Patients can suppress urgency by relaxing, standing in place or sitting down (rather than rushing to the toilet), and tightening pelvic floor muscles to prevent leakage. Many also benefit by knowing that the urge will build for a minute or so and then recede, similar to a wave on the beach. Thus, they only need to hold on for a minute or so. Once the patient has maintained daytime urinary control for three consecutive days, the voiding interval can be extended by one half hour and the process repeated until a satisfactory result or continence is achieved. Biofeedback can complement bladder retraining and is helpful for some patients.

In a patient who cannot follow the retraining regimen, a technique of prompted voiding is used. It reduces incontinence frequency by up to 50% in institutionalized elderly patients. The patient is asked at 2-hour intervals about the need to void; a patient who responds yes is escorted to the toilet and given positive reinforcement after voiding (negative reinforcement is avoided). Prompted voiding should not be pursued in those who do not respond.

If the voiding diary reveals nocturia and nocturnal incontinence, the cause should be determined (see Table 99-3). Nocturnal diuresis attributable to heart failure lessens with diuretic therapy. Peripheral edema without heart failure may respond to pressure-gradient stockings and daytime leg elevation. Diuresis not due to peripheral edema may respond to a changed pattern of fluid intake or to administration of a rapidly acting diuretic in the late afternoon or early evening. For the patient with detrusor hyperactivity with impaired contractility and uninhibited contractions provoked only at high volumes, catheterization just before bedtime removes the residual urine, increasing functional bladder capacity and often restoring continence and sleep.

Pharmacotherapy can augment behavior therapy but not replace it, because drugs generally do not abolish uninhibited contractions (see Table 99-5). The efficacy of each drug in the table is about the same. Drugs with a rapid onset of action (eg, oxybutynin [not the extended-release form]) can be used prophylactically if incontinence occurs at predictable times. Occasionally, combining low doses of two drugs with complementary actions (eg, oxybutynin and imipramine) maximizes benefits and minimizes adverse effects. Some of these drugs can be administered intravesically but only in patients who can catheterize themselves. All bladder relaxant drugs may cause urinary retention. Intentionally inducing urinary retention and using intermittent catheterization may be reasonable for patients whose incontinence (eg, DHIC) defies other remedies and for whom intermittent catheterization is feasible.

Augmentation cystoplasty increases bladder capacity by incorporating a section of intestine or stomach into the bladder. This treatment is reserved for severe cases of intractable detrusor hyperreflexia, especially those associated with a poorly compliant contracted bladder, and is contraindicated in frail patients. Neuromodulation, in which electrodes are implanted around the spinal nerve roots, is a promising new and investigational technique.

Pads and special undergarments may be needed for refractory incontinence. Many products are available, and the choice can be tailored to the patient. Condom catheters can be helpful for some men but often lead to penile skin breakdown and decreased motivation to become dry and may not be feasible for men with a small or retracted penis. New external collection devices may be effective in women. Indwelling urethral catheters are not recommended for detrusor overactivity because they usually exacerbate contractions. If a catheter is necessary (eg, to allow healing of a pressure sore in a patient with refractory detrusor overactivity), a narrow one with a small balloon should be used to minimize irritability and consequent leakage around the catheter. If bladder spasms persist, oxybutynin or tolterodine can be used. Drugs with more potent anticholinergic adverse effects (eg, belladonna suppositories) should be avoided in the elderly.

Outlet incompetence may be lessened by weight loss in an obese patient, by treatment of precipitating conditions (eg, atrophic vaginitis, coughing), and, in some women, by insertion of a pessary. Pelvic muscle exercises (eg, Kegel's exercises) are often effective, especially if used at the time of stress. Patients must contract the pelvic muscles but not the thigh, abdominal, or buttock muscles; re-instruction is often necessary, and biofeedback is often useful. In women < 75 years, cure rate is 10 to 25% and improvement occurs in an additional 40 to 50%, especially if the patient is motivated, does the exercises as instructed, and receives written instructions and/or follow-up visits for encouragement. Whether women > 75 years can achieve similar success is unknown.

Pessaries, available in many sizes and shapes, (see Figure 118-4) may be useful if the patient wishes to defer surgery or is at a high operative risk. Contraceptive diaphragms may ameliorate stress incontinence. Tampons are occasionally useful in elderly women with a narrow introitus. Newer devices, such as urethral inserts or caps, are also becoming available.

Additional nonpharmacologic treatment consists of a toileting and fluid regimen that maintains bladder volume below the leakage threshold. This approach is often appropriate for elderly women, whose sphincter deficiency is more often mild and the result of atrophy.

Pharmacotherapy with an -adrenergic agonist (eg, sustained-release phenylpropanolamine 25 to 75 mg po bid [removed from the US market in 2000]) may be beneficial, especially when given with estrogen. These drugs may be more effective in women with intrinsic sphincter deficiency. Imipramine 10 to 25 mg po 1 to 4 times daily may be used in patients with stress and urge incontinence and no evidence of postural hypotension.

Surgery to correct urethral hypermobility may be needed if other treatment methods fail or are unacceptable. Anterior colporrhaphy is less likely to cure stress incontinence than are other bladder neck suspension techniques. Many elderly women cannot tolerate a Marshall-Marchetti-Krantz procedure, which entails lengthy abdominal surgery and a prolonged recovery time. An alternative suprapubic procedure, the Burch colposuspension, requires less extensive surgery, corrects anterior vaginal wall laxity, and is highly successful. However, the procedure may exacerbate posterior vaginal wall weakness and cause stranguria (the need to strain to void) and urinary retention in some women with a very weak bladder. Vaginal bladder neck suspensions (eg, Pereyra, Stamey, and Raz procedures) are relatively minor procedures but are often less durable than Burch procedures. A different approach (pubovaginal sling) is often required for intrinsic sphincter deficiency and can also be used in the absence of such deficiency. However, morbidity is higher, and chronic urinary retention is more likely to be precipitated than with procedures usually used to correct urethral hypermobility.

Another treatment for sphincter deficiency, especially for men who have had a prostatectomy, is implantation of an artificial sphincter. With patient selection, about 70% of patients regain continence; of the rest, most use only one or two pads/day, but reoperation or revision may be needed in 20 to 40%. Another approach is periurethral injection of bulking agents. With glutaraldehyde cross-linked bovine collagen, short-term improvement or cure occurs in 50 to 95% of women but much less often in men. Although bulking agents are appealing (injection requires only local anesthesia and little time), success usually involves multiple injections, and long-term data are lacking. Experience with persons > 75 is limited, and urinary retention (often leading to catheterization) is a risk.

In men, if all other interventions fail, a condom catheter, penile clamp, penile sheath (such as a McGuire prosthesis, similar to an athletic supporter), or self-adhesive sheath (especially if lined with a polymer gel or cellulose) may be useful. Some collection devices for women are available. Thin superabsorbent polymer gel pads can more readily absorb the smaller amount of leakage usually associated with stress incontinence. Electrical stimulation, a promising alternative for women, is under investigation.

Outlet obstruction in men is treated with oral -adrenergic blockers (eg, prazosin 1 to 2 mg bid to qid, terazosin 1 to 10 mg/day, doxazosin 1 to 8 mg/day, or tamsulosin 0.4 to 0.8 mg/day), which relieve symptoms and may improve postvoiding residual volume, outlet resistance, and urinary flow rate. Effects occur within days to weeks.

The 5-reductase inhibitor finasteride 5 mg/day po decreases prostate size, obstructive events, and the need for transurethral resection of the prostate in glands > 50 g. At least a 3-month trial is necessary to determine if finasteride is effective. Some investigators have suggested combination therapy with an -adrenergic blocker, but evidence for this approach is equivocal. Recent reports suggest that phytotherapy with saw palmetto may be useful for symptoms of prostatism, but further studies are needed.

Transurethral resection of the prostate or suprapubic or retropubic prostatectomy may be used if bothersome symptoms persist. Alternative approaches (eg, bladder neck incision with bilateral prostatotomy) have made surgical decompression feasible for even the most frail patient.

Urethral stents are promising, but long-term follow-up data are lacking. Adverse effects include stent migration and urinary urgency (usually subsiding after a few weeks to months). Promising new transurethral techniques include microwave hyperthermia, laser therapy, and needle ablation, but long-term data are lacking.

In women, surgery usually is required for a large cystocele, and an outlet suspension procedure should be performed if urethral hypermobility coexists. If the bladder neck is incompetent or the urethral closure pressure is < 10 cm H₂O, a different surgical approach may be required. Primary bladder neck obstruction is easily corrected in even the most frail woman. Distal urethral stenosis can be treated with dilation and estrogen. More extensive intervention may be necessary if meatal stenosis is present; alternatively, dilation can be repeated frequently. However, most women who undergo dilation do not have urethral stenosis; they have an underactive detrusor. For these women, dilation is usually not helpful and may be harmful.

Detrusor underactivity is managed by reducing residual volume, eliminating hydronephrosis (if present), and preventing urosepsis. For patients with retention of > 800 mL, an indwelling catheter is used to decompress the bladder for >= 7 to 14 days, while potential contributors to impaired detrusor function (eg, fecal impaction, drug adverse effects) are eliminated.

If decompression does not fully restore bladder function, augmented voiding techniques may help: double voiding or implementation of Credé's maneuver (application of suprapubic pressure during voiding) or the Valsalva maneuver. Bethanechol 40 to 200 mg/day po in divided doses is occasionally useful for a patient whose bladder contracts poorly due to an anticholinergic drug that cannot be discontinued (eg, a tricyclic antidepressant). Residual volume should be monitored so that bethanechol can be discontinued if ineffective.

If the detrusor is completely acontractile after decompression, any intervention is likely to be futile, and the patient should undergo intermittent catheterization or have an indwelling urethral catheter placed. Antibiotic or methenamine mandelate prophylaxis against UTI is probably warranted with intermittent catheterization if the patient has frequent symptomatic UTIs or has an abnormal heart valve or an orthopedic prosthesis; such prophylaxis is not useful with indwelling catheterization. If intermittent catheterization is performed in an institutional setting, a sterile rather than clean technique should be used because of the prevalence and virulence of bacteria in such settings.

Nursing and Caregiver Issues

Appropriate care of urinary incontinence is often multidisciplinary. Many diagnostic and therapeutic procedures are often performed by physical therapists, physicians, or nurses. Nurses must also teach patients and caregivers about incontinence. Home health care nurses, nursing home nurses, and hospital-based nurses have partial responsibility for recognizing incontinence and creating care plans.