* This is the Professional Version. *
Urinary Incontinence in Adults
Urinary incontinence is involuntary loss of urine; some experts consider it present only when a patient thinks it is a problem. The disorder is greatly underrecognized and underreported. Many patients do not report the problem to their physician, and many physicians do not ask about incontinence specifically. Incontinence can occur at any age but is more common among the elderly and among women, affecting about 30% of elderly women and 15% of elderly men.
Incontinence greatly reduces quality of life by causing embarrassment, stigmatization, isolation, and depression. Many elderly patients are institutionalized because incontinence is a burden to caregivers. In bedbound patients, urine irritates and macerates skin, contributing to sacral pressure ulcer formation. Elderly people with urgency are at increased risk of falls and fractures.
Incontinence may manifest as near-constant dribbling or as intermittent voiding with or without awareness of the need to void. Some patients have extreme urgency (irrepressible need to void) with little or no warning and may be unable to inhibit voiding until reaching a bathroom. Incontinence may occur or worsen with maneuvers that increase intra-abdominal pressure. Postvoid dribbling is extremely common and probably a normal variant in men. Identifying the clinical pattern is sometimes useful, but causes often overlap and much of treatment is the same.
Urge incontinence is uncontrolled urine leakage (of moderate to large volume) that occurs immediately after an urgent, irrepressible need to void. Nocturia and nocturnal incontinence are common. Urge incontinence is the most common type of incontinence in the elderly but may affect younger people. It is often precipitated by use of a diuretic and is exacerbated by inability to quickly reach a bathroom. In women, atrophic vaginitis, common with aging, contributes to thinning and irritation of the urethra and urgency.
Stress incontinence is urine leakage due to abrupt increases in intra-abdominal pressure (eg, with coughing, sneezing, laughing, bending, or lifting). Leakage volume is usually low to moderate. It is the 2nd most common type of incontinence in women, largely because of complications of childbirth and development of atrophic urethritis. Men can develop stress incontinence after procedures such as radical prostatectomy. Stress incontinence is typically more severe in obese people because of pressure from abdominal contents on the top of the bladder.
Overflow incontinence is dribbling of urine from an overly full bladder. Volume is usually small, but leaks may be constant, resulting in large total losses. Overflow incontinence is the 2nd most common type of incontinence in men.
Functional incontinence is urine loss due to cognitive or physical impairments (eg, due to dementia or stroke) or environmental barriers that interfere with control of voiding. For example, the patient may not recognize the need to void, may not know where the toilet is, or may not be able to walk to a remotely located toilet. Neural pathways and urinary tract mechanisms that maintain continence may be normal.
Mixed incontinence is any combination of the above types. The most common combinations are urge with stress incontinence and urge or stress with functional incontinence.
The disorder tends to differ among age groups. With aging, bladder capacity decreases, ability to inhibit urination declines, involuntary bladder contractions (detrusor overactivity) occur more often, and bladder contractility is impaired. Thus, voiding becomes more difficult to postpone and tends to be incomplete. Postvoid residual volume increases, probably to ≤ 100 mL (normal < 50 mL). Endopelvic fascia weakens.
In postmenopausal women, decreased estrogen levels lead to atrophic urethritis and atrophic vaginitis and to decreasing urethral resistance, length, and maximum closure pressure.
In men, prostate size increases, partially obstructing the urethra and leading to incomplete bladder emptying and strain on the detrusor muscle. These changes occur in many normal, continent elderly people and may facilitate incontinence but do not cause it.
In younger patients, incontinence often begins suddenly, may cause little leakage, and usually resolves quickly with little or no treatment. Often, incontinence has one cause in younger patients but has several in the elderly.
Conceptually, categorization into reversible (transient) or established causes may be useful. However, causes and mechanisms often overlap and occur in combination.
There are several causes of transient incontinence (see Table: Causes of Transient Incontinence). A useful mnemonic for many transient causes is DIAPPERS (with an extra P): D elirium, I nfection (commonly, symptomatic UTIs), A trophic urethritis and vaginitis, P harmaceuticals (eg, those with alpha-adrenergic, cholinergic, or anticholinergic properties; diuretics; sedatives), P sychiatric disorders (especially depression), E xcess urine output (polyuria), R estricted mobility, and S tool impaction.
Causes of Transient Incontinence
Established incontinence is caused by a persistent problem affecting nerves or muscles. Mechanisms usually used to describe these problems are bladder outlet incompetence or obstruction, detrusor overactivity or underactivity, detrusor-sphincter dyssynergia, or a combination (see Table: Causes of Established Incontinence). However, these mechanisms are also involved in some transient causes.
Causes of Established Incontinence
Some Neurologic Causes
Some Nonneurologic Causes
Bladder outlet incompetence
Lower motor neuron lesion (rare)
In men, radical prostatectomy*
Intrinsic sphincter deficiency
In women, multiple vaginal deliveries, pelvic surgery (eg, hysterectomy), age-related changes (eg, atrophic urethritis)
In men, prostate surgery
Bladder outlet obstruction
Spinal cord lesion causing detrusor-sphincter dyssynergia (rare)
Anterior urethral stricture
Urethral diverticula (rarely) or large bladder diverticula (very rarely)
Bladder neck suspension surgery
In women, cystocele (if large)
Outlet obstruction or incompetence
Autonomic neuropathy (eg, due to diabetes, alcoholism, or vitamin B12 deficiency)
Spinal neural tube defect (less often, may cause overactivity)
Surgical damage (eg, anteroposterior resection)
Chronic bladder outlet obstruction
Idiopathic (common among women)
Spinal cord lesion
Brain lesion affecting pathways to the pontine micturition center
Voiding dysfunction of childhood (poor relaxation of the sphincter with bladder contraction can result from the fear of bed wetting or soiling of clothes)
*Other prostate surgical procedures rarely cause established incontinence.
Outlet incompetence is a common cause of stress incontinence. In women, it is usually due to weakness of the pelvic floor or of the endopelvic fascia. Such weakness commonly results from multiple vaginal deliveries, pelvic surgery (including hysterectomy), age-related changes (including atrophic urethritis), or a combination. As a result, the vesicourethral junction descends, the bladder neck and urethra become hypermobile, and pressure in the urethra falls below that of the bladder. In men, a common cause is damage to the sphincter or to the bladder neck and posterior urethra after radical prostatectomy.
Outlet obstruction is a common cause of incontinence in men, although most men with obstruction are not incontinent. Obstruction in men commonly results from benign prostatic hyperplasia, prostate cancer, or urethral stricture. In both sexes, fecal impaction can cause obstruction. In women, outlet obstruction can result from previous surgery for incontinence or from a prolapsed cystocele that causes the urethra to kink during straining to void.
Obstruction leads to a chronically overdistended bladder, which loses its ability to contract; then the bladder does not empty completely, resulting in overflow. Obstruction also may lead to detrusor overactivity and urge incontinence. If the detrusor muscle loses its ability to contract, overflow incontinence may follow. Some causes of outlet obstruction (eg, large bladder diverticula, cystoceles, bladder infections, calculi, and tumors) are reversible.
Detrusor overactivity is a common cause of urge incontinence in elderly and younger patients. The detrusor muscle contracts intermittently for no apparent reason, usually when the bladder is partially or nearly full. Detrusor overactivity may be idiopathic or may result from dysfunction of the frontal micturition inhibitory center (commonly due to age-related changes, dementia, or stroke) or outlet obstruction. Detrusor overactivity (hyperactivity) with impaired contractility is a variant of urge incontinence characterized by urgency, frequency, a weak flow rate, urinary retention, bladder trabeculation, and a postvoid residual volume of > 50 mL. This variant may mimic prostatism in men or stress incontinence in women.
Detrusor underactivity causes urinary retention and overflow incontinence in about 5% of patients with incontinence. It may be caused by injury to the spinal cord or to nerve roots supplying the bladder (eg, by disk compression, tumor, or surgery), by peripheral or autonomic neuropathies, or by other neurologic disorders (see Table: Causes of Established Incontinence). Anticholinergics and opioids greatly decrease detrusor contractility; these drugs are common transient causes. The detrusor may become underactive in men with chronic outlet obstruction as the detrusor is replaced by fibrosis and connective tissue, preventing the bladder from emptying even when the obstruction is removed. In women, detrusor underactivity is usually idiopathic. Less severe detrusor weakness is common among elderly women. Such weakness does not cause incontinence but can complicate treatment if other causes of incontinence coexist.
Detrusor-sphincter dyssynergia (loss of coordination between bladder contraction and external urinary sphincter relaxation) may cause outlet obstruction, with resultant overflow incontinence. Dyssynergia is often due to a spinal cord lesion that interrupts pathways to the pontine micturition center, which coordinates sphincter relaxation and bladder contraction. Rather than relaxing when the bladder contracts, the sphincter contracts, obstructing the bladder outlet. Dyssynergia causes severe trabeculation, diverticula, a “Christmas tree” deformation of the bladder, hydronephrosis, and renal failure.
Functional impairment (eg, cognitive impairment, reduced mobility, reduced manual dexterity, coexisting disorders, lack of motivation), particularly in the elderly, may contribute to established incontinence but rarely causes it.
Most patients, embarrassed to mention incontinence, do not volunteer information about it, although they may mention related symptoms (eg, frequency, nocturia, hesitancy). All adults should therefore be screened with a question such as “Do you ever leak urine?”.
Clinicians should not assume that incontinence is irreversible just because it is long-standing. Also, urinary retention must be excluded before treatment for detrusor overactivity is started.
History focuses on duration and patterns of voiding, bowel function, drug use, and obstetric and pelvic surgical history. A voiding diary can provide clues to causes. Over 48 to 72 h, the patient or caregiver records volume and time of each void and each incontinent episode in relation to associated activities (especially eating, drinking, and drug use) and during sleep. The amount of urine leakage can be estimated as drops, small, medium, or soaking; or by pad tests (measuring the weight of urine absorbed by feminine pads or incontinence pads during a 24-h period).
If the volume of most nightly voids is much smaller than functional bladder capacity (defined as the largest single voided volume recorded in the diary), the cause is a sleep-related problem (patients void because they are awake anyway) or a bladder abnormality (patients without bladder dysfunction or a sleep-related problem awaken to void only when the bladder is full).
Of men with obstructive symptoms (hesitancy, weak urinary stream, intermittency, feeling of incomplete bladder emptying), about one third have detrusor overactivity without obstruction.
Urgency or an abrupt gush of urine without warning or without preceding increase in intra-abdominal pressure (often called reflex or unconscious incontinence) typically indicates detrusor overactivity. The term overactive bladder is sometimes used to describe urinary urgency (with or without incontinence) that is often accompanied by urinary frequency and nocturia.
Neurologic, pelvic, and rectal examinations are the focus.
Neurologic examination involves assessing mental status, gait, and lower extremity function and checking for signs of peripheral or autonomic neuropathy, including orthostatic hypotension. Neck and upper extremities should be checked for signs of cervical spondylosis or stenosis. The spinal column should be checked for evidence of prior surgeries and for deformities, dimples, or hair tufts suggesting neural tube defects.
Innervation of the external urethral sphincter, which shares the same sacral roots as the anal sphincter, can be tested by assessing:
Volitional anal sphincter contraction (S2 to S4)
The anal wink reflex (S4 to S5), which is anal sphincter contraction triggered by lightly stroking perianal skin
The bulbocavernosus reflex (S2 to S4), which is anal sphincter contraction triggered by pressure on the glans penis or clitoris
However, the absence of these reflexes is not necessarily pathologic.
Pelvic examination in women can identify atrophic vaginitis and urethritis, urethral hypermobility, and pelvic floor weakness with or without pelvic organ prolapse. Pale, thin vaginal mucosae with loss of rugae indicate atrophic vaginitis. Urethral hypermobility can be seen during coughing when the posterior vaginal wall is stabilized with a speculum. A cystocele, an enterocele, a rectocele, or uterine prolapse suggests pelvic floor weakness (see Pelvic Relaxation Syndromes). When the opposite wall is stabilized with a speculum, bulging of the anterior wall indicates a cystocele, and bulging of the posterior wall indicates a rectocele or enterocele. Pelvic floor weakness does not suggest a cause, unless a large, prolapsed cystocele is present.
Rectal examination can identify fecal impaction, rectal masses, and, in men, prostate nodules or masses. Prostate size should be noted but correlates poorly with outlet obstruction. Suprapubic palpation and percussion to detect bladder distention are usually of little value except in extreme acute cases of urinary retention.
Urinary stress testing can be done on the examination table if stress incontinence is suspected; this method has a sensitivity and specificity of > 90%. The bladder must be full; a patient sits upright or close to upright with the legs spread, relaxes the perineal area, and coughs vigorously once:
If cough triggers incontinence, the maneuver can be repeated while the examiner places 1 or 2 fingers inside the vagina to elevate the urethra (Marshall-Bonney test); incontinence that is corrected by this maneuver may respond to surgery.
Results can be false-positive if patients have an abrupt urge to void during the test.
Results can be false-negative if patients do not relax, the bladder is not full, the cough is not strong, or a large cystocele is present (in women). In women with large cystoceles, the test should be repeated with the patient supine and the cystocele reduced, if possible
Urinalysis, urine culture, and measurement of BUN and serum creatinine are required. Other tests may include serum glucose and calcium (with albumin for estimation of protein-free calcium levels) if the voiding diary suggests polyuria, electrolytes if patients are confused, and vitamin B12 levels if clinical findings suggest a neuropathy.
Postvoid residual volume should be determined by catheterization or ultrasonography (preferred). Postvoid residual volume plus voided volume estimates total bladder capacity and helps assess bladder proprioception. A volume <50 mL is normal; < 100 mL is usually acceptable in patients > 65 but abnormal in younger patients; and > 100 mL may suggest detrusor underactivity or outlet obstruction.
Urodynamic testing is indicated when clinical evaluation combined with the appropriate tests is not diagnostic or when abnormalities must be precisely characterized before surgery.
Cystometry may help diagnose urge incontinence, but sensitivity and specificity are unknown. Sterile water is introduced into the bladder in 50-mL increments using a 50-mL syringe and a 12- to 14-F urethral catheter until the patient experiences urgency or bladder contractions, detected by changes in fluid level in the syringe. If < 300 mL causes urgency or contractions, detrusor overactivity and urge incontinence are likely.
Peak urinary flow rate testing with a flow meter is used to confirm or exclude outlet obstruction in men. Results depend on initial bladder volume, but a peak flow rate of < 12 mL/sec with a urinary volume of ≥ 200 mL and prolonged voiding suggest outlet obstruction or detrusor underactivity. A rate of ≥ 12 mL/sec excludes obstruction and may suggest detrusor overactivity. During testing, patients are instructed to place their hand on their abdomen to check for straining during urination, especially if stress incontinence is suspected and surgery is contemplated. Straining suggests detrusor weakness that may predispose patients to postoperative retention.
In cystometrography, pressure-volume curves and bladder sensation are recorded while the bladder is filled with sterile water; provocative testing (with bethanechol or ice water) is used to stimulate bladder contractions.
Electromyography of perineal muscle is used to assess sphincter innervation and function. Urethral, abdominal, and rectal pressures may be measured.
Pressure-flow video studies, usually done with voiding cystourethrography, can correlate bladder contraction, bladder neck competency, and detrusor-sphincter synergy, but equipment is not widely available.
Specific causes are treated, and drugs that can cause or worsen incontinence are stopped or the dosing schedule is altered (eg, a diuretic dose is timed so that a bathroom is near when the drug takes effect). Other treatment is based on type of incontinence. Regardless of type and cause, some general measures are usually helpful.
Patients are instructed to limit fluid intake at certain times (eg, before going out, 3 to 4 h before bedtime), to avoid fluids that irritate the bladder (eg, caffeine-containing fluids), and to drink 48 to 64 oz (1500 to 2000 mL) of fluid a day (because concentrated urine irritates the bladder).
Some patients, especially those with restricted mobility or cognitive impairment, benefit from a portable commode. Others use absorbent pads or specialized padded undergarments. These products can greatly improve the quality of life of patients and their caregivers. However, they should not be substituted for measures that can control or eliminate incontinence, and they must be changed often to avoid skin irritation and development of UTIs.
Patients may benefit from bladder training (to change voiding habits) and changes in fluid intake. Bladder training usually involves timed voiding (every 2 to 3 h) while awake. Over time, this interval can be increased to every 3 to 4 h while awake. Prompted voiding is used for cognitively impaired patients; they are asked about every 2 h whether they need to void or whether they are wet or dry. A voiding diary helps establish how often and when voiding is indicated and whether patients can sense a full bladder.
Pelvic muscle exercises (eg, Kegel exercises) are often effective, especially for stress incontinence. Patients must contract the pelvic muscles (pubococcygeus and paravaginal) rather than the thigh, abdominal, or buttock muscles. The muscles are contracted for 10 sec, then relaxed for 10 sec 10 to 15 times tid. Re-instruction is often necessary, and biofeedback is often useful. In women < 75 yr, cure rate is 10 to 25%, and improvement occurs in an additional 40 to 50%, especially if patients are motivated; do the exercises as instructed; and receive written instructions, follow-up visits for encouragement, or both.
Pelvic floor electrical stimulation is an automated version of Kegel exercises; it uses electrical current to inhibit detrusor overactivity and contract pelvic muscles. Advantages are improved compliance and contraction of the correct pelvic muscles, but benefits over behavioral changes alone are unclear.
Drugs are often useful (see Table: Drugs Used to Treat Incontinence). Such drugs include anticholinergics and antimuscarinics, which relax the detrusor, and alpha-agonists, which increase sphincter tone. Drugs with strong anticholinergic effects should be used judiciously in the elderly. Alpha-antagonists and 5-alpha-reductase inhibitors may be used to treat outlet obstruction in men with urge or overflow incontinence.
Drugs Used to Treat Incontinence
Treatment aims to reduce detrusor overactivity; it begins with bladder training, Kegel exercises, and relaxation techniques. Biofeedback can be used with these treatments. Drugs may also be needed, as may intermittent self-catheterization (eg, when postvoid residual volume is large). Infrequently, sacral nerve stimulation, intravesical therapies, and surgery are used.
Bladder training helps patients tolerate and ultimately inhibit detrusor contractions. Regular voiding intervals are gradually lengthened (eg, 30 min every 3 days that urinary control is maintained) to improve tolerance of detrusor contractions. Relaxation techniques can improve emotional and physical responses to the urge to void. Relaxing, standing in place or sitting down (rather than rushing to the toilet), and tightening pelvic floor muscles can help patients suppress the urge to void.
Drugs (see Table: Drugs Used to Treat Incontinence) should supplement, not replace, behavioral changes. The most commonly used are oxybutynin and tolterodine; both are anticholinergic and antimuscarinic and are available in extended-release forms that can be taken po once/day. Oxybutynin is available as a skin patch that is changed twice/wk as well as topical gels that are applied to the skin daily.
Newer drugs with anticholinergic and antimuscarinic properties include solifenacin and darifenacin, which are taken po once/day, and trospium, which is taken once/day or bid. Drugs may be required to suppress urgency symptoms due to detrusor overactivity (hyperactivity) with impaired contractility. Drugs with a rapid onset of action (eg, immediate-release oxybutynin) can be used prophylactically if incontinence occurs at predictable times. Combinations of drugs may increase both efficacy and adverse effects, possibly limiting this approach in the elderly. OnabotulinumtoxinA is administered via cystoscopic injection into the detrusor muscle and is useful in treating urge incontinence refractory to other treatments in patients with neurologic causes (eg, multiple sclerosis, spinal cord dysfunction).
Sacral nerve stimulation is indicated for patients with severe urge incontinence refractory to other treatments. It is thought to work by centrally inhibiting bladder sensory afferents. The procedure begins with percutaneous nerve stimulation of the S3 nerve roots for at least 3 days; if patients respond, a neurostimulator is permanently implanted under the buttock skin. Posterior tibial nerve stimulation (PTNS) is a similar technique of electrical neuromodulation for the treatment of voiding dysfunction that was developed as a less invasive alternative to traditional sacral nerve stimulation. A needle is inserted above the medial malleolus near the posterior tibial nerve followed by the application of low voltage stimulation in 30-min sessions given weekly for 10 to 12 wk. The durability of PTNS is uncertain.
Rarely, intravesical instillation of capsaicin or resiniferatoxin (a capsaicin analog) is used when urge incontinence results from spinal cord injuries and other CNS disorders. This experimental treatment desensitizes C-fiber bladder afferents responsible for reflex bladder emptying.
Surgery is a last resort, usually used only for younger patients with severe urge incontinence refractory to other treatments. Augmentation cystoplasty, in which a section of intestine is sewn into the bladder to increase bladder capacity, is most common. Intermittent self-catheterization may be required if augmentation cystoplasty results in weak bladder contractions or poor coordination of abdominal pressure (Valsalva maneuver) with sphincter relaxation. Detrusor myomectomy may be done to decrease undesired bladder contractions. As a last resort, a urinary diversion can be created to divert the urine away from the bladder. Choice of procedure is based on presence of other disorders, physical limitations, and patient preference.
Treatment includes bladder training and Kegel exercises. Drugs, surgery, other procedures, or, in women, occlusive devices are also usually needed. Treatment is generally directed at outlet incompetence but includes treatments for urge incontinence if detrusor overactivity is present. Avoiding physical stresses that provoke incontinence can help. Losing weight may help lessen incontinence in obese patients.
Drugs (see Table: Drugs Used to Treat Incontinence) include pseudoephedrine, which may be useful in women with outlet incompetence; imipramine, which may be used for mixed stress and urge incontinence or for either separately; and duloxetine. If stress incontinence is due to atrophic urethritis, topical estrogen (0.3 mg conjugated or 0.5 mg estradiol once/day for 3 wk, then twice/wk after) is often effective.
Surgery and other procedures provide the best chance of cure when noninvasive treatments are ineffective. Bladder neck suspension is used to correct urethral hypermobility. Suburethral slings, injection of periurethral bulking agents, or surgical insertion of an artificial sphincter is used to treat sphincter deficiency. Choice depends on the patient’s ability to tolerate surgery and need for other surgeries (eg, hysterectomy, cystocele repair) and on local experience.
Occlusive devices may be used in elderly women with or without bladder or uterine prolapse if surgical risks are high or if prior surgery for stress incontinence was ineffective. Various mesh slings can be used. Pessaries may be effective; they elevate the bladder neck, elevate the vesicourethral junction, and increase urethral resistance by pressing the urethra against the pubic symphysis. Newer, possibly more acceptable alternatives include silicone suction caps over the urethral meatus, intraurethral occlusive devices inserted with an applicator, and intravaginal bladder neck support prostheses. Removable intraurethral plugs are under study.
Exercise regimens using vaginal cones— in which progressively heavier cones are inserted into the vagina and retained for 15 min bid by contracting pelvic floor muscles—are also under study.
Treatment depends on whether the cause is outlet obstruction, detrusor underactivity, or both.
Outlet obstruction due to benign prostatic hyperplasia or cancer is treated with drugs or surgery; that due to urethral stricture is treated with dilation or stenting. Cystoceles in women are treated with surgery or can be reduced using a pessary; unilateral suture removal or urethral adhesiolysis may be effective if cystoceles resulted from surgery. If urethral hypermobility coexists, bladder neck suspension should be done.
Detrusor underactivity requires bladder decompression (reduction of residual volume) by intermittent self-catheterization or, rarely, temporary use of an indwelling catheter (see Bladder Catheterization). Several weeks of decompression may be required to restore bladder function. If bladder function is not fully restored, maneuvers to augment voiding are used. Examples include
A completely acontractile detrusor requires intermittent self-catheterization or use of an indwelling catheter. Using antibiotics or methenamine mandelate to prevent UTIs in patients who require intermittent self-catheterization is controversial but probably indicated if patients have frequent symptomatic UTIs or a valvular or orthopedic prosthesis. Such prophylaxis is not helpful with indwelling catheters.
Additional treatments that may induce bladder contraction and promote emptying include electrical stimulation and the cholinergic agonist bethanechol. However, bethanechol is usually ineffective and has adverse effects (see Table: Drugs Used to Treat Incontinence).
Absorbent pads, special undergarments, and intermittent self-catheterization may be needed. Indwelling urethral catheters are an option for patients who cannot walk to the toilet or who have urinary retention and cannot self-catheterize; these catheters are not recommended for urge incontinence because they may exacerbate detrusor contractions. If a catheter is necessary (eg, to allow healing of a pressure ulcer in patients with refractory detrusor overactivity), a narrow catheter with a small balloon should be used because it will minimize irritability; irritability can force urine out, even around a catheter.
For men who can comply with treatment, condom catheters may be preferable because they reduce risk of UTIs; however, these catheters may cause skin breakdown and reduce motivation to become dry. New external collection devices may be effective in women. If involuntary bladder contractions persist, oxybutynin or tolterodine can be used. If mobility is restricted, measures to prevent skin irritation and breakdown due to urine are essential (see Pressure Ulcers : Prevention).
Because patients often do not volunteer that they are incontinent, ask about it specifically.
Incontinence is not a normal consequence of aging and should always be investigated.
The 4 types of urinary incontinence are urge, stress, overflow, and functional.
Even some longstanding causes of incontinence are reversible.
Do at least a urinalysis, urine culture, serum BUN and creatinine, and measurement of postvoid residual volume on all incontinent patients.
Consider bladder training and Kegel exercises.
Direct drug therapy toward correcting the mechanism of bladder dysfunction.
* This is the Professional Version. *