Health Articles

Impacted stool is implicated as a cause of urinary incontinence in up to 10% of older patients seen in hospitals or referred to incontinence clinics. The mechanism may involve stimulation of opioid receptors or a mechanical disturbance of the bladder or urethra. Patients usually present with symptoms of either urge or overflow incontinence and typically have associated fecal incontinence as well. Removing the impacted stool restores continence.

Incontinence can result from not being able to get to the toilet. Many treatable conditions can restrict mobility, including arthritis, hip deformity, physical deconditioning, postural or postprandial hypotension, claudication, spinal stenosis, heart failure, poor eyesight, fear of falling, a stroke, foot problems, and drug-induced disequilibrium or confusion. Restricted mobility may simply be a matter of the patient being restrained in a bed or a chair. A diligent search often identifies these or other correctable causes. If it does not, a urinal or bedside commode may improve or resolve the incontinence.

Causes of excessive urine output include high fluid intake; diuretics (including caffeine and alcohol), metabolic abnormalities (eg, hyperglycemia and hypercalcemia); and disorders associated with fluid overload, including heart failure, peripheral venous insufficiency, hypoalbuminemia (especially in malnourished debilitated elderly), and drug-induced peripheral edema (eg, that associated with nonsteroidal anti-inflammatory drugs and some calcium channel blockers). Factors associated with peripheral edema are likely to be present when incontinence occurs at night.

Although psychologic causes of incontinence have not been well studied in any age group, they are probably less common in older persons than in younger ones. Initial intervention is directed at the psychologic disturbance, usually depression or lifelong neurosis. Persistent incontinence warrants further evaluation.

Drugs are a major cause of transient incontinence in the elderly . Many of these agents also are used to treat incontinence, underscoring the fact that most medications used by the elderly are “double-edged swords.” The long-acting sedative-hypnotics, such as diazepam and flurazepam whose half-lives can exceed 100 h, can cloud an older patient’s sensorium. Alcohol has the double effect of clouding the sensorium and inducing a diuresis. Loop diuretics such as furosemide or bumetanide can provoke leakage by inducing a brisk diuresis; tnethylxanthine agents such as theophylline and caffeine may have a similar effect in frail persons.
Drugs with anticholinergic side effects present particular problems and include major tranquilizers, most antidepressants, some antiparkinsonian agents (not L-dopa or selegiline but trihexyphenidyl and benztropine mesylate), antihistamines, disopyramide, and gastrointestinal antispasmodics. Opioids are not anticholinergic but nonetheless decrease detrusor contractility. A reduction in detrusor contractility can lead to urinary retention and overflow incontinence. Anticholinergic properties occur in many nonprescription preparations (eg, antihistamines for colds or insomnia) that people take without consulting a physician, and elderly persons often may take more than one.
As direct smooth muscle relaxants, calcium channel blockers may increase residual volume and lead to overflow incontinence, particularly in older women with detrusor weakness and a weak urethral sphincter or in men with urethral obstruction. The dihydropyridine class of these drugs also may cause peripheral edema, which exacerbates nocturia and nocturnal incontinence.
By blocking receptors for smooth muscle contraction at the bladder neck, α-adrenoceptor antagonist antihypertensives may induce stress incontinence in older women in whom urethral length and closure pressure have decreased. Thus, before interventions for stress incontinence are considered in such women, an alternative antihypertensive drug should be tried and the incontinence should be reevaluated.
In men with otherwise asymptomatic prostatic enlargement, α-adrenoceptor agonists in nonprescription preparations such as decongestants may provoke acute retention, especially if the preparation also contains an antihistamine (anticholinergic). For example, urinary retention may be precipitated in an older man who takes a cold capsule, long-acting nose drops, and a hypnotic (usually an antihistamine). How often this results in an unnecessary or premature prostatectomy is unknown.
Vincristine can cause a partially reversible neuropathy that leads to urinary retention. The prostaglandin Ei analog misoprostol has been associated with stress incontinence, possibly through its action on urethral smooth muscle tone. The cough associated with angiotensin converting enzyme inhibitors may exacerbate what otherwise would be mild or not bothersome stress incontinence.

These disorders are often a source of lower urinary tract symptoms, including incontinence, in women. As many as 80% of elderly women attending an incontinence clinic have physical evidence of atrophic vaginitis characterized by mucosal atrophy, friability, erosions, and telangiectasia. Atrophic urethritis leads to epithelial and submucosal thinning of the urethra, which may cause local irritation and loss of the mucosal seal. Incontinence associated with atrophic urethritis is characterized usually by urgency and occasionally by a sense of “scalding” dysuria. In demented persons, atrophic urethritis may produce agitation.
Atrophic urethritis and vaginitis can be treated with systemic or topical low-dose estrogen (eg, conjugated estrogen 0.3 to 0.625 mg orally once a day or vaginally in a cream containing 0.625 mg estrogen per gram). While the duration of therapy is not well established, one approach is to administer a low dose of estrogen daily for 1 to 2 mo and then to taper it. Eventually, most patients can be treated as infrequently as two to four times per month. After 6 mo, estrogen can be discontinued entirely in some patients, although recurrence of atrophy is common. Treatment has another benefit: it may ameliorate recurrent cystitis and dyspareunia. Since the estrogen dose is low and given briefly, it has little or no carcinogenic effect. However, if long-term estrogen therapy is required and the patient has an intact uterus, a progestin probably should be added to the regimen (see Ch. 83). Mammography should be performed before initiating hormone therapy, which is con-traindicated in women with a history of breast cancer.

The eight reversible causes of transient incontinence can be recalled using the mnemonic DIAPPERS (misspelled with an extra P; see TABLE 15-1). These causes should be assiduously sought in every incontinent elderly patient. Identification of these factors is important in all settings because they are easily treatable and contribute to other morbidity. Continence often can be regained by those who become incontinent in the context of acute illness.
Delirium: In a delirious patient, incontinence is merely an associated symptom that abates once the underlying cause of delirium is identified and treated.
Infection: Symptomatic urinary tract infection causes transient incontinence when dysuria and urgency are so severe that the person is unable to reach the toilet before voiding. Asymptomatic infection, which is much more common in the elderly and occurs even in noncatheter-ized persons, is usually not a cause of incontinence. However, because older patients can present atypically, incontinence is occasionally the only symptom of a urinary tract infection. Thus, if an otherwise asymptomatic urinary tract infection is found on the initial evaluation of incontinence, bacteriuria should be treated and the result documented in the patient’s record to prevent futile and unnecessary therapy in the future. However, because treatment may lead to the emergence of resistant organisms, bacteriuria should be treated only when it occurs with otherwise unexplained new onset incontinence, fever, leukocytosis, dysuria, or (particularly in demented or debilitated patients) inanition or agitation. Sexually active women with persistent dysuria, despite negative urinalysis and adequate estrogen treatment, may have Chlamydia trachomatis infection and should be tested or treated with doxy-cycline. Pyuria without bacteriuria should be further evaluated with a urine culture for mycobacteria and with a purified protein derivative (PPD) skin test for tuberculosis.

Transient incontinence is common in the elderly, accounting for up to one third of the incontinence in community-dwelling persons and up to half of the incontinence in hospitalized patients. Transient incontinence becomes persistent if its cause is left untreated; the incontinence cannot be considered chronic merely because it is of long-standing duration. The risk of transient incontinence is increased if an older person suffers from a pathologic condition or is taking a medication that could cause incontinence. For example, a person with a weak bladder who takes an anticholinergic agent is more likely to develop overflow incontinence; a person with detrusor overactivity or impaired mobility who is taking a loop diuretic is more likely to develop urge incontinence.

Incontinence can be categorized by duration of symptoms, by clinical presentation, or by physiologic abnormality. Determining whether incontinence is of recent onset (transient) or chronic (established) is important because, although some overlap exists, the differential diagnosis of each differs. Categorizing the problem as urge incontinence, stress incontinence, or overflow incontinence offers a framework around which to organize the differential diagnosis, diagnostic evaluation, and treatment options. The clinical presentation may point to an underlying physiologic abnormality as the actual cause of the incontinence, knowledge of which offers the clearest guide to treatment.

Continence requires not only the integrity of lower urinary tract function but also adequate mentation, mobility, motivation, and manual dexterity.
The lower urinary tract changes with age, even without disease. Bladder capacity, the ability to postpone voiding, and urinary flow rate appear to decline in both sexes. Uninhibited contractions become more prevalent. The postvoiding residual volume increases but probably to no more than 50 to 100 mL. Maximum urethral closure pressure and urethral length probably decline in women, and prostate size increases in most men. The pattern of fluid excretion also changes: younger persons excrete most of their daily ingested fluid before bedtime, whereas many elderly people—even those who do not have peripheral venous insufficiency, renal disease, heart failure, or prostatism—excrete most of theirs during the night. Because of this and an increased prevalence of sleep disorders, most healthy elderly persons have one or two episodes of nocturia every night.
Although none of these age-related changes causes incontinence, each predisposes to it. And an older person is more likely to encounter additional pathologic, physiologic, or pharmacologic insults, which further increase the risk of incontinence. The corollary is equally important. The new onset or exacerbation of incontinence in an older person is likely due to a precipitant outside the lower urinary tract that is often amenable to medical intervention. Treatment of the precipitant alone may be sufficient to restore continence, even if a urinary tract abnormality coexists. For example, in a woman with age-related detrusor overactivity, a flare-up of hip arthritis that impairs mobility may convert urinary urgency to incontinence. Treating the arthritis rather than the uninhibited contractions may not only restore continence but will lessen pain and improve mobility.