The Impact of Age on Incontinence

At any age, continence depends on not only the integrity of lower urinary tract function but also the presence of adequate mentation, mobility, motivation, and manual dexterity. Although incontinence in younger patients is rarely associated with deficits outside the urinary tract, such deficits occur commonly in older patients. It is crucial to detect them, both because they exacerbate and, occasionally, even cause incontinence in the elderly, and because design of an efficacious intervention requires that they be addressed.

In addition, the lower urinary tract changes with age, even in the absence of disease. Data from continent elderly are sparse and longitudinal data virtually nonexistent. However, it appears that although bladder capacity does not change with age (Pfisterer et al, 2006b), bladder sensation, contractility, and the ability to postpone voiding decline in both sexes, while urethral length and maximum closure pressure, as well as striated muscle cells in the rhabdosphincter and urogenital diaphragm, probably decline with age in women (Diokno et al, 1988; Resnick, 1988; Resnick et al, 1995; Strasser et al, 1999; Perucchini et al, 2002; Pfisterer et al, 2006a, 2006b; Trowbridge et al, 2007; Betschart et al, 2008). The prostate enlarges in most men, and appears to cause urodynamic obstruction in half (Resnick et al, 1995). In both sexes, the prevalence of involuntary detrusor contractions increases, whereas the postvoid residual (PVR) volume probably increases but to no more than 50 to 100 mL (Diokno et al, 1988; Resnick, 1988; Resnick et al, 1995; Bonde et al, 1996). In addition, the elderly often excrete most of their fluid intake at night, even in the absence of venous insufficiency, renal disease, heart failure, or prostatism (Miller, 2000; Morgan et al, 2000). This fact, coupled with an age-associated increase in sleep disorders, leads to one to two episodes of nocturia in the majority of healthy elderly (Miller, 2000; Morgan et al, 2000). Finally, at the cellular level, detrusor smooth muscle develops a “dense band pattern” characterized by dense sarcolemmal bands with depleted caveolae (Elbadawi et al, 1993a, 1993b, 1997a). This depletion may mediate the age-related decline in bladder contractility. In addition, an “incomplete dysjunction pattern” develops, characterized by scattered protrusion junctions, albeit not in chains; these changes may underlie the high prevalence of involuntary detrusor contractions (vide infra) (Resnick et al, 1995; Hailemariam et al, 1997; Elbadawi et al, 1997a).

None of these age-related changes causes incontinence, but they do predispose to it. This predisposition, coupled with the increased likelihood that an older person will encounter an additional pathologic, physiologic, or pharmacologic insult, explains why the elderly are so likely to become incontinent. The implications are equally important. The onset or exacerbation of incontinence in an older person is probably due to precipitant(s) outside the lower urinary tract that are amenable to medical intervention. Furthermore, treatment of the precipitant(s) alone may be sufficient to restore continence, even if there is coexistent urinary tract dysfunction. For instance, flare of hip arthritis in a woman with age-related detrusor overactivity may be sufficient to convert her urinary urgency into incontinence. Treatment of the arthritis, rather than the involuntary detrusor contractions, will not only restore continence but also lessen pain and improve mobility. These principles, depicted in Figures 76-1 and 76-2 (Resnick, 1996; Resnick and Marcantonio, 1997), provide the rationale in the older patient for adding a set of transient causes to the established lower urinary tract causes of incontinence. Because of their frequency, ready reversibility, and association with morbidity beyond incontinence, the transient causes are discussed first.

Figure 76–1 Incontinence results when the ability to compensate for bladder dysfunction is inadequate. For instance, in the intact older person, detrusor overactivity or sphincter weakness may not cause leakage if the patient is more attuned to bladder fullness, drinks less, voids more often, eliminates precipitants such as coughing, and stays close to a toilet. This explains how older patients may remain continent despite such abnormalities, and also suggests alternative therapeutic approaches independent of the urinary tract.

(From Resnick NM. An 89-year-old woman with urinary incontinence. JAMA 1996;276:1832–40.)

Figure 76–2 This graph shows why treatment of urinary incontinence (UI) in older adults has to differ and is often easier than in younger adults. Both of these patients with detrusor overactivity (DO) have the same frequency of leakage. However, in the younger patient with intact compensatory mechanisms, such leakage reflects solely the contribution of the DO. In the older adult, other comorbid conditions make it more difficult to appreciate bladder fullness, adjust fluid output, and reach the bathroom. Such conditions magnify the impact of DO and will be unaffected by bladder relaxant therapy. But addressing them will result in a marked improvement in the UI even without treatment of the DO and will make DO therapy, if still required, more effective. LUT, lower urinary tract.

(From Resnick NM, Marcantonio ER. How should clinical care of the aged differ? Lancet 1997;350:1157–58.)

Causes of Transient Incontinence

Incontinence is transient in up to one third of community-dwelling elderly and in up to half of acutely hospitalized patients (Resnick, 1988; Herzog and Fultz, 1990). Although most of the transient causes lie outside the lower urinary tract, three points warrant emphasis. First, the risk of transient incontinence is increased if, in addition to physiologic changes of the lower urinary tract, the older person also suffers from pathologic changes. Anticholinergic agents are more likely to cause overflow incontinence in persons with a weak or obstructed bladder, while excess urine output is more likely to cause urge incontinence in persons with detrusor overactivity and/or impaired mobility (Fantl et al, 1990; Diokno et al, 1991). Second, although termed “transient,” these causes of incontinence may persist if left untreated and cannot be dismissed merely because incontinence is longstanding. Third, similar to the situation for established causes (vide infra), identification of “the most common cause” is of little value. The likelihood of each cause depends on the individual, the clinical setting (community, acute hospital, nursing home), and referral pattern. Moreover, geriatric incontinence is rarely due to just one of these causes. Trying to disentangle which of the multiple abnormalities is “the” cause is more useful for metaphysics than for clinical practice.

The causes of transient incontinence can be recalled easily using the mnemonic “DIAPERS” (Table 76–1). In the setting of delirium (an acute and fluctuating confusional state due to virtually any drug or acute illness), incontinence is merely an associated symptom that abates once the underlying cause of confusion is identified and treated. The patient needs medical rather than bladder management (Resnick, 1988).

Table 76–1 Causes of Transient Incontinence

Symptomatic urinary tract infection causes transient incontinence when dysuria and urgency are so prominent that the older person is unable to reach the toilet before voiding. Asymptomatic bacteriuria, which is much more common in the elderly, does not cause incontinence (Brocklehurst et al, 1968; Resnick, 1988; Baldassare and Kaye, 1991; Ouslander et al, 1995). Because illness can present atypically in older patients, however, incontinence is occasionally the only atypical symptom of a urinary tract infection (UTI). Thus, if otherwise asymptomatic bacteriuria is found on initial evaluation, it should be treated and the result recorded in the patient’s record to prevent future futile therapy.

Atrophic urethritis/vaginitis frequently causes lower urinary tract symptoms, including incontinence. Up to 80% of elderly women attending an incontinence clinic have atrophic vaginitis, characterized by vaginal mucosal atrophy, friability, erosions, and punctate hemorrhages (Robinson and Brocklehurst, 1984). Incontinence associated with this entity usually is associated with urgency and, occasionally, a sense of “scalding” dysuria that mimics a urinary tract infection, but both symptoms may be unimpressive. In demented individuals, atrophic vaginitis may present as agitation. Atrophic vaginitis also can exacerbate stress incontinence.

The importance of recognizing atrophic vaginitis is that it may respond to low-dose estrogen (Fantl et al, 1996; Cardozo et al, 2004). Moreover, as for other causes of transient incontinence, treatment has additional benefits; in the case of atrophic urethritis, treatment ameliorates dyspareunia and reduces the frequency of recurrent cystitis (Resnick, 1988; Raz and Stamm, 1993; Cardozo et al, 1998; Eriksen, 1999).

Reports from two large-scale randomized prospective trials, however, have recently challenged long-standing assumptions about the benefits and risks of hormone therapy. The Women’s Health Initiative (WHI) randomized more than 27,000 women, aged 50 to 79 years, to oral conjugated equine estrogen (CEE) 0.625 mg, with or without medroxyprogesterone (MPA) 2.5 mg (Hendrix et al, 2005). The Heart and Estrogen/Progestin Replacement Study (HERS) randomized nearly 2800 postmenopausal women of the same age to the same regimen (Grady et al, 2001). Both studies found that hormone therapy was associated with worsening of pre-existing incontinence. WHI investigators also found that hormone therapy, whether prescribed as CEE alone or with MPA, was associated with increased incidence of new incontinence. Because both studies also found that hormone therapy did not protect against heart disease, they advised against using hormone therapy for urinary incontinence.

In trying to apply the results of the WHI and HERS trials, several caveats should be noted. Postmenopausal hormone levels differ substantially, and in some individuals they are similar to levels seen in the follicular phase of premenopausal women (Kuchel et al, 2001). Tissue sensitivity also varies. Thus it is surprising that neither WHI nor HERS randomized or stratified results by the presence or absence of atrophic vaginitis, nor did investigators examine patients to determine whether the dose administered was sufficient to treat the condition if it was present. Dropout rates in WHI were also high: 42% in the combined hormone therapy group and 54% in the estrogen-alone group. In addition, incontinence data were based on self-report, which can be problematic in older adults, both for reproducibility and for determining the type of incontinence (Resnick et al, 1994; Kirschner-Hermanns et al, 1998). Urodynamic testing was not performed. Moreover, although drugs used to treat heart disease in such patients can cause or exacerbate incontinence (e.g., diuretics, α blockers, calcium channel blockers, and angiotensin-converting enzyme inhibitors (ACEI), their impact was not reported. Finally, other hormone doses, types, and routes of administration were not evaluated. For example, a recent randomized placebo-controlled study with ultralow-dose transdermal estrogen (0.014 mg) revealed no substantial effect on either the frequency of incontinence or the risk of developing at least weekly incontinence (Waetjen et al, 2005).

There is less evidence available from recent studies of nursing home patients, but limitations of sample size; selection bias; route, dose adequacy, and type of hormone used; and characterization and stratification by type of urinary infection (UI) all similarly preclude meaningful conclusions (DuBeau, 2001; Ouslander et al, 2001a).

The apparent lack of efficacy for conjugated equine estrogen demonstrated in these two studies, as well as the risks associated with long-term use of higher doses, must be balanced against the other benefits cited above—the lower doses and shorter duration of treatment advised for treatment of atrophic vaginitis, and the shorter life expectancy of many older women in whom the prevalence and severity of atrophic vaginitis are highest. Moreover, data from other randomized double-blind trials, which employed different estrogen preparations (estriol, estradiol, or quinestradol), demonstrated significant reduction in incontinence among nursing home residents (Judge, 1969) and postmenopausal women with sensory urge incontinence (Walter et al, 1978; Moehrer et al, 2003). Thus clinical judgment is warranted, and local administration of other types of estrogen may be best. Unfortunately, the use of vaginal estrogen has not yet been well-studied.

With adequate treatment, symptoms of atrophic vaginitis remit in a few days to several weeks, but the intracellular response takes longer (Semmens et al, 1985). The duration of therapy has not been well established (Pandit and Ouslander, 1997). One approach is to insert a ring containing estradiol. The advantage is that it is small and delivers the dose locally. Because it does not increase systemic estrogen concentrations, it is often considered for women with a past history of breast cancer. The disadvantage is that, despite its small size, it is not always feasible or well tolerated by frail older women, especially those with pronounced vaginal stenosis. Another option is to administer a low dose of estradiol orally or vaginally for 1 to 2 months and then taper it. Most patients probably can be weaned to a dose given as infrequently as 2 to 4 times per month. After 6 months, estrogen can be discontinued entirely in some patients, but recrudescence is common. Because the dose is low and given briefly, the carcinogenic effect is likely slight, if any. However, if long-term treatment is selected, a progestin probably should be added if the patient has a uterus. Hormone treatment (except for administration by a vaginal ring) is contraindicated for women with a history of breast cancer. For those without such a history, mammography should be performed prior to initiating hormone therapy. There appears to be a slightly increased risk of breast cancer among women using oral estrogen daily for more than 5 years, but fortunately, such high-dose, frequent, and long-term therapy is rarely required.

Pharmaceuticals are one of the most common causes of geriatric incontinence, precipitating leakage by a variety of mechanisms (Table 76–2 and Tsakiris et al, 2008). Experts often cite dosages and serum levels below which side effects are uncommon. Unfortunately, such rules are of limited use in the elderly, because they are generally derived from studies of healthy younger persons who have no other diseases and take no other medications. Of note, many of these agents also are used in the treatment of incontinence, underscoring the fact that most medications are “double-edged swords” for the elderly.

Table 76–2 Commonly Used Medications That May Affect Continence

* Examples include amlodipine (Norvasc), nifedipine, nicardipine, isradipine, felodipine, nimodipine.

Long-acting sedative/hypnotics, whose half-life can exceed 100 hours, are associated not only with incontinence (Landi et al, 2002) but also with falling, hip fractures, driving accidents, depression, and confusion. Alcohol causes similar problems, but, for a variety of reasons, physicians frequently fail to identify alcohol use by older people as a source of symptoms, including incontinence. Sequelae of alcohol abuse are often absent or attributed to other causes. In addition, because of age-related alterations in the pharmacokinetics and pharmacodynamics of alcohol disposal, as well as interactions with other commonly used drugs, as few as one or two drinks can pose a problem for older individuals.

Because anticholinergic agents are prescribed so often for the elderly, and are used even without prescription (e.g., sedating antihistamines used for allergies, coryza, and insomnia), it is important to ask about them. They cause or contribute to incontinence in several ways. In addition to provoking overt urinary retention, these agents often induce subclinical retention. The resultant decrease in available bladder capacity (i.e., total capacity minus residual) allows it to be reached more quickly, exacerbating incontinence due to DO, as well as that due to functional impairment. By increasing bladder capacity (and often residual volume), anticholinergic agents also may aggravate leakage due to stress incontinence by further increasing the challenge to the sphincter mechanism. Additionally, many of these drugs decrease mobility (e.g., antipsychotics that induce extrapyramidal stiffness) and precipitate confusion. Finally, several agents intensify the dry mouth that many elderly already suffer owing to an age-related decrease in salivary gland function; the resultant increased fluid intake contributes to incontinence. Attempts should be made to discontinue anticholinergic agents, or to substitute with ones having less anticholinergic effect (e.g., a selective serotonin uptake inhibitor [SSRI] for a tricyclic antidepressant; risperidone for chlorpromazine). Limited data suggest that bethanechol may be useful for nonobstructed patients whose urinary retention is associated with use of an anticholinergic that cannot be discontinued (Everett, 1975).

In men with asymptomatic prostatic obstruction, α-adrenergic agonists can provoke acute retention. Particularly problematic are nonprescribed decongestants. They often contain an (anticholinergic) antihistamine and are frequently taken with a nonprescribed hypnotic, all of which are also sedating antihistamines. Because older individuals often fail to mention non-prescribed agents to a physician, urinary retention due to use of a decongestant, nose drops, and a hypnotic may result in premature or even unnecessary prostatectomy.

By blocking receptors at the bladder neck, α-adrenergic antagonists (many antihypertensives) may induce stress incontinence in older women (Mathew et al, 1988; Marshall and Beevers, 1996) in whom urethral length and closure pressure decline with age. Because hypertension affects half of the elderly, use of these agents may increase. Before considering interventions for stress incontinence in such women, one should substitute an alternative agent and reevaluate the incontinence.

Calcium channel blockers also can cause incontinence. As smooth muscle relaxants, they may increase residual volume and may occasionally lead to overflow incontinence, particularly in obstructed men with coexisting detrusor weakness. The dihydropyridine class of these agents (e.g., nifedipine, amlodipine, nicardipine, isradipine, nimodipine) also can cause peripheral edema, which can exacerbate nocturnal polyuria and nocturnal incontinence.

Angiotensin-converting enzyme inhibitors (ACEI) are prescribed increasingly for age-associated conditions such as myocardial infarction, congestive heart failure, and hypertension. Because the risk of developing an ACEI-induced cough increases with age, these agents may exacerbate what otherwise would be minimal stress incontinence in older women.

A few reports impugn cholinesterase inhibitors, such as donepezil (Aricept) or rivastigmine, as a cause of urinary incontinence (Hashimoto et al, 2000; Starr, 2007). The association is plausible, because these agents block the breakdown of acetylcholine within the neuroeffector junctional cleft. However, the incontinence often ceases even if the drug is continued, the number of cases is small, and the descriptions and evaluations of these cases are sparse. In addition, prospective trials in which these agents were evaluated for their cognitive impact did not note an increase in incontinence. Nonetheless, the association has not been well-evaluated to date, and because incontinence may improve or resolve on decreasing the drug dose or discontinuation, such an association is worth keeping in mind.

Excess urine output commonly contributes to or even causes geriatric incontinence. Causes include excessive fluid intake; diuretics (including theophylline-containing fluids, lithium, and alcohol); metabolic abnormalities (e.g., hyperglycemia and hypercalcemia); and disorders associated with fluid overload, including congestive heart failure, peripheral venous insufficiency, hypoalbuminemia (especially in malnourished debilitated elderly), and drug-induced peripheral edema associated with an increasing array of medications, including nonsteroidal anti-inflammatory drugs (NSAIDs), dihydropyridine calcium channel blockers, thiazolidinediones (“glitazones”), pramipexole and ropinirol (for Parkinson disease), amantadine (for Parkinson disease and influenza), and β blockers. Fluid overload is a likely contributor when incontinence is associated with nocturia.

Restricted mobility commonly contributes to geriatric incontinence. It can result from numerous treatable conditions, including arthritis, hip deformity, deconditioning, postural or postprandial hypotension, claudication, spinal stenosis, heart failure, poor eyesight, fear of falling, stroke, foot problems, drug-induced disequilibrium or confusion, or being restrained in a bed or chair (Resnick, 2004). A careful search will often identify these or other correctable causes. If not, a urinal or bedside commode may still improve or resolve the incontinence.

Finally, stool impaction is implicated as a cause of urinary incontinence in up to 10% of older patients admitted to acute hospitals or referred to incontinence clinics (Resnick, 1988); the mechanism may involve stimulation of opioid receptors (Hellstrom and Sjoqvist, 1988). Patients present with urge or overflow incontinence and typically have associated fecal incontinence as well. Disimpaction restores continence.

These seven reversible causes of incontinence should be assiduously sought in every elderly patient. In one series of hospitalized elderly patients, when these causes were identified, continence was regained by most of those who became incontinent in the context of acute illness (Resnick, 1988). Regardless of their frequency, their identification is important in all settings because they are easily treatable and contribute to morbidity beyond incontinence.

Established Incontinence

Diagnostic Approach

Evaluation

The evaluation should identify transient and established causes of incontinence, assess the patient’s environment and available support, and detect uncommon but serious conditions that may underlie incontinence, including lesions of the brain and spinal cord, carcinoma of the bladder or prostate, hydronephrosis, bladder calculi, detrusor-sphincter dyssynergia, and decreased bladder compliance. Assessment must be tailored to the patient’s clinical status and goals, and tempered by the realization that not all detected conditions can be cured, that simple interventions may be effective even in the absence of a diagnosis, and that for many elderly patients, diagnostic tests are themselves often interventions. Because the evaluation generally requires a comprehensive approach, it should be conducted over more than one visit to ease the burden and obviate further evaluation in those who respond to simple measures.

History

In addition to the assessment outlined in Chapter 64, evaluation of the older patient should search for transient causes of incontinence (including nonprescribed medications) and functional impairment. It should be augmented by medical records, as well as input from caregivers. Functional assessment focuses on both basic activities of daily living (ADLs: i.e., transferring from a bed, walking, bathing, toileting, eating, and dressing) and more advanced “instrumental” activities of daily living (IADLs: i.e., shopping, cooking, driving, managing finances, using the telephone). The assessment is accomplished by using a questionnaire, which can be completed by the patient or caregiver prior to the evaluation, and by objective evaluation of the patient from the beginning of the encounter, noting affect, mobility, ability to sit and rise from a chair, ability to provide a coherent history, and amount of time and assistance required to dress and undress.

Of course, as for younger individuals, it also is important to characterize the voiding pattern and the type of incontinence. Although the clinical type of incontinence most often associated with detrusor overactivity (DO) is urge incontinence, “urge” is neither a sensitive nor specific symptom; it is absent in 20% of older patients with detrusor overactivity, and the figure is higher in demented patients (Resnick et al, 1989). “Urge” is also reported commonly by patients with stress incontinence, outlet obstruction, and overflow incontinence.

A better term for the symptom associated with DO is “precipitancy,” which can be defined in two ways. For patients with no warning of imminent urination (“reflex” or “unconscious” incontinence), the abrupt gush of urine in the absence of a stress maneuver can be termed precipitant leakage, and it is almost invariably due to DO. For those who do sense a warning, it is of less value to focus on the leakage, because the presence and volume of leakage in this situation depend on bladder volume, amount of warning, toilet accessibility, the patient’s mobility, and whether the patient can overcome the relative sphincter relaxation accompanying detrusor contraction (Dyro and Yalla, 1986). Instead, precipitancy should be defined as the abrupt sensation that urination is imminent, whatever the interval or amount of leakage that follows; defined in these two ways, precipitancy is both a sensitive and specific symptom (Resnick, 1990).

Similar to the situation for urgency, other symptoms ascribed to DO also can be misleading in the older person unless explored carefully. Urinary frequency (greater than seven diurnal voids) is common (Brocklehurst et al, 1968; Diokno et al, 1986; Resnick, 1988), and may be due to voiding habit, preemptive urination to avoid leakage, overflow incontinence, sensory urgency, a stable but poorly compliant bladder, excessive urine production, depression, anxiety, or social reasons (Resnick, 1990). Conversely, incontinent individuals may severely restrict their fluid intake so that even in the presence of DO they do not void frequently. Thus the significance of urinary frequency, or its absence, can be determined only in the context of more information.

Nocturia also can be misleading unless it is first defined (e.g., two episodes may be normal for the individual who sleeps 10 hours but not for one who sleeps 4 hours) and then approached systematically (Table 76–3). The three general reasons for nocturia—excessive urine output, sleep-related difficulties, and urinary tract dysfunction—can be differentiated by careful questioning and a voiding diary that includes voided volumes (Fig. 76–3). The record of voided volumes is inspected to determine the available bladder capacity (the largest single voided volume) and then compares this capacity to the volume of each nighttime void. For instance, if the available bladder capacity is 400 mL and each of three nightly voids is approximately 400 mL, the nocturia is due to excessive production of urine at night. If the volume of most nightly voids is much smaller than bladder capacity, nocturia reflects either: (1) a sleep-related problem (the patient voids because she is awake anyway), or (2) a problem with the lower urinary tract. Similar to excess urine output, sleep-related nocturia may also be due to treatable causes, including age-related sleep disorders, pain (e.g., bursitis, arthritis), dyspnea, depression, caffeine, or a short-acting hypnotic (e.g., triazolam). Bladder-related causes of nocturia are displayed in the table. Whatever the cause, the nocturnal component of incontinence can generally be ameliorated.

Table 76–3 Causes of Nocturia

Volume Related

Age-related Excess intake/alcohol Diuretic, caffeine, theophylline, lithium Endocrine/metabolic Diabetes mellitus/insipidus Hypercalcemia Peripheral edema Congestive heart failure Low albumin states Peripheral vascular disease Venous insufficiency Drugs (e.g., NSAIDs [indomethacin, COX-2 inhibitors], nifedipine)

Sleep Related

Insomnia Obstructive sleep apnea (causes polyuria as well) Restless legs syndrome Pain Dyspnea Depression Drugs

Lower Urinary Tract–Related

Small bladder capacity Detrusor overactivity Prostate related Overflow incontinence Decreased bladder compliance Sensory urgency

COX-2, cyclooxygenase; NSAIDs, nonsteroidal anti-inflammatory drugs.

Adapted from Resnick NM. Noninvasive diagnosis of the patient with complex incontinence. Gerontology 1990;36(Suppl. 2):8–18.

Figure 76–3 Voiding diary of an incontinent 75-year-old man. Urodynamic evaluation excluded urethral obstruction and confirmed a diagnosis of detrusor hyperactivity with impaired contractility (DHIC). Note the 24-hour urine output of nearly 3 L, due to the belief that drinking 10 glasses of fluid/day was “good for my health.” (He did not mention this until queried about the voiding record). Given the typical voided volume of 150 to 250 mL and a measured postvoid residual (PVR) of 150 mL, excess fluid intake was overwhelming his usual bladder capacity of 400 mL (150 + 250 mL). Although involuntary bladder contractions were present, the easily reversible volume component of the problem—combined with the risk of precipitating urinary retention with an anticholinergic agent—prompted treatment with volume restriction alone. After daily urinary output dropped to 1500 mL, frequency abated and incontinence resolved.

(Adapted from DuBeau CE, Resnick NM. Evaluation of the causes and severity of geriatric incontinence: a critical appraisal. Urol Clin North Am 1991;18:243–56.)

The symptoms of “prostatism” also warrant comment. Owing to the high prevalence of medication use, nocturnal polyuria (Reynard et al, 1998), constipation, and DHIC, as well as the impairment of bladder contractility that accompanies aging, “prostatic” symptoms are even less specific in older men than in younger men (DuBeau and Resnick, 1991).

When asking about leakage with stress maneuvers, it is important to ensure that the absence of such leakage is not due to simply the lack of coughing or sneezing. For those without such precipitants, it is useful to inquire about instantaneous leakage with lifting or bending over to put on a shoe or stockings.

Finally, patients or their caregivers should be asked which voiding symptom is most bothersome. For example, although a woman may have both stress and urge incontinence, the urge component may be her worst problem and should become the focus of evaluation and treatment. A man with “prostatism” may be most bothered by nocturia (DuBeau et al, 1995), which may be remedied without any consideration of his prostate (see Fig. 76–3). Failure to address symptom bother can lead to frustration for patient and provider alike.

Voiding Diary

One of the most helpful components of the history is the voiding diary. Kept by the patient or caregiver for 48 to 72 hours, the diary records the time of each void and incontinent episode. No attempt is made to alter voiding pattern or fluid intake. Many formats have been proposed; a sample is shown in Figure 76–3.

To record voided volumes at home, individuals use a measuring cup, coffee can, pickle jar, or other large-mouth container. Information regarding the volume voided provides an index of functional bladder capacity and, together with the pattern of voiding and leakage, can suggest the cause of leakage. For example, incontinence occurring only between 8 AM and noon may be caused by a morning diuretic. Incontinence that occurs at night in a demented man with congestive heart failure, but not during a 4-hour nap in his wheelchair, is likely due to neither dementia nor prostatic obstruction but to postural diuresis associated with his heart failure. A woman with volume-dependent stress incontinence may leak only on the way to void after a full night’s sleep, when her bladder contains greater than 400 mL—more than it ever does during her continent waking hours. A patient with impaired mobility may become incontinent if polyuria develops.

The voiding diary should also guide therapy. For instance, in a patient with DO or prostatic obstruction, excess nocturnal excretion may result in nocturnal incontinence, which is more severe and troublesome than daytime leakage; successful therapy must address the excess excretion. By contrast, another patient with the same urinary tract dysfunction and excretion—but with the ability to hold more urine when asleep—might be bothered more by daytime leakage. Shifting nocturnal excretion to the daytime will exacerbate his problem.

Targeted Physical Examination

Similar to the history, the physical examination is essential to detect transient causes, comorbid disease, and functional impairment. In addition to the standard neurourologic examination, one should check for signs of neurologic diseases that are more common in older people, such as delirium, dementia, stroke, Parkinson disease, cord compression, and neuropathy (autonomic or peripheral), as well as for atrophic vaginitis and general medical illnesses, such as heart failure and peripheral edema. The rectal exam checks for fecal impaction, masses, sacral reflexes, symmetry of the gluteal creases, and prostate consistency and nodularity; as noted in Chapter 92, the palpated size of the prostate is unhelpful. Many neurologically unimpaired elderly patients are unable to volitionally contract the anal sphincter, but, if they can, it is evidence against a spinal cord lesion. The absence of the anal wink is not necessarily pathologic in the elderly, nor does its presence exclude an underactive detrusor (due to diabetic neuropathy, for example).

Stress Testing and PVR Measurement

Several caveats apply to performing the stress test and measuring the PVR in older patients. Stress testing is performed optimally when the bladder is full, and the patient is relaxed (check the gluteal folds to corroborate) and in as close to the upright position as possible. The cough or strain should be vigorous and single, so one can determine whether leakage coincides with the increase in abdominal pressure or follows it. Stress-related leakage may be missed if any of these conditions is not met. Delayed leakage typical of stress-induced DO should be differentiated from leakage typical of stress incontinence, which is instantaneous and ceases as soon as abdominal pressure declines. To be useful diagnostically, leakage must replicate the symptom for which help is sought,

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