Health Articles

If the cause of the incontinence still cannot be determined, urodynamic evaluation should be considered. Urodynamic evaluation is reproducible and safe, even in frail and debilitated people. Although its precise role remains to be determined, multichannel urodynamic testing is probably warranted in older patients when diagnostic uncertainty may affect therapy, when empiric therapy has failed and other approaches could be tried, or when surgical correction is being contemplated. Unfortunately, although simple to perform and up to 75% sensitive for detrusor overactivity with normal contractility, bedside cystometry cannot differentiate primary detrusor overactivity from that secondary to stress incontinence or obstruction (and therefore not of primary importance). Moreover, sensitivity and reproducibility are lower in nursing home patients, and the test is neither sensitive nor specific for detrusor hyperactivity with impaired contractility, the most common cause of incontinence in the nursing home population for whom this test might be the most useful.

Electrolyte, BUN, and creatinine levels should be measured, and a urinalysis and urine culture should be obtained in all patients. If the voiding record suggests polyuria, serum concentrations of glucose and calcium (and albumin, to allow calculation of free calcium levels in sick, malnourished patients) are measured as well. The age-associated decline in glomerular filtration rate—30% by the eighth decade—is not associated with an increase in serum creatinine because of a concomitant decrease in muscle mass; thus normal creatinine levels do not imply a normal glomerular filtration rate (see Ch. 63).
In any patient with sterile hematuria or suprapubic or perineal discomfort or in a patient at high risk for bladder carcinoma (eg, unexplained recent onset of urgency or urge incontinence, exposure to industrial dyes), urine cytology or cystoscopy should be performed.

Urge is neither a sensitive nor a specific symptom; 20% of patients with detrusor overactivity (and an even higher percentage of patients who also have dementia) do not have urge. Although urge incontinence is most often associated with detrusor overactivity, it is also common in patients with outlet incompetence (stress incontinence), outlet obstruction, and detrusor underactivity (overflow incontinence).
Precipitancy is the abrupt sensation that urination is imminent, whatever the interval and amount of leakage that follows. Defined in this way, precipitancy is both sensitive and specific for detrusor overactivity. 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 also can be considered precipitant leakage and is almost invariably due to detrusor overactivity. For those who do sense a warning, it is of less value to focus on the leakage; whether and how much the patient leaks depends on bladder volume, the amount of warning, the accessibility of a toilet, the patient’s mobility, and whether the relative sphincter relaxation that accompanies detrusor contraction can be overcome.
Urinary frequency (more than seven diurnal voids) is common in the elderly. It may be due to preemptive voiding habits, overflow incontinence, sensory urgency, a stable but poorly compliant bladder, depression, anxiety, or excessive urine production (eg, because of diabetes, hypercalcemia, or high fluid intake). Conversely, incontinent persons may severely restrict their fluid intake, so that even if they have detrusor overactivity 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, another common symptom in the elderly, can be misleading (eg, two episodes may be normal for the person who sleeps 10 h but not for one who sleeps 4 h). It must be evaluated systematically. The three general reasons for true nocturia—excessive urine output, sleep-related difficulties, and bladder dysfunction—can be differentiated by thorough questioning and a voiding record that includes voided volumes (see above discussion and TABLE 15-5). Voided volumes help determine the functional bladder capacity (the largest single voided volume) and should be compared with the volume of each nighttime void. For example, if the functional bladder capacity is 400 mL and each of three nightly voids is about 400 mL, the nocturia is due to excessive production of urine at night. If the volume of most nightly voids is much can be determined in any position, although its extent may be underestimated if the patient is examined only in the supine position. Pelvic floor muscle laxity indicates little about the cause of leakage. Detrusor overactivity may exist in addition to a cystocele, and stress incontinence may exist without a cystocele. Thus, knowledge of pelvic muscle laxity is useful primarily to the surgeon in choosing the best type of operation. The one exception occurs in the woman with a large cystocele; its descent may kink the urethra and cause obstruction.
The Q-tip test for pelvic floor laxity is not helpful in the assessment of incontinence. The Bonney (or Marshall) test is also of limited usefulness. The test is used to determine whether leakage can be prevented by stabilizing (but not occluding) the bladder base and thereby preventing its herniation through the urogenital diaphragm. Two fingers are placed in the lateral vaginal fornices, and the patient is asked to cough. Urethralhypermobility is likely if leakage is prevented. However, vaginal stenosis is common, and inaccurate finger placement may occlude the urethra and thereby lead to a false-positive result. Even if the test is performed correctly, a false-positive result may occur if leakage was due to a cough-induced detrusor contraction and (when the bladder is empty) does not recur when the bladder base is elevated.
Stress incontinence is best assessed with a provocative stress test. When performed properly, this test has a sensitivity and specificity exceeding 90%, even in the elderly. 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. A false-negative result may occur if the patient does not relax, if the bladder is not full, if the cough is not strong, or if the test is conducted in the upright position in a woman with a large cystocele. In the last case, the test should be repeated in the supine position with the cystocele reduced, if possible.
Whether leakage occurs coincidentally with the stress maneuver or is delayed for a few seconds or more should be noted. Delayed leakage suggests detrusor overactivity (triggered by coughing) rather than outlet incompetence. A stress test should not be performed when the patient has an abrupt urge to void, because the urge may be due to an uninhibited contraction. If the contraction is accompanied by physiologic sphincter relaxation and the patient then coughs, she will leak instantaneously, prompting the physician to misdiagnose a detrusor abnormality as outlet incompetence.
The vagina should be inspected for signs of atrophic vaginitis, which is characterized by indications of inflammation such as mucosal friability, petechiae, telangiectasia, and vaginal erosions. Loss of rugal folds and a thin, shiny mucosa are signs of vaginal atrophy rather than the inflammation of atrophic vaginitis (see also GENITAL ATROPHY in Ch. 83). A cytologic maturation index showing 100% parabasal cells ;ilso indicates atrophy but not necessarily atrophic vaginitis. Treatment of atrophic vaginitis is discussed under TRANSIENT INCONTINENCE, above.
Finally, the pelvic examination provides an opportunity to obtain a Papanicolaou smear; many elderly women have never been screened for cervical carcinoma.
Observation Of micturition; An observation of how a patient voids is part of the physical examination and provides much information about bladder and urethral function. When feeling full, the patient should first forestall voiding for several minutes to see if the sensation passes or if precipitant leakage occurs. The examiner should explain the reason for observing micturition and accompany the patient to a toilet that is equipped with a receptacle to measure the volume voided. If the patient will not allow the examiner to observe voiding, then the flow rate can be assessed either by using a uroflow machine (uroflowmeter) or by audibly monitoring the flow with a portable audio monitor (such as that used to monitor a baby’s room at home) and then asking the patient to place a hand on the abdomen to check for straining during urination.
Straining should be searched for especially if stress incontinence is suspected and surgery is contemplated, since straining suggests detrusor weakness that might predispose the patient to postoperative retention. If detrusor overactivity is suspected, it may be triggered by offering fluids; by having the patient change posture, cough, or hop; or by jouncing the heels (if the patient is unable to stand). If detrusor overactivity is precipitated, whether and how quickly the patient can interrupt the urine stream should be determined; rapid and complete interruption augurs well for bladder retraining.
The examination concludes with determination of the postvoiding residual volume, either by catheterization or ultrasound estimate. Adding the postvoiding residual volume to the voided volume provides an estimate of total bladder capacity (if the patient felt full before voiding) and a crude assessment of bladder proprioception. A postvoiding residual volume > 50 to 100 mL suggests either bladder weakness or outlet obstruction, but smaller amounts do not exclude either diagnosis, especially if the patient strained to void or double voided. Thus, observation of micturition or listening to the voided stream is important. If straining is observed, the patient is asked whether it is typical.
Incidentally, relying on the ease of catheterization to establish the presence of obstruction can be misleading. Difficult catheter passage may be caused by urethral tortuosity, a false passage, or catheter-induced spasm of the distal sphincter, whereas catheter passage may be easy even in severely obstructed patients.

Detrusor underactivity: An underactive detrusor sufficient to cause urinary retention and overflow incontinence is found in only about 5% to 10% of incontinent older persons. Injury may have occurred to the nerves supplying the bladder (eg, by disk compression or tumor involvement). Detrusor underactivity is also caused by the autonomic neuropathy of diabetes, pernicious anemia, Parkinson’s disease, alcoholism, or tabes dorsalis. Alternatively, the detrusor may be replaced by fibrosis and connective tissue in men with chronic outlet obstruction, so that the bladder fails to empty normally even when the obstruction is removed. Detrusor weakness may also occur in women, but the cause is unknown.
Symptoms of severe detrusor underactivity (eg, urgency, frequency, and 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 older women. Although mild weakness does not cause incontinence, it can complicate treatment when it occurs with other causes of incontinence.
diuretic. Incontinence that occurs at night in a demented person with heart failure, but does not occur during a 4-h daytime nap in the wheelchair, is probably attributable to the postural diuresis associated with 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 > 400 mL—more than it ever does during her continent waking hours. A patient may also void frequently because of polyuria.

Although outlet obstruction is the second most common cause of incontinence in older men, most men with obstruction are not incontinent. Common causes of outlet obstruction include benign prostatic hyperplasia, prostate cancer, and urethral stricture. Outlet obstruction can also occur in women, but anatomic obstruction is uncommon in women who have not had previous surgery for incontinence or who do not have a large cystocele that prolapses and kinks the urethra when straining to void. Patients who are incontinent because of obstruction most often present with postvoid dribbling. However, if secondary detrusor overactivity develops, urge incontinence may result, and if detrusor decompensation supervenes, overflow incontinence may ensue.
Obstruction that results from neurologic disease is invariably associated with a spinal cord lesion. In this situation, interruptions occur in pathways to the pontine micturition center (see FIG. 15-1), where outlet relaxation is coordinated with bladder contraction. Then, rather than relaxing when the bladder contracts, the outlet contracts simultaneously, leading to severe outlet obstruction (causing severe trabecu-lation, diverticula, and a “Christmas tree” deformation of the bladder; hydronephrosis; and renal failure—a constellation termed detrusor-sphincter dyssynergia).

Detrusor overactivity: The leading urinary tract cause of incontinence in older persons is detrusor overactivity, a generic term for uninhibited bladder contractions. The distinction between detrusor overactivity associated with a CNS lesion (detrusor hyperreflexia) and that which is not (detrusor instability) is often less clear in older patients. Uninhibited contractions may occur incidental to normal aging, a past stroke, prostatic outlet obstruction, or stress incontinence—even in persons with Alzheimer’s disease. No reliable way is known to determine the source of such contractions. While detrusor overactivity is the primary urinary tract cause of incontinence in demented patients, it is also the most common cause in nondemented patients. Two studies have failed to find a definite association between cognitive status and detrusor overactivity. Moreover, demented patients may also be incontinent because of transient causes (see TRANSIENT INCONTINENCE, above) or other urinary tract abnormalities.
Detrusor overactivity is characterized by frequent and precipitant voiding. The urge to void comes on abruptly. The volume of leakage is usually moderate to large, nocturnal frequency and incontinence are common, sacral sensation and reflexes are preserved, voluntary control of the anal sphincter is intact, and the postvoiding residual volume is generally low. A residual volume > 50 to 100 mL in a patient with detrusor overactivity suggests outlet obstruction (although the residual may be nil in early obstruction), detrusor hyperactivity with impaired contractility, or pooling of urine in a cystocele (in a woman) or large bladder diverticulum. A large residual volume is also found in patients with Parkinson’s disease, spinal cord injury, or diabetic neuropathy.
Detrusor overactivity in the elderly exists as two physiologic subsets: one in which contractile function is preserved and one in which it is impaired. The latter condition is termed detrusor hyperactivity with impaired contractility (DHIC) and is the most common cause of established incontinence in frail elderly persons. Because the bladder is weak in DHIC, urinary retention is common. Even without urinary retention, DHIC mimics virtually every other lower urinary tract cause of incontinence. For example, if the uninhibited contraction is triggered by or occurs coincidentally with a stress maneuver, DHIC may be misdiagnosed as stress incontinence. Alternatively, because DHIC is associated with urgency, frequency, a weak flow rate, significant residual urine, and bladder trabeculation, it may mimic prostatism in men. Finally, bladder weakness may interfere with anticholinergic therapy of DHIC if urinary retention is induced. Thus, alternative therapeutic approaches are often required (see TREATMENT CONSIDERATIONS, below).
Outlet incompetence: The second most common cause of incontinence in older women is outlet incompetence, which is manifested as stress incontinence. Leakage without a bladder contraction occurs coincidentally with stress maneuvers such as coughing, laughing, bending, and lifting.
In women, stress incontinence is usually caused by pelvic muscle laxity. A less common cause is intrinsic sphincter deficiency, also known as type 3 stress incontinence, which is usually due to operative trauma but also can result from nothing more than urethral atrophy. Women with intrinsic sphincter deficiency may leak even when sitting or standing quietly. This is a helpful diagnostic and therapeutic point, since many women become dry when bladder volume is kept below the leakage threshold (eg, 200 to 400 mL). A third but rare cause of stress incontinence is urethral instability, in which the sphincter abruptly and paradoxically relaxes without an apparent detrusor contraction. Most older women who are thought to have urethral instability probably have DHIC instead.
In men, stress incontinence is usually due to sphincter damage after transurethral or radical prostatectomy. In both sexes, stress-associated leakage also can occur in association with urinary retention, but in this situation, leakage is not the result of outlet incompetence.

If leakage persists after transient causes of incontinence have been addressed, lower urinary tract causes must be considered (see TABLE 15-3). Lower urinary tract malfunction generally is similar in older and younger patients, although older persons rarely develop fistulas or impaired detrusor compliance.