Hospital Practice

ISSN: 2154-8331 (Print) 2377-1003 (Online) Journal homepage: http://www.tandfonline.com/loi/ihop20

Urinary Incontinence in Older Adults Neil M. Resnick To cite this article: Neil M. Resnick (1992) Urinary Incontinence in Older Adults, Hospital Practice, 27:10, 139-184, DOI: 10.1080/21548331.1992.11705514 To link to this article: http://dx.doi.org/10.1080/21548331.1992.11705514

Published online: 17 May 2016.

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Urinary Incontinence in Older Adults

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NEIL M. RESNICK

Harvard University

A frequent and largely neglected problem, incontinence in the elderly can often be ameliorated or cured. Transient incontinence is usually secondary to intercurrent disease and thus should be addressed by treatment of that pathology. Established incontinence is most often due to detrusor hyperactivity. Behavioral intervention and bladder relaxants are management options.

Urinary incontinence affects 15% to 30% of older adults living in the community, about half of them on a daily to weekly basis. In acute care hospitals, about 35% of the elderly are incontinent daily, while more than 50% of those in a long-term facility are incontinent. The medical and psychological toll is high; the economic cost is an estimated $14 billion per year. Nevertheless, incontinence remains a largely neglected problem. Most people do not seek medical attention for incontinence, and even when they do, most physicians have little experience in the correct evaluation of the problem. This is unfortunate, because incontinence is no more an inevitable aspect of aging than is chest pain or diabetes; the symptoms reflect a variety of underlying conditions. Moreover, study after study has documented that incontinence can be ameliorated and even cured, often without invasive tests or surgery, even in frail elderly patients.

Lower Urinary Tract Anatomy and Physiology The detrusor muscle of the bladder and the urethral outlet act as a coordinated unit that permits the storage and expulsion of urine (Figure 1). The detrusor is innervated primarily by the parasympathetic nervous system and increases its contractile force and frequency in response to increased cholinergic activity. The sympathetic nervous system innervates both the bladder and urethra, with its effect determined by local receptors. Adrenergic receptors are sparse in the body of the bladder; those present are /3-receptors. Receptors at the bladder base and proximal urethra are a-recep-

tors; their stimulation contracts the bladder neck and proximal urethra. The somatic (voluntary) nervous system innervates the urogenital diaphragm and striated urethral sphincter, although the striated sphincter probably receives other innervation as well. Detrusor relaxation and sphincter closure mediate the storage of urine. Relaxation is accomplished by central nervous system inhibition of parasympathetic tone, while closure involves an increase in a-adrenergic and somatic neural activity. Voiding is mediated by detrusor contraction and sphincter relaxation; contraction requires the parasympathetic nervous system, relaxation the inhibition of sympathetic and somatic impulses to the outlet. Bladder capacity, the ability to postpone voiding, urethral compliance, and urinary flow rate probably decline with age in both sexes, while maximum urethral closure pressure and urethral length probably decline in women. Postvoiding residual volume and prevalence of uninhibited bladder contractions appear to increase. Often overlooked, the pattern of fluid excretion is altered as well. Younger persons excrete the bulk of their daily ingested fluid before bedtime; older persons excrete most of theirs during the night. One or two episodes of nocturia per night may be normal and not necessarily a sign of prostatism or cardiac failure. While none of these changes alone causes incontinence, each makes the older person more vulnera-

Dr. Resnick is Assistant Professor of Medicine, Harvard Medical School, and Chief of Gerontology, Brigham and Women's Hospital, Boston. Hospital Practice October 15, 1992

139

Disorders of Storage

Disorders of Emptying

Bladder empties completely but at inappropriate timesbladder size is normal

Bladder empties incompletelybladder is distended

@ Detrusor Overactivity

Detrusor Underactivity (Overflow Incontinence)

(Urge, Reflex, or Mixed Incontinence)

Decompensated Outlet Obstruction (Overflow Incontinence)

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@ Outlet Incompetence (Stress or Mixed Incontinence)

Figure 1. The four pathophysiologic mechanisms under-

lying urinary incontinence can be divided into disorders of storage and disorders of emptying. In the former, the patient cannot retain urine because either the outlet is open when it should be closed or the bladder muscle contracts when it should not (detrusor overactivity). Compensated outlet obstruction is a secondary cause of detrusor over-

ble to any additional pathologic or pharmacologic insult. This vulnerability, coupled with the increased likelihood that an older person will encounter such a challenge, explains the higher incidence of incontinence. An important corollary is that the new onset or exacerbation of incontinence in an older person is likely to reflect events outside the lower urinary tract-conditions usually amenable to medical therapy. 140

Hospital Practice October 15. 1992

activity. Disorders of emptying are marked by retention of some urine, eventuating in overflow incontinence. The cause may be detrusor underactivity or decompensated outlet obstruction. Obstruction can be due to spinal cord damage that resuHs in simuHaneous contraction of bladder and outlet or to mechanical causes, such as prostatic enlargement in men or large cystocele in women.

Transient Causes ofIncontinence Incontinence is due to transient causes in up to one third of elderly incontinent persons living in the community and up to one half of those in acute care hospitals. By definition, it is not the result of a fixed urinary tract disease; often it is secondary to intercurrent pathology and is alleviated by treatment of that pathology. The mnemonic we use to

recall the major reversible causes of incontinence in older adults is DIAPPERS (Table 1 ). Delirium induces incontinence in large part because the patient is unaware of the need to void; once the underlying problem is treated, the confusion resolves and the incontinence abates. Symptomatic urinary tract infection causes transient incontinence when the associated dysuria and frequency impede the patient's ability to reach

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the toilet, but asymptomatic bacteriuria does not appear to cause incontinence. Atrophic vaginitis is present in more than 80% of elderly women attending incontinence clinics. It can cause urge incontinence and leakage associated with stress maneuvers, as well as dyspareunia and recurrent cystitis. However, the vaginitis responds readily to treatment with lowdose estrogen, orally (0.3 mg of conjugated estrogen per day) or topically. The duration of theraPY has not been established; my colleagues and I give the low dose for one to two months and then taper, decreasing the dose each month by one pill per week. Pharmaceuticals capable of inducing incontinence are frequently used to treat older patients (Table 2). Let me expand the list by noting that among

Table 1. Causes of Transient Incontinence Delirium/confusional state I nfection-urinary (symptomatic)

A trophic urethritis/vaginitis P harmaceuticals P sychological, especially depression E xcessive excretion (e.g., CHF, hyperglycemia) R estricted mobility S tool impaction

Moreover, the elderly often use more than one such drug concurrently in the form of an overthe-counter preparation, which many do not regard as "medicines" worth mentioning to the physician. By inhibiting the cholinergic nervous system, these agents decrease bladder contractility, and problems of

the drugs with anticholinergic properties are antidepressants, antipsychotics, antihistamines, some antiparkinsonian agents (not the combination drug carbidopa-levodopa), antispasmodics, antiarrhythmics, and opiates. Thus, at least seven categories of medication have anticholinergic side effects.

Table 2. Medications That May Affect Continence Type of Medication

Examples

Potential Effects

Potent diuretics

Furosemide

Polyuria, frequency, urgency

Anticholinergics

Antihistamines, trihexyphenidyl, benztropine, dicyclomine, disopyramide

Urinary retention, overflow incontinence, delirium, fecal impaction

Psychotropics Antidepressants

Amitriptyline, desipramine

Anticholinergic actions, sedation

Narcotic analgesics

Morphine

Urinary retention, fecal impaction, sedation, delirium

a-Adrenergic blockers

Prazosin, terazosin

Urethral relaxation (stress incontinence in women)

a-Adrenergic agonists

Decongestants

Urinary retention in men

Calcium channel blockers

All

Urinary retention

------------------------------------------------------------------------- -------------------------------Anticholinergic actions, sedation, rigidity, immobility Thioridazine, haloperidol Anti psychotics -------------------------------------------------------------------------------------------------------Sedation, delirium, immobility Diazepam, flurazepam Sedatives/hypnotics

Alcohol

Polyuria, frequency, urgency, sedation, delirium, immobility

Vincristine

Urinary retention

Adapted from Resnick NM: Geriatric medicine and the elderly patient. In Current Medical Diagnosis and Treatment, Tierney LT et al (Eds), Appleton & lange, Norwalk, Conn (in press)

Hospital Practice October 15. 1992

141

urinary retention and overflow incontinence may result. Adrenergically active drugs affect the lower urinary tract because the bladder neck and proximal urethra derive much of their innervation from the sympathetic nervous system. The proximal urethra contains mostly a-adrenergic receptors; its

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Table 3. Causes of Established Incontinence Detrusor Overactivity

CNSdamage Stroke Alzheimer's disease Parkinson's disease Multiple sclerosis Local bladder irritation Cystitis (interstitial, infection, radiation, chemotherapy) Tumor Stone Outlet incompetence Outlet obstruction Outlet Incompetence

Pelvic floor muscle laxity Intrinsic sphincter incompetence Outlet Obstruction

Prostatic enlargement Urethral stricture (males) Spinal cord damage (bladder and outlet contract simultaneously) Large cystocele Detrusor Underactivity

Peripheral nerve damage Tumor involvement Disk compression Neuropathy Diabetic Alcoholic Syphilitic

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Hospital Practice October 15, 1992

tone can be increased by a-agonists and decreased by a-antagonists. a-Antagonists are contained in many antihypertensive agents; in an older woman with age-related weakening and shortening of the urethra, such drugs may precipitate stress incontinence. On the other hand, nonprescription preparations containing a-agonists (such as decongestants) may provoke acute urinary retention in a man with otherwise asymptomatic prostate enlargement-especially if the preparation contains an antihistamine with anticholinergic properties. Calcium channel blockers reduce smooth muscle contractility throughout the body, including the bladder. They not infrequently induce mild urinary retention and, occasionally, severe retention. Although severe depression is an uncommon cause of incontinence, excessive urine output is a frequent contributor. Many older people believe they need eight to 10 glasses of water per day to remain healthy. When combined with decreased bladder capacity, and especially with decreased mobility, excessive urine output may be sufficient to result in incontinence. Other causes of excessive output include diuretics (e.g., caffeine, theophylline, and alcohol) and disorders associated with excess fluid accumulation (e.g., congestive heart failure, low albumin states, venous insufficiency, and malnutrition). Drugs that cause fluid retention, such as NSAlDs and some calcium channel blockers, may also cause excessive output. Incontinence due to restricted mobility results not only from the inability to ambulate per se but also from visual impairment, muscle deconditioning, orthostatic and post-

prandial hypotension, claudication, and arthritis-all of which are treatable. Finally, stool impaction accounts for up to 10% of geriatric incontinence. A clinical clue is fecal oozing and overflow urinary incontinence. Whatever the cause, disimpaction restores continence. These transient causes should be assiduously sought in every incontinent elderly patient. In our series of hospitalized patients, continence was regained by three fourths of those who became incontinent in the context of acute illness. Regardless ofthe frequency, identification is important in all settings because the causes are a source of morbidity beyond the urinary tract and because transient incontinence will persist if untreated. An 83-year-old woman referred to us by the sleep laboratory was thought to have a sleep disorder and had been treated with an antidepressant. Although it had little effect on the sleep disorder. the drug was continued and the patient became incontinent. We eliminated the tricyclic antidepressant, and the incontinence, which had persisted for nine months, abated.

Established Incontinence Even with a normal urinary tract, established incontinence (Table 3) may be associated with either severe cognitive impairment or immobility. The patient who cannot reach the bathroom, or does not know where the bathroom is, needs help. On the other hand, demented patients usually also have a lower urinary tract disorder. Among the myths associated with geriatric incontinence is that detrusor hyperactivity is the primary lower urinary tract cause ofthe problem (continues)

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I NC0

NTINENCE

(continued)

in patients with severe dementia. In a prospective study of about 100 representative institutionalized patients, however, we found no significant association between detrusor hyperactivity and dementia. Detrusor hyperactivity is the cause of established incontinence in two thirds of incontinent elderly persons regardless of their cognitive status. Another myth maintains that incontinence in demented persons is untreatable, when in fact it may be caused by urinary tract infection, fecal impaction, or medications. For the rest, a simple toileting program will go a long way to control incontinence. Prospective studies of demented nursing home patients have shown that the incontinent often can be restored to dryness, merely by two-hourly reminders of the need to void. Thus, although treatments may differ, incontinence even in demented persons is treatable in up to two thirds and amenable to palliation in most others.

Lower Urinary Tract Dysfunction Urologic causes of incontinence (see Table 3) are best understood if divided into bladder and urethral dysfunction. The bladder either contracts when it should not, because of detrusor hyperactivity, or fails to contract when, or as well as, it should because of detrusor underactivity. Outlet resistance is high when it should be low because of outlet obstruction, or low when it should be high because of outlet incompetence. The two categories are not mutually exclusive: Both outlet obstruction and outlet incompetence can lead to secondary detrusor hyperactivity.

Detrusor hyperactivity, a condition in which the bladder escapes central inhibition and contracts reflexly, is the most common of the established causes in the elderly. Detrusor hyperactivity presents clinically as urge incontinence. It may result from an upper motor neuron lesion, as in stroke, Alzheimer's II disease, Parkinson's disease, or multiple sclerosis. Alternatively, the etiology of the hyperactivity may be in the urinary tract itself, where a source of irritation, such as cystitis, a bladder tumor, or a stone, overwhelms the ability of even the normal brain to inhibit bladder contraction. Detrusor hyperactivity exists as two subtypes-one in which contractile function is preserved, and one in which it is not. The latter, detrusor hyperactivity with impaired contractility, is known as DHIC. Detrusor underactivity may result from injury to the nerves supplying the bladder, such as disk compression, tumor involvement, or the autonomic neuropathy of diabetes. Alternatively, the bladder muscle may become weak due to degeneration of detrusor muscle, nerve, or both. This can occur in men with chronic outlet obstruction, and in such cases the bladder will fail to empty normally even after the obstruction is removed; it also may occur for reasons we still do not understand. Outlet incompetence is often the cause of incontinence in older women. The usual reason is pelvic floor muscle laxity, with consequent urethral hypermobility, so that the bladder base and proximal urethra "herniate" into the pelvic area through the urogenital diaphragm. Herniation produces an unequal transmission of abdominal pressure

to the bladder and urethra, causing stress incontinence each time the patient coughs or laughs. A small minority of those with stress incontinence have sphincter incompetence; it is so weak that the hydrostatic weight of a full bladder overcomes outlet resistance even at rest. Outlet obstruction may be associated with a spinal cord lesion. Pathways that coordinate outlet opening with bladder contraction are interrupted. Rather than relaxing when the bladder contracts, the outlet contracts simultaneously, leading to severe obstruction, hydronephrosis, and renal failure. Alternatively and much more commonly, obstruction results from prostatic enlargement or urethral stricture in men; anatomic obstruction is uncommon in women in the absence of a large cystocele. Clinically, it is useful to divide the four basic pathophysiologic mechanisms into two categories: disorders of storage (detrusor hyperactivity or outlet incompetence) in which the bladder empties completely but at inappropriate times; and disorders of expulsion (detrusor underactivity or outlet obstruction) in which the bladder empties inadequately, leading to progressive urine accumulation until overflow occurs. In disorders of storage, the bladder is normal in size; in emptying disorders, it is distended.

Evaluation of the Incontinent Patient The first step (Table 4) is to characterize the patient's usual voiding pattern, to find out if abnormal symptoms, such as straining to void or a sense of incomplete emptying, are present. (continues) Hospital Practice October 15. 1992

14 7

INC 0 NT! N EN C E

(continued)

These are usually taken as evidence of outlet obstruction or a weak bladder. However, many elderly persons strain at the end of voiding to empty the last few drops, and others have been straining so long they are unawareofit.

The physician elicits a detailed description ofthe incontinence, as for any symptomatic condition: onset, frequency, severity, pattern, precipitants, palliating features, and associated manifestations. Does the patient have leakage at night? Patients with detrusor hyperactivity gush intermittently both day and night;

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Table 4. Clinical Evaluation of the Incontinent Patient History Type (urge, reflex, stress, overflow, or mixed) Frequency, severity, duration Pattern (diurnal, nocturnal, or both; after medications) Associated symptoms (straining to void, incomplete emptying, dysuria) Alteration in bowel habit or sexual function Other relevant factors (cancer, diabetes, acute illness, urinary tract infections, neurologic disease, pelvic or lower urinary tract surgery-especially abdominoperineal resection and radical hysterectomy, which can cause decreased detrusor compliance) Medications, including nonprescription agents Functional assessment Physical Examination Other medical conditions (e.g., congestive heart failure or peripheral edema) Stress-induced leakage when bladder is full Observe or listen to voiding Palpable bladder distention after voiding Pelvic examination (atrophic vaginitis or urethritis, pelvic muscle laxity, pelvic mass) Rectal examination (perineal skin breakdown, resting tone and voluntary control of anal sphincter, prostate nodules, fecal impaction) Neurologic examination (mental status and elemental examination, including sacral reflexes and perineal sensation) Subsequent Studies Voiding or incontinence chart Metabolic survey (serum levels of electrolytes, calcium, glucose, and creatinine) Measurement of postvoiding residual volume Urinalysis and culture

Renal ultrasound• Urine cytologic study• Measured urine flow• ?Cystoscopy• •Selected cases only

those with pure stress incontinence are usually dry at night. A most useful part of the history is the voiding record kept by the patient, family, or nursing staff (Table 5). Such charts note the time of each voiding for a 48hour period. Incontinence between 8 A.M. and noon may be caused by a morning diuretic. Or if a wheelchair-bound man with congestive heart failure wets himself frequently at night but stays dry during a four-hour daytime nap in his wheelchair, the problem is probably postural diuresis rather than prostatic enlargement. The presentation suggests the type of incontinence: Urge incontinence, most common in the elderly, is characterized by leakage of a large volume preceded by an abrupt but intense warning of seconds to minutes. Reflex incontinence, or leakage not preceded by a warning, is seen less often. More likely is stress incontinence, in which leakage occurs only simultaneously with increases in abdominal pressure. Ovelj7.ow incontinence, in which there is continuous dribbling from the weight of urine in a distended bladder, is the least common cause. Each ofthese types correlates relatively well with the pathophysiologic mechanisms already mentioned: urge andreflex incontinence with detrusor hyperactivity, stress incontinence with outlet incompetence, overflow incontinence with outlet obstruction or detrusor underactivity. However, there are pitfalls. The frrst is differentiation of urge from stress incontinence. Some women awaken with a strong urge and lose large amounts of urine while rushing to the toilet. The problem may be urge incontinence, but one has to probe further for corroborative symp(conttnues)

150

Hospital Practice October 15. 1992

Table 5. Voiding Diary of an Incontinent 75-Year-Oid Man*

Day Day 1

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Day2

Time

Volume Voided (m/)

Are You Wet or Dry?

Approximate Volume of Incontinence

3:50P.M.

240

Wet

Slight

6:05P.M.

210

Dry

8:15P.M.

150

Dry

10:20 P.M.

150

Wet

10:30 P.M.

30

Dry

3:15A.M.

270

Dry

6:05A.M.

300

Dry

7:40A.M.

200

Dry

9:50A.M.

?

Dry

11:20 A.M.

200

Dry

12:50P.M.

180

Dry

1:40 P.M.

240

Dry

3:35P.M.

160

Wet

Slight

6:00P.M.

170

Wet

Slight

8:20P.M.

215

Wet

Slight

10:25 P.M.

130

Dry

Tablespoonful

Comments

Running water

Bowel movement

Running water

*Urodynamic evaluation confirmed a diagnosis of detrusor hyperactivity with impaired contractility. 24-Hour urine output of nearly 3 liters reflected patient"s belief that drinking 10 glasses of fluid/day was "good for his health." Excess fluid intake was overwhelming his (normal) bladder capacity. Although uninhibited contractions were present, the easily reversible volume component, coupled with the risk of precipitating urinary retention with an anticholinergic agent, prompted treatment with volume restriction alone. Frequency abated and incontinence resolved.

INC 0 NT IN EN C E

(continued)

toms, such as frequency. nocturnal incontinence, and incontinence while sitting quietly. If these are absent. the patient may actually have stress leakage apparent only with the large volumes that accumulate overnight. Whether the man with prostatism has irritative or obstructive symptoms, the physician can be easily misled. Several investigators have found that one third of the patients referred for surgical treatment of prostatism actually have an abnormality other than obstruction as the cause of their incontinence. Often the problem is an overac-

tive detrusor, which, if unaccompanied by outlet obstruction, may be exacerbated by surgical intervention (Table 6).

Targeted Physical Examination The examination is directed to check for signs of neurologic disease-dementia, delirium, stroke, Parkinson's disease, and autonomic or peripheral neuropathy. One looks for bladder distention (pointing to an emptying disorder) and for stress leakage (Figure 2). The latter is assessed by asking the patient with a full bladder to assume a position as close to upright as possi-

ble, to relax, spread the legs, and cough vigorously (but only a single cough). The diagnosis of stress incontinence can be missed if any of these maneuvers is omitted. Ifleakage occurs, it is necessary to note whether it is coincident with the stress maneuver or delayed for more than a few seconds. If delayed, such leakage suggests detrusor hyperactivity (triggered by coughing) rather than outlet incompetence. In the rectal examination, one checks for fecal impaction and masses. The size ofthe prostate is less important to assess because, as determined by palpation, it correlates poorly with the (continues)

Hospital Practice October 15. 1992

157

AEROBID'/AEROBID'-M (flunisolide) Effective asthma control BID

For oral inhalation only CONTRAINOICATIONS AEROBIO/AEROBIO-M Inhaler rs conlraindrcaled mlhe p11mary lrealmenl of slalus aslhmalicus or olher acule episodes ol aslhma where inlensivemeasuresare reqwed Hypersensilivily lo any oflhe rngredienls ollhis prepara110n conlraindicales ils use

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WARNINGS Particular care is needed in pa11en1s who are lransferred from syslemrcally aclrve cor11cosleroids lo AEROBIO/AEROBIO-M Inhaler becausedealhsdueloadrenalrnsulllciencyhaveoccurredrnasthmalicpalrenlsduringandafterlransferfromsyslemlc corticosleroids lo aerosol corlicosleroids After wrlhdrawal from syslemic cortrcosleroids, a number ol monlhs are requrred for recovery ol hypolhalamic-pilullary-adrenal (HPA) lunclion Ouring lhis period ol HPA suppress ron, palienls may exhibif signs and sympfoms ol adrenal insuffiCiency when exposed fo lrauma, surgery or rnfect1ons. particularly gaslroenleritis Allhough AEROBIO/AEROBIO-M Inhaler may provrde control ol asthmatic symptoms du11ng these episodes it does NOT provide the systemicsteroidthatis necessaryforcopingwiththeseemergencies Ouring periods ol stress or 1 severe asthmatrc aftack, patients who have been wrthdrawn from system1c cortrcosterords should be inslrucledloresumesystemrcsteroids(intargedoses)immedialelyandtocontacttherrphysicianforfurlherinstruclion. These palientsshouldatsobeinstructedtocarryawarningcardindicatinglhallheymayneedsupptementarysyslemicsleroidsduring periods of stress or asevere asthma aftack. To assess the risk of adrenal insufficiency in emergency Situations. routine tests of adrenatcorticatlunction, inctudingmeasurementofeartymornrngrestingcortlsottevets.shoutdbepertormedperiodicallyinall patients An early morning resting cortisol level may be accepted as normal 1l1t Ia IIs at or near the normal mean level. Localized infections with Candida albicans or Aspergillus mger have occurred in the mouth and pharynx and occasionally in the larynx. Positive cultures for oral Candida may be present in up to 34% of patients Although the frequency of clrnically apparent infection is considerably tower. these mfections may require treatment with appropr~ate ant1lungat therapy or discontinuance wilh AEROBID/AERDBIO-M Inhaler AEROBID/AERDBIO-M Inhaler is nol to be regarded as a bronchodilator and is not indicaled lor rapid relief of bronchospasm. Palients should be instructed to contact their physician immedralely when episodes ol asthma lhal are not responsive lo bronchoditatorsoccurduringthecourseoltreatment. Dur~ngsuchepisodes. patientsmrayrequrretherapywithsyslemiccorticosleroids There is no evrdence that control ol asthma can be achieved by admrmstrat1on of the drug mamounts greater than the recommended doses, whrch appear to be lhe lherapeutic equivalent ol approximately 10 mg/day of oral prednrsone. Theoretically, lhe use of inhaled corticosteroids wilh allernate-day prednisone systemrc treatment should be accompanred by more HPA suppression thanatherapeulicallyequivalentregimenofeitheratone Transfer of patients from systemic steroid therapy to AEROBIO/AEROBIO-M Inhaler may unmask allergic conditions previously suppressed bythesystemicsterord therapy, eg, rhinitls.conjunctrvitis.andeczema Children who are on immunosuppressant drugs are more susceptible to mfections than healthy children Chrcken pox and measles, forexampte,canhaveamoreseriousorevenfalalcourseinchlldrenonrmmunosuppressanlcorticosferoids. In such children. or inadultswhohavenothadthesediseases. particular care should betakentoavoidexposure. If exposed, therapywilhvaricella zoster immune globulin (VZIG) or pooled intravenous immunoglobulin (IVIG) as appropr~ate may be indicated If chicken pox devetops,treatmentwithantrviratagenlsmaybeconsldered PRECAUTIONS General: Because of lhe relatively high molar dose olltunrsotide per activat1on in this preparation, and because ollhe evidence suggesting h1gher levels ol syslemic absorption with ltunrsotide than with other comparable inhaled corticosleroids (see CLINICAL PHARMACOLOGY seclion), palients lreated with AEROBIO/AEROBIO-M should be observed carefully for any evidence ol systemic corticosteroid effect, including suppression of bone growth in children Part1cutar care should be taken rn observing patients postoperalively or during periods ol slress for evrdence of adecrease in adrenal function During Withdrawal from oral steroidS, some palienls may experience symptoms of syslemicalty aclrve stero1d withdrawal, eg., jornt and/or muscular pain, lassitude and depression, despile maintenance or even improvemenl of respiratory function (see DOSAGE AND ADMINISTRATION for delails) In responsrve patienls, flunisolide may permit control ol asthmatic symptoms without suppressron of HPA function. Since ffunisotide IS absorbed into the circulation and can be systemically actrve, the benelicrat effects of AEROBID/AERDBID-M Inhaler in mmimi11ng or preventing HPA dysfunction may be expected only when recommended dosages are not exceeded The long-term elfects of the drug in human subjects are strlt unknown. In partrcutar, the local effects of the agent on developmental or immunologic processes in lhe mouth, pharynx, trachea. and lung are unknown There is also no information about the possible long-termsystemiceffectsoftheagent The potentral elfects of the drug on acute, recurrent. or chronic pulmonary mfections. mctud1ngactive or quiescent tuberculosis, are not known Srmrtarty, the potential elfects of tong-term admmrstratron of the drug on lung or other trssues are unknown Pulmonary infillrates wrth eosinophilia may occur in patients on AEROBID/AEROBID-M Inhaler therapy Allhough il is possible !hat in some patrents th1s state may become manifest because ol systemrc sterord wrthdrawat when inhalatronat steroids are administered.acausatrverotelorthedrugand/oritsvehictecannotberuledout Carcinogenesis: Long-term studies were conducted mm1ce and rats usmg oral admmrstration to evaluate the carcinogenic potenliat olthedrug. There was an rncreaserntheincidenceofputmonaryadenomas inm1ce. but not in rats female rats receiving Ihe highest oral dose had an rncreased rncidence of mammary adenocarcrnoma compared to control rats An rncreased incidenceollhislumortypehasbeen reported for other corticosteroids Impairment of Fertility: female rats receiving high doses ol flcmsolrde (200 meg/kg/day) showed some evidence of impaired fertility. Reproductive performance rn the tow (8 meg/kg/day) and mrd-dose (40 meg/kg/day) groups was comparable to controls Pregnancy: Pregnancy Category C As wilh other corticosterords, flunisolrde has been shown to be teralogenic in rabbits and rats at doses o140 and 200 meg/kg/day respeclively II was also feloloxic in lhese animal reproductive sludies. There are no adequate and well-controlled studies in pregnant women ftunrsotide should be used during pregnancy only il the potential benefit rustifiesthepotentialrisktothefetus. Nursing Mothers: ll1s not known whether this drug is excreted " human milk Because other cort1costero1ds are excreted in human milk, caution should be exercised when ftumsotrde is admimstered to nursrng women ADVERSE REACTIONS Adverse evenls reported in controlled clinical t11als and long-term open studies in 514 patients treated w1th AEROBID/AEROBID-M are described below. 01 those patrents. 463 were treated for 3 months or longer 4071or 6 months or longer, 287 for 1 year or longer, and 1221or 2years or longer

~~:~~l~s!;:~';::~~~:1f~~t~1r; ;~~i~~1t~;r;~~~ of sterord-dependent patrents rn whom the dose of oral sleroid was berng tapered

1

Incidence 10% or greater Gastrointestinal.' diarrhea (10%). nausea and/or vomrtrng (25%). upset stomach (10%), General. flu (10%): Mouth and Throat sorethroat (20%), Nervous Syslem headache (25%), Respiratory cold symptoms (15%), nasal congest1on (15%), upper resprratory rnlectron (25%), SpeCial Senses.· unpleasant taste (10%) Incidence 3-9% Cardiovascular patpitatrons: Gas/rmnteslinal. abdominal pain heartburn General chesl pain, decreased appet1te, edema, lever: Moulh and Throat Candida infectiOn. Nervous System druiness. !flllabllity. nervousness. shakiness. Reproductive menstrual disturbances, Respiratory chest congestion, cough." hoarseness: rhrnrtis, runny nose, sinus congest1on, srnus drainage srnus rnfeclron, srnus1trs. sneeZing, sputum. wheeZing" Skm eczema, rtching (prurrtus), rash, Specral Senses. ear rnfect1on, loss ol smellorlaste Incidence 1-3% General: chills. rncreased appetrte and werght garn. matarse. peripheral edema sweatrng weakness CardiOvascular hypertension. tachycardra, Gastromtestmal. constrpat1on. dyspepsra, gas Hemic/Lymph caprllary lragrtrty. en arged lymph nodes: Mouth .and Throal: dry throat, glossitis, mouth irntat1on, pharyngrt1s, phlegm, 11roat rrrrtatron. Nervous Syslem anxiety, depression, farntness. fatigue, hyperactivity. hypoactrvrty, rnsomnra, moodiness, numbness, vertrgo, Respiratory bronchitiS. chest trghtness: dyspnea, ep1stax1s, head stuff!ness, laryngitis. nasal1mtat1on. pleunsy. pneumon1a s1nus discomfort. Skm acne. h1ves or urt1caria. SpeCJal Senses· blurred VISIOn. earache. eye d1scomfor!. eye mfec!lon Incidence less lhan 1%, judged by rnvestrgators as possibly or probably drug-related abdomrnat fullness, shortness of breath 'The incidences as shown ol cough, wheezing, and chest tightness were JUdged by investigators to be possrbtyor probably drugrelated. In placebo-controlled trials, the overall rncidences oftheseadverseevents(regardtessofinvestlgators' judgement of drug relationship) were srmilar lor drug and placebo-treated groups They may be related to the veh1cte or delivery system CAUTION: federal taw prohibrts drspensrng without prescriptiOn See full prescrrbing information for precautrons concernrng the transfer ol pat rents from oral sterords to AEROBID'/AEROBID'-M Not recommended lor chronrc use With alternate-day prednrsone regrmens References: I Nalional HeJrt, Lung, and Blood lnstilute National Asthma Education Program Exper/ Panel Report-Gwdelrnes lor the D~agnosrs and Management of Asthma Bethesda. Md US Dept of Health and Human Servrces 1991 2 Physicians' Desk Reference' 45th ed Oradell NJ Med1cat Economrcs Co Inc: 1991 955 1862. 2026 3 Data on frle Mid. by: 3M Health Care For: FOREST PHARMACEUTICALS, INC.

~id~a3~t~~5~~4Ctr

© 1992 forest Pharmaceutrcais. Inc

INCONTINENCE

presence or absence of outlet obstruction. The remainder of the rectal examination is actually a detailed neurourologic examination, since the same nerve roots (S2-S4) innervate both the external urethral and anal sphincters. For assessment of motor innervation, the patient is asked to volitionally contract and relax the anal sphincter. Many neurologically unimpaired elderly patients are unable to do so; if they can, it is evidence against a cord lesion. Motor innervation is assessed further by testing the anal wink (S4-S5) and bulbocavernosus reflexes (S2-S4). However, absence of these reflexes in older people is not necessarily pathologic, nor does their presence exclude an underactive detrusor due, for instance, to a diabetic neuropathy. Finally, the afferent supply is assessed by testing the perineal sensation. In women, one must perform a pelvic examination to check for pelvic floor muscle laxity (cystocele, rectocele, enterocele, or uterine prolapse) and pelvic masses. Atrophic vaginitis also must be sought. It is characterized by mucosal friability, petechiae, telangiectasia, and vaginal erosions; loss of rugal folds and the presence of a thin mucosa are signs of vaginal atrophy rather than atrophic vaginitis. The examination concludes when the patient voids and is catheterized for determination of postvoid residual volume. Adding the residual to the voided volume provides an assessment of total bladder capacity. A residual volume greater than 50 to 100 ml suggests either bladder weakness or outlet obstruction, but lower volumes do not (continues)

ffildlli'll p

~ ~~~~~:~~.o~:~:,~:;:;~~~~c-

AER-031-92 ~ UAD LABORATORIES ~ Division of Forest Pharmaceuticals, Inc. Jackson, Mississippi 39209

Revrsed 9/92

(continued)

160

INC 0 NT IN EN C E

(continued)

exclude either diagnosis, especially if the patient has strained to void. Thus, it is important first to observe or listen to the voided stream to interpret the results. A urine sample obtained by catheter is sent for urinalysis and culture, and blood urea nitrogen and creatinine levels are measured.

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Urodynamic Evaluation Sophisticated multichannel video urodynamic studies can pinpoint the pathophysiologic mechanism of incontinence, but they are invasive and expensive. For most elderly patients, a carefully performed clinical evaluation is sufficient to establish an initial working diagnosis. In a prospective and blinded study, we correctly predicted the urodynamically determined cause

of incontinence in more than 90% of cases. The difference between our experience and that of some others may in part be related to our use of all components ofthe clinical evaluation rather than relying on a single sign or symptom. If the cause of the patient's incontinence cannot be determined by clinical means, urodynamic study is the next step to consider. In general, this entails simultaneous measurement of bladder, urethral, and rectal pressures during the filling and emptying phases of the cycle. Optimally, the study is fluoroscopically monitored, and periurethral electromyography is occasionally required. Urodynamic evaluation probably should be performed in the older patient in several situations: when diagnostic uncertainty may affect therapy; when empiric therapy has failed and other approaches

Table 6. Predominant lower Urinary Tract Causes of Incontinence in the Very Elderly (Based on 94 Patients) Diagnosis

Women

Men Number(%)

Detrusor hyperreflexia With normal contractility

24 (31)

3 (18)

With impaired contractility

23 (30)

7 (41)

------------------------------- ------------------- ---------------Underactive detrusor

6 (8)

0

Stress incontinence

16 (21)

0

Outlet obstruction

3 (4)

5 (29)

Sensory urgency

1 (1)

0

Normal

1 (1)

0

Mixed*

3 (4)

2 (12)

77 (100)

17 (100)

Total

*Stress incontinence and either detrusor hyperreflexia with normal contractility or detrusor hyperreflexia with impaired contractility.

164

Hospital Practice October 15. 1992

need to be tried; and when surgical intervention is planned. With the requisite skill and experience, it can be done safely even in frail elderly patients and can be extremely helpful. As mentioned, there are two subtypes of detrusor hyperactivity. Patients may have the classic variety, in which detrusor function is preserved, or DHIC, in which the bladder is overactive but contracts poorly (Figure 3). DHIC was responsible for incontinence in one third of our consecutively evaluated nursing home residents, and it was seen in older patients in other settings as well. DHIC is not only a frequent cause of incontinence but also can pose a diagnostic dilemma. In addition to presenting as urge incontinence, it can present as urinary retention and may mimic prostatic obstruction in men and stress incontinence in women. Because of this mimicry of urethral obstruction or incompetence, national guidelines recently issued by the U.S. DHHS Agency for Health Care Policy Research recommend that urodynamic evaluation be done prior to operation in older patients undergoing surgery for suspected stress incontinence or urethral obstruction. DHIC also may have pathophysiologic implications, since we are currently unable to explain why this is such a common cause of incontinence in older persons and is seldom found in those under 70. There are two potential mechanisms ofDHIC: the weak bladder becomes uninhibited after a neurologic or other insult, or the uninhibited bladder that has been strong over the years becomes weaker because of progressive degenerative changes. Both hypotheses are currently under investigation by various groups.

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Abdominal Pressure S em H 2 0

Abdominal Pressure 1OS em H 2 0

Abdominal Pressure 1OS em H 2 0

110 em H 2 0

Normal

Stress Incontinence

Figure 2. Pure stress incontinence occurs simultaneously and exclusively in association with increases in abdominal pressure. The mechanism is an incompetent outlet, which most often results from laxity of the pelvic floor muscles.

Treatment Detrusor hyperactivity. The cornerstone of management of detrusor hyperactivity, the most common urinary cause of urge incontinence, is behavioral intervention. The clinician's ap-

When abdominal pressure increases (e.g., during coughing), the proximal urethra and bladder neck "herniate" through the urogenital diaphragm, permitting transmission of unequal pressure to the bladder and urethra.

proach addresses two basic categories of patients. For the cognitively intact and compliant patient, one uses a diary to determine the longest interval between voidings. If the patient is wet every three hours, he or she is instructed to void every two

hours during the day until continence has been maintained for three consecutive days. The interval is then progressively lengthened by half-hour increments until an interval offour to five hours is reached, at which point-for reasons still not well Hospital Practice October 15, 1992

165

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understood-incontinence will generally resolve. Patients are also taught ways to cope with bladder spasms. which generally occur as an abrupt, intense urge to void. Others have tried biofeedback techniques, but these require expertise and sophisticated equipment. Whether patients who have failed behavioral intervention as outlined will be helped by biofeedback is not yet known. For patients who are cognitively impaired, the technique of prompted voiding has been subjected to careful trials in nursing homes and found effective. Either the patient can be asked to void at frequent and regular intervals (e.g., every one to two hours) or the voiding record can be analyzed to predict when leakage is likely to occur; the patient is asked if he or she needs to void and is escorted in advance. Patients are rewarded with positive verbal reinforcement for awareness of their continence status. A randomized controlled study, conducted in two nursing homes, found a 50% decrease in incontinence on the first day of such prompted voiding; the decrease persisted as long as the technique was used. In about 25% of nursing home patients, complete continence can thus be restored using such techniques. Bladder suppressant medications are added as necessary (Table 7). As part ofthe Agency for Health Care Policy and Research mandate to recommend management guidelines, we did a comprehensive review of the drugs used to treat urge incontinence due to detrusor hyperactivity. First to be proved effective in randomized controlled trials were the anticholinergic drugs propantheline and dicyclomine. Drugs with mixed actions combining both smooth muscle re166

Hospital Practice October 15, 1992

Figure 3. Pressure tracing from patient with detrusor hyperactivity {top), in which the bladder escapes central inhibition and contracts reflexly, shows strong contraction associated with rapid rise in detrusor pressure beginning at point 1; at point 2, the urethra was mechanically occluded and there followed a further rapid rise in pressure. In contrast, the lower pressure tracing, wHh point 1 indicating start of pressure rise and point 2 urethral occlusion, is from patient who has detrusor hyperactivity with impaired contractility. In DHIC, the bladder Is uninhibited but weak, and the pressure rise is generally attenuated.

laxant and anticholinergic properties, such as oxybutynin and terodiline, also proved effective in several trials. (Terodiline has since been withdrawn from the European market, and U.S. clinical trials were suspended after reports of possible association with onset oftorsade de pointes.) The third category of drugs useful for urge incontinence includes the tricyclic antidepressants, particularly those with anticholinergic side effects. Each of

the following has been subjected to controlled trials and appears to work: imipramine, nortriptyline, desipramine, and doxepin. The most anticholinergic of the tricyclic antidepressants, amitriptyline, has not been tested for urge incontinence in controlled trials, and we suggest avoiding it in the elderly because of its greater anticholinergic properties and because it is a potent inducer of orthostatic hy(conttnuesJ

Table 7. Study Findings on Drugs for Urge Incontinence*

Propantheline

Oxybutynin

Terodiline

Tricyclic Antidepressants

Number of randomized controlled trials

5

6

7

3

Trials at nursing home sites

3

1

0

1

Number of patients

259

309

278

265

Female patients (%)

82

90

94

-

15-30 mgtid-qid; ± 60 mgqhs

5 mgbid-qid

12.5-25 mg

4 days-4 weeks

Cure ('}{,)t

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Dose tested

bid-tid

Imipramine, 25-100 mg, total daily dose

1-4weeks

3-8weeks

3-8weeks

0-5

28-44

18-33

31

Urinary incontinence reduction (%)t

0-53

9-56

14-83

20-77

Side effects (%)*

0-50

2-66

14-40

0-70

Dropouts (%l*

(0-9)

(3-45)

(2-8)

Study duration

*Includes drugs used for overactive detrusor with demonstrated efficacy in at least two randomized, blinded, placebo-controlled trials tPercent cure or reduction of baseline urinary incontinence frequency while on active drug minus percent while on placebo *figures are the difference in percent of side effects on active drug compared with placebo. Figures in parentheses are percent of dropouts in trial ascribed to drug minus percent ascribed to placebo.

INC ONTI NE N C E

(continued)

potension. There have not been any controlled trials of the calcium channel blockers for use in incontinence. Controlled trials of flavoxate have not yet proved it effective. How then to choose which bladder relaxant to use? In older patients we consider side effects we most want to engender or avoid. In a depressed person who is also incontinent, the agent of choice might be an antidepressant. In another patient with orthostatic hypotension, we would avoid an antidepressant, since it might worsen the hypotension. For the patient who has confusion or dementia, an anticholinergic such as propantheline would be less desirable because of its propensity to exacerbate confusion; a drug without 178

Hospital Practice October 15. 1992

CNS side effects, such as a calcium channel blocker, would be preferable. For the patient with hypertension, angina pectoris, or abnormalities of cardiac diastolic relaxation, a calcium channel blocker also might be the treatment of choice. Some drugs with combined properties, such as oxybutynin, have a rapid onset of action and can be used to prevent incontinence at predictable times. Finally, combinations of drugs with different actions, such as an anticholinergic with a calcium channel blocker, may allow the use of lower doses with enhanced benefit. Whichever agent is selected, however, the patient must be monitored for urinary retention. With respect to DHIC, we do not yet know the treatment im-

plications. Since there already is bladder weakness, it may be easier to suppress the spasms with a bladder relaxant alone. On the other hand, it may be more difficult to treat, since the relaxant might turn the bladder off completely and thereby precipitate overflow incontinence. We are nearing completion of a prospective, randomized crossover trial on this issue. Pending the trial results, patients are treated individually. If straining during voiding empties the bladder, only a totleting regimen may be required. If that fails, we will cautiously add a bladder relaxant if it is not contraindicated by urinary retention and a high residual volume. If these interventions do not work, we recommend intermittent selfcatheterization when feasible. (continues)

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INC 0 NT IN EN C E

(continued)

Stress incontinence in women is usually attributed to pelvic floor laxity and urethral hypermobility. The goal is to strengthen the urethral supports, and pelvic floor exercises can be used. The patient is instructed to sit on the toilet and begin voiding. Once voiding has started, she is asked to interrupt the stream by contracting the sphincter for as long as possible. Most elderly women are able to do so for no more than a second or two, but after a few weeks of effort, most can prolong the contraction. Once the woman recognizes which muscles to contract, she can do the exercises at any time and during any activity. The best regimen has yet to be determined. My associates and I advise patients, if they can, to increase the duration of muscle contraction to about 10 seconds, contract the muscle as many as 25 times per set, and complete three to four sets per day. If not contraindicated, treatment with an a-adrenergic agonist, such as phenylpropanolamine, may be added and is often beneficial, especially when administered with estrogen for women (Table 8). Imipramine, which affects the bladder and the outlet, is a reasonable choice for patients with both stress and urge incontinence if postural hypotension has been excluded. If these methods fail, or if the patient prefers it, surgical correction may be considered. Surgery may be performed successfully in most elderly patients once urethral hypermobility has been confirmed. A small minority will have intrinsic sphincter deficiency. Strengthening the urethral supports will not help; the urethra itself must be tightened. Since in180

Hospital Practice October 15. 1992

trinsic sphincter deficiency is often less severe in older compared with younger women, it often responds to drugs such as estrogen, given with an a-adrenergic stimulant. Restoration of premenopausal estrogen levels results in growth of the urothelium, which (when combined with a-adrenergic stimulation) helps to coapt the urethra. Some data suggest that administration of estrogen also enhances the number of a-adrenergic receptors and, thereby, the ability of the urethra to contract. However, correction of intrinsic sphincter deficiency usually requires a surgical approach (pubovagtnal sling) in which actual compression of the urethra is carried out. This operation is more likely to result in chronic urinary retention with an obstructed urethra in an older woman, particularly because the strength of the detrusor muscle seems to decline with age. There are several interventions for patients who have intrinsic sphincter deficiency. One generic category is the urethral bulking procedure, e.g., submucosal injection of a compound to help coaptation of the urethra. This can be done in the physician's office, but the process may have to be repeated at intervals. The agent currently used in this procedure is Teflon; collagen, which is easier to inject, is still under investigation The other surgical option is insertion of an artificial sphincter. Until recently, more than 90% of the experience had been in men, in whom insertion is generally easier because the device is placed at a lower level, around the bulbous urethra. In women, the insertion has to be more proximal and therefore is more difficult, but it seems to be a feasible operation for appropriate candidates. The potential risks

include compression of the urethra, which could cause erosion or infection, in which case the device must be removed. However, in centers that specialize in implantation of such devices, those adverse effects occur in less than 10% of patients. Urethral obstruction in men is usually caused by a stricture, carcinoma, or prostate enlargement; urethral obstruction is rare in women. The quicker operative procedures (e.g., prostatotomy with bladder neck incision) have made surgical decompression possible for even the most frail patients. These procedures, as well as transurethral prostatectomy in some cases, can be performed under local anesthesia. In women with a large cystocele, which can kink the urethra and thereby block it, surgical correction should include an outlet suspension if urethral hypermobility is also present. Prior urodynamic evaluation is helpful: If bladder neck incompetence or low urethral closure pressure is observed, a different surgical approach may be required to avoid sphincteric incompetence. Rarely, distal urethral stenosis may be the cause of obstruction; the stenosis can be dilated and treated with estrogen. It should be noted that most women who undergo dilation do not have urethral stenosis but rather an underactive detrusor; for these women, dilation usually is not helpful and may be harmful.

Another approach to the obstructed man is the administration of a-adrenergic antagonists, such as prazosin. A number of double-blind placebo-controlled trials have documented the symptomatic efficacy of these agents, and in some trials, the postvoiding residual volume,

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outlet resistance, and urinary flow rate have improved as well. However, the trials did not include men with urinary retention. These agents are not panaceas for outlet obstruction. Rather, each allows the physician to treat the problem symptomatically until more definitive therapy is necessary or feasible. Detrusor underactivity is associated with a large postvoiding residual volume and overflow incontinence. Before it can be diagnosed, one must exclude outlet obstruction. The first step is to ensure protection of the upper urinary tract, since overflow incontinence with a high bladder pressure can result in hydro~

nephrosis and renal insufficiency. After excluding hydronephrosis, the bladder should be decompressed for at least one to two weeks, and a search for reversible causes of urinary retention should be undertaken. Once the bladder has been adequately decompressed, a urodynamic evaluation can be done. Patients with outlet obstruction will have a disproportionately high voiding pressure and a low flow rate; those without obstruction will have a low voiding pressure commensurate with a low flow rate. Patients with obstruction are referred for an operation, if they are candidates. Augmented voiding techniques (such as double voiding

and the Crede or Valsalva maneuver) may help patients without obstruction if they are able to initiate a detrusor contraction. When this is insufficient, pharmacotherapy is added. Bethanechol is the traditional drug, but as yet there is not enough evidence that it is effective in this setting. An alternative option is to use an a-adrenergic antagonist, such as prazosin, to reduce outlet resistance. For patients unable to void at all, the augmented voiding techniques are fruitless and drugs appear to have no role. Thus, such patients need either intermittent catheterization or an indwelling catheter. Intermittent (continues)

Table 8. Study Findings on Drugs for Stress Incontinence* Estrogen supp ementat1on (Postmenopausal)

a-Adrenerg1c Agonists

Phenylpropanolamine

Quinestradol

Piperazine Estrone

Estriol

8

1

1

2

248

18

36

25

Average age (range)

55 (33-90)

79.6 (66-92)

57.2 (47-72)

62 (42-76)

Dose tested

50mgbid

0.25 mgqid

3mg

4mg

4 weeks (2-6)

4weeks

3 months

5 weeks (4-12)

~14

0

0

0; 14 (S)

19-60

89

20

0;29

(S in 5 randomized controlled trials)

(S)

Not significant

(S)

5-33

0

11

11-28

(~.3)

(0)

Number of randomized controlled trials Number of patients

Study duration (range) Cure (%)t

Percent urinary incontinence reduction > placebot

Side effects (%) Dropouts (%l*

*

(0; 0)

*All female subjects, randomized controlled trials tPercent of subjects cured or improved while on active drug minus percent while on placebo *Figures are the difference in percent of side effects on active drug compared with placebo. Figures in parentheses are the percent of dropouts in trial ascribed to drug minus percent ascribed to placebo. (In some papers it was not mentioned or information is incomplete.) S=significant difference between active drug and placebo

Hospital Practice October 15. 1992

181

Ideal Therapy For:

!ifsmokers lif'J:Iderly Patients [!(Maintenance Patients

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Professional Use lnformatton

BRIEF SUMMARY CONTllAINOICATIONS There are no known contramdtcatiOns to the use of sucralfate

PRECAI/TIONS Duodenal ulcer tS a chrontc. recurrent d•sease Whtle short-term treatment w•th sucralfate can result m complete healing of the ulcer, a successful course of treatment wtth sucrallate should not be expected to alter the postheallng frequency or severity of duodenal ulceratton

Special Populations: Chronic Renal Fatlure and Dialysis Patients. When sucralfate ts admmtstered orally, small amounts of aluminum are absorbed from the gastromtesllnal tract Concomttant use of sucralfate with other products that contain alumtnum. such as alummum-contatntng antactds. may tncrease the total body burden of alummum Pattents wtth normal renal functiOn rece1v1ng the recommended doses of sucralfate and alumtnum'"(:ontatmng products adequately excrete alummum tn the unne Patients wtth chrontc renal failure or those receiving aialysts have tmpatred excretton ol absorbed alumtnum In addttton. alumtnum does not cross d1alysts membranes because tt 1s bound to albumm and transfemn plasma protems Alummum accumulatiOn and toxtctty (alumtnum osteodystrophy. osteomalaCia. encephalopathy) have been descnbed tn pattents w1th renal tmpMment Sucralfate should be used Wtlh cautton m pattents Wtth chrontcrenalfatlure Drug lnteracttons: Some studtes have shown that Simultaneous sucralfate admtmstratiOn tn healthy volunteers recuced the extent of absorpt1on (btoavatlabtlity) of smgle doses of the followmg drugs ctmettdtne. ctprofloxactn. dtgoxtn. norfloxacm. phenytotn. rantttdiOe. tetracycline. and theophylline The mechantsm of these mteracttons appears to be nonsystemtc tn nature. presum· ably resulttng from sucralfate bmdtng to the concom1tant agent 10 the gastrotn· testinal tract. In all cases studted to date (ctmettdme, ctprofloxacm. dtQOKtn. and ranitidinet dostng the concomttant medtcat1on 2 hours before sucralfate elimtnated the tnteract,on Because of the potenttal of CARAFA TE to alter the absorption of some drugs. CARAFATE should be admtntstered separately from other drugs when alterations tn btoavatlabtlity are felt to be cnttcal In these cases. pattents should be monttored appropnately CarcinogeneSIS, Mutagenests, lmpatrment of F9rtility. Chrontc oral :o-.tctty studtes of 24 morths' duratiOn were conducted 10 mtce and rats at doses up to 1 gm/kg (12 ttmes the human dose! There was no evtdence of drug-related tumongentctty A reproductton study tn rats at doses up to 38 ttmes the human dose dtd not reveal any mdtcatton of lerttltty tmpamnent MutagentCtty studtes "oNere not conducted Pregnancy: Te•atogentc effects Pregnancy Category B Teratogemctty studtes have been performed tn mtce. rats. and rabbitS at doses up to 50 ttmes the human dose and have revealed no evtdence of harm to the fetus due to sucralfate There are. however, no adeQuate and well-controlled studtes tn pregnant women Because ammal reoroductton studtes are not always predtcttve of human response. this drug should be used dunng pregnancy only tf clearly needed Nursing Mothers: It ts not known whether th1s drug tS excreted tn human mtlk Because many drugs are excreted 10 human mtlk. cautton should be exerCISed when sucratfate 'S admtntstered to a nurstng woman Pediatric Use: Safety and effect1veness m chtldren have not been establtshed ADVERSE REACTIONS Adverse react1ons to sucralfate tn cl!mcal tnals "oNere m1nor and only rarely led

~~~~;~~~~~~; ~~~~~r~~~~ss:;:sr~:!~~n~; tJ~)t1ents treated wtth Consttpatton was the most freQuent complatnt (2%) Other adverse effects repo~ tn le~s than 0 5% of the pattents are listed below by body system Gastromtestmal. d1arrhea. nausea. vomtltng. gastrtc dtscomfort. tnd1gest1on. _ flatulence.drymouth Dermatological: pruntus. rash Nervous system: dtwness. sleep1ness. verttgo Other: back patn. headache Postmarketing reports of hypersensttlvtty reacllans. tncluding urticana !htves). angtoedema. resptratory dlff,culty, and rhtn1!1s have been recetved However. a causal relattonsh1p has not been established

Issued 3/91

INCONTINENCE

(continued)

catheterization is preferred and requires only clean, rather than sterile, catheter insertion. The patient can purchase a supply inexpensively. The one or two catheters that are used during the day can be carried in a pocket or purse. The catheters are cleaned daily, allowed to air-dry at night, and may be used repeatedly. Prophylaxis against urinary tract infection is probably warranted if the patient has more than an occasional symptomatic infection. Despite the benefits and proven feasibility of intermittent catheterization, many elderly patients choose indwelling catheterization instead. The attendant complications of indwelling catheterization include bladder and urethral erosion, bladder stones, and bladder cancer, as well as urosepsis. On the other hand, because overflow incontinence due to detrusor underactivity is relatively uncommon, indwelling catheters are proba-

bly required in only 1% to 2% of patients, even those in nursing homes. It should be noted that the elderly are likely to have more than one type of incontinence. Symptoms of urge incontinence, for example, may develop in a woman with a history of stress incontinence. The mixed incontinence differs from stress-induced detrusor hyperactivity, since the symptoms of urge and stress reflect both a hyperactive detrusor and a loss of outlet integrity. Urodynamic evaluation is often helpful in cases of mixed incontinence. Overall, incontinence in the elderly requires a comprehensive approach to identify and treat all reversible factors and then target therapy to the causes within the lower urinary tract. If the physician is prepared to devote interest and understanding to the problem, most patients show substantial improvement and many can have full continence restored. D

Selected Reading Urinary Incontinence Guideline Panel: Urinary Incontinence in Adults: Clinical Practice Guideline. AHCPR Pub. No. 92-0038, DHHS, Rockville, Md,1992 Resnick NM, Yalla SV, Laurino E: The pathophysiology of urinary Incontinence among institutionalized elderly persons. N Eng! J Med 320: 1, 1989 Resnick NM, Yalla SV: Management of urinary Incontinence In the elderly. NEnglJMed313:800,1985 Resnick NM, Yalla SV: Detrusor hyperactivity with impaired contractile function: An unrecognized but common cause of incontinence In elderly patients. JAMA 257: 3076, 1987 Resnick NM: Voiding dysfunction and urinary Incontinence. In Neurourology and Urodynamics: Principles and Practice, Yalla SV et al (Eds). MacMillan, New York, 1988, pp 303-330 Fantl JA et al: Efficacy ofbladder training In older women with urinary incontinence. JAMA 265: 609, 1991 Schnelle J: Treatment of urinary Incontinence In nursing home patients by prompted voiding. JAm Gerlatr Soc 38: 356, 1990

'"MARION Ml:RRELL DOW IN( ..

,

KANSAS

CIT¥

MO

WeinAJ: Pharmacologic treatment of incontinence. JAm Gerlatr Soc 38:317,1990

64114