Janimine

Urinary incontinence, defined as involuntary urine loss of sufficient quantity or frequency to be a problem, is common among the elderly. An estimated 8 to 12 million persons in the United States suffer from incontinence.[1] Approximately 20 percent of the community-dwelling elderly, half of the institutionalized elderly and nearly 75 percent of the hospitalized elderly have this problem.[2]

The consequences of urinary incontinence are great, affecting the patient, the family and the caregivers, and the disorder exacts a cost in the form of shame, guilt and social withdrawal on the part of the patient, in addition to its tremendous financial. burden.[3] The estimated cost of urinary incontinence in this country, including medical, social and psychologic consequences, exceeds $10 billion annually.[4]

Despite the apparently high prevalence of incontinence, many patients are hesitant to raise the subject with their physician. As a result, urinary incontinence is underreported. Therefore, physicians must be diligent about raising the topic during office visits and physical examinations.

Clinical evaluation of the incontinent patient should include a complete history, with particular focus on voiding patterns; a physical examination with attention to the genitourinary system, and laboratory tests and investigative studies, such as assessment of postvoid residual volume.[3,5,6,] A number of effective pharmacologic and nonpharmacologic approaches are available for the treatment of urinary incontinence. Nonpharmacologic treatments were discussed in a previous article in American Family Physician.[7] This article describes the current pharmacologic options for the treatment of urinary incontinence.

Diagnosis

Once urinary incontinence has been identified, the next step is to distinguish between transient and established forms of the disorder. Transient (acute) incontinence has a number of potential causes, including infection, drug side effects, acute delirium, atrophy, anxiety, depression and restricted mobility. An appropriate treatment plan should include efforts to reverse the underlying condition (e.g., withdrawal of offending medications, treatment of infection). Table 1[5] summarizes the reversible causes of urinary incontinence in an easy-to-remember mnemonic,

DIAPPERS

Established (chronic) urinary incontinence can be divided into four common subtypes: overflow, stress, urge and mixed incontinence. Selection of an appropriate therapy depends on identification of the type of incontinence and an understanding of the normal physiologic function of the bladder and its outlet.

Physiology of the Bladder

The dynamic muscular wall of the bladder is the detrusor muscle. This three-layered bundle of smooth muscle is responsive to parasympathetic stimulation, causing contraction, and to beta-adrenergic stimulation, allowing relaxation when combined with inhibitory sympathetic tone. Detrusor contractions are initiated by a reflex arc from the brainstem nucleus, unless inhibited by a higher cortical control.

The smooth muscle of the bladder neck and proximal urethra is rich in alpha-adrenergic receptors; when stimulated, it assists in bladder continence. This smooth muscle allows relaxation of the bladder outlet in conjunction with detrusor contraction. In addition, the skeletal muscles of the pelvic floor are under voluntary control by way of the pudendal nerve. These muscles are able to counter the effects of intra-abdominal pressure on the bladder to prevent unintentional emptying.[8]

Figure 1 illustrates the normal anatomy of the bladder and bladder outlet. Normal physiology (Figures 2a through 2d) should be kept in mind as the pharmacologic therapies for each type of urinary incontinence are discussed.

Overflow Incontinence

Overflow incontinence occurs when the bladder is unable to empty normally and becomes overdistended, resulting in frequent, if not constant, loss of urine. The disorder derives from neurologic problems that inhibit detrusor activity, such as those associated with diabetes, vitamin [B.sub.12] deficiency and herniated intervertebral disc. In addition, overflow incontinence may occur as a result of obstruction in the outflow of urine, such as from prostatic enlargement, strictures of the urethra and bladder neck, tumors, uninhibited contractions of the urethral sphincter and certain medications.[3,7]

The diagncsis of overflow incontinence is made by palpation of a distended bladder following voiding or by measurement of a postvoid residual volume in excess of 100 mL. In men, palpation of an enlarged prostate may suggest the clinical diagnosis of overflow incontinence. Urologic evaluation, including ultrasound assessment of bladder volume and uroflowmetry, may help confirm the diagnosis.

Drug treatment of overflow incontinence should be considered only after any existing outflow obstruction has been corrected. Alternative therapies include intermittent self-catheterization, double-voiding and Credes maneuver.

A cholinergic agonist, such as bethanechol (Urecholine), has a relatively localized effect on the urinary tract. It is helpful in the treatment of nonobstructive bladder atony. Bethanechol is contraindicated in patients with hyperthyroidism, peptic ulcer or bronchial asthma. It should be avoided in patients who may be at increased risk from its vagotonic effects (i.e., those with cardiac disease or severe obstructive pulmonary disease).[9]

Alpha-adrenergic agents, such as prazosin (Minipress) and terazosin (Hytrin), were originally designed to treat hypertension. However, their alpha blockade also produces a decrease in bladder neck and urethral tone, allowing for improved outflow of urine from the bladder. These drugs are gaining wider use in patients with overflow problems due to prostatic hypertrophy or sphincter hyperspasticity who are not surgical candidates.[9,10] Side effects include lightheadedness, orthostatic hypotension or syncope from vigorous lowering of blood pressure.

Stress Incontinence

Stress incontinence results when bladder outlet mechanisms are inadequate to counter intravesicular pressure. Causes include direct damage to the bladder neck or urethra from surgery or trauma, sphincter weakness secondary to neurologic injury and decreased pelvic floor competence as a result of normal aging, multiparity or surgery.

The diagnosis of stress incontinence is made on the basis of a history of small amounts of urine lost immediately after an increase in intra-abdominal pressure, such as during coughing, sneezing, laughing, heaving or straining. The urine loss usually stops immediately when elevation of intra-abdominal pressure ceases.

Physical examination may reveal weakness and protrusion of the anterior vaginal wall, urethra and, possibly, bladder. Having the patient perform a Valsalva's maneuver (in either the supine or standing position) while the bladder is full may confirm leakage. Postvoid residual urine volume is normal (less than 100 mL).

A variety of nonpharmacologic treatments, such as pelvic floor exercises and biofeedback, are available to help increase outlet resistance.[7] Drug therapy may be used as an adjunct to nonpharmacologic treatment or as initial therapy in some patients. Alpha agonists, commonly used in cold preparations, are also useful in stimulating increased smooth muscle tone at the bladder outlet.[11] Phenylpropanolamine has been used extensively in treating stress incontinence, with documented success. Pseudoephedrine and ephedrine are also effective in treating stress incontinence.

Imipramine (Janimine, Tofranil), a tricyclic antidepressant, has anticholinergic and direct relaxant effects on the detrusor muscle, plus an alpha-adrenergic effect on the bladder outlet.[3] For this reason, imipramine is commonly used to treat stress incontinence or mixed urge and stress incontinence.[12] Care must be taken to monitor the patient for the numerous side effects associated with this class of drugs (e.g., postural hypotension, sedation, constipation).

Topical estrogen therapy is considered mildly helpful in postmenopausal women, because of its potential for increasing the tone of the bladder outlet, although studies have failed to prove this conclusively.

If severe, stress incontinence may fail to respond to pharmacologic therapy and may require surgery.[7]

Urge Incontinence

Urge incontinence is the most common form of urinary incontinence in elderly persons, accounting for up to 70 percent of cases. It occurs when an urge to void is perceived but the mechanism for inhibiting the detrusor contraction is ineffective. This type of incontinence is commonly referred to as detrusor hyperactivity. Among its causes are central nervous system lesions (stroke), demyelinating diseases that prevent bladder inhibition and local irritating factors (urinary tract infection, bladder tumors). In most cases, however, no clear etiology is identifiable.

The diagnosis of urge incontinence is made in the presence of a normal postvoid residual volume and a history of an irresistible urge to void. The urge may be precipitated by a change in posture, a sudden laugh or cough, or by stimulation from the sound or feel of water. The amount of urine lost may vary from a few drops to the entire bladder contents. The urine loss begins several seconds after the triggering event and usually continues beyond the trigger, as long as the detrusor contraction persists.

A variety of nonpharmacologic approaches are available to help control urge incontinence.[3] When these measures are inadequate, anticholinergic and bladder-relaxant medications have proved useful. Anticholinergic medications inhibit detrusor contraction and may produce increased bladder capacity.[3] Propantheline (Pro-Banthine) has been widely used, although it may produce unacceptable side effects such as dry mouth and eyes, constipation and confusion. Imipramine, already mentioned for stress incontinence, has anticholinergic effects that reduce involuntary detrusor contractions, but it must be used with caution because of side effets.[12]

Bladder relaxants act directly on the bladder muscle to inhibit involuntary contractions in a manner distinct from an anticholinergic effect. Oxybutynin (Ditropan), flavoxate (Urispas) and dicyclomine (Bentyl) have proved effective in decreasing bladder contractility with relatively few anticholinergic side effects.[12]

Calcium antagonists appear to offer a direct means of preventing smooth muscle contraction of the bladder wall, but no clear evidence is found in the literature.[9] This potential effect may be a factor to consider when choosing a drug for the treatment of hypertension or heart disease.

Estrogen replacement therapy appears to have a greater effect on urge incontinence, urgency, nocturia and frequency than on stress incontinence.[3] Estrogen may be given in oral (Premarin), transdermal (Estraderm) or intravaginal (Estrace, Premarin) forms. There appears to be no particular advantage to one form over the others in relation to the effects on the bladder. The relative risks and benefits of estrogen replacement therapy must be considered for each patient. Concomitant use of a progesterone medication must be considered in patients with an intact uterus.[13]

Table 2 lists drugs and dosages recommended for the treatment of incontinence. As With any medication use in elderly patients, it is important to begin at a low dosage and increase the dosage slowly, being mindful of adverse side effects (Table 3).

COPYRIGHT 1992 American Academy of Family Physicians
COPYRIGHT 2004 Gale Group