Source:Disorders of bladder emptying
Drugs can impair bladder emptying by a variety of mechanisms. Agents which antagonize or block cholinergic receptors in the bladder body can result in decreased contractility. Although this is a common and desirable direct effect of many medications used for the treatment of overactive bladder, such as tolterodine and oxybutinin, these medications may also cause new-onset, unwanted voiding dysfunction, impaired bladder emptying, and, in some instances, urinary retention. Other anticholinergic medications, such as dicyclomine, hyoscyamine, and atropine, may be used in the treatment of GI conditions such as irritable bowel syndrome, with unwanted side effects on the lower urinary tract as discussed earlier. In fact, oxybutynin was primarily used for the treatment of gastrointestinal hypermotility disorders for years before its application in the treatment of overactive bladder [5] . Other agents with significant anticholinergic properties that can result in voiding dysfunction include those that are used for symptomatic relief of upper respiratory illnesses, such as antihistamines (diphenhydramine, hydoxyzine, meclizine), a number of antipsychotics especially in the phenothiazine class (chlorpromazine, thioridazine, fluphenazine), and tricyclic antidepressants (amitriptyline, nortriptyline) [6] [7] [8] . Scopolamine, an agent for the treatment of motion sickness can also result in retention at the bladder level by a potent anticholinergic effect. Centrally acting muscarinic receptor antagonists, such as benztropine and trihexypohenidyl, gain access to the CNS and are used to treat Parkinson's disease and the extrapyramidal side effects of antipsychotics. Their effects on the bladder are similar to those of other anticholinergics.
Stimulation or activation of á-adrenergic receptors at the bladder neck may precipitate voiding dysfunction. These agents may increase effective outlet resistance that can impair bladder emptying. This results in the clinical appearance of an elevated postvoid residual urine or even frank urinary retention. These effects are probably most commonly seen in patients with pre-existing detrusor dysfunction (impaired contractility) or some degree of anatomic or functional bladder outlet obstruction. Alpha agonists are commonly found as ingredients in medications that are used to treat symptomatic upper respiratory illness (pseudoephedrine), and as appetite suppressants. Amphetamines (dextroamphetamine), used to treat a variety of psychiatric and other medical illnesses may have direct effects on the alpha receptors at the bladder neck level, and may promote urinary retention and voiding dysfunction by increasing outlet resistance as well.
Opioids and narcotic analgesics can be associated with voiding dysfunction and urinary retention. Acting at the brain and spinal cord levels, opioids may inhibit or suppress the micturition reflex and increase the tone of the external sphincter. This may be a common, but incompletely, recognized source of postoperative voiding dysfunction and transient urinary retention.
Urologic Clinics of North America
Volume 30 "¢ Number 1 "¢ February 2003
Urologic complications of nonurologic medications
Arthur Thomas, MD
Christopher Woodard, MD
Eric S. Rovner, MD *
Alan J. Wein, MD