Each week we will aim to bring out a concise email that provides 4-5 key pieces of information addressing a specific issue in clinical therapeutics.
This week: Medication-related urinary retention
Urinary retention is defined as the inability to empty the bladder completely. The condition can be chronic or acute. Risk factors for acute urinary retention include increasing age, male gender, conditions such as Benign Prostatic Hypertrophy (BPH), prostate cancer, diabetes mellitus & constipation, surgery or the use of certain medications. As much as 10% cases of acute urinary retention may relate to medication use.
- Many drug classes have anticholinergic properties. Anticholinergics block the parasympathetic pathway, resulting in reduced contractions of the detrusor muscle of the bladder. Anticholinergic drugs include but are not limited to antihistamines, antidepressants (in particular tricyclic antidepressants), antipsychotics, benztropine, oxybutynin, hyoscine butylbromide, tiotropium and ipratropium.
- Opioids can cause urinary retention by a number of mechanisms. Inhibition of the parasympathetic nerves of the bladder decreases the sensation of bladder fullness and increased tone of the sphincter increases outflow resistance. Confusion and constipation may also contribute to urinary retention.
- Calcium channel blockers such as diltiazem and verapamil reduce bladder contractions by inhibiting calcium influx in the smooth muscle.SNRIs and reboxetine have been associated with urinary retention. Both serotonin and noradrenaline are involved in control of micturition. The mechanism by which urinary retention is caused is likely to be central and peripheral activation of adrenoreceptors and 5-HT2 receptors.
- Besides tricyclic antidepressants, other antidepressants including SSRIs, SNRIs, and reboxetine have been associated with urinary retention. Both serotonin and noradrenaline are involved in control of micturition. The mechanism by which urinary retention is caused is likely to be central and peripheral activation of adrenoreceptors and 5-HT2 receptors.
Please consider these issues when preparing or interpreting RMMR reports or education sessions. Contributions of content or suggested topics are welcome and should be sent directly to firstname.lastname@example.org.