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Acute urinary retention is a common painful urologic emergency characterized by an inability to pass urine, with lower abdominal distention or pain. Most patients with urinary retention are elderly men with benign prostatic hyperplasia.1,2 The incidence and risk of this etiology increase with age, with 1 in 10 men in their 70s having an episode of acute urinary retention and 1 in 3 men having one in their 80s. There is a 20% recurrence rate within 6 months of an episode of urinary retention due to benign prostatic hyperplasia.2 Acute urinary retention in women is relatively uncommon, accounting for only 3 out of 100,000 cases of acute urinary retention each year, with the most common causes being bladder masses, gynecologic surgery, and pelvic prolapse.3


The voiding process, or micturition, involves the complex integration and coordination of high cortical neurologic (sympathetic, parasympathetic, and somatic) and muscular (detrusor and sphincter smooth muscle) functions. As the bladder fills, sensory input is transmitted to cortical centers in the brain, which responds by coordinating voluntary urination. The contraction of bladder detrusor muscle (by cholinergic muscarinic receptors) and relaxation of both the internal sphincter of the bladder neck and the urethral sphincter (through α-adrenergic inhibition) are both necessary for successful voiding.4 Continent urine storage in the bladder requires both relaxation of the detrusor muscle (through β-adrenergic stimulation and parasympathetic inhibition) and contraction of the bladder neck and internal sphincter (through α-adrenergic stimulation).

Urinary retention is the inability to void voluntarily despite a distended bladder resulting from dysfunction of the detrusor muscle and/or coordination of the bladder outlet. If extrinsic compression is the cause of the outlet obstruction (e.g., benign prostatic hyperplasia), the patient may report a history of a weakened urine stream despite forceful and prolonged detrusor contraction. In chronic decompensation of urination, diminished detrusor muscle contractility is more pronounced, with a large amount of residual urine volume, compared to acute decompensation. After prolonged complete bladder outlet obstruction, postobstructive acute kidney injury follows.5 Upon relief of prolonged obstruction, postobstructive diuresis occurs in 0.5% to 50% of acute urinary retention cases, depending on duration and comorbidities.6 This form of diuresis represents the normal physiologic response to excess volume and solutes accumulated during the period of prolonged obstruction.5 Absence of diuresis in patients with significant elevation in serum creatinine predicts poor kidney recovery.7


The most common presentation is an elderly male with inability to void for several hours and lower abdominal distention or pain, secondary to benign prostatic hyperplasia. Consider urinary retention in patients complaining of lower abdominal pain, even if they do not offer urinary complaints. Also consider urinary retention as an underlying risk factor when finding a urinary tract infection.

The causes of urinary retention (Tables 92-1, 92-2...

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