Acute urinary retention is a common painful urologic emergency characterized by a sudden 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 increase with age. There is a 20% recurrence within 6 months after an episode of urinary retention.² Few data are available for women. In men with spontaneous urinary retention, the mortality rate at 1 year increases from 4.1% in patients age 45 to 54 years to 32.8% in those age 85 years and older.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 sensory impulse of bladder distention transmits to cortical centers, these areas of the brain smoothly coordinate voluntary urination. 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). The contraction of bladder detrusor muscle (by cholinergic muscarinic receptors) and relaxation of both the internal sphincter of bladder neck and the urethral sphincter (through α-adrenergic inhibition) contribute to smooth urination.⁶

Any causes that interfere with the neurologic control of the voiding process can result in voiding dysfunction. Urinary retention is the inability to void voluntarily despite a distended bladder and results from the dysfunction of the detrusor muscle and its coordination with the control of the bladder outlet. As bladder outlet obstruction progressively increases, the urine stream decreases in strength and size 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.

The causes of urinary retention (Tables 92-1, 92-2 and 92-3) are categorized into several domains: obstructive, neurogenic, traumatic, infectious, operative, psychogenic, childhood, extraurinary, and pharmacologic.^4,5,6,7 A detailed history of the present illness and physical examination, especially the neurologic examination, supported by imaging and urodynamic studies, reveal the cause in the majority of patients.

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.

Collect past medical history to look for a history of prostatism, prostate or urinary bladder cancer, bladder calculi, indwelling urethral catheter or injury to urethra, prostate surgery, or pelvic radiation therapy. Ask about history of urinary urgency, frequency, or hesitancy; decreased force and caliber of stream; terminal dribbling; nocturia; and incontinence (typically due to overflow phenomena). Gross hematuria may indicate infection, bladder calculi, or urinary tract neoplasm. A patient with urethral stricture may have a history of Foley catheter insertion, cystoscopy, trauma, or previous radiation therapy or infection. Collect any history of new medications, including common cold preparations, anticholinergics (including bronchodilators), sympathomimetic agents, and psychogenic and other potential agents (Table 92-3). Obtain a detailed neurologic history, looking for a causative lesion from high cortical function down to peripheral nerves that determine end-organ function. Identify possible spinal cord injury by determining recent activities including any remote trauma.