Priapism: Ischemic Vs Nonischemic

Priapism is a persistent penile erection unrelated to sexual stimulation, classified into ischemic (low-flow, veno-occlusive) and nonischemic (high-flow, arterial) subtypes with fundamentally different pathophysiologies and clinical urgencies. Normal erection physiology involves parasympathetic stimulation (S2-S4 nerve roots via the pelvic splanchnic nerves) releasing nitric oxide from non-adrenergic, non-cholinergic nerve terminals and endothelial cells. Nitric oxide activates guanylyl cyclase, increasing cyclic GMP, which relaxes cavernosal smooth muscle and dilates helicine arteries, flooding the corpora cavernosa with arterial blood. Expansion of the sinusoids compresses the subtunical venular plexus against the rigid tunica albuginea, trapping blood within the corpora and producing rigidity — this is the corporal veno-occlusive mechanism. Detumescence normally occurs when sympathetic alpha-1 adrenergic stimulation contracts cavernosal smooth muscle, reduces arterial inflow, and reopens venous outflow channels. Ischemic priapism occurs when venous outflow obstruction persists beyond the normal erectile cycle: trapped deoxygenated blood becomes progressively acidotic and hypoxic (corporal blood gas shows pO2 <30 mmHg, pCO2 >60 mmHg, pH <7.25 — resembling venous blood gases), creating a compartment syndrome within the corpora cavernosa. After 4-6 hours, smooth muscle hypoxia and acidosis cause...