Clinical meaning
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 endothelial damage and interstitial edema; after 24-48 hours, smooth muscle necrosis, thrombosis, and irreversible corporal fibrosis develop, leading to permanent erectile dysfunction. This time-dependent progression makes ischemic priapism a urological emergency. The most common cause is sickle cell disease: deoxygenated hemoglobin S polymerizes within erythrocytes, causing sickling, which obstructs the narrow corporal sinusoidal spaces and impedes venous drainage. Other causes include phosphodiesterase-5 inhibitor use (excessive cGMP accumulation preventing detumescence), intracavernosal injection therapy (alprostadil), and medications with alpha-adrenergic blocking properties (trazodone, antipsychotics — preventing the sympathetic detumescence mechanism). Nonischemic priapism results from unregulated arterial inflow, typically from a traumatic cavernosal artery-sinusoidal fistula created by perineal or penile trauma (straddle injury). Because arterial blood continuously perfuses the corpora, the blood is well-oxygenated (corporal blood gas shows arterial values: pO2 >90 mmHg, normal pH), the erection is typically partial and non-painful, and there is no ischemic urgency — the tissue is not at risk for necrosis. Penile Doppler ultrasound confirms the diagnosis: ischemic priapism shows absent or minimal cavernosal artery flow, while nonischemic priapism demonstrates high-velocity turbulent flow at the fistula site. Treatment of ischemic priapism follows a stepwise approach: corporal aspiration of stagnant blood (using a large-bore needle through the glans or lateral corpus), followed by intracavernosal injection of a sympathomimetic alpha-1 agonist (phenylephrine 100-500 mcg, diluted, every 3-5 minutes) to constrict cavernosal smooth muscle and restore venous outflow. If phenylephrine fails, surgical shunting creates a communication between the corpus cavernosum and the corpus spongiosum (distal shunt: Winter, Al-Ghorab) or the saphenous vein (proximal shunt) to bypass the veno-occlusive obstruction.