What is the pathophysiology of priapism?

Updated: Dec 26, 2019
  • Author: Osama Al-Omar, MD, MBA, FACS, FEBU; Chief Editor: Edward David Kim, MD, FACS  more...
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The penis has 3 corporeal bodies: 2 corpora cavernosa and 1 corpus spongiosum. Erection is the result of smooth-muscle relaxation and increased arterial flow into the corpora cavernosa, causing engorgement and rigidity (see image below). In priapism, the corpus spongiosum and glans penis are typically not engorged.

Priapism. Corporeal relaxation causes external pre Priapism. Corporeal relaxation causes external pressure on the emissary veins exiting the tunica albuginea, trapping blood in the penis and causing erection.

Engorgement of the corpora cavernosa compresses the venous outflow tracts (ie, subtunical venules), trapping blood within the corpora cavernosa. The major neurotransmitter that controls erection is nitric oxide, which is secreted by the endothelium that lines the corpora cavernosa (see image below). These events occur in both normal and pathologic erections.

Priapism. Sexual stimulation causes the release of Priapism. Sexual stimulation causes the release of nitric oxide (NO) via stimulation of nonadrenergic noncholinergic neurons. NO-activated intracellular guanylate cyclase, converting guanosine triphosphate (GTP) to cyclic guanosine monophosphate (cGMP), causes relaxation of cavernosal arteries and increased penile blood flow, resulting in erection.

Pathophysiologically, priapism can be of either a low-flow (ischemic) or a high-flow (nonischemic) type. Low-flow priapism, which is by far the most common type, results from failure of venous outflow, whereas high-flow priapism results from uncontrolled arterial inflow. Clinically, differentiation of low-flow from high-flow priapism is critical, because treatment for each is different.

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