Priapism pathophysiology

Ricciardi R, Jr., Bhatt GM, Cynamon J et al (1993) Delayed high flow priapism pathophysiology and management. J Urol 149 119-121... 

In broad terms, priapism may be regarded as an alteration of imbalance between arterial inflow and outflow. Burnett (2003) has recently reviewed the pathophysiology of priapism and suggested derangements in the diverse systems of regulatory control in erectile function. These dysregulatory functions include possible overactivity of the veno-occlusive mechanism, arterial inflow, or neurogenic processes that can affect inflow or outflow. Conversely, the problem may be secondary to malfunction of the normal contractile activities of cavernosal smooth muscle cells. 

A mechanism for the pathophysiology of high-flow priapism is described by Bastuba et al. (1994). Unlike a traditional arteriovenous fistula, the condition is described as an arterial-lacunar fistula where the helicine arteries are bypassed, and the blood passes directly into the lacunar spaces. The high-flow in the lacunar space creates shear stress in adjacent areas, leading to increased nitric oxide release, activation of the cGMP pathway, smooth muscle relaxation and trabecular dilatation. These authors also postulate that the delay in onset of high-flow priapism may be secondary to a delay in the complete necrosis of the arterial wall after the initial trauma or secondary to clot formation at the site of injury followed by the normal lytic pathway, which progresses in a few days. 

As described in Chapter 9, priapism is an uncommon medical condition defined as persistent tumescence or erection not associated with sexual desire or stimulation (Pautler and Brock 2001). Different pathophysiologies have been described. Low-flow or ischemic priapism is characterized by complete painful erection secondary to inadequate venous outflow leading to hypoxia, acidosis and pain (Lue et al. 1986 Pautler and Brock 2001). High-flow priapism is usually associated with penile or perineal blunt trauma and cavernosal artery tear (Pautler and Brock 2001). Patients... 

Van der Horst C, Stuebinger H, Seif C et al (2003) Priapism-etiology, pathophysiology and management. Int Braz J Urol 29 391-400... 

Shamloul R, Kamel I (2005) A broken intracavernous needle successful ultrasound-guided removal. J Sex Med 2 147-148 Witt MA, Goldstein I, Saenz de Tejada I, et al (1990) Traumatic laceration of intracavernosal arteries the pathophysiology of nonischemic, high flow, arterial priapism. J Urol 143 129-132... 

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