Priapism: Pathogenesis
Post-cavernosal venous occlusion
↑ nitric oxide from cavernous nerve plexus and cavernosal sinus endothelia
Impaired detumescence (erection-ending) pathways
Post-cavernosal venous drainage is mechanically obstructed e.g. sickle cell disease, dialysis etc.
Ischemic (Low-flow):
Inadequate venous function
Blood pools in corpora cavernosa
Cavernosal cell metabolism uses O2 and releases CO2 into pooled blood
Trabecular smooth muscle relaxes
Cavernosal artery smooth muscle relaxes
Lack of norepinephrine action on penile SM
Post-cavernosal venules are compressed against tunica albuginea
Trabecular smooth muscle and cavernosal artery smooth muscle do not contract
↑ pressure in corpora
↑PCO2 ↓pH
Acidosis
↓PO2
Tissue hypoxia
Tissue damage
Irreversible fibrosis leading to erectile dysfunction
Priapism
Prolonged erection lasting more than 4 hours; in absence of sexual stimulation; not relieved by ejaculation
Trauma to penis or adjacent areas
Authors:
Arsalan Ahmad
Reviewers:
Alec Mitchell
Darren Desantis*
Yan Yu*
* MD at time of publication
Cavernosal artery is damaged
Excessive, unregulated arterial blood flow into corpora cavernosa
Pain
Non-ischemic (High-flow):
Uncontrolled arterial flow
↑ volume of blood in corpora
↑ pressure in corpora
Legend:
Pathophysiology
Mechanism
Sign/Symptom/Lab Finding
Complications
Published September 22, 2019 on www.thecalgaryguide.com