Case Presentation: 37-year-old Hispanic male presented with an episode of painful priapism with history of a car accident in 2005 which resulted in spinal injury. Since then, he has had more than 20 recurrent episodes of priapism. He reported having multiple phenylephrine injections, aspirations and two shunt procedures performed in the past without improvement in symptoms. Exam revealed an erect but not completely rigid penis. Venous Blood Gas from the corpus cavernosum showed pH of 7.37 indicating high flow (non-ischemic) priapism. He received 2 doses of phenylephrine, 1 dose of terbutaline and penile aspiration with little effect on pain and erection. He was admitted to the medicine service for further management. Urology team recommended consultation by Interventional Radiology for angiography and/or embolization. He underwent pelvic aortogram, bilateral internal iliac arteriogram, and left external pudendal arteriogram. A left internal pudendal arterio-cavernosal fistula was identified and subsequently embolized. Patient reported improvement in pain and resolution in priapism. He was seen in Urology clinic for follow up where he reported having more episodes of priapism since the embolization so consideration was given to repeating the procedure. Further investigations including work up for sickle cell anemia and spinal imaging were recommended. Unfortunately, he was lost to further follow up.

Discussion: Priapism, a painful condition in which the penis is erect for a period of more than 4 hours that is unrelated to sexual stimulation. It is categorized as ischemic (low flow) priapism and non-ischemic (high flow) priapism. Low-flow priapism needs emergent attention as ischemia can set in from lack of oxygenated blood flow. It is usually caused by blood disorders like sickle cell anemia and leukemia; and medications like anti-depressants, alpha blockers, antipsychotics, testosterone etc. Less commonly seen is non-ischemic priapism which is usually painless with a tumescent non-rigid penis as oxygenated blood flow is maintained. A cavernous blood gas sampling is necessary to distinguish the two types of priapism. pH below 7.25 indicates ischemic condition whereas pH above 7.25 and oxygen level above 60 mmHg indicates non-ischemic priapism. Non ischemic priapism is typically caused by congenital malformation or formation of arteriovenous malformation from genital trauma. In most males, the penis is supplied by the penile artery, a branch off the internal pudendal artery which arises from the anterior internal iliac artery. When arteriovenous malformations develop in these vessels, uncontrolled arterial overflow can result in recurrent high- flow priapism as described in our patient. These conditions are extremely rare. Selective embolization and coiling have shown to be favorable treatment modalities with high success rates.

Conclusions: This case highlights the importance of recognition of posttraumatic high flow priapism and unveils the role of selective internal pudendal artery angiography and embolization as a diagnostic and therapeutic means of management.