Priapism can be defined as a painful prolonged penile erection in the absence of sexual stimulation. Two subtypes of priapism have been described based on their underlying cause. Ischemic priapism is characterized by a veno-occlusive state in which inadequate venous outflow creates an acidotic hypoxic environment leading to a painful prolonged erection. This more common type of priapism has become a well-recognized clinical entity because of the widespread use of intracavernous agents for erections. Ischemic priapism is a urologic emergency. The second subtype, arterial or high-flow priapism, is much less common. Injury to a cavernosal artery, usually after perineal or direct penile trauma, results in uncontrolled high arterial inflow within the corpora cavernosa. Patients with arterial priapism seek medical attention later than those with ischemic priapism. This is due to the fact that non-ischemic erections cause less pain and discomfort.

Ischemic priapism should be considered a serious medical condition as it can lead to permanent penile fibrosis and erectile dysfunction. When effectively treated early (within 6-12 hours) little risk of permanent injury exists. Tissue injury is visible after 12 hours of ischemia, characterized as interstitial edema. Within 24 hours, there is destruction of the sinusoidal endothelium and adherence. All men using vasoactive drugs for penile self-injection should be instructed to seek medical attention if their erection persists longer than 3-4 hours. Other causes of ischemic priapism include sickle cell anemia, medication induced, and pelvic malignancy.

The agent of choice for the treatment of ischemic priapism is Neosynephrine (phenylephrine) used in a concentration of 500ug/cc. 100 ug (or 0.2 cc) of phenylephrine is injected into the cavernous body each 2 minutes until the penis is flaccid. At this concentration, little impact on the systemic BP is seen in most men. Detumescence is often seen by 2-5 minutes and will first be noted with return of the arterial pulsations of the penis. In some cases, aspiration of blood of the fully rigid penis may be needed to attain detumescence. Once the rigidity is decreased a more effective delivery of the alpha-agonist is possible. However it is important to understand that even in most cases when a fully rigid erection is present simply injecting the neosynephrine will succeed in reversing the patient. Cases refractory to conservative management may require surgical shunting procedures to return the penis to a flaccid state. One exception is with sickle cell anemia. Priapism in these patients should be initially treated with oxygenation, hydration, analgesia and transfusions to reduce the concentration of hemoglobin S below 30%.

Non-ischemic priapism is not considered a medical emergency. Treatment is tailored to the circumstance that induced this condition. In some cases conservative therapy will allow the injured cavernous artery to seal off and restore normal blood flow to the corporal bodies. In other more established cases embolization or even open repair of the cavernous vessels might be needed. Use of super selective arteriography allow for the exact determination of the site of injury and treatment through embolization. There remains a low risk of impotence associated with high flow priapism. This must be considered in treating these individuals.

The long-term sequela of priapism includes penile scarring and fibrosis, penile deformity and ED. Strategies to avoid these complications include education of the patient on an injection program and rapid treatment of priapism as it occurs.