Penile erection is established by relaxation of smooth muscle of cavernosal arteries and tissue. This leads to increased arterial inflow and decreased venous outflow (figure 3). Priapism can occur at any age and has a wide variety of causes. It mostly involves the corpora cavernosa, although some cases have been reported with the involvement of the corpus spongiosum and the glans penis2.
Ischemic priapism, also known as low-flow or veno-occlusive priapism, is the most common type of priapism. The prolonged erection is caused by impaired relaxation and paralysis of cavernosal smooth muscle. This in turn results in a compartment syndrome in which hypoxia and acidosis may lead to structural damage of erectile tissue. In adults, the administration of medication is usually the cause of low-flow priapism2. Quick management is necessary to decrease the risk of irreversible damage.
Non-ischemic priapism, also known as high-flow or arterial priapism is less common and is usually the result of a fistula between the cavernosal artery and corpus cavernosum. Trauma is the most common cause of high-flow priapism in adults. The trauma will result in a laceration of the perforating arteries from the penile artery. On clinical presentation, the erection is incomplete and not painful, in contrast to the low-flow priapism. Due to the inflow of oxygenated blood in the corpus carvernosum, the cavernosal blood gas sample has a high p02 (> 90 mmHg) and pH (>7.4) levels2. Spontaneous resolution of priapism is reported in many cases3 and observation or compression therapy is therefore the initial treatment. In case of persistent priapism, the treatment is selective trans-arterial embolisation of the arterio-lacunar fistula. Different embolic agents are used, all with a high rate of technical and clinical success. The choice of embolic agent should be based on operator experience and fistula characteriscs2. In this case, Spongostan, a temporary embolic agent was used with both technical and clinical success. While embolizing the fistula, caution must be given of potential communication of the contralateral internal pudendal artery contributing to persistent filling of the fistula.