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Clinical History: 35-year-old man status post failed renal transplant for end-stage renal disease and acute onset of painless priapism following atraumatic case of sexual intercourse approximately two days prior to presentation.
Findings: (Fig. 1) Cavernosal arteries with high resistance flow bilaterally and peak systolic velocity of 0.9 meters per second on right (Fig. 1a) and 0.82 meters per second on left. (Fig. 1b) Diastolic flow is reversed.
(Fig. 2) Selective arteriographic images of left internal pudendal artery (closed arrow) demonstrate both patency and normal caliber of common penile artery (arrowhead), dorsal penile artery (open arrow) and both cavernosal arteries (Fig.2a) (curved arrows). Post embolization images demonstrate occlusion of cavernosal branches filling from left internal pudendal artery. The dorsal penile artery remains intact (Fig. 2b).
(Fig. 3a and b) Penile ultrasound obtained approximately 24 hours following the embolization procedure demonstrates significant interim decrease in systolic velocities in the cavernosal arteries. The systolic velocities now measure approximately 0.2 to 0.24 meters per second. There is forward flow in diastole.
Diagnosis: Arterial (high flow) priapism.
Discussion: Priapism is an uncommon condition of prolonged, persistent and occasionally painful penile erection. It is primary or idiopathic in 60% of cases. 20% of secondary priapism are hematologic in origin (Sickle cell disease, leukemia, heparin therapy); Other causes are neurogenic, traumatic, and infectious. Idiopathic causes and Sickle cell disease account for approximately 80% of all cases. Nearly three quarters of adult cases are idiopathic, while two-thirds of pediatric cases are due to Sickle cell disease.
On the basis of etiology, priapism can be broadly divided into low flow (veno-occlusive) and high flow (arterial) varieties. The former involves a physiologic or mechanical obstruction to venous drainage of the penis which causes a build-up of viscous, poorly oxygenated blood within the corpora cavernosa. The origin of priapism in these cases may be secondary to multiple areas of sludging and thrombosis. The major causes of veno-occlusive priapism are complication of Sickle cell disease, hematopoietic malignancy or a hypercoagulable state.
Arterial priapism is a physiologically distinct entity which is markedly less common than the veno-occlusive form. Arterial priapism results from unregulated inflow of arterial blood into the lacunar spaces of corpora cavernosae from a lacerated cavernous artery, bypassing regulatory function of helicine arterioles. Etiology of increased arterial inflow may be secondary to arteriovenous fistula, frank arterial laceration with extravasation or a pseudoaneurysm. Although most cases of high flow priapism are secondary to blunt or penetrating trauma to the perineum or penis, a large majority of cases, especially in adults, may be idiopathic, without history of pertinent trauma or findings of anatomic abnormalities.
It is imperative to distinguish between the two types of priapism, since effective therapy differs for each. The majority of patients with veno-occlusive forms may be treated by means of cavernosal aspiration and irrigation or with several shunt procedures, whereby the venous blood from the corpora cavernosae is diverted and drained through a variety of surgically created shunts.
Arterial priapism may be treated with arterial ligation or percutaneous embolization. Other therapeutic modalities, such as sustained perineal compression and ice packs or intracavernous administration of alpha-adrenergic agonists have proven to be less effective.
We report a case of iatrogenic high-flow priapism which was not relieved by corporal irrigation and mechanical means, as outlined above, but benefited from superselective, percutaneous embolization of a cavernosal artery. We elected to utilize gelfoam embolization material since it is absorbed over time from deposition site, thereby decreasing, at least in principle, the risk of permanent impotence which is an important unwanted side effect of penile arterial occlusion. Following embolization, the patient experienced rapid resolution of tumescence to approximately 50% of the original level. Clinical follow-up approximately 12 hours following the procedure demonstrated an essentially flaccid penis, with only minimal residual erection remaining. The patient reported satisfaction with the procedure.
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