T. Gregory Walker, MD • Philip W. Grant, MD • Irwin Goldstein, MD • Robert J. Krane, MD • Alan J. Greenfield, MD
"High-Flow" Priapism: Treatment with Superselective Transcatheter Embolizationl Hemodynamically, most cases of priapism occur as a result of venous outflow obstruction producing engorgement of the corpora cavernosa. In a small number of patients, however, the cause is uncontrolled arterial inflow, often from direct arterial trauma. The authors report two cases of arterial or "high-flow" priapism that were successfully treated with selective transcatheter embolization with autologous clot. Index terms: Arteries, injuries, 969.412 • Arteries, therapeutic blockade, 969.1299 • Arteries, pudendal, 969.1222 • Penis, 847.482 Radiology 1990; 174:1053-1054
is defined as a prolonged and often painful erection, unrelated to sexual stimulation. Although at least 50% of cases are considered idiopathic, trauma, numerous chronic diseases, and drugs have all been identified as causes of this disorder (1). Hemodynamically, most cases of priapism occur as a result of engorgement of the corpora cavernosa from intrinsic or extrinsic venous outflow obstruction, termed "veno-occlusive" priapism (2). However, in a small number of patients the cause is related to uncontrolled arterial inflow, usually due to direct trauma and laceration of one of the cavernosal arteries. This form has been termed "high-flow" or arterial priapism (3). We report two cases of high-flow priapism that were caused by direct penile trauma. In both patients, an arterial injury was identified with angiography, and the priapism was successfully treated with superselective transcatheter occlusion of the bleeding artery. DRIAPISM
CASE REPORTS
1 From the Departments of Radiology (T.G.W., P.W.G., A.J.G.) and Urology (I.G., R.J.K.), Boston University Medical Center, Boston University School of Medicine, 88 E Newton St, Boston, MA 02118. Received March 1, 1989; revision requested March 25; revision received April 4; accepted April 5. Address reprint requests to T.G.W. RSNA, 1990
A 50-year-old man with a history of impotence for several years had been placed on a self-administered regimen of intracorporal papaverine /phentolamine injections. He subsequently presented with a 2-day history of painless priapism that occurred after an unusually painful injection. On physical examination, the corporal bodies were turgid and not tender, while the glans and spongiosum were soft and compressible. The priapism was initially treated with corporal aspiration, repeated intracorporal injection of phenylephrine and epinephrine, and two separate corporal-glandular shunts, with only temporary, partial detumescence. Selective internal pudendal arteriography performed 6 days after priapism helped identify extravasation of contrast material arising from the deep penile artery (Fig la). A decision was made to occlude the feeding artery with transcatheter embolization.
From a left femoral artery approach, a catheter was advanced over the aortic bifurcation, and the tip was positioned in the right internal pudendal artery. A 3-F Tracker catheter (Target Therapeutics, Los Angeles) was advanced coaxially into the common penile artery, proximal to the feeding vessel (Fig lb), and 2 cm 3 of autologous clot was introduced. This resulted in occlusion of the common penile artery and its distal branches (Fig lc). Within minutes of embolization, there was partial detumescence, and the priapism had resolved at the time of discharge 24 hours later. The patient has been followed up for 4 months, and there has been no recurrence. Additionally, the patient now reports restoration of the same quality of premorbid erection that was achieved with the intracorporal injection regimen. We have encountered another patient who presented with high-flow priapism after blunt perineal trauma. The condition in this 37-year-old man had failed to respond to corporal aspiration, phenylephrine injection, and irrigation. Partial, temporary detumescence was achieved with two corporal-glandular shunts. He subsequently underwent selective pudendal arteriography, which demonstrated extravasation into the corporal crus from a lacerated proximal cavernosal arterial branch (Fig 2a). He was also successfully treated on the 6th day of the priapism with autologous clot embolization by means of the same transcatheter technique (Fig 2b). Normal premorbid erectile function was present in this patient at 14 months, with no recurrence of the priapism.
DISCUSSION Considerable difficulty has been encountered in the effective treatment of priapism, partly because of an incomplete understanding of the pathophysiologic features of the condition. Various treatments have been employed, including aspiration, ice packs, heparin, pressure dressings, spinal anesthesia, arterial ligation, and surgical shunting. The success rates of these methods have varied, and complications have included im1053
c b. Figure 1. (a) Selective internal pudendal arteriogram shows intracorporal contrast material extravasation (arrows) arising from deep penile artery. (b) Catheter tip is selectively positioned in distal common penile artery immediately before embolization. (c) After selective embolization with autologous clot, occlusion of the distal common penile artery (arrow) and branches is seen. Extravasation is no longer present. a.
paired function, impotence, and penile fibrosis and necrosis (2,4,5). With improved understanding of erectile physiology, it is more frequently possible to identify the cause of an individual case of priapism and thus tailor the treatment appropriately. In the cases we report, a high-flow state was suggested by the clinical findings, the aspiration of bright red blood from the corpora, and the failure of adrenergic agonist administration and corporal-glandular shunting. Angiograms demonstrated intrapenile contrast material extravasation arising from a lacerated cavernosal artery. Thus, the cause was confirmed as one in which arterial inflow—unrestrained by the normal regulatory mechanisms—directly enters the lacunar spaces of the corpora and results in a sustained erection. When increased arterial blood flow is thought to be a component of priapism, treatment has been aimed at reducing or normalizing the arterial blood supply to the penis (3). In the past, this treatment was accomplished with ligation of one or both internal pudendal arteries but was associated with impotence and gangrene (3,6). Effective treatment for high-flow priapism should ideally abolish the abnormal, uncontrolled arterial inflow while erectile function is preserved. Therapy with transcatheter embolization has previously been used successfully in two cases of posttraumatic priapism thought to be due to increased arterial inflow (6,7), as well as in several cases of idiopathic priapism (8). In all cases, the internal pudendal artery was embolized with autologous clot, a temporary occlusive agent, and the priapism was re1054 • Radiology
.
a.
b. Figure 2. (a) Selective arteriogram of an accessory pudendal artery shows contrast material extravasation from two arterial branches at base of penis (arrows). No arterial contribution to the penile vasculature from the internal pudendal artery is seen. (b) After selective embolization with 0.5 cm 3 of autologous clot, active extravasation is no longer present. Collection of contrast material (straight arrows) at base of penis is the residual from injections before embolization. The common penile (curved arrow) and distal penile arteries are intact. Priapism resolved almost immediately.
lieved. The use of autologous clot permits rapid restoration of blood flow after clot lysis, minimizes complications, and potentially allows for recovery of normal sexual function (8). More selective catheter placement and subsequent vessel occlusion than has been previously reported was possible in each of our patients. This was in part due to the availability of newer catheter systems but was also possible because a site of extravasation was identified in each patient. In both cases, the priapism resolved, and premorbid erectile function subsequently returned. In patients with posttraumatic priapism, a high-flow arterial cause should be considered and appropriately investigated. Prompt diagnosis may prevent unnecessary shunt surgery and permit treatment with selective embolization therapy. n
References 1. LaRocque MA, Cosgrove MD. Pri4ism: a review of 46 cases. J Urol 1974; 112:770773. 2. Hinman F Jr. Priapism: reasons for failure of therapy. J Urol 1960; 83:420-428. 3. Puppo P, Belgrano E, Germinale F, Bottino P, Guiliani L. Angiographic treatment of high-flow priapism. Eur Urol 1985; 11:397400. 4. Grace DA, Winter CC. Priapism: an appraisal of management of 23 patients. J Urol 1968; 99:301-310. 5. Cosgrove MD, LaRocque MA. Shunt surgery for priapism: review of results. Urology 1974; 4:1-5. 6. Wear JB Jr, Crummy AB, Munson BO. A new approach to the treatment of priapism. J Urol 1977; 117:252-254. 7. Crummy AB, Ishizuka H, Masden PO. Post-traumatic priapism: successful treatment with autologous clot embolization. AJR 1979; 133:329-330. 8. Belgrano E, Puppo P, Quattrini S, Trombetta C, Bottino P, Giuliani L. Percutaneous temporary embolization of the internal pudendal arteries in idiopathic priapism: two additional cases. J Urol 1984; 131:756758.
March 1990 • Part 2
"High-Flow" Priapism: Treatment with Superselective Transcatheter Embolizationl Hemodynamically, most cases of priapism occur as a result of venous outflow obstruction producing engorgement of the corpora cavernosa. In a small number of patients, however, the cause is uncontrolled arterial inflow, often from direct arterial trauma. The authors report two cases of arterial or "high-flow" priapism that were successfully treated with selective transcatheter embolization with autologous clot. Index terms: Arteries, injuries, 969.412 • Arteries, therapeutic blockade, 969.1299 • Arteries, pudendal, 969.1222 • Penis, 847.482 Radiology 1990; 174:1053-1054
is defined as a prolonged and often painful erection, unrelated to sexual stimulation. Although at least 50% of cases are considered idiopathic, trauma, numerous chronic diseases, and drugs have all been identified as causes of this disorder (1). Hemodynamically, most cases of priapism occur as a result of engorgement of the corpora cavernosa from intrinsic or extrinsic venous outflow obstruction, termed "veno-occlusive" priapism (2). However, in a small number of patients the cause is related to uncontrolled arterial inflow, usually due to direct trauma and laceration of one of the cavernosal arteries. This form has been termed "high-flow" or arterial priapism (3). We report two cases of high-flow priapism that were caused by direct penile trauma. In both patients, an arterial injury was identified with angiography, and the priapism was successfully treated with superselective transcatheter occlusion of the bleeding artery. DRIAPISM
CASE REPORTS
1 From the Departments of Radiology (T.G.W., P.W.G., A.J.G.) and Urology (I.G., R.J.K.), Boston University Medical Center, Boston University School of Medicine, 88 E Newton St, Boston, MA 02118. Received March 1, 1989; revision requested March 25; revision received April 4; accepted April 5. Address reprint requests to T.G.W. RSNA, 1990
A 50-year-old man with a history of impotence for several years had been placed on a self-administered regimen of intracorporal papaverine /phentolamine injections. He subsequently presented with a 2-day history of painless priapism that occurred after an unusually painful injection. On physical examination, the corporal bodies were turgid and not tender, while the glans and spongiosum were soft and compressible. The priapism was initially treated with corporal aspiration, repeated intracorporal injection of phenylephrine and epinephrine, and two separate corporal-glandular shunts, with only temporary, partial detumescence. Selective internal pudendal arteriography performed 6 days after priapism helped identify extravasation of contrast material arising from the deep penile artery (Fig la). A decision was made to occlude the feeding artery with transcatheter embolization.
From a left femoral artery approach, a catheter was advanced over the aortic bifurcation, and the tip was positioned in the right internal pudendal artery. A 3-F Tracker catheter (Target Therapeutics, Los Angeles) was advanced coaxially into the common penile artery, proximal to the feeding vessel (Fig lb), and 2 cm 3 of autologous clot was introduced. This resulted in occlusion of the common penile artery and its distal branches (Fig lc). Within minutes of embolization, there was partial detumescence, and the priapism had resolved at the time of discharge 24 hours later. The patient has been followed up for 4 months, and there has been no recurrence. Additionally, the patient now reports restoration of the same quality of premorbid erection that was achieved with the intracorporal injection regimen. We have encountered another patient who presented with high-flow priapism after blunt perineal trauma. The condition in this 37-year-old man had failed to respond to corporal aspiration, phenylephrine injection, and irrigation. Partial, temporary detumescence was achieved with two corporal-glandular shunts. He subsequently underwent selective pudendal arteriography, which demonstrated extravasation into the corporal crus from a lacerated proximal cavernosal arterial branch (Fig 2a). He was also successfully treated on the 6th day of the priapism with autologous clot embolization by means of the same transcatheter technique (Fig 2b). Normal premorbid erectile function was present in this patient at 14 months, with no recurrence of the priapism.
DISCUSSION Considerable difficulty has been encountered in the effective treatment of priapism, partly because of an incomplete understanding of the pathophysiologic features of the condition. Various treatments have been employed, including aspiration, ice packs, heparin, pressure dressings, spinal anesthesia, arterial ligation, and surgical shunting. The success rates of these methods have varied, and complications have included im1053
c b. Figure 1. (a) Selective internal pudendal arteriogram shows intracorporal contrast material extravasation (arrows) arising from deep penile artery. (b) Catheter tip is selectively positioned in distal common penile artery immediately before embolization. (c) After selective embolization with autologous clot, occlusion of the distal common penile artery (arrow) and branches is seen. Extravasation is no longer present. a.
paired function, impotence, and penile fibrosis and necrosis (2,4,5). With improved understanding of erectile physiology, it is more frequently possible to identify the cause of an individual case of priapism and thus tailor the treatment appropriately. In the cases we report, a high-flow state was suggested by the clinical findings, the aspiration of bright red blood from the corpora, and the failure of adrenergic agonist administration and corporal-glandular shunting. Angiograms demonstrated intrapenile contrast material extravasation arising from a lacerated cavernosal artery. Thus, the cause was confirmed as one in which arterial inflow—unrestrained by the normal regulatory mechanisms—directly enters the lacunar spaces of the corpora and results in a sustained erection. When increased arterial blood flow is thought to be a component of priapism, treatment has been aimed at reducing or normalizing the arterial blood supply to the penis (3). In the past, this treatment was accomplished with ligation of one or both internal pudendal arteries but was associated with impotence and gangrene (3,6). Effective treatment for high-flow priapism should ideally abolish the abnormal, uncontrolled arterial inflow while erectile function is preserved. Therapy with transcatheter embolization has previously been used successfully in two cases of posttraumatic priapism thought to be due to increased arterial inflow (6,7), as well as in several cases of idiopathic priapism (8). In all cases, the internal pudendal artery was embolized with autologous clot, a temporary occlusive agent, and the priapism was re1054 • Radiology
.
a.
b. Figure 2. (a) Selective arteriogram of an accessory pudendal artery shows contrast material extravasation from two arterial branches at base of penis (arrows). No arterial contribution to the penile vasculature from the internal pudendal artery is seen. (b) After selective embolization with 0.5 cm 3 of autologous clot, active extravasation is no longer present. Collection of contrast material (straight arrows) at base of penis is the residual from injections before embolization. The common penile (curved arrow) and distal penile arteries are intact. Priapism resolved almost immediately.
lieved. The use of autologous clot permits rapid restoration of blood flow after clot lysis, minimizes complications, and potentially allows for recovery of normal sexual function (8). More selective catheter placement and subsequent vessel occlusion than has been previously reported was possible in each of our patients. This was in part due to the availability of newer catheter systems but was also possible because a site of extravasation was identified in each patient. In both cases, the priapism resolved, and premorbid erectile function subsequently returned. In patients with posttraumatic priapism, a high-flow arterial cause should be considered and appropriately investigated. Prompt diagnosis may prevent unnecessary shunt surgery and permit treatment with selective embolization therapy. n
References 1. LaRocque MA, Cosgrove MD. Pri4ism: a review of 46 cases. J Urol 1974; 112:770773. 2. Hinman F Jr. Priapism: reasons for failure of therapy. J Urol 1960; 83:420-428. 3. Puppo P, Belgrano E, Germinale F, Bottino P, Guiliani L. Angiographic treatment of high-flow priapism. Eur Urol 1985; 11:397400. 4. Grace DA, Winter CC. Priapism: an appraisal of management of 23 patients. J Urol 1968; 99:301-310. 5. Cosgrove MD, LaRocque MA. Shunt surgery for priapism: review of results. Urology 1974; 4:1-5. 6. Wear JB Jr, Crummy AB, Munson BO. A new approach to the treatment of priapism. J Urol 1977; 117:252-254. 7. Crummy AB, Ishizuka H, Masden PO. Post-traumatic priapism: successful treatment with autologous clot embolization. AJR 1979; 133:329-330. 8. Belgrano E, Puppo P, Quattrini S, Trombetta C, Bottino P, Giuliani L. Percutaneous temporary embolization of the internal pudendal arteries in idiopathic priapism: two additional cases. J Urol 1984; 131:756758.
March 1990 • Part 2
