Case Report Urol Int 1992;49:227-229
Department of Urology, University of California School of Medicine, San Francisco, Calif., USA
High-Flow Priapism and Gians Hypervascularization following Deep Dorsal Vein Arterialization for Vasculogenic Impotence
Key Words
Abstract
Impotence Microsurgery Arteriovenous shunt, surgical Postoperative complications Priapism
Microsurgical penile revascularization is becoming an increasingly applied technique in patients with arteriogenic or mixed arteriogenic and venogenic impotence. Deep dorsal vein arterialization has been used successfully in selected patients. Aside from failure of the procedure and the occasional prob lems associated with vascular surgery, priapism and glans hypervasculariza tion are specific complications of deep dorsal vein arterialization. Priapism in these cases is ‘high-flow’; the functional arterial-cavernous fistula can over come the maintenance of the flaccid state and cause persistent erection. Gians hypervascularization, a syndrome of glans enlargement, skin changes and pain secondary to excessive retrograde filling of the glans penis and corpus spongio sum, can result in urethral compression and glans ulceration. Along with the presentation of the case of a man who suffered both complications, we discuss their pathophysiology, prevention, and treatment.
Vasculogenic impotence, if mild, may be adequately managed with vacuum erection devices or intracavernosal injections. Sometimes the degree of arteriogenic insuf ficiency and/or venous leakage is too great; microvascular surgery aimed at overcoming either lesion may then be indicated in selected patients. In 1973, Michal et al. [ 1] first reported the technique of epigastric artery to cavernous body anastomosis for the treatment of vasculogenic impotence. Michal’s operation was hampered by frequent occlusion of the anastomosis and postoperative priapism [2, 3]. Since then, numerous techniques have been devised for revascularization of the penis. Arterialization of the deep dorsal vein by anasto
Received: March 5. 1992 Accepted: March 17. 1992
mosis with a vein graft from the femoral artery was first described by LeVeen and Diaz [2], Virag [4] has compiled six variations of the procedure (table 1). Deep dorsal vein arterialization (DDVA), though a therapeutic improve ment over Michal’s procedure, can still be associated with priapism [5, 6]. Another potential complication of DDVA is glans hypervascularization [7]. We report the case of a man who suffered both pria pism and glans hypervascularization after undergoing a modification of the Virag II DDVA. The pathophysiology and therapeutic options arc discussed.
I om F. Luc. MI) Department of Urology, U-575 University of California San Francisco. CA 94143-0738 (USA)
© 1992 S. Kargcr AG. Basel 0042-1138/92/0494-0227 $2.75/0
Downloaded by: Univ. of Michigan, Taubman Med.Lib. 141.211.4.224 - 7/9/2017 10:28:23 PM
J. Stuart Wolf, Jr. Tom F. Lue
Table 1. Virag procedures for deep dorsal vein arterialization [4]
I
Inferior epigastric artery to deep dorsal vein, proximal dorsal vein open Inferior epigastric artery to deep dorsal vein, proximal dorsal vein ligated Saphenous vein graft to deep dorsal vein, proximal dorsal vein ligated Virag I procedure plus dorsal vein to cavernous body shunt Virag II procedure plus dorsal vein to cavernous body shunt Virag III procedure plus dorsal vein to cavernous body shunt
II III IV V VI
nounced pulsations of the cavernous bodies. The diagnoses of highflow priapism and glans hypervascularization were made. In the operating room, one of the two major branches of the deep dorsal vein noted previously was ligated. The intracavernous pres sure fell from 45 to 30 mm Hg with the ligation, and pulsations in several of the circumflex veins of the penis were noticeably dimin ished. There was significant detumcsccnce. At 6 months’ follow-up. the patient no longer has evidence of priapism or glans hypcrvascularization. Although he has suffered no permanent sequcllac. he still reports inability to achieve adequate erections.
Discussion
A 34-year-old man presented with lifelong erectile dysfunction. He reported only rare partial morning erections with complete inability to achieve rigid erections. History was significant for occa sional cigarette use. Physical examination was unremarkable. Base line Doppler ultrasonography revealed both cavernous arteries to be 0.04 cm in diameter. Five minutes after the intracavernosal injection of 10 pg prostaglandin E|, which resulted in only a soft erection, cavernosal artery diameter was unchanged and peak flow velocity was only 17 cm/s. The same values were obtained after genital self-stimu lation, which indicated a moderate degree of arterial insufficiency. Cavernosometry was performed after the injection of 0.5 ml of a papaverine, phentolamine, and prostaglandin E| mixture ( 12 mg/ml. I mg/ml, and 9 gg/ml. respectively). Initial intracavernous pressure was 5 mm Hg: 10 min after injection it was 35 mm Hg. Infusion of normal saline at 40 ml/min increased the pressure to 200 mm Hg. When the infusion was stopped, the intracavernous pressure dropped to 75 mm Hg in 30 s, to 58 mm Hg after l min, and to 48 mm Hg after 5 min. Cavernosography revealed leakage via the dorsal vein only. The diagnosis of combined arteriogenic and venogenic impo tence was made. At operation the deep dorsal vein was noted to derive from 2 main branches converging at the midshaft of the penis. The infrapubic deep dorsal vein was ligated, divided, and mobilized up to this major confluence. A valvulotome was passed retrograde to ablate several valves. At a distal branch the instrument would not pass easi ly, so the vein was opened distally and the ablation performed antegradely. The vein was ligated at the venotomy site and all venous tributaries from the glans were carefully tied off. Through a lower midline abdominal incision, the left inferior epi gastric artery was divided at the level of the umbilicous and mobi lized from its origin. It was brought down to the penis through the external inguinal ring and anastomosed to the deep dorsal vein end to end. proximal to the major branching point. There was no evi dence of glans engorgement or unusual degree of tumescence after the clamps were released. Postoperatively, there was some edema of the penile skin but no frank priapism. On postoperative day 3, Doppler ultrasonography demonstrated a peak flow of 67 cm/s at the anastomosis. Three weeks later the patient reported penile pain and swelling. Examina tion revealed a firmly erect penis as well as engorgement and purplish discoloration of the glans. There was significant bullous edema of the glans, with some skin sloughing. The patient denied a change in his urinary stream. Repeat Doppler ultrasonography revealed pro
228
Wolf/Lue
Surgical revascularization of the penis is in its infancy. The procedures are performed at only a few centers and have yet to be standardized. Selection criteria remain indistinct. Since the treatment of impotence is purely elective, the consideration of complications is para mount. Aside from failure of the procedure and occa sional complications of vascular surgery (anastomotic dis ruption, hematoma, wound infection, etc.), the specific problems that merit scrutiny arc priapism and glans hypervascularization. Priapism, the state of prolonged erection not associ ated with sexual excitement, can be classified as either low-flow or high-fiow depending on the state of the caver nous system [8], The former, resulting from a decrease of venous outflow from the corpora, is the most common. It is represented by most cases of spontaneous priapism or priapism induced by intracavernosal injection of agents. Although low-flow priapism can frequently be managed with aspiration and instillation of sympathomimetics, a shunting procedure is often required to treat priapism of more than 48 h duration [9], High-flow priapism is caused by a persistent increase of vascular inflow, rather than a decrease of outflow. It is usually associated with a traumatic event that creates an arterial-cavernous fistula, resulting in excessive filling of the erectile bodies [10]. All penile revascularization pro cedures, except for the arterial-arterial procedures, are based on the creation of a functional arterial-cavernous fistula. Too small a fistula will be ineffective in providing erectile capability. Too large a fistula may overcome the physiologic maintenance of the flaccid state and result in a persistent erection. Because of the variations in vascular anatomy, it is often difficult to predict the course of blood flow beyond the anastomosis or guage the exact effect of the fistula. In DDVA, ligation of circumflex veins or different parts of the deep dorsal vein might redirect flow in a more optimal
Priapism and Glans Hypervascularization
Downloaded by: Univ. of Michigan, Taubman Med.Lib. 141.211.4.224 - 7/9/2017 10:28:23 PM
Case Report
course, but the placement of ligatures will vary with each patient. Until a reliable technique is developed to predict the effect of vacular manipulations, postoperative pria pism will remain a potential complication of penile revas cularization. Unfortunately, the remedy, ligation or band ing of all or part of the anastomosis, often results in the return of impotence [5, 6], Transcatheter embolization, applied successfully in other forms of high-flow priapism [10], might be useful here as well. Gians hypervascularization is a complication unique to those revascularization procedures which direct ar terial flow into the penile venous system. This category would include DDVA, where glans hypervascularization occurred in 12.5 % of cases in one series [11]. Gians hyper vascularization results from the retrograde blood flow being directed excessively into the glans penis and corpus spongiosum, with subsequent engorgement of these struc tures. The Hauri procedure, since it involves a dorsal penile artery to deep dorsal vein anastomosis at the site of the inferior epigastric artery anastomosis, can also result in high venous flow to the glans. Indeed, Hauri [12] has reported 2 cases of glans hypervascularization in patients undergoing his procedure.
Glans enlargement, skin changes, pain and urethral compression may be the result of this excessive blood flow. If left untreated, ulcerations may develop [13]. Ben nett [5] reports that the condition can be recognized intraoperatively, but we and Biedcrman [14] have found that the presentation can be delayed as well. Treatment consists of ligation of all or part of the anastomosis (as in our case), additional venous ligatures, or banding of the inflow vessel. Transcathcter embolization of the bypass graft has also been applied [ 15], The result of intervention is often impotence, but Biedermann [14] reports success ful treatment of glans hypervascularization with preserva tion of penile revascularization in some patients. Avoiding ablation of the distalmost valve in the deep dorsal vein or ligating the deep dorsal vein near the glans are measures recommended to prevent glans hypervascu larization [5], Our patient developed this condition de spite ligation of the deep dorsal vein distally and careful interruption of all venous tributaries to the glans. Until the drainage system of the penis can be manipulated in a constant fashion, glans hypervascularization will occur in some patients undergoing DDVA.
References 5 Bennett AH: Venous arterialization for erectile impotence. Urol Clin North Am 1988:15:111113.
6 Wagenknecht LV: Microsurgical arterializa tion for vascular impotence. Eur Urol 1989:16: 262-266. 7 Virag R: The treatment of angiogenic impo tence. Int Angiol 1984;3:275-279. 8 Hauri D. Spycher M. Bruhlmann W: Erection and priapism: A new physiopathological con cept. Urol Int 1983:38:138-145. 9 Lue TF. Hellstrom WJG. McAninch JW. Tanagho EA: Priapism: A refined approach to diagnosis and treatment. J Urol 1986:136:104108. 10 Witt MA. Goldstein 1. de Tejada IS. Greenfield A, Krane RJ: Traumatic laceration ofintracavernosal arteries: The pathophysiology of non ischemic, high flow, arterial priapism. J Urol 1990:143:129-132.
11 Virag R. Zwang G. Dermange H, Legman M: Vasculogenic impotence: A review of 92 cases with 54 surgical operations. Vase Surg 1983; 15: 9-17. 12 Hauri D: A new operative technique in vascu logenic erectile impotence. World J Urol 1986: 4:237-249. 13 Fritsch P. Grubauer G. Hilty N. Biedermann H: Ilypervaskularisationssyndrom des Penis nach Artérialisation der Vena dorsalis penis wegen erektiler Impotenz. Hautarzt 1989:40: 434-436. 14 Biedermann H: Ergebnisse mikro(gefass)chirurgischer Eingriffe bei vascular bedingten Erektionsstörungen. Wien Klin Wochenschr 1989;101:723-728. 15 Wilms G. Oyen R. Claes L, Boeckx W, Baert AL. Baert L: Glans ischemia after penis revas cularization: Therapeutic embolization. Cardiovasc Interval Radiol 1990;13:304-305.
229
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1 Michal V. Kramar R. Pospical J. Hejha! L: Prima tepenna anastomaza na corpora caver nosa penis v. leebe ercctivini impotence. Rozhl Chir 1973:52:587. 2 LeVeen HH. Diaz C: Treatment by corpus cavernosum revascularization: in Zorgniotti AW. Rossi G (eds): Vasculogenic Impotence: Proc 1st Int Conf Corpus cavernosum Revasculari zation. Springfield, Thomas. 1980. chap 25. pp 217-233. 3 Michal V. Kramar K. Hcjhal L: Revasculariza tion procedures of the cavernous bodies: in Zorgniotti AW, Rossi G (eds): Vasculogenic Impotence: Proc 1st lnt Conf Corpus caverno sum Revascularization. Springfield. Thomas. 1980. chap 27. pp 239-255. 4 Virag R: Revascularization of the penis; in Bennett AH (cd): Management of Male Impo tence. Baltimore. Williams & Wilkins. 1982. chap 17. pp 219-233.
Department of Urology, University of California School of Medicine, San Francisco, Calif., USA
High-Flow Priapism and Gians Hypervascularization following Deep Dorsal Vein Arterialization for Vasculogenic Impotence
Key Words
Abstract
Impotence Microsurgery Arteriovenous shunt, surgical Postoperative complications Priapism
Microsurgical penile revascularization is becoming an increasingly applied technique in patients with arteriogenic or mixed arteriogenic and venogenic impotence. Deep dorsal vein arterialization has been used successfully in selected patients. Aside from failure of the procedure and the occasional prob lems associated with vascular surgery, priapism and glans hypervasculariza tion are specific complications of deep dorsal vein arterialization. Priapism in these cases is ‘high-flow’; the functional arterial-cavernous fistula can over come the maintenance of the flaccid state and cause persistent erection. Gians hypervascularization, a syndrome of glans enlargement, skin changes and pain secondary to excessive retrograde filling of the glans penis and corpus spongio sum, can result in urethral compression and glans ulceration. Along with the presentation of the case of a man who suffered both complications, we discuss their pathophysiology, prevention, and treatment.
Vasculogenic impotence, if mild, may be adequately managed with vacuum erection devices or intracavernosal injections. Sometimes the degree of arteriogenic insuf ficiency and/or venous leakage is too great; microvascular surgery aimed at overcoming either lesion may then be indicated in selected patients. In 1973, Michal et al. [ 1] first reported the technique of epigastric artery to cavernous body anastomosis for the treatment of vasculogenic impotence. Michal’s operation was hampered by frequent occlusion of the anastomosis and postoperative priapism [2, 3]. Since then, numerous techniques have been devised for revascularization of the penis. Arterialization of the deep dorsal vein by anasto
Received: March 5. 1992 Accepted: March 17. 1992
mosis with a vein graft from the femoral artery was first described by LeVeen and Diaz [2], Virag [4] has compiled six variations of the procedure (table 1). Deep dorsal vein arterialization (DDVA), though a therapeutic improve ment over Michal’s procedure, can still be associated with priapism [5, 6]. Another potential complication of DDVA is glans hypervascularization [7]. We report the case of a man who suffered both pria pism and glans hypervascularization after undergoing a modification of the Virag II DDVA. The pathophysiology and therapeutic options arc discussed.
I om F. Luc. MI) Department of Urology, U-575 University of California San Francisco. CA 94143-0738 (USA)
© 1992 S. Kargcr AG. Basel 0042-1138/92/0494-0227 $2.75/0
Downloaded by: Univ. of Michigan, Taubman Med.Lib. 141.211.4.224 - 7/9/2017 10:28:23 PM
J. Stuart Wolf, Jr. Tom F. Lue
Table 1. Virag procedures for deep dorsal vein arterialization [4]
I
Inferior epigastric artery to deep dorsal vein, proximal dorsal vein open Inferior epigastric artery to deep dorsal vein, proximal dorsal vein ligated Saphenous vein graft to deep dorsal vein, proximal dorsal vein ligated Virag I procedure plus dorsal vein to cavernous body shunt Virag II procedure plus dorsal vein to cavernous body shunt Virag III procedure plus dorsal vein to cavernous body shunt
II III IV V VI
nounced pulsations of the cavernous bodies. The diagnoses of highflow priapism and glans hypervascularization were made. In the operating room, one of the two major branches of the deep dorsal vein noted previously was ligated. The intracavernous pres sure fell from 45 to 30 mm Hg with the ligation, and pulsations in several of the circumflex veins of the penis were noticeably dimin ished. There was significant detumcsccnce. At 6 months’ follow-up. the patient no longer has evidence of priapism or glans hypcrvascularization. Although he has suffered no permanent sequcllac. he still reports inability to achieve adequate erections.
Discussion
A 34-year-old man presented with lifelong erectile dysfunction. He reported only rare partial morning erections with complete inability to achieve rigid erections. History was significant for occa sional cigarette use. Physical examination was unremarkable. Base line Doppler ultrasonography revealed both cavernous arteries to be 0.04 cm in diameter. Five minutes after the intracavernosal injection of 10 pg prostaglandin E|, which resulted in only a soft erection, cavernosal artery diameter was unchanged and peak flow velocity was only 17 cm/s. The same values were obtained after genital self-stimu lation, which indicated a moderate degree of arterial insufficiency. Cavernosometry was performed after the injection of 0.5 ml of a papaverine, phentolamine, and prostaglandin E| mixture ( 12 mg/ml. I mg/ml, and 9 gg/ml. respectively). Initial intracavernous pressure was 5 mm Hg: 10 min after injection it was 35 mm Hg. Infusion of normal saline at 40 ml/min increased the pressure to 200 mm Hg. When the infusion was stopped, the intracavernous pressure dropped to 75 mm Hg in 30 s, to 58 mm Hg after l min, and to 48 mm Hg after 5 min. Cavernosography revealed leakage via the dorsal vein only. The diagnosis of combined arteriogenic and venogenic impo tence was made. At operation the deep dorsal vein was noted to derive from 2 main branches converging at the midshaft of the penis. The infrapubic deep dorsal vein was ligated, divided, and mobilized up to this major confluence. A valvulotome was passed retrograde to ablate several valves. At a distal branch the instrument would not pass easi ly, so the vein was opened distally and the ablation performed antegradely. The vein was ligated at the venotomy site and all venous tributaries from the glans were carefully tied off. Through a lower midline abdominal incision, the left inferior epi gastric artery was divided at the level of the umbilicous and mobi lized from its origin. It was brought down to the penis through the external inguinal ring and anastomosed to the deep dorsal vein end to end. proximal to the major branching point. There was no evi dence of glans engorgement or unusual degree of tumescence after the clamps were released. Postoperatively, there was some edema of the penile skin but no frank priapism. On postoperative day 3, Doppler ultrasonography demonstrated a peak flow of 67 cm/s at the anastomosis. Three weeks later the patient reported penile pain and swelling. Examina tion revealed a firmly erect penis as well as engorgement and purplish discoloration of the glans. There was significant bullous edema of the glans, with some skin sloughing. The patient denied a change in his urinary stream. Repeat Doppler ultrasonography revealed pro
228
Wolf/Lue
Surgical revascularization of the penis is in its infancy. The procedures are performed at only a few centers and have yet to be standardized. Selection criteria remain indistinct. Since the treatment of impotence is purely elective, the consideration of complications is para mount. Aside from failure of the procedure and occa sional complications of vascular surgery (anastomotic dis ruption, hematoma, wound infection, etc.), the specific problems that merit scrutiny arc priapism and glans hypervascularization. Priapism, the state of prolonged erection not associ ated with sexual excitement, can be classified as either low-flow or high-fiow depending on the state of the caver nous system [8], The former, resulting from a decrease of venous outflow from the corpora, is the most common. It is represented by most cases of spontaneous priapism or priapism induced by intracavernosal injection of agents. Although low-flow priapism can frequently be managed with aspiration and instillation of sympathomimetics, a shunting procedure is often required to treat priapism of more than 48 h duration [9], High-flow priapism is caused by a persistent increase of vascular inflow, rather than a decrease of outflow. It is usually associated with a traumatic event that creates an arterial-cavernous fistula, resulting in excessive filling of the erectile bodies [10]. All penile revascularization pro cedures, except for the arterial-arterial procedures, are based on the creation of a functional arterial-cavernous fistula. Too small a fistula will be ineffective in providing erectile capability. Too large a fistula may overcome the physiologic maintenance of the flaccid state and result in a persistent erection. Because of the variations in vascular anatomy, it is often difficult to predict the course of blood flow beyond the anastomosis or guage the exact effect of the fistula. In DDVA, ligation of circumflex veins or different parts of the deep dorsal vein might redirect flow in a more optimal
Priapism and Glans Hypervascularization
Downloaded by: Univ. of Michigan, Taubman Med.Lib. 141.211.4.224 - 7/9/2017 10:28:23 PM
Case Report
course, but the placement of ligatures will vary with each patient. Until a reliable technique is developed to predict the effect of vacular manipulations, postoperative pria pism will remain a potential complication of penile revas cularization. Unfortunately, the remedy, ligation or band ing of all or part of the anastomosis, often results in the return of impotence [5, 6], Transcatheter embolization, applied successfully in other forms of high-flow priapism [10], might be useful here as well. Gians hypervascularization is a complication unique to those revascularization procedures which direct ar terial flow into the penile venous system. This category would include DDVA, where glans hypervascularization occurred in 12.5 % of cases in one series [11]. Gians hyper vascularization results from the retrograde blood flow being directed excessively into the glans penis and corpus spongiosum, with subsequent engorgement of these struc tures. The Hauri procedure, since it involves a dorsal penile artery to deep dorsal vein anastomosis at the site of the inferior epigastric artery anastomosis, can also result in high venous flow to the glans. Indeed, Hauri [12] has reported 2 cases of glans hypervascularization in patients undergoing his procedure.
Glans enlargement, skin changes, pain and urethral compression may be the result of this excessive blood flow. If left untreated, ulcerations may develop [13]. Ben nett [5] reports that the condition can be recognized intraoperatively, but we and Biedcrman [14] have found that the presentation can be delayed as well. Treatment consists of ligation of all or part of the anastomosis (as in our case), additional venous ligatures, or banding of the inflow vessel. Transcathcter embolization of the bypass graft has also been applied [ 15], The result of intervention is often impotence, but Biedermann [14] reports success ful treatment of glans hypervascularization with preserva tion of penile revascularization in some patients. Avoiding ablation of the distalmost valve in the deep dorsal vein or ligating the deep dorsal vein near the glans are measures recommended to prevent glans hypervascu larization [5], Our patient developed this condition de spite ligation of the deep dorsal vein distally and careful interruption of all venous tributaries to the glans. Until the drainage system of the penis can be manipulated in a constant fashion, glans hypervascularization will occur in some patients undergoing DDVA.
References 5 Bennett AH: Venous arterialization for erectile impotence. Urol Clin North Am 1988:15:111113.
6 Wagenknecht LV: Microsurgical arterializa tion for vascular impotence. Eur Urol 1989:16: 262-266. 7 Virag R: The treatment of angiogenic impo tence. Int Angiol 1984;3:275-279. 8 Hauri D. Spycher M. Bruhlmann W: Erection and priapism: A new physiopathological con cept. Urol Int 1983:38:138-145. 9 Lue TF. Hellstrom WJG. McAninch JW. Tanagho EA: Priapism: A refined approach to diagnosis and treatment. J Urol 1986:136:104108. 10 Witt MA. Goldstein 1. de Tejada IS. Greenfield A, Krane RJ: Traumatic laceration ofintracavernosal arteries: The pathophysiology of non ischemic, high flow, arterial priapism. J Urol 1990:143:129-132.
11 Virag R. Zwang G. Dermange H, Legman M: Vasculogenic impotence: A review of 92 cases with 54 surgical operations. Vase Surg 1983; 15: 9-17. 12 Hauri D: A new operative technique in vascu logenic erectile impotence. World J Urol 1986: 4:237-249. 13 Fritsch P. Grubauer G. Hilty N. Biedermann H: Ilypervaskularisationssyndrom des Penis nach Artérialisation der Vena dorsalis penis wegen erektiler Impotenz. Hautarzt 1989:40: 434-436. 14 Biedermann H: Ergebnisse mikro(gefass)chirurgischer Eingriffe bei vascular bedingten Erektionsstörungen. Wien Klin Wochenschr 1989;101:723-728. 15 Wilms G. Oyen R. Claes L, Boeckx W, Baert AL. Baert L: Glans ischemia after penis revas cularization: Therapeutic embolization. Cardiovasc Interval Radiol 1990;13:304-305.
229
Downloaded by: Univ. of Michigan, Taubman Med.Lib. 141.211.4.224 - 7/9/2017 10:28:23 PM
1 Michal V. Kramar R. Pospical J. Hejha! L: Prima tepenna anastomaza na corpora caver nosa penis v. leebe ercctivini impotence. Rozhl Chir 1973:52:587. 2 LeVeen HH. Diaz C: Treatment by corpus cavernosum revascularization: in Zorgniotti AW. Rossi G (eds): Vasculogenic Impotence: Proc 1st Int Conf Corpus cavernosum Revasculari zation. Springfield, Thomas. 1980. chap 25. pp 217-233. 3 Michal V. Kramar K. Hcjhal L: Revasculariza tion procedures of the cavernous bodies: in Zorgniotti AW, Rossi G (eds): Vasculogenic Impotence: Proc 1st lnt Conf Corpus caverno sum Revascularization. Springfield. Thomas. 1980. chap 27. pp 239-255. 4 Virag R: Revascularization of the penis; in Bennett AH (cd): Management of Male Impo tence. Baltimore. Williams & Wilkins. 1982. chap 17. pp 219-233.
