•
•
Nonsurgical Treatment of Arteriovenous Malformations of the Trunk and Limb by Transcatheter Arterial Embolization 1
Diagnostic Radiology
Robert J. Stanley, M.D. and Enrique Cublllo, M.D. Two patients with large arteriovenous malformations (AVM) were successfully treated by transcatheter selective arterial embolization with Gelfoam. An extensive lumbar retroperitoneal acquired AVM was markedly reduced, eliminating any clinical evidence of a persistent left-to-right shunt. A large localized congenital AVM of the thigh in the second patient completely disappeared. Transient post-procedure fever developed in the first patient. Prolonged fever and pulmonary infarction complicated the second case with complete recovery in three weeks. The advantages of Gelfoam as an embolizing agent are discussed. The technique appears to be a reasonable alternative to extensive and sometimes mutilative surgery. INDEX TERMS:
Embolism, therapeutic. Malformations, arteriovenous
Radiology 115:609-612, June 1975
• HE SURGICAL management of both congenital and acquired arteriovenous malformations (fistulas) of the trunk and extremities is generally unsuccessful when limited to ligation of the main feeding and draining vessels, and sometimes successful when extirpative surgery is employed (3, 5). The surgical results are considerably better in the treatment of acute acquired posttraumatic arteriovenous fistulas of the limbs and trunk, before extensive collateral circulation through the area of the fistula has developed. The purpose of this report is to describe a new approach to the management of large, chronic trunk and limb arteriovenous malformations, involving the selective embolization of the main feeding arteries with small particles of sterile absorbable gelatin sponge (Geltoarnj.i' Two patients, one with a large congenital arteriovenous malformation of the left proximal thigh and another with an extensive post-surgical retroperitoneal arteriovenous malformation (fistula) in the left inferior lumbar area, were evaluated arteriographically in the past year. In both cases prior surgery had failed to eliminate or reduce the arteriovenous malformation (AVM). Gelfoam embolization was performed in both patients with virtually total elimination of the thigh AVM and hemodynamically significant reduction of the retroperitoneal AVM.
T
CASE REPORTS CASE 1: A 37-year-old white woman was first hospitalized in 1959, at the age of 23, for the treatment of a suspected chorioepithelioma of the uterus. Panhysterectomy was performed. Shortly thereafter, during lumbar laminectomy for suspected metastases, massive hemorrhage was encountered and bleeding was controlled with difficulty by packing the wound. Several days later prior to removal of the packs, the patient suffered a cardiac arrest during the induction of anesthesia and was resuscitated with open cardiac massage. Permanent lower limb paraplegia developed at that time.
In the three years prior to her first admission to Barnes Hospital progressive cardiomegaly developed and loud bruits were noted in the lower abdomen and lumbar region. In September 1973, cardiac catheterization, cardiac output determination and abdominal aortography performed at another hospital revealed a significant left-toright shunt based on oxygen saturation studies. Cardiac output was 10.85 liters/min. and a large arteriovenous fistula from the lower abdominal aorta to the inferior vena cava was found. Selective studies to determine the main feeders were not performed. Subsequently during the patient's first admission to the Barnes Medical Center in November 1973, surgical closure of a large fistula between the aorta and vena cava as well as ligation of several large arterial feeders, including the right internal iliac artery, were performed. Postoperatively the intensity of the abdominal bruits remained the same, heart size was unchanged, borderline congestive heart failure was present at rest, and persistence of the large AVM was suspected. In February 1974, the left internal iliac artery was selectively catheterized via a right femoral percutaneous approach and was demonstrated to be the dominant feeder of an extensive network of dilated vessels in the left sacroiliac and lower lumbar area (Fig. 1). Rapid shunting to lumbar veins, the left common iliac vein and inferior vena cava was apparent at one and one-half seconds. An aortogram at that time demonstrated that several lower lumbar arteries also contributed to the AVM. After considering the alternatives, it was decided to attempt selective embolization of the main feeding arteries. On March 19, 1974, the retroperitoneal AVM was again studied angiographically. Gelatin· sponge emboli' were prepared from sterile Gelfoam. Multiple 1-mm squares of Gelfoam were suspended in a saline solution. Ten to fifteen individual particles, suspended in saline, were drawn up into a syringe and injected into the main feeding branches arising from the internal iliac artery. After each shower of Gelfoam emboli, an arteriogram was obtained to assess the effect. Diminished flow through the AVM was evident after the second embolic shower. Six separate injections of Gelfoam emboli were made before adequate plugging of the AVM had been obtained. The final arteriogram revealed the presence of emboli within many vessels (Fi~. 2). No shunt into the venous system was evident and delayed flow was present in most of the branches of the internal iliac artery. The postoperative period was marked by moderate fever initially, but the patient remained essentially free of symptoms. No complica-
1 From the Mallinckrodt Institute of Radiology, Washington University School of Medicine, and the Department of Radiology,St. Lukes's Hospital, St. Louis, Mo. Accepted for publication in January 1975. dk 2 Upjohn Company, Kalamazoo, Mich.
609
610
ROBERT
J.
STANLEY AND ENRIQUE CUBILLO
June 1975
Fig. 1. CASE 1. Left common iliac arteriogram, mid arterial phase. The internal iliac artery (arrow) is greatly enlarged compared to the external iliac. Iliolumbar and superior gluteal branches of the internal iliac are markedly enlarged and give rise to innumerable tortuous vessels, which are already shunting the contrast material into venous structures. The common iliac vein and inferior vena cava are faintly visible at this time. Fig. 2. CASE 1. Final post-embolization selective internal iliac arteriogram, late arterial phase. Extensive network of vessels previously seen arising from branches of the internal iliac artery is no longer filling. The flow of contrast medium through the vessels is delayed. Emboli can be visualized in numerous branches. No rapid venous shunting is apparent. By advancing the catheter out the internal iliac artery, embolization of the vesical, obturator and pudendal branches has been avoided.
tions were encountered and the patient was discharged on the fifth post-procedure day. On January 20, 1975, approximately ten and one-half months after the embolization procedure, the patient again underwent cardiac catheterization. Cardiac output was found to be 5.3 liters/min. No abdominal bruits were audible but faint lumbar bruits persisted. Heart size had returned to normal and the patient was asymptomatic. No need to attempt further correction of the arterial venous fistula was felt to be indicated. CASE 2: In June 1974, a 29-year-old woman was admitted for the second time to St. Luke's Hospital after having had an operation for a large AVM of the left thigh two years earlier. On the first admission a femoral arteriogram had demonstrated that the 20 cm in diameter mass on the medial aspect of the left thigh was a large arterial venous malformation supplied primarily by the deep femoral artery. A large venous component was present. The operation consisted of ligation of the deep femoral artery at its origin. On this admission the AVM was found to be slightly larger than before. The deep femoral artery was again the primary feeder of the anomaly, having been reconstituted by multiple enlarged muscular branches of the superficial femoral artery (Fig. 3). A second component of the AVM was identified in the left side of the pelvis, fed primarily by inferior branches of the left internal iliac artery. Encouraged by the results of the first case, selective embolization was again attempted. Approaching the left superficial femoral artery from a right femoral percutaneous route, the muscular branches supplying the AVM via the previously ligated deep femoral artery were selectively catheterized. As before, multiple small pieces of Gelfoam suspended in saline were injected into the AVM. A total of
three size 50 Gelfoam sponges was used to produce complete occlusion of the malformation. Progress was assessed by intermediate arteriograms. The final arteriogram revealed complete occlusion of the AVM and absence of the venous phase (Fig. 4). Delayed flow was present in the primary arterial feeders. No arteriographic or clinical evidence of embolization of the distal superficial femoral artery or its branches to the lower leg and foot was present at the completion of the procedure. A shaking chill was noted at the end of the procedure and moderate fever on the following day. Accompanying the onset of fever, severe generalized swelling of the left lower extremity developed without evidence of impaired arterial or venous circulation. Increase in local skin temperature over the AVM was noted. Serial blood Cultures were negative. Wide-spectrum antibiotics were prophylactically administered. On the fourth post-procedure day a pulmonary embolus to the right lung was diagnosed and anticoagulation with heparin was initiated. The subsequent clinical course was consistent with an evolving pulmonary infarction. The patient made a gradual recovery over the next three weeks, during which time an initially persistent fever in the range of 39°C slOWly lysed to normal. At the time of the patient's discharge from the hospital, three and one-half weeks after the embolization procedure, the originally large pulsatile mass in the left thigh had completely disappeared. No bruit or other detectable abnormality remained. No further residual abnormality was noted during a 10-week follow-up examination. In December 1974, six months after the embolization procedure, no physical evidence of the prior, huge AVM could be detected.
Diagnostic Radiology
Fig. 3. CASE 2. A. Superficial femoral arteriogram, mid arterial phase. The catheter (short arrow) is positioned in the midsuperficial femoral artery. Numerous enlarged muscular branches reconstitute flow to the previously ligated deep femoral artery (long arrow) which provides the dominant blood 'flow to the arteriovenous malformation evident in the medial aspect of the upper thigh. B. Late arterial phase. The bulk of the huge arteriovenous malformation is now opacified. The previously ligated proximal end of the deep femoral artery is visible (arrow). Rapid filling of the deep femoral vein as well as other unnamed venous structures in the medial aspect of the proximal thigh is evident. Fig. 4. CASE 2. A. Final arteriogram post embolization, mid arterial phase. Marked decrease in flow through muscular branches of superficial femoral artery. Delayed filling of deep femoral artery. Essentially no filling of AVM. B. Venous phase. Markedly delayed flow in the deep femoral artery. Numerous emboli plug the dominant feeding vessel to the AVM. Flow is no longer present through the AVM and scattered lucencies in the region of the AVM represent large plugs of Gelfoam emboli within the vascular network.
611
612
ROBERT J. STANLEY AND ENRIQUE CUBILLO
DISCUSSION
Arteriovenous malformations (fistulas) can be divided into congenital and acquired types. The congenital arteriovenous malformations (fistulas) are clinically divided into a localized and diffuse type. CASE 2 represents a form of a localized congenital AVM. In a review by Flanc (5), the overall success rate in the surgical treatment of localized congenital A VMs is approximately 500/0. He points out, however, that 75% of these surgical cures involve the amputation of a digit, a hand, or even an entire limb. Surgical treatment when there is diffuse involvement is generally less successful and conservative measures are preferred. The success of surgical treatment of acquired arteriovenous fistulas depends more often upon how quickly the fistula is recognized. Chronicity leads to extensive collateral circulation, compromising the chance for surgical cure (1, 3, 4). Selective embolization of cerebral arteriovenous malformations, carotid-cavernous fistulas, and vascular tumors at the base of the skull and in the paranasal sinuses have been reported (2, 6, 8-11). Opaque plastic spheres, muscle tissue, and Gelfoam particles have been used as emboli. Of the three, particles of Gelfoam suspended in saline are the easiest to inject through a catheter, permitting large showers of ..e mboli in a short period of time. Gelfoam has been used extensively in neurosurgery as a hemostatic agent and earlier studies found it to be both nonantigenic and nonirritating. Gelatin sponges implanted in monkeys were found to induce a slight cellular reaction similar to one induced by a simple blood c10~. The sponge disappeared from the site of implantation in 20 to 45 days, by a process of tissue digestion and phagocytosis (7). The decision to attempt transcatheter embolic occlusion of these two large AVMs was based on (a) the lack of reasonable surgical alternatives, (b) the nature of the hemodynamics of abnormal arteriovenous communications (4, 5), and (c) the fact that the dominant feeding vessels could be subselectively catheterized, minimizing the chance of inadvertent embolization of normal areas. Three potential complications were evident: 1) that the Gelfoam emboli could pass through to the venous side immediately, resulting in pulmonary embolus and infarction; 2) that the stasis within the venous component of the A VM might result in venous thrombosis and late migration of the venous thrombus into the pulmonary circulation; 3) that a minor breakdown in sterile technique could result in bacteremia and septicemia from the embolization procedure. In neither case was there clinical evidence of the first potential complication, but the pulmonary embolus and infarction which occurred on the fourth day in CASE 2 could well have resulted from the second suggested potential complication. Whether prophylactic anticoagulation, starting 12 to 24 hours after
June 1975
the embolization procedure, would obviate the risk of pulmonary embolus and infarction without diminishing the desired effect on the AVM can only be speculated upon at this time. Certainly, close monitoring is indicated to detect and treat pulmonary embolism at the earliest possible time. The fever which developed in both patients within 24 hours of the procedure was thought to be related to muscle and associated tissue breakdown, . since Gelfoam has not been found to be pyrogenic (7). In CASE 1 the febrile episode was short-lived and produced no symptoms. In CASE 2 the fever was alarmingly prolonged. In spite of negative serial blood cultures, wide-spectrum 'antibiotics were administered. The fact that substantially more Gelfoam was used in CASE 2, inducing a greater tissue reaction, could possibly have some bearing on the prolonged fever. In view of the results in these first two cases, we feel that the technique of transcatheter Gelfoam embolization of large chronic AVMs in the trunk and limbs should be given strong consideration as a primary form of treatment, when the dominant arterial feeder(s) can be clearly identlfled and subselectively catheterized. The potential for sparing the patient extensive and sometimes mutilative surgery is exemplified here. Mallinckrodt Institute of Radiology Washington University School of Medicine 510 South Kingshighway St. Louis, MO. 63110
REFERENCES 1. Bell D, Cockshott WP: Angiography of traumatic arteriovenous fistulae. Clin Radiol16: 241-247, Jul 1965 2. Boulos R, Kricheff II, Chase NE: Value of cerebral angiography in the embolization treatment of cerebral arteriovenous malformations. Radiology 97: 65-70, Oct 1970 3. Creech 0 Jr, Gantt J, Wren H: Traumatic arteriovenous fistula at unusual sites. Ann Surg 161: 908-920, Jun 1965 4. Holman E: Contributions to cardiovascular physiology gleaned from clinical and experimental observations of abnormal arteriovenous communications. J Cardiovasc Surg 3:48-63, Feb 1962 5. Flanc C: Congenital arterio-venous fistulas of the extremities. Aust NZ J Surg 37: 222-232, Feb 1968 6. Ishimori S, Hattori M, Shibata Y, et al: Treatment of carotid-cavernous fistula by Gelfoam embolization. J Neurosurg 27: 315-319, Oct 1967 7. Light RU, Prentice HR: Surgical investigation of a new absorbable sponge derived from gelatin for use in hemostasis. J Neurosurg 2: 435-445, Sep 1945 8. Luessenhop ,AJ, Kachmann R Jr, Shevlin W, et al: Clinical evaluation of artificial embolization in the management of large cerebral arteriovenous malformations. J Neurosurg 23:400-417, Oct 1965 9. Picard L, Djindjian R, Manelfe C: L'embolisation dans les malformations vasculaires cephaliques dependant de la carotide externe. Presented at the 10th Symposium Neuroradiologicum, Uruguay, March 1974. To be published in Acta Radiol 10. Robles C, Carrasco-Zanini J: Treatment of cerebral arteriovenous malformations by muscle embolization. J Neurosurg 29: 603-608, Dec 1968 11. Sedzimir CS, Occleshaw JV: Treatment of carotid-cavernous fistula by muscle embolization and Jaeger's maneuver. J Neurosurg 27: 309-314, Oct 1967
•
Nonsurgical Treatment of Arteriovenous Malformations of the Trunk and Limb by Transcatheter Arterial Embolization 1
Diagnostic Radiology
Robert J. Stanley, M.D. and Enrique Cublllo, M.D. Two patients with large arteriovenous malformations (AVM) were successfully treated by transcatheter selective arterial embolization with Gelfoam. An extensive lumbar retroperitoneal acquired AVM was markedly reduced, eliminating any clinical evidence of a persistent left-to-right shunt. A large localized congenital AVM of the thigh in the second patient completely disappeared. Transient post-procedure fever developed in the first patient. Prolonged fever and pulmonary infarction complicated the second case with complete recovery in three weeks. The advantages of Gelfoam as an embolizing agent are discussed. The technique appears to be a reasonable alternative to extensive and sometimes mutilative surgery. INDEX TERMS:
Embolism, therapeutic. Malformations, arteriovenous
Radiology 115:609-612, June 1975
• HE SURGICAL management of both congenital and acquired arteriovenous malformations (fistulas) of the trunk and extremities is generally unsuccessful when limited to ligation of the main feeding and draining vessels, and sometimes successful when extirpative surgery is employed (3, 5). The surgical results are considerably better in the treatment of acute acquired posttraumatic arteriovenous fistulas of the limbs and trunk, before extensive collateral circulation through the area of the fistula has developed. The purpose of this report is to describe a new approach to the management of large, chronic trunk and limb arteriovenous malformations, involving the selective embolization of the main feeding arteries with small particles of sterile absorbable gelatin sponge (Geltoarnj.i' Two patients, one with a large congenital arteriovenous malformation of the left proximal thigh and another with an extensive post-surgical retroperitoneal arteriovenous malformation (fistula) in the left inferior lumbar area, were evaluated arteriographically in the past year. In both cases prior surgery had failed to eliminate or reduce the arteriovenous malformation (AVM). Gelfoam embolization was performed in both patients with virtually total elimination of the thigh AVM and hemodynamically significant reduction of the retroperitoneal AVM.
T
CASE REPORTS CASE 1: A 37-year-old white woman was first hospitalized in 1959, at the age of 23, for the treatment of a suspected chorioepithelioma of the uterus. Panhysterectomy was performed. Shortly thereafter, during lumbar laminectomy for suspected metastases, massive hemorrhage was encountered and bleeding was controlled with difficulty by packing the wound. Several days later prior to removal of the packs, the patient suffered a cardiac arrest during the induction of anesthesia and was resuscitated with open cardiac massage. Permanent lower limb paraplegia developed at that time.
In the three years prior to her first admission to Barnes Hospital progressive cardiomegaly developed and loud bruits were noted in the lower abdomen and lumbar region. In September 1973, cardiac catheterization, cardiac output determination and abdominal aortography performed at another hospital revealed a significant left-toright shunt based on oxygen saturation studies. Cardiac output was 10.85 liters/min. and a large arteriovenous fistula from the lower abdominal aorta to the inferior vena cava was found. Selective studies to determine the main feeders were not performed. Subsequently during the patient's first admission to the Barnes Medical Center in November 1973, surgical closure of a large fistula between the aorta and vena cava as well as ligation of several large arterial feeders, including the right internal iliac artery, were performed. Postoperatively the intensity of the abdominal bruits remained the same, heart size was unchanged, borderline congestive heart failure was present at rest, and persistence of the large AVM was suspected. In February 1974, the left internal iliac artery was selectively catheterized via a right femoral percutaneous approach and was demonstrated to be the dominant feeder of an extensive network of dilated vessels in the left sacroiliac and lower lumbar area (Fig. 1). Rapid shunting to lumbar veins, the left common iliac vein and inferior vena cava was apparent at one and one-half seconds. An aortogram at that time demonstrated that several lower lumbar arteries also contributed to the AVM. After considering the alternatives, it was decided to attempt selective embolization of the main feeding arteries. On March 19, 1974, the retroperitoneal AVM was again studied angiographically. Gelatin· sponge emboli' were prepared from sterile Gelfoam. Multiple 1-mm squares of Gelfoam were suspended in a saline solution. Ten to fifteen individual particles, suspended in saline, were drawn up into a syringe and injected into the main feeding branches arising from the internal iliac artery. After each shower of Gelfoam emboli, an arteriogram was obtained to assess the effect. Diminished flow through the AVM was evident after the second embolic shower. Six separate injections of Gelfoam emboli were made before adequate plugging of the AVM had been obtained. The final arteriogram revealed the presence of emboli within many vessels (Fi~. 2). No shunt into the venous system was evident and delayed flow was present in most of the branches of the internal iliac artery. The postoperative period was marked by moderate fever initially, but the patient remained essentially free of symptoms. No complica-
1 From the Mallinckrodt Institute of Radiology, Washington University School of Medicine, and the Department of Radiology,St. Lukes's Hospital, St. Louis, Mo. Accepted for publication in January 1975. dk 2 Upjohn Company, Kalamazoo, Mich.
609
610
ROBERT
J.
STANLEY AND ENRIQUE CUBILLO
June 1975
Fig. 1. CASE 1. Left common iliac arteriogram, mid arterial phase. The internal iliac artery (arrow) is greatly enlarged compared to the external iliac. Iliolumbar and superior gluteal branches of the internal iliac are markedly enlarged and give rise to innumerable tortuous vessels, which are already shunting the contrast material into venous structures. The common iliac vein and inferior vena cava are faintly visible at this time. Fig. 2. CASE 1. Final post-embolization selective internal iliac arteriogram, late arterial phase. Extensive network of vessels previously seen arising from branches of the internal iliac artery is no longer filling. The flow of contrast medium through the vessels is delayed. Emboli can be visualized in numerous branches. No rapid venous shunting is apparent. By advancing the catheter out the internal iliac artery, embolization of the vesical, obturator and pudendal branches has been avoided.
tions were encountered and the patient was discharged on the fifth post-procedure day. On January 20, 1975, approximately ten and one-half months after the embolization procedure, the patient again underwent cardiac catheterization. Cardiac output was found to be 5.3 liters/min. No abdominal bruits were audible but faint lumbar bruits persisted. Heart size had returned to normal and the patient was asymptomatic. No need to attempt further correction of the arterial venous fistula was felt to be indicated. CASE 2: In June 1974, a 29-year-old woman was admitted for the second time to St. Luke's Hospital after having had an operation for a large AVM of the left thigh two years earlier. On the first admission a femoral arteriogram had demonstrated that the 20 cm in diameter mass on the medial aspect of the left thigh was a large arterial venous malformation supplied primarily by the deep femoral artery. A large venous component was present. The operation consisted of ligation of the deep femoral artery at its origin. On this admission the AVM was found to be slightly larger than before. The deep femoral artery was again the primary feeder of the anomaly, having been reconstituted by multiple enlarged muscular branches of the superficial femoral artery (Fig. 3). A second component of the AVM was identified in the left side of the pelvis, fed primarily by inferior branches of the left internal iliac artery. Encouraged by the results of the first case, selective embolization was again attempted. Approaching the left superficial femoral artery from a right femoral percutaneous route, the muscular branches supplying the AVM via the previously ligated deep femoral artery were selectively catheterized. As before, multiple small pieces of Gelfoam suspended in saline were injected into the AVM. A total of
three size 50 Gelfoam sponges was used to produce complete occlusion of the malformation. Progress was assessed by intermediate arteriograms. The final arteriogram revealed complete occlusion of the AVM and absence of the venous phase (Fig. 4). Delayed flow was present in the primary arterial feeders. No arteriographic or clinical evidence of embolization of the distal superficial femoral artery or its branches to the lower leg and foot was present at the completion of the procedure. A shaking chill was noted at the end of the procedure and moderate fever on the following day. Accompanying the onset of fever, severe generalized swelling of the left lower extremity developed without evidence of impaired arterial or venous circulation. Increase in local skin temperature over the AVM was noted. Serial blood Cultures were negative. Wide-spectrum antibiotics were prophylactically administered. On the fourth post-procedure day a pulmonary embolus to the right lung was diagnosed and anticoagulation with heparin was initiated. The subsequent clinical course was consistent with an evolving pulmonary infarction. The patient made a gradual recovery over the next three weeks, during which time an initially persistent fever in the range of 39°C slOWly lysed to normal. At the time of the patient's discharge from the hospital, three and one-half weeks after the embolization procedure, the originally large pulsatile mass in the left thigh had completely disappeared. No bruit or other detectable abnormality remained. No further residual abnormality was noted during a 10-week follow-up examination. In December 1974, six months after the embolization procedure, no physical evidence of the prior, huge AVM could be detected.
Diagnostic Radiology
Fig. 3. CASE 2. A. Superficial femoral arteriogram, mid arterial phase. The catheter (short arrow) is positioned in the midsuperficial femoral artery. Numerous enlarged muscular branches reconstitute flow to the previously ligated deep femoral artery (long arrow) which provides the dominant blood 'flow to the arteriovenous malformation evident in the medial aspect of the upper thigh. B. Late arterial phase. The bulk of the huge arteriovenous malformation is now opacified. The previously ligated proximal end of the deep femoral artery is visible (arrow). Rapid filling of the deep femoral vein as well as other unnamed venous structures in the medial aspect of the proximal thigh is evident. Fig. 4. CASE 2. A. Final arteriogram post embolization, mid arterial phase. Marked decrease in flow through muscular branches of superficial femoral artery. Delayed filling of deep femoral artery. Essentially no filling of AVM. B. Venous phase. Markedly delayed flow in the deep femoral artery. Numerous emboli plug the dominant feeding vessel to the AVM. Flow is no longer present through the AVM and scattered lucencies in the region of the AVM represent large plugs of Gelfoam emboli within the vascular network.
611
612
ROBERT J. STANLEY AND ENRIQUE CUBILLO
DISCUSSION
Arteriovenous malformations (fistulas) can be divided into congenital and acquired types. The congenital arteriovenous malformations (fistulas) are clinically divided into a localized and diffuse type. CASE 2 represents a form of a localized congenital AVM. In a review by Flanc (5), the overall success rate in the surgical treatment of localized congenital A VMs is approximately 500/0. He points out, however, that 75% of these surgical cures involve the amputation of a digit, a hand, or even an entire limb. Surgical treatment when there is diffuse involvement is generally less successful and conservative measures are preferred. The success of surgical treatment of acquired arteriovenous fistulas depends more often upon how quickly the fistula is recognized. Chronicity leads to extensive collateral circulation, compromising the chance for surgical cure (1, 3, 4). Selective embolization of cerebral arteriovenous malformations, carotid-cavernous fistulas, and vascular tumors at the base of the skull and in the paranasal sinuses have been reported (2, 6, 8-11). Opaque plastic spheres, muscle tissue, and Gelfoam particles have been used as emboli. Of the three, particles of Gelfoam suspended in saline are the easiest to inject through a catheter, permitting large showers of ..e mboli in a short period of time. Gelfoam has been used extensively in neurosurgery as a hemostatic agent and earlier studies found it to be both nonantigenic and nonirritating. Gelatin sponges implanted in monkeys were found to induce a slight cellular reaction similar to one induced by a simple blood c10~. The sponge disappeared from the site of implantation in 20 to 45 days, by a process of tissue digestion and phagocytosis (7). The decision to attempt transcatheter embolic occlusion of these two large AVMs was based on (a) the lack of reasonable surgical alternatives, (b) the nature of the hemodynamics of abnormal arteriovenous communications (4, 5), and (c) the fact that the dominant feeding vessels could be subselectively catheterized, minimizing the chance of inadvertent embolization of normal areas. Three potential complications were evident: 1) that the Gelfoam emboli could pass through to the venous side immediately, resulting in pulmonary embolus and infarction; 2) that the stasis within the venous component of the A VM might result in venous thrombosis and late migration of the venous thrombus into the pulmonary circulation; 3) that a minor breakdown in sterile technique could result in bacteremia and septicemia from the embolization procedure. In neither case was there clinical evidence of the first potential complication, but the pulmonary embolus and infarction which occurred on the fourth day in CASE 2 could well have resulted from the second suggested potential complication. Whether prophylactic anticoagulation, starting 12 to 24 hours after
June 1975
the embolization procedure, would obviate the risk of pulmonary embolus and infarction without diminishing the desired effect on the AVM can only be speculated upon at this time. Certainly, close monitoring is indicated to detect and treat pulmonary embolism at the earliest possible time. The fever which developed in both patients within 24 hours of the procedure was thought to be related to muscle and associated tissue breakdown, . since Gelfoam has not been found to be pyrogenic (7). In CASE 1 the febrile episode was short-lived and produced no symptoms. In CASE 2 the fever was alarmingly prolonged. In spite of negative serial blood cultures, wide-spectrum 'antibiotics were administered. The fact that substantially more Gelfoam was used in CASE 2, inducing a greater tissue reaction, could possibly have some bearing on the prolonged fever. In view of the results in these first two cases, we feel that the technique of transcatheter Gelfoam embolization of large chronic AVMs in the trunk and limbs should be given strong consideration as a primary form of treatment, when the dominant arterial feeder(s) can be clearly identlfled and subselectively catheterized. The potential for sparing the patient extensive and sometimes mutilative surgery is exemplified here. Mallinckrodt Institute of Radiology Washington University School of Medicine 510 South Kingshighway St. Louis, MO. 63110
REFERENCES 1. Bell D, Cockshott WP: Angiography of traumatic arteriovenous fistulae. Clin Radiol16: 241-247, Jul 1965 2. Boulos R, Kricheff II, Chase NE: Value of cerebral angiography in the embolization treatment of cerebral arteriovenous malformations. Radiology 97: 65-70, Oct 1970 3. Creech 0 Jr, Gantt J, Wren H: Traumatic arteriovenous fistula at unusual sites. Ann Surg 161: 908-920, Jun 1965 4. Holman E: Contributions to cardiovascular physiology gleaned from clinical and experimental observations of abnormal arteriovenous communications. J Cardiovasc Surg 3:48-63, Feb 1962 5. Flanc C: Congenital arterio-venous fistulas of the extremities. Aust NZ J Surg 37: 222-232, Feb 1968 6. Ishimori S, Hattori M, Shibata Y, et al: Treatment of carotid-cavernous fistula by Gelfoam embolization. J Neurosurg 27: 315-319, Oct 1967 7. Light RU, Prentice HR: Surgical investigation of a new absorbable sponge derived from gelatin for use in hemostasis. J Neurosurg 2: 435-445, Sep 1945 8. Luessenhop ,AJ, Kachmann R Jr, Shevlin W, et al: Clinical evaluation of artificial embolization in the management of large cerebral arteriovenous malformations. J Neurosurg 23:400-417, Oct 1965 9. Picard L, Djindjian R, Manelfe C: L'embolisation dans les malformations vasculaires cephaliques dependant de la carotide externe. Presented at the 10th Symposium Neuroradiologicum, Uruguay, March 1974. To be published in Acta Radiol 10. Robles C, Carrasco-Zanini J: Treatment of cerebral arteriovenous malformations by muscle embolization. J Neurosurg 29: 603-608, Dec 1968 11. Sedzimir CS, Occleshaw JV: Treatment of carotid-cavernous fistula by muscle embolization and Jaeger's maneuver. J Neurosurg 27: 309-314, Oct 1967
