Ethanol Embolization of Arteriovenous Fistulas: A Primary Mode of Therapy1 Wayne F. Yakes, M D James M. Luethke, M D Jean Jacques Merland, M D Kevin M. Rak, M D Dick D. Slater, M D Harris W . Hollis, M D Steve H. Parker, M D Alfredo Casasco, M D Armand Aymard, M D Jonathan Hodes, M D Kenneth D. Hopper, M D A. Thomas Stavros, M D Thomas E. Carter, M D
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Index terms: Alcohol Arteries, therapeutic 9*.1299 ' arteriOvenous, 9*.149,9*.494 Fistula, therapeutic blockade, 9*.1299
JVIR 1990; 1:89-96 Abbreviations: AP = anteroposterior, AV = arteriovenous, AVF = arteriovenous fistula, AVM = arteriovenous malformaangiogra. tion, DSA = digital phy, IBCA = isobutyl-2-cyanoacrylate.
From the Departments of Radiology (W.F.Y., J.M.L., K.M.R., D.D.S.) and Surgery (H.W.H., T.E.C.), Fitzsimons Army Medical Center, Aurora, CO 80045~5001; Service de Neuroradiologie e t D'Angiographic Therapeutique, University of Paris, Paris (J.J.M., A.C., A.A., J.H.); Imaging Associates, Englewood, Colo (S,H.P,, A,T,S,); and the Department of Radiology, Perm State University, Hershey, Pa (K.D.H.). Received October 9,1989; revision requested December 10; revision received April 4,1990; accepted May 20. Address reprint requests to W.F.Y. The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the Department of the Army or the Department of Defense.
@ SCVIR, 1990
Arteriovenous fistulas (AVFs) can be posttraumatic or congenital vascular malformations. In the initial arteriographic evaluation, chronic AVFs potentially can be confused with arteriovenous malformations (AVMs). The authors studied five patients with a single AVF and one patient with numerous AVFs. Three patients had undergone surgery for treatment of their AVFs, one patient had undergone isobutyl-2-cyanoacrylate (IBCA) embolization, and two patients had undergone no prior therapy. The AVFs recurred in the three patients who had undergone surgery and in the patient who had undergone IBCA embolization. All patients underwent ethanol embolization of their AVFs. Angiograms obtained immediately after embolization documented closure of all AVFs. At follow-up, none of the embolized lesions have recurred. The authors conclude that ethanol embolotherapy can cure these problematic lesions. Extreme caution, however, must be employed with the use of intravascular ethanol because nontarget embolization can potentially result in tissue devitalization. In this study, two patients developed a small focal area of skin necrosis that did not require skin grafting and healed with conservative management.
AnTEnlovENous fistulas (AVFs)
are vascular malformations of congenital or posttraumatic origins, usutrauma Or penetrating injury. At arteriography chronic AVFs may be confused with arteriovenous malformations (AVMs) because the multiple enlarged feeding arteries can simulate an AVM nidus near the arteriovenous (AV) connection. Surgical intervention in AVFs is a difficult operation with a high rate of recurrence, and it can lead to hemorrhagic complications, neural injury, and functional loss (1).With the aid of improved catheter systems and superselective techniques, embolotherapy is gaining acceptance as an excellent alternative in the treatment of AVFs. Vasoocclusive devices, such as spring coils, detachable balloons, and particulate agents, have been used to treat AVFs (2-7). At least two renal AVFs have been treated with absolute ethanol as the sole embolic agent (8). TOthe best of our knowledge, ours is the first series in which
absolute ethanol was used to treat AVFS in other locations. PATIENTS AND METHODS Six patients with AVFs, three men and three women (age range, 30-54 years; mean age, 36 years) underwent treatment. Three patients (patients 1, 2, and 3) had posttraumatic AVFs, and three patients (patients 4,5, and 6) had congenital AVFs. Patient 1 had undergone a single surgical procedure previously, and patients 2 and 4 had undergone multiple surgical procedures. No surgery proved curative, as the AVF and the symptoms recurred in all three patients. Patient 2 had undergone multiple failed embolization procedures as well, and patient 6 had a recurrent AVF after embolization with isobutyl-2-cyanoacrylate (IBCA). Three patients (patients 1,2, and 4) presented with pain. Two patients (patients 3 and 6) suffered from swelling and atrophic skin
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changes. Two patients (patients 1and 2) additionally suffered from lower limb claudication. Patient 2 also suffered from a markedly increased resting cardiac output of 18 Llmin, which led to significant cardiac sequelae. Patient 5 had hereditary hemorrhagic telangiectasia and a pulmonary AVF. Patient 6 suffered a significant hemorrhage from a recurrent AVF of the right ear. Patient 1 (Fig 1) had a posttraumatic AVF in the left anterior tibial compartment secondary to a knife injury 18 years earlier. Patient 2 (Fig 2) had multiple posttraumatic AVFs extending from the right lower pelvis to the ipsilateral distal popliteal region, secondary to a high-velocity bullet injury. Patient 3 had an AVF of the fourth finger, secondary to blunt trauma 20 years earlier. Patient 4 (Fig 3) had a congenital AVF and a venous malformation involving the anterior tibial compartment of the right lower extremity. Patient 5 (Fig 4) had a large congenital right pulmonary AVF. Patient 6 had a recurrent AVF of the right ear. Prior to ethanol embolotherapy, all patients underwent baseline selective biplane arteriography with cut-film and digital subtraction angiographic (DSA) techniques. Selective and superselective angiographic studies were required to accurately define the abnormal AV connection. From these baseline studies, transcatheter arterial routes, retrograde venous routes, and direct percutaneous puncture routes were planned to embolize the AVF exactly at the AV connection, thereby ablating the high- to lowpressure vascular shunt. Direct percutaneous puncture embolizations were employed to circumvent tortuosity and other anatomic obstacles related to prior surgical vascular ligations. In patient 1, two direct percutaneous arterial catheters were placed in the proximal and distal ligated stumps of the anterior tibial artery, and one retrograde venous 7-F occlusion balloon catheter (Medi-tech/ Boston Scientific, Watertown, Mass) was placed in the draining anterior tibial vein to occlude flow during em-
Y :
D~ETHL
PLITERL "-E L T INJECT CffLF
a. b. C. Figure 1. Patient 1. (a)Lateral radiograph of the left lower extremity. Note the bone bridging between the tibia and fibula. (b) Anteroposterior (AP) DSA study of the popliteal artery. Note the hypertrophied anterior tibial artery (arrow) supplying the AVF. (c) AP selective DSA study of the anterior tibial artery. Note the large pseudoaneurysm at the AV connection. Note the distal continuation of the transected anterior tibial artery below the AVF (arrows).Note the large anterior tibial vein draining the fistula inferiorly (arrowheads) (Fig 1continues).
right ear, direct percutaneous puncbolization and for 10 minutes after embolization. In patient 2, only retro- ture of the primary outflow vein was performed just distal to the AV congrade venous approaches to the mulnection, with the needle tip directed tiple AVFs were used to occlude flow toward the AVF. External manual with either a 5-F Berenstein catheter compression of the ear outflow vein (Medi-tech/Boston Scientific) or 5-F against the petrous bone, posterior to or 7-F occlusion balloon catheters, thereby inducing vascular stasis. Em- the external auditory canal, induced bolization was performed through the vascular stasis. Retrograde ethanol embolization of the AVF was then persame occlusion balloon catheter, formed. The external manual compreswhich remained inflated for 10 minsion was maintained for 10 minutes. utes. In three embolizations in paNo medetermined ethanol volumes tient 2, a thigh blood pressure cuff infor embolization were considered. flated to 250 mm Hg for 10 minutes The amount of ethanol used was estiwas also required to induce vascular mated from the flow-volume characstasis. Patient 3 underwent direct teristics of the individual AVF treatpercutaneous puncture embolization ed. Occluding spring coil emboli with use of a 21-gauge butterfly nee(Cook, Bloomington, Ind) of various dle with no need to occlude flow. Unsizes were used as a temporary means der real-time color flow Doppler ulto occlude the inflow arterial feeder trasound (US) guidance (Acuson, prior to ethanol embolotherapy at Mountain View, Calif), patient 4 unseveral retrograde venous transcathderwent embolization via direct per" eter embolizations to prevent uncutaneous puncture with use of a 21wanted nontarget arterial embolizagauge butterfly needle. A thigh blood tion proximal to the fistula (patients pressure cuff inflated to 250 mm Hg 1and 2). Three occluding spring coil was used to induce vascular stasis in patient 4. In patient 5, a 7-F occlusion emboli were used to stabilize the thrombosis in a large pulmonary AVF balloon catheter was placed in the pulmonary artery to occlude flow and in an attempt to prevent unwanted forward migration of the clot to the permit injection of ethyl alcohol. In patient 6 with a recurrent AVF of the left side of the heart and the systemic
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RESULTS
Figure 1 (continued). (d) AP popliteal arteriogram obtained 1month after surgery. The AVF has recurred, but the pseudoaneurysm has thrombosed. Note ligation of the anterior tibial artery proximal and distal to the fistula (arrows).Note the nonocclusive ligature on the draining anterior tibial vein (arrowhead).(e) AP DSA study of the popliteal artery immediately after embolization. Note the closure of the AVF. (f) AP popliteal arteriogram obtained 12 months after ethanol embolotherapy. The AVF remains thrombosed with no evidence of recanalization. arterial circulation (patient 5). Patient 3 did not require vascular occlusion for thrombosis of her AVF. For those patients who required vascular occlusion by means of an occlusion balloon catheter and/or blood pressure cuffs inflated above systolic pressure, the duration of occlusion was 10 minutes. To determine the volume of ethanol used during embolization and the rate of injection, test injections of contrast material were performed with fluoroscopic monitoring. The amount of ethanol used was based on the amount of contrast material required to fill the fistula without opacifying normal vessels. In those embolizations requiring vascular stasis, test injections of contrast material were performed and monitored with fluoroscopy while vascular occlusion was employed. Again, delivery of the volume of contrast material required to opacify only the AVF at a particular rate of manual injection was practiced several times. Once the volume and manual injection rate were determined for contrast material, the procedure was repeated for ethanol. Several ethanol injections
were usually required to completely thrombose the AVF. Arteriograms or retrograde venous angiograms were obtained after all ethanol embolizations. Follow-up angiograms were obtained in patients 1 and 2. Patient 4 did not require follow-up arteriography because color flow Doppler US accurately depicted the AVF prior to ethanol embolotherapy and was used to document persistent thrombosis at follow-up. Informed consent was obtained from each patient. All patients were counseled extensively as to the potential complications of intravascular ethanol embolization. All patients were closely followed up to identify any immediate or delayed complications. Later clinical follow-up visits were required to evaluate improvement, worsening, or recurrence of symptoms. Patients 1and 2 underwent follow-up arteriography. Patient 2 also underwent follow-up retrograde venography. Patient 4 underwent follow-up color flow Doppler US examination. Patients 3, 5, and 6 will return for follow-up angiography at 6 months after embolization.
Six patients underwent 27 embolization procedures: one transcatheter arterial, 21 transcatheter retrograde vein, and five direct percutaneous puncture embolizations. Angiograms obtained immediately after embolization documented the acute thrombosis of the AVFs embolized in all patients. No embolization of nontarget vessels was identified. In patients who underwent transcatheter retrograde vein embolization, no angiographic evidence or clinical signs and symptoms of deep vein thrombosis or venous insufficiency were found. All follow-up arterial and venous studies in patients 1and 2 showed persistent AVF thrombosis with no evidence of fistula recanalization or neovascular recruitment. Persistent thrombosis was documented on all angiographic studies from these two patients (range, 12-16 months; mean, 14 months). Color flow Doppler US follow-up studies at 7 months depicted persistent AVF thrombosis in patient 4. Therefore, persistent AVF thrombosis was documented in patients l , 2, and 4 (range, 7-16 months; mean, 11months). All patients, except patient 2, had a single AVF and required only a single embolization session to ablate the fistula. Patient 2 had numerous AVFs and required multistaged ethanol embolizations. In addition to pain and claudication in his right lower extremity, this patient also had a significantly increased cardiac output of 18 Llmin. After five ethanol embolizations, the patient's cardiac output was reduced to a more tolerable 9 L/ min. Further, the patient no longer requires any cardiac medications. His therapy is ongoing. Intravascular ethanol embolotherapy can cause pain that may not be controlled by the usual premedication regimens. Patients 1,2,3, and 5 were given increased doses of intravenously administered meperidine and diazepam during the procedure as needed. These four patients experienced significant pain that responded to the
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Figure 2. Patient 2. (a) AP pelvic arteriogram, early phase. Note the significant vascular hypertrophy of the entire right iliofemoral arterial system. (b) AP pelvic arteriogram, late phase. Note the early filling of the enlarged right iliofemoral venous system (arrows) during the arterial phase, secondary to the vascular shunting caused by multiple AVFs. (c) AP deep femoral arteriogram of the proximal thigh, early phase. Note the arterial hypertrophy. (d) AP deep femoral arteriogram, late phase. Note the early filling of the deep femoral venous system (arrows) secondary to the extensive AV shunting (Fig 2 continues).
increased doses of medication. Patients 4 and 6 received neuroleptic sedation administered intravenously by an anesthesiologist and did not remember a painful experience. Among 27 embolization procedures, there were two complications. Patient 2 has undergone 20 ethanol embolization procedures to date. After the second ethanol embolization, there was a small area of skin breakdown (2 X 2 cm) with a secondary infection. The patient completely recovered after institution of local wound care and antibiotic therapy. No complications occurred in this patient after the other ethanol embolizations. Patient 4 underwent ethanol embolization via a direct percutaneous puncture of an AVF of the right anterior tibia1 compartment. The patient suffered a small area of skin breakdown (2 X 3 cm) that caused secondary superficial saphenous vein phlebitis. The patient recovered completely with local wound care and antibiotic therapy. In this patient series, the total complication rate is 7.5%.
DISCUSSION
c.
Differentiation between AVFs and AVMs is important prior to an embolization procedure (3). Clinically and
angiographically, both types of vascular malformations can be strikingly similar and difficult to differentiate.
d. AVMs are congenital vascular malformations supplied by hypertrophied (macrofistulous) inflow arteries
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Figure 2 (continued). (e) AP superficial femoral arteriogram, early phase. Note the multi~ledistal collateral vessels (arrows) shunting through multiple AVFs. (f) AP superficial femoral arteriogram, late phase. Note that the superficial femoral artery is opacified (arrows), and simultaneously the deep femoral vein (arrowheads) is opacified secondary to multiple tortuous vessels shunting through many AVFs. Because of the many overlapping arteries and veins, it is exceedingly difficult to delineate discrete AVFs without selective arteriograms and retrograde venograms. (g) AP retrograde vein angiogram from a DSA study shows reflux of contrast material into multiple tortuous inflow arterial channels (arrowheads). Note the bullet fragment. Two AVFs are seen on this retrograde venous study (large straight arrows). Each AVF drains into a single vein (small straight arrows), which then merges and drains into a larger deep femoral vein (curved arrow). (h) AP retrograde vein angiogram obtained after selective ethanol embolization of each AVF. No reflux of contrast material into the tortuous inflow arteries occurs because each AVF has thrombosed. Note that contrast material is seen only in the two small veins that initially drained the two AVFs (straight arrows). The larger deep femoral vein (curved arrow) remains patent. No complications occurred.
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as well as microfistulous connections, which usually are not evident a t arteriography. These feeding arteries connect to an immature interlacing network of primitive vascular spaces termed the AVM nidus. Hypertrophied outflow veins drain the AVM nidus. Because there is no intervening capillary bed, a prominent high-pres-
sure to low-pressure vascular shunt is present. AVFs are single direct AV connections without an intervening capillary bed. AVFs are most commonly acquired lesions secondary to blunt or penetrating trauma, with injury to an artery and adjacent vein. In the healing process a fistula forms between
the artery and vein. This situation is stimulated by preferential vascular shunting through the AVF from the higher-pressure arterial system to the lower-pressure venous system. The vascular shunt may increase with long-standing AVFs with resultant neovascular recruitment in response to this shunt. This may cause confusion at angiography as the multiple tortuous inflow arteries and dilated outflow veins may simulate an AVM nidus near the AV connection (2,3).
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Figure 3. Patient 4. (a) AP popliteal arteriogram from a DSA study. Note the hypertrophied inflow artery (arrowheads) arising from the posterior tibial artery, which supplies the AVF (large straight arrow). Note enlarged outflow venous varix (small straight arrows) and the previous surgical ligation and resection of the anterior tibial artery (curved arrow). (b) Lateral popliteal arteriogram. Note the hypertrophied inflow artery (arrowheads)supplying the AVF (large arrow) and the enlarged outflow venous varix (small arrows). (c) AP direct puncture angiogram obtained before embolization. Note opacification of the venous varix and outflow vein. (d) AP popliteal arteriogram obtained after ethanol embolization. Note absence of the hypertrophied feeder compared with a. Note the misregistration artifact of the thrombosed venous varix (arrows).
The natural history of AVFs can be extremely varied. Like AVMs, AVFs can remain unknown clinically and be well tolerated by the patient. Examples include the iatrogenic AVF constructed for the dialysis patient or the asymptomatic renal AVF incidentally found at aortography. At the opposite end of the spectrum is the patient who suffers recurrent bouts of congestive heart failure and is incapacitated by his AVF. Vascular steal alone can cause symptoms in the tissues or organs adjacent to the AVF. The natural historv of the AVF depends on the size of the shunt throughAthefistula. When the shunt is large, hemodynamic consequences such as an increased heart rate, cardiomegaly, abnormally increased cardiac output, and bouts of congestive heart failure can be extremely problematic. Treatment of AVFs requires complete occlusion of the AV connection. Like AVMs, proximal arterial ligations and distal venous ligations will always fail. This surgical approach only removes possible vascular access routes for endovascular ablation of
the AVF. It is mandatory that any surgical or embolization procedure be directed at the complete ablation of the AVF at the AV connection. Various vascular occlusive devices, including spring coils, detachable balloons, polyvinyl alcohol, and silk sutures, have been successful in occluding AVFs (3-7). Recurrence of AVFs has been reported after the use of detachable balloons (9). In high-flow AVFs, care must be maintained in the closure of the fistula. Normal perfusion pressure breakthrough phenomenon is a potential complication after closure of any AVF (10). There is one previous report of the use of absolute ethanol to treat two
patients with renal AVFs. Ours is the first patient series in which ethanol is used to embolize AVFs in other locations. On the basis of our current success in treating AVMs with absolute ethanol, we applied the same principles to treatment of AVFs (11-13). Ethanol is superior to many embolic agents because it is easy to use, and it incites an intense thrombosis to the level of the smallest caliber vessel.
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a. b. Figure 4. Patient 5. (a) AP right pulmonary arteriogram obtained before embolization shows the AVF (arrow). (b) AP right pulmonary arteriogram obtained after ethanol and coil embolization demonstrates absence of the AVF (arrow).
Precisely because of these superb thrombotic properties, embolization of nontarget vessels must be eliminated to minimize the risks of neuropathy and devitalization of normal tissues. Temporary vascular occlusion and the predetermined volume and rate of manual injection of ethanol provide some control and help lessen the likelihood of nontarget embolization. Two patients experienced skin necrosis following ethanol embolization. Patient 4 (Fig 3) had undergone several surgical procedures in a failed attempt to treat an AVF of the anterior tibial compartment. At her last surgery, the entire anterior tibial compartment was completely excised along with the anterior tibial artery, veins, and nerve. This left the patient with a permanent foot drop and compromised arterial and venous systems of the anterior tibial region. The AVF, however, recurred and caused renewed pain and swelling. The AVF was thrombosed after ethanol embolization by means of direct percutaneous puncture. A small area of skin ne-
crosis occurred in a circumferential area around the puncture site, which led to a secondary infection. Several mechanisms could be responsible for the small focal area of skin necrosis. Because of the compromised arterial vascularity, ethanol-induced edema or thrombosis of end vessels could further compromise the tissues, worsen the ischemia, and lead to necrosis. Venous thrombosis may also play a role. Also, ethanol could leak from the vessel puncture site after removal of the percutaneous needle and cause inflammatory changes in ischemic tissues that could lead to necrosis. These mechanisms that could be responsible for the skin necrosis are difficult to prevent when ethanol is the embolic agent. Patient 2 had multiple AVFs of the thigh secondary to a high-velocity bullet injury. This resulted in markedly decreased exercise tolerance and intermittent pain, exacerbated by low-pressure environments, such as the poorly pressurized cabins he had flown in on some military airlifts. He also had a cardiac output of 18 L/min.
Multiple surgeries had no effect. Particulate arterial embolization caused multiple pulmonary emboli that, in turn, caused the patient to become comatose for 9 days. A vascular surgeon recommended bilateral lower extremity amputation and a right hemipelvectomy, in hopes of resecting all of the AVFs and returning the patient's cardiac output to normal. Instead, ethanol embolotherapy was instituted. After five retrograde venous embolizations, the patient's cardiac output was reduced to a more tolerable 9 Llmin. After the second embolization, a small area of bruising was seen subcutaneously. The patient was observed for 14 days, and no skin necrosis occurred. The patient was then taken by military airlift back to his home in Houston. However, this flight 15 days after embolization caused renewed symptoms of pain and swelling so severe that the patient was confined to a litter by the time he arrived in Texas. During the next 2 days, the patient noted that the skin overlying the area of bruising broke down and became secondarily infected. He was then readmitted, and his wound healed with local wound care and antibiotic therapy. The precise pathophysiologic mechanisms responsible for the skin necrosis in this case are uncertain. Edema associated with low cabin pressure may have further compromised an area of skin with a vascular supply that was already precarious from the embolization. Vascular spasm may have also played a role. This phenomenon was also observed in a patient with an AVM of the foot who did very well after embolization. However, during the flight home 3 days after embolization, the patient experienced acute pain and swelling, resulting in prolonged postembolization edema of the foot. It is also important to remember that the sympathetic nerves to the lower extremities run parallel to the arteries and their branches. Sympathetic function can be destroyed by ischemic injury or direct neurotoxic effects of ethanol, resulting in loss of vasomotor tone and severe swelling,
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discoloration, and pain. In a t least one case of superselective transarterial embolization of a renal cell carcinoma metastasis to the femur, a 1-2 mL injection of ethanol led to "chemical syrnpathectomy," severe swelling (days later), and reddish purple discoloration of the entire extremity below the level of embolization. The patient became bedridden (Becker GJ, personal communication, 1990). However, these vasomotor changes lasted only 3 weeks. They may have been self-limited due to recovery of the peripheral sympathetic nerves. Alternatively, the clinical improvement may have represented a response to orally administered carbamazepine. Additionally, improvement of sympathetic nervous function may have resulted, in part, from resolution of surrounding tissue edema. Tissue ischemia and injury can occur with any embolization procedure. These complications are especially possible with the use of intravascular ethanol. Despite the fact that nontarget embolization was not observed during any procedures in our series, two instances of skin necrosis occurred. Although these complications were unfortunate, the regions were small and manageable, unlike the patients' AVFs. In each case, the risk of skin necrosis must be given due consideration, but not out of proportion with the patient's primary problem. We have found that patients with extremely problematic vascular malformations who have undergone multiple traumatic failed therapies tend to accept the very real risk of skin necrosis-provided there is a reasonable chance of curing the underlying lesion with embolization and curing the skin necrosis with wound care, skin grafts, or myocutaneous flaps. In summary, absolute ethanol acutely thrombosed problematic AVFs that recurred after surgery and embolization with agents other than ethanol. All patients experienced symptomatic improvement after closure of the fistula with ethanol embolotherapy. Two patients had small areas of skin necrosis after embolization
that resulted in local bacterial infections that required antibiotic therapy. For both patients the injuries healed with conservative management; neither required skin or myocutaneous grafts. At follow-up, two patients are cured of their AVF (patients 1and 4), and one patient is currently undergoing ethanol embolotherapy for multiple AVFs, with significant clinical improvement after 20 embolization procedures (patient 2). Follow-up studies in patient 2 have documented persistent closure of all AVFs embolized. Patients 3,5, and 6 are considered initially cured, but they will return at 6 months to document persistent AVF closure. Ethanol embolotherapy has proved efficacious in the treatment of problematic AVFs that recurred after surgery and those AVFs in patients who had not undergone prior therapy. Extreme caution and meticulous technique must be exercised with the use of ethanol to minimize the risks of tissue devitalization. Acknowledgments: The authors thank Nona Marie Yakes, BA, Julia Ann Criado, Frances Yakes, MA, and Lynnen Yakes for their exemplary efforts and inspiration in the preparation and completion of this manuscript. References 1. Fowl RJ, Kempczinski FJ, Bailey WW, Dickhoner WA. Management of a complex, posttraumatic, pelvic arteriovenous fistula with the use of cardiopulmonary bypass: case report and review of the literature. Vasc Surg 1987; 6:257-261. 2. Trout HH, Tievsky AL, Rieth KG, Druy EM, Giordano JM. Arteriovenous fistula simulating arteriovenous malformation. Otolaryngol Head Neck Surg 1987; 97:322-325. 3. Lawdahl RB, Routh WD, Vitek JJ, McDowell HA, Gross GM, Keller FS. Chronic arteriovenous fistulas masquerading as arteriovenous malformations: diagnostic considerations and therapeutic implications. Radiology 1989; 17O:lOll-1015. 4. Debrun G, Legre J , Kasbarian M, Tapias PL, Caron JP. Endovascular occlusion of vertebral fistulae by detachable balloons with conservation
of the vertebral blood flow. Radiology 1979; 130:141-147. Layne TA, Finck EJ, Boswell WD. Transcatheter occlusion of the arterial supply to arteriovenous fistulas with Gianturco coils. AJR 1978; 131: 1027-1030. Halbach VV, Higashida RT, Hieshima GB. Treatment of vertebral arteriovenous fistulas. AJR 1988; 150:405-412. White RI, Lynch-Nyhan A, Terry P, et al. Pulmonary arteriovenous malformations: techniques and longterm outcome of embolotherapy. Radiology 1988; 169:663-669. Sasaki M, Tadokoro S, Kimura S, Mori M, Kosuda S, Tachnibana M. Two cases of renal arteriovenous fistula treated by transcatheter embolization with absolute ethanol. Hinyokika Kiyo 1984; 30:295-298. Keller FS, King CE. Delayed detachable balloon migration: a cause of recurrent arteriovenous fistula. J Intervent Radio1 1986; 1:37-39. Halbach VV, Higashida RT, Hieshima GB, Norman D. Normal perfusion pressure breakthrough occurring during treatment of carotid and vertebral fistulas. AJNR 1987; 8:751756. Yakes WF, Pevsner P, Reed M, Donohue HJ, Ghaed N. Serial embolizations of an extremity arteriovenous malformation with alcohol via direct percutaneous puncture. AJR 1986; 146:1038-1040. Yakes WF, Haas DK, Parker SH, et al. Symptomatic vascular malformations: ethanol embolotherapy. Radiology 1989; 170:1059-1066. Yakes WF, Parker SH, Gibson MD, Haas DK, Pevsner PH, Carter TE. Alcohol embolotherapy of vascular malformations. Semin Intervent Radiol 1989: 6:146-161.
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Index terms: Alcohol Arteries, therapeutic 9*.1299 ' arteriOvenous, 9*.149,9*.494 Fistula, therapeutic blockade, 9*.1299
JVIR 1990; 1:89-96 Abbreviations: AP = anteroposterior, AV = arteriovenous, AVF = arteriovenous fistula, AVM = arteriovenous malformaangiogra. tion, DSA = digital phy, IBCA = isobutyl-2-cyanoacrylate.
From the Departments of Radiology (W.F.Y., J.M.L., K.M.R., D.D.S.) and Surgery (H.W.H., T.E.C.), Fitzsimons Army Medical Center, Aurora, CO 80045~5001; Service de Neuroradiologie e t D'Angiographic Therapeutique, University of Paris, Paris (J.J.M., A.C., A.A., J.H.); Imaging Associates, Englewood, Colo (S,H.P,, A,T,S,); and the Department of Radiology, Perm State University, Hershey, Pa (K.D.H.). Received October 9,1989; revision requested December 10; revision received April 4,1990; accepted May 20. Address reprint requests to W.F.Y. The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the Department of the Army or the Department of Defense.
@ SCVIR, 1990
Arteriovenous fistulas (AVFs) can be posttraumatic or congenital vascular malformations. In the initial arteriographic evaluation, chronic AVFs potentially can be confused with arteriovenous malformations (AVMs). The authors studied five patients with a single AVF and one patient with numerous AVFs. Three patients had undergone surgery for treatment of their AVFs, one patient had undergone isobutyl-2-cyanoacrylate (IBCA) embolization, and two patients had undergone no prior therapy. The AVFs recurred in the three patients who had undergone surgery and in the patient who had undergone IBCA embolization. All patients underwent ethanol embolization of their AVFs. Angiograms obtained immediately after embolization documented closure of all AVFs. At follow-up, none of the embolized lesions have recurred. The authors conclude that ethanol embolotherapy can cure these problematic lesions. Extreme caution, however, must be employed with the use of intravascular ethanol because nontarget embolization can potentially result in tissue devitalization. In this study, two patients developed a small focal area of skin necrosis that did not require skin grafting and healed with conservative management.
AnTEnlovENous fistulas (AVFs)
are vascular malformations of congenital or posttraumatic origins, usutrauma Or penetrating injury. At arteriography chronic AVFs may be confused with arteriovenous malformations (AVMs) because the multiple enlarged feeding arteries can simulate an AVM nidus near the arteriovenous (AV) connection. Surgical intervention in AVFs is a difficult operation with a high rate of recurrence, and it can lead to hemorrhagic complications, neural injury, and functional loss (1).With the aid of improved catheter systems and superselective techniques, embolotherapy is gaining acceptance as an excellent alternative in the treatment of AVFs. Vasoocclusive devices, such as spring coils, detachable balloons, and particulate agents, have been used to treat AVFs (2-7). At least two renal AVFs have been treated with absolute ethanol as the sole embolic agent (8). TOthe best of our knowledge, ours is the first series in which
absolute ethanol was used to treat AVFS in other locations. PATIENTS AND METHODS Six patients with AVFs, three men and three women (age range, 30-54 years; mean age, 36 years) underwent treatment. Three patients (patients 1, 2, and 3) had posttraumatic AVFs, and three patients (patients 4,5, and 6) had congenital AVFs. Patient 1 had undergone a single surgical procedure previously, and patients 2 and 4 had undergone multiple surgical procedures. No surgery proved curative, as the AVF and the symptoms recurred in all three patients. Patient 2 had undergone multiple failed embolization procedures as well, and patient 6 had a recurrent AVF after embolization with isobutyl-2-cyanoacrylate (IBCA). Three patients (patients 1,2, and 4) presented with pain. Two patients (patients 3 and 6) suffered from swelling and atrophic skin
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changes. Two patients (patients 1and 2) additionally suffered from lower limb claudication. Patient 2 also suffered from a markedly increased resting cardiac output of 18 Llmin, which led to significant cardiac sequelae. Patient 5 had hereditary hemorrhagic telangiectasia and a pulmonary AVF. Patient 6 suffered a significant hemorrhage from a recurrent AVF of the right ear. Patient 1 (Fig 1) had a posttraumatic AVF in the left anterior tibial compartment secondary to a knife injury 18 years earlier. Patient 2 (Fig 2) had multiple posttraumatic AVFs extending from the right lower pelvis to the ipsilateral distal popliteal region, secondary to a high-velocity bullet injury. Patient 3 had an AVF of the fourth finger, secondary to blunt trauma 20 years earlier. Patient 4 (Fig 3) had a congenital AVF and a venous malformation involving the anterior tibial compartment of the right lower extremity. Patient 5 (Fig 4) had a large congenital right pulmonary AVF. Patient 6 had a recurrent AVF of the right ear. Prior to ethanol embolotherapy, all patients underwent baseline selective biplane arteriography with cut-film and digital subtraction angiographic (DSA) techniques. Selective and superselective angiographic studies were required to accurately define the abnormal AV connection. From these baseline studies, transcatheter arterial routes, retrograde venous routes, and direct percutaneous puncture routes were planned to embolize the AVF exactly at the AV connection, thereby ablating the high- to lowpressure vascular shunt. Direct percutaneous puncture embolizations were employed to circumvent tortuosity and other anatomic obstacles related to prior surgical vascular ligations. In patient 1, two direct percutaneous arterial catheters were placed in the proximal and distal ligated stumps of the anterior tibial artery, and one retrograde venous 7-F occlusion balloon catheter (Medi-tech/ Boston Scientific, Watertown, Mass) was placed in the draining anterior tibial vein to occlude flow during em-
Y :
D~ETHL
PLITERL "-E L T INJECT CffLF
a. b. C. Figure 1. Patient 1. (a)Lateral radiograph of the left lower extremity. Note the bone bridging between the tibia and fibula. (b) Anteroposterior (AP) DSA study of the popliteal artery. Note the hypertrophied anterior tibial artery (arrow) supplying the AVF. (c) AP selective DSA study of the anterior tibial artery. Note the large pseudoaneurysm at the AV connection. Note the distal continuation of the transected anterior tibial artery below the AVF (arrows).Note the large anterior tibial vein draining the fistula inferiorly (arrowheads) (Fig 1continues).
right ear, direct percutaneous puncbolization and for 10 minutes after embolization. In patient 2, only retro- ture of the primary outflow vein was performed just distal to the AV congrade venous approaches to the mulnection, with the needle tip directed tiple AVFs were used to occlude flow toward the AVF. External manual with either a 5-F Berenstein catheter compression of the ear outflow vein (Medi-tech/Boston Scientific) or 5-F against the petrous bone, posterior to or 7-F occlusion balloon catheters, thereby inducing vascular stasis. Em- the external auditory canal, induced bolization was performed through the vascular stasis. Retrograde ethanol embolization of the AVF was then persame occlusion balloon catheter, formed. The external manual compreswhich remained inflated for 10 minsion was maintained for 10 minutes. utes. In three embolizations in paNo medetermined ethanol volumes tient 2, a thigh blood pressure cuff infor embolization were considered. flated to 250 mm Hg for 10 minutes The amount of ethanol used was estiwas also required to induce vascular mated from the flow-volume characstasis. Patient 3 underwent direct teristics of the individual AVF treatpercutaneous puncture embolization ed. Occluding spring coil emboli with use of a 21-gauge butterfly nee(Cook, Bloomington, Ind) of various dle with no need to occlude flow. Unsizes were used as a temporary means der real-time color flow Doppler ulto occlude the inflow arterial feeder trasound (US) guidance (Acuson, prior to ethanol embolotherapy at Mountain View, Calif), patient 4 unseveral retrograde venous transcathderwent embolization via direct per" eter embolizations to prevent uncutaneous puncture with use of a 21wanted nontarget arterial embolizagauge butterfly needle. A thigh blood tion proximal to the fistula (patients pressure cuff inflated to 250 mm Hg 1and 2). Three occluding spring coil was used to induce vascular stasis in patient 4. In patient 5, a 7-F occlusion emboli were used to stabilize the thrombosis in a large pulmonary AVF balloon catheter was placed in the pulmonary artery to occlude flow and in an attempt to prevent unwanted forward migration of the clot to the permit injection of ethyl alcohol. In patient 6 with a recurrent AVF of the left side of the heart and the systemic
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RESULTS
Figure 1 (continued). (d) AP popliteal arteriogram obtained 1month after surgery. The AVF has recurred, but the pseudoaneurysm has thrombosed. Note ligation of the anterior tibial artery proximal and distal to the fistula (arrows).Note the nonocclusive ligature on the draining anterior tibial vein (arrowhead).(e) AP DSA study of the popliteal artery immediately after embolization. Note the closure of the AVF. (f) AP popliteal arteriogram obtained 12 months after ethanol embolotherapy. The AVF remains thrombosed with no evidence of recanalization. arterial circulation (patient 5). Patient 3 did not require vascular occlusion for thrombosis of her AVF. For those patients who required vascular occlusion by means of an occlusion balloon catheter and/or blood pressure cuffs inflated above systolic pressure, the duration of occlusion was 10 minutes. To determine the volume of ethanol used during embolization and the rate of injection, test injections of contrast material were performed with fluoroscopic monitoring. The amount of ethanol used was based on the amount of contrast material required to fill the fistula without opacifying normal vessels. In those embolizations requiring vascular stasis, test injections of contrast material were performed and monitored with fluoroscopy while vascular occlusion was employed. Again, delivery of the volume of contrast material required to opacify only the AVF at a particular rate of manual injection was practiced several times. Once the volume and manual injection rate were determined for contrast material, the procedure was repeated for ethanol. Several ethanol injections
were usually required to completely thrombose the AVF. Arteriograms or retrograde venous angiograms were obtained after all ethanol embolizations. Follow-up angiograms were obtained in patients 1 and 2. Patient 4 did not require follow-up arteriography because color flow Doppler US accurately depicted the AVF prior to ethanol embolotherapy and was used to document persistent thrombosis at follow-up. Informed consent was obtained from each patient. All patients were counseled extensively as to the potential complications of intravascular ethanol embolization. All patients were closely followed up to identify any immediate or delayed complications. Later clinical follow-up visits were required to evaluate improvement, worsening, or recurrence of symptoms. Patients 1and 2 underwent follow-up arteriography. Patient 2 also underwent follow-up retrograde venography. Patient 4 underwent follow-up color flow Doppler US examination. Patients 3, 5, and 6 will return for follow-up angiography at 6 months after embolization.
Six patients underwent 27 embolization procedures: one transcatheter arterial, 21 transcatheter retrograde vein, and five direct percutaneous puncture embolizations. Angiograms obtained immediately after embolization documented the acute thrombosis of the AVFs embolized in all patients. No embolization of nontarget vessels was identified. In patients who underwent transcatheter retrograde vein embolization, no angiographic evidence or clinical signs and symptoms of deep vein thrombosis or venous insufficiency were found. All follow-up arterial and venous studies in patients 1and 2 showed persistent AVF thrombosis with no evidence of fistula recanalization or neovascular recruitment. Persistent thrombosis was documented on all angiographic studies from these two patients (range, 12-16 months; mean, 14 months). Color flow Doppler US follow-up studies at 7 months depicted persistent AVF thrombosis in patient 4. Therefore, persistent AVF thrombosis was documented in patients l , 2, and 4 (range, 7-16 months; mean, 11months). All patients, except patient 2, had a single AVF and required only a single embolization session to ablate the fistula. Patient 2 had numerous AVFs and required multistaged ethanol embolizations. In addition to pain and claudication in his right lower extremity, this patient also had a significantly increased cardiac output of 18 Llmin. After five ethanol embolizations, the patient's cardiac output was reduced to a more tolerable 9 L/ min. Further, the patient no longer requires any cardiac medications. His therapy is ongoing. Intravascular ethanol embolotherapy can cause pain that may not be controlled by the usual premedication regimens. Patients 1,2,3, and 5 were given increased doses of intravenously administered meperidine and diazepam during the procedure as needed. These four patients experienced significant pain that responded to the
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Figure 2. Patient 2. (a) AP pelvic arteriogram, early phase. Note the significant vascular hypertrophy of the entire right iliofemoral arterial system. (b) AP pelvic arteriogram, late phase. Note the early filling of the enlarged right iliofemoral venous system (arrows) during the arterial phase, secondary to the vascular shunting caused by multiple AVFs. (c) AP deep femoral arteriogram of the proximal thigh, early phase. Note the arterial hypertrophy. (d) AP deep femoral arteriogram, late phase. Note the early filling of the deep femoral venous system (arrows) secondary to the extensive AV shunting (Fig 2 continues).
increased doses of medication. Patients 4 and 6 received neuroleptic sedation administered intravenously by an anesthesiologist and did not remember a painful experience. Among 27 embolization procedures, there were two complications. Patient 2 has undergone 20 ethanol embolization procedures to date. After the second ethanol embolization, there was a small area of skin breakdown (2 X 2 cm) with a secondary infection. The patient completely recovered after institution of local wound care and antibiotic therapy. No complications occurred in this patient after the other ethanol embolizations. Patient 4 underwent ethanol embolization via a direct percutaneous puncture of an AVF of the right anterior tibia1 compartment. The patient suffered a small area of skin breakdown (2 X 3 cm) that caused secondary superficial saphenous vein phlebitis. The patient recovered completely with local wound care and antibiotic therapy. In this patient series, the total complication rate is 7.5%.
DISCUSSION
c.
Differentiation between AVFs and AVMs is important prior to an embolization procedure (3). Clinically and
angiographically, both types of vascular malformations can be strikingly similar and difficult to differentiate.
d. AVMs are congenital vascular malformations supplied by hypertrophied (macrofistulous) inflow arteries
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Figure 2 (continued). (e) AP superficial femoral arteriogram, early phase. Note the multi~ledistal collateral vessels (arrows) shunting through multiple AVFs. (f) AP superficial femoral arteriogram, late phase. Note that the superficial femoral artery is opacified (arrows), and simultaneously the deep femoral vein (arrowheads) is opacified secondary to multiple tortuous vessels shunting through many AVFs. Because of the many overlapping arteries and veins, it is exceedingly difficult to delineate discrete AVFs without selective arteriograms and retrograde venograms. (g) AP retrograde vein angiogram from a DSA study shows reflux of contrast material into multiple tortuous inflow arterial channels (arrowheads). Note the bullet fragment. Two AVFs are seen on this retrograde venous study (large straight arrows). Each AVF drains into a single vein (small straight arrows), which then merges and drains into a larger deep femoral vein (curved arrow). (h) AP retrograde vein angiogram obtained after selective ethanol embolization of each AVF. No reflux of contrast material into the tortuous inflow arteries occurs because each AVF has thrombosed. Note that contrast material is seen only in the two small veins that initially drained the two AVFs (straight arrows). The larger deep femoral vein (curved arrow) remains patent. No complications occurred.
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as well as microfistulous connections, which usually are not evident a t arteriography. These feeding arteries connect to an immature interlacing network of primitive vascular spaces termed the AVM nidus. Hypertrophied outflow veins drain the AVM nidus. Because there is no intervening capillary bed, a prominent high-pres-
sure to low-pressure vascular shunt is present. AVFs are single direct AV connections without an intervening capillary bed. AVFs are most commonly acquired lesions secondary to blunt or penetrating trauma, with injury to an artery and adjacent vein. In the healing process a fistula forms between
the artery and vein. This situation is stimulated by preferential vascular shunting through the AVF from the higher-pressure arterial system to the lower-pressure venous system. The vascular shunt may increase with long-standing AVFs with resultant neovascular recruitment in response to this shunt. This may cause confusion at angiography as the multiple tortuous inflow arteries and dilated outflow veins may simulate an AVM nidus near the AV connection (2,3).
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Figure 3. Patient 4. (a) AP popliteal arteriogram from a DSA study. Note the hypertrophied inflow artery (arrowheads) arising from the posterior tibial artery, which supplies the AVF (large straight arrow). Note enlarged outflow venous varix (small straight arrows) and the previous surgical ligation and resection of the anterior tibial artery (curved arrow). (b) Lateral popliteal arteriogram. Note the hypertrophied inflow artery (arrowheads)supplying the AVF (large arrow) and the enlarged outflow venous varix (small arrows). (c) AP direct puncture angiogram obtained before embolization. Note opacification of the venous varix and outflow vein. (d) AP popliteal arteriogram obtained after ethanol embolization. Note absence of the hypertrophied feeder compared with a. Note the misregistration artifact of the thrombosed venous varix (arrows).
The natural history of AVFs can be extremely varied. Like AVMs, AVFs can remain unknown clinically and be well tolerated by the patient. Examples include the iatrogenic AVF constructed for the dialysis patient or the asymptomatic renal AVF incidentally found at aortography. At the opposite end of the spectrum is the patient who suffers recurrent bouts of congestive heart failure and is incapacitated by his AVF. Vascular steal alone can cause symptoms in the tissues or organs adjacent to the AVF. The natural historv of the AVF depends on the size of the shunt throughAthefistula. When the shunt is large, hemodynamic consequences such as an increased heart rate, cardiomegaly, abnormally increased cardiac output, and bouts of congestive heart failure can be extremely problematic. Treatment of AVFs requires complete occlusion of the AV connection. Like AVMs, proximal arterial ligations and distal venous ligations will always fail. This surgical approach only removes possible vascular access routes for endovascular ablation of
the AVF. It is mandatory that any surgical or embolization procedure be directed at the complete ablation of the AVF at the AV connection. Various vascular occlusive devices, including spring coils, detachable balloons, polyvinyl alcohol, and silk sutures, have been successful in occluding AVFs (3-7). Recurrence of AVFs has been reported after the use of detachable balloons (9). In high-flow AVFs, care must be maintained in the closure of the fistula. Normal perfusion pressure breakthrough phenomenon is a potential complication after closure of any AVF (10). There is one previous report of the use of absolute ethanol to treat two
patients with renal AVFs. Ours is the first patient series in which ethanol is used to embolize AVFs in other locations. On the basis of our current success in treating AVMs with absolute ethanol, we applied the same principles to treatment of AVFs (11-13). Ethanol is superior to many embolic agents because it is easy to use, and it incites an intense thrombosis to the level of the smallest caliber vessel.
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a. b. Figure 4. Patient 5. (a) AP right pulmonary arteriogram obtained before embolization shows the AVF (arrow). (b) AP right pulmonary arteriogram obtained after ethanol and coil embolization demonstrates absence of the AVF (arrow).
Precisely because of these superb thrombotic properties, embolization of nontarget vessels must be eliminated to minimize the risks of neuropathy and devitalization of normal tissues. Temporary vascular occlusion and the predetermined volume and rate of manual injection of ethanol provide some control and help lessen the likelihood of nontarget embolization. Two patients experienced skin necrosis following ethanol embolization. Patient 4 (Fig 3) had undergone several surgical procedures in a failed attempt to treat an AVF of the anterior tibial compartment. At her last surgery, the entire anterior tibial compartment was completely excised along with the anterior tibial artery, veins, and nerve. This left the patient with a permanent foot drop and compromised arterial and venous systems of the anterior tibial region. The AVF, however, recurred and caused renewed pain and swelling. The AVF was thrombosed after ethanol embolization by means of direct percutaneous puncture. A small area of skin ne-
crosis occurred in a circumferential area around the puncture site, which led to a secondary infection. Several mechanisms could be responsible for the small focal area of skin necrosis. Because of the compromised arterial vascularity, ethanol-induced edema or thrombosis of end vessels could further compromise the tissues, worsen the ischemia, and lead to necrosis. Venous thrombosis may also play a role. Also, ethanol could leak from the vessel puncture site after removal of the percutaneous needle and cause inflammatory changes in ischemic tissues that could lead to necrosis. These mechanisms that could be responsible for the skin necrosis are difficult to prevent when ethanol is the embolic agent. Patient 2 had multiple AVFs of the thigh secondary to a high-velocity bullet injury. This resulted in markedly decreased exercise tolerance and intermittent pain, exacerbated by low-pressure environments, such as the poorly pressurized cabins he had flown in on some military airlifts. He also had a cardiac output of 18 L/min.
Multiple surgeries had no effect. Particulate arterial embolization caused multiple pulmonary emboli that, in turn, caused the patient to become comatose for 9 days. A vascular surgeon recommended bilateral lower extremity amputation and a right hemipelvectomy, in hopes of resecting all of the AVFs and returning the patient's cardiac output to normal. Instead, ethanol embolotherapy was instituted. After five retrograde venous embolizations, the patient's cardiac output was reduced to a more tolerable 9 Llmin. After the second embolization, a small area of bruising was seen subcutaneously. The patient was observed for 14 days, and no skin necrosis occurred. The patient was then taken by military airlift back to his home in Houston. However, this flight 15 days after embolization caused renewed symptoms of pain and swelling so severe that the patient was confined to a litter by the time he arrived in Texas. During the next 2 days, the patient noted that the skin overlying the area of bruising broke down and became secondarily infected. He was then readmitted, and his wound healed with local wound care and antibiotic therapy. The precise pathophysiologic mechanisms responsible for the skin necrosis in this case are uncertain. Edema associated with low cabin pressure may have further compromised an area of skin with a vascular supply that was already precarious from the embolization. Vascular spasm may have also played a role. This phenomenon was also observed in a patient with an AVM of the foot who did very well after embolization. However, during the flight home 3 days after embolization, the patient experienced acute pain and swelling, resulting in prolonged postembolization edema of the foot. It is also important to remember that the sympathetic nerves to the lower extremities run parallel to the arteries and their branches. Sympathetic function can be destroyed by ischemic injury or direct neurotoxic effects of ethanol, resulting in loss of vasomotor tone and severe swelling,
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discoloration, and pain. In a t least one case of superselective transarterial embolization of a renal cell carcinoma metastasis to the femur, a 1-2 mL injection of ethanol led to "chemical syrnpathectomy," severe swelling (days later), and reddish purple discoloration of the entire extremity below the level of embolization. The patient became bedridden (Becker GJ, personal communication, 1990). However, these vasomotor changes lasted only 3 weeks. They may have been self-limited due to recovery of the peripheral sympathetic nerves. Alternatively, the clinical improvement may have represented a response to orally administered carbamazepine. Additionally, improvement of sympathetic nervous function may have resulted, in part, from resolution of surrounding tissue edema. Tissue ischemia and injury can occur with any embolization procedure. These complications are especially possible with the use of intravascular ethanol. Despite the fact that nontarget embolization was not observed during any procedures in our series, two instances of skin necrosis occurred. Although these complications were unfortunate, the regions were small and manageable, unlike the patients' AVFs. In each case, the risk of skin necrosis must be given due consideration, but not out of proportion with the patient's primary problem. We have found that patients with extremely problematic vascular malformations who have undergone multiple traumatic failed therapies tend to accept the very real risk of skin necrosis-provided there is a reasonable chance of curing the underlying lesion with embolization and curing the skin necrosis with wound care, skin grafts, or myocutaneous flaps. In summary, absolute ethanol acutely thrombosed problematic AVFs that recurred after surgery and embolization with agents other than ethanol. All patients experienced symptomatic improvement after closure of the fistula with ethanol embolotherapy. Two patients had small areas of skin necrosis after embolization
that resulted in local bacterial infections that required antibiotic therapy. For both patients the injuries healed with conservative management; neither required skin or myocutaneous grafts. At follow-up, two patients are cured of their AVF (patients 1and 4), and one patient is currently undergoing ethanol embolotherapy for multiple AVFs, with significant clinical improvement after 20 embolization procedures (patient 2). Follow-up studies in patient 2 have documented persistent closure of all AVFs embolized. Patients 3,5, and 6 are considered initially cured, but they will return at 6 months to document persistent AVF closure. Ethanol embolotherapy has proved efficacious in the treatment of problematic AVFs that recurred after surgery and those AVFs in patients who had not undergone prior therapy. Extreme caution and meticulous technique must be exercised with the use of ethanol to minimize the risks of tissue devitalization. Acknowledgments: The authors thank Nona Marie Yakes, BA, Julia Ann Criado, Frances Yakes, MA, and Lynnen Yakes for their exemplary efforts and inspiration in the preparation and completion of this manuscript. References 1. Fowl RJ, Kempczinski FJ, Bailey WW, Dickhoner WA. Management of a complex, posttraumatic, pelvic arteriovenous fistula with the use of cardiopulmonary bypass: case report and review of the literature. Vasc Surg 1987; 6:257-261. 2. Trout HH, Tievsky AL, Rieth KG, Druy EM, Giordano JM. Arteriovenous fistula simulating arteriovenous malformation. Otolaryngol Head Neck Surg 1987; 97:322-325. 3. Lawdahl RB, Routh WD, Vitek JJ, McDowell HA, Gross GM, Keller FS. Chronic arteriovenous fistulas masquerading as arteriovenous malformations: diagnostic considerations and therapeutic implications. Radiology 1989; 17O:lOll-1015. 4. Debrun G, Legre J , Kasbarian M, Tapias PL, Caron JP. Endovascular occlusion of vertebral fistulae by detachable balloons with conservation
of the vertebral blood flow. Radiology 1979; 130:141-147. Layne TA, Finck EJ, Boswell WD. Transcatheter occlusion of the arterial supply to arteriovenous fistulas with Gianturco coils. AJR 1978; 131: 1027-1030. Halbach VV, Higashida RT, Hieshima GB. Treatment of vertebral arteriovenous fistulas. AJR 1988; 150:405-412. White RI, Lynch-Nyhan A, Terry P, et al. Pulmonary arteriovenous malformations: techniques and longterm outcome of embolotherapy. Radiology 1988; 169:663-669. Sasaki M, Tadokoro S, Kimura S, Mori M, Kosuda S, Tachnibana M. Two cases of renal arteriovenous fistula treated by transcatheter embolization with absolute ethanol. Hinyokika Kiyo 1984; 30:295-298. Keller FS, King CE. Delayed detachable balloon migration: a cause of recurrent arteriovenous fistula. J Intervent Radio1 1986; 1:37-39. Halbach VV, Higashida RT, Hieshima GB, Norman D. Normal perfusion pressure breakthrough occurring during treatment of carotid and vertebral fistulas. AJNR 1987; 8:751756. Yakes WF, Pevsner P, Reed M, Donohue HJ, Ghaed N. Serial embolizations of an extremity arteriovenous malformation with alcohol via direct percutaneous puncture. AJR 1986; 146:1038-1040. Yakes WF, Haas DK, Parker SH, et al. Symptomatic vascular malformations: ethanol embolotherapy. Radiology 1989; 170:1059-1066. Yakes WF, Parker SH, Gibson MD, Haas DK, Pevsner PH, Carter TE. Alcohol embolotherapy of vascular malformations. Semin Intervent Radiol 1989: 6:146-161.
