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Vascular complications post orthotopic liver transplantation
Vascular Complications Post Orthotopic Liver Transplantation A. Eid, S. Lyass, M. Venturero, Y. Ilan, R. Safadi, G. Zamir, Y. Berlatzky, and O. Jurim
L
IVER transplantation is the treatment of choice for selected patients with end-stage liver disease. Vascular complications after orthotopic liver transplantation (OLT) are serious events that may lead to graft loss or patient death.1 The aim of this study is to review these complications in our program. MATERIALS AND METHODS From October 1991 to May 1998, 63 OLT in 57 patients were performed at Hadassah Hebrew University Medical Center. These included 58 whole liver transplantations, four reduced size, and one living-related liver transplantation. There were 25 females and 32 males with a mean age of 40.7 year (range 3.5– 68). The follow-up was a mean of 21 months (range of 0.1–78). In 52 OLT donor liver arterial inflow was based on recipient hepatic artery (HA), and in 10 OLT on recipient aorta (Ao). In one OLT, this information was not available. Portal vein (PV) reconstruction was by end-to-end anastomosis in all transplants except in one OLT with recipient PV thrombosis (PVT), in which an interposition donor iliac vein was used. Inferior vena cava (IVC) reconstruction was performed in a standard manner in 53 OLT, and piggy-back in 10 OLT. Vascular complications were diagnosed based on clinical, ultrasonographic, angiographic, and operative findings. Statistical analysis was performed using Fisher’s exact test with significance accepted at P , .05.
RESULTS
Vascular complications developed in nine OLT (14%) including hepatic artery thrombosis (HAT) in six OLT, suprahepatic IVC stenosis in two OLT, and PVT in one OLT. One patient developed HAT secondary to primary graft failure that was successfully treated by retransplantation. In three patients, HAT developed early (within 1 week post-OLT), and in two patients it was late (at 3 months and 3 years). Three HAT occurred in the Ao group, compared to two in the HA groups (P 5 .026). In the early group, two patients underwent urgent thrombectomy with revascularization, eventually dying from septic complications with patent hepatic artery. The third patient was treated non operatively. She developed biliary stricture which was successfully managed radiologically. Both patients in the late group presented with biliary sepsis; one died awaiting retransplantation and the second died following retransplantation. The overall mortality rate of HAT in this series was 80%. Two patients developed suprahepatic IVC stenosis post-OLT. One patient presented with intractable ascitis and the second as Budd-Chiari syndrome. They were
successfully treated by balloon dilation and cavo-atrial shunt, respectively.2 PV thrombosis occurred in one patient. This complication was noted during successful retransplantation for primary graft failure with an earlier normal duplex ultrasonography of the portal vein. DISCUSSION
HAT is the most common vascular complication that may occur early (within 1 month) or late after OLT.3 At the time of diagnosis, this complication can be completely asymptomatic or it may present by deteriorating liver function, gram negative bacteremia, biliary necrosis, with bile leak, liver abscess, or graft necrosis.4 The incidence of early HAT of 4.7% in our series compares favorably with the literature.1,3,5 Multiple risk factors for HAT include technical difficulties, prolonged cold ischemia time, pediatric recipient, whole liver allograft, positive cross match, and the use of aortic conduit.6 It is interesting to note that in our series, and in accordance with the experience of Soin et al, anastomosis of donor vessels to recipient aorta was a significant risk factor for HAT to occur following liver transplantation.7 HAT carries a dismal prognosis even if it occurs late after transplantation.4 Although some patients remain asymptomatic with no complications, the majority will require surgical therapy to prevent graft loss or patient death from septic complications. The optimal surgical treatment for HAT is still debatable. Traditionally, retransplantation has been the cornerstone of therapy. Unfortunately, this approach is restricted by a limited donor pool. Therefore, and due to recent innovations in duplex ultrasound technology permitting a timely diagnosis of HAT, various centers have adopted urgent thrombectomy and revascularization of the graft as an alternative approach, with good results especially for early thrombosis and in asymptomatic patients.3,8 Following this approach, however, some patients will still require retransplantation, especially for ischemic biliary From the Hadassah Hebrew University Medical Center, Jerusalem, Israel. Address reprint requests to Dr Ahmed Eid, Department of Surgery and Transplantation Unit, Hadassah Medical Center, PO Box 12000, Jerusalem 91120, Israel.
© 1999 by Elsevier Science Inc. 655 Avenue of the Americas, New York, NY 10010
0041-1345/99/$–see front matter PII S0041-1345(99)00148-7
Transplantation Proceedings, 31, 1903–1904 (1999)
1903
1904
damage. It is difficult to draw definite conclusions based on our current series, however, due to the lack of a back-up system for urgent retransplantation in our center, we tend to adopt the revascularization approach for cases with early HAT. Anastomotic complications of the IVC following OLT are very rare.9 They usually present as Budd-Chiari like syndrome and respond to balloon dilatation angioplasty. Some cases of complete anastomotic obstruction may require bypass procedure or retransplantation.2 REFERENCES 1. Lopez Santamaria M, Vazquez J, Gamez M, et al: J Pediatr Surg 31:600, 1996
EID, LYASS, VENTURERO ET AL 2. Eid A, Rhamimov R, Ilan Y, et al: Liver Transplant Surg (in press) 3. Sheiner PA, Varma CV, Guarrera JV, et al: Transplantation 64:1295, 1997 4. Valente JF, Alonso MH, Weber FL, et al: Transplantation 61:61, 1996 5. Pinna AD, Smith CV, Furukawa H, et al: Transplantation 62:1584, 1996 6. Lallier M, St VD, Dubois J, et al: J Pediatr Surg 30:1122, 1995 7. Soin AS, Friend PJ, Rasmussen A, et al: Br J Surg 83:637, 1996 8. Langnas AN, Marujo W, Stratta RP, et al: Transplantation 51:86, 1991 9. Langnas AN, Marujo W, Stratta RP, et al: Am J Surg 161:76, 1991
L
IVER transplantation is the treatment of choice for selected patients with end-stage liver disease. Vascular complications after orthotopic liver transplantation (OLT) are serious events that may lead to graft loss or patient death.1 The aim of this study is to review these complications in our program. MATERIALS AND METHODS From October 1991 to May 1998, 63 OLT in 57 patients were performed at Hadassah Hebrew University Medical Center. These included 58 whole liver transplantations, four reduced size, and one living-related liver transplantation. There were 25 females and 32 males with a mean age of 40.7 year (range 3.5– 68). The follow-up was a mean of 21 months (range of 0.1–78). In 52 OLT donor liver arterial inflow was based on recipient hepatic artery (HA), and in 10 OLT on recipient aorta (Ao). In one OLT, this information was not available. Portal vein (PV) reconstruction was by end-to-end anastomosis in all transplants except in one OLT with recipient PV thrombosis (PVT), in which an interposition donor iliac vein was used. Inferior vena cava (IVC) reconstruction was performed in a standard manner in 53 OLT, and piggy-back in 10 OLT. Vascular complications were diagnosed based on clinical, ultrasonographic, angiographic, and operative findings. Statistical analysis was performed using Fisher’s exact test with significance accepted at P , .05.
RESULTS
Vascular complications developed in nine OLT (14%) including hepatic artery thrombosis (HAT) in six OLT, suprahepatic IVC stenosis in two OLT, and PVT in one OLT. One patient developed HAT secondary to primary graft failure that was successfully treated by retransplantation. In three patients, HAT developed early (within 1 week post-OLT), and in two patients it was late (at 3 months and 3 years). Three HAT occurred in the Ao group, compared to two in the HA groups (P 5 .026). In the early group, two patients underwent urgent thrombectomy with revascularization, eventually dying from septic complications with patent hepatic artery. The third patient was treated non operatively. She developed biliary stricture which was successfully managed radiologically. Both patients in the late group presented with biliary sepsis; one died awaiting retransplantation and the second died following retransplantation. The overall mortality rate of HAT in this series was 80%. Two patients developed suprahepatic IVC stenosis post-OLT. One patient presented with intractable ascitis and the second as Budd-Chiari syndrome. They were
successfully treated by balloon dilation and cavo-atrial shunt, respectively.2 PV thrombosis occurred in one patient. This complication was noted during successful retransplantation for primary graft failure with an earlier normal duplex ultrasonography of the portal vein. DISCUSSION
HAT is the most common vascular complication that may occur early (within 1 month) or late after OLT.3 At the time of diagnosis, this complication can be completely asymptomatic or it may present by deteriorating liver function, gram negative bacteremia, biliary necrosis, with bile leak, liver abscess, or graft necrosis.4 The incidence of early HAT of 4.7% in our series compares favorably with the literature.1,3,5 Multiple risk factors for HAT include technical difficulties, prolonged cold ischemia time, pediatric recipient, whole liver allograft, positive cross match, and the use of aortic conduit.6 It is interesting to note that in our series, and in accordance with the experience of Soin et al, anastomosis of donor vessels to recipient aorta was a significant risk factor for HAT to occur following liver transplantation.7 HAT carries a dismal prognosis even if it occurs late after transplantation.4 Although some patients remain asymptomatic with no complications, the majority will require surgical therapy to prevent graft loss or patient death from septic complications. The optimal surgical treatment for HAT is still debatable. Traditionally, retransplantation has been the cornerstone of therapy. Unfortunately, this approach is restricted by a limited donor pool. Therefore, and due to recent innovations in duplex ultrasound technology permitting a timely diagnosis of HAT, various centers have adopted urgent thrombectomy and revascularization of the graft as an alternative approach, with good results especially for early thrombosis and in asymptomatic patients.3,8 Following this approach, however, some patients will still require retransplantation, especially for ischemic biliary From the Hadassah Hebrew University Medical Center, Jerusalem, Israel. Address reprint requests to Dr Ahmed Eid, Department of Surgery and Transplantation Unit, Hadassah Medical Center, PO Box 12000, Jerusalem 91120, Israel.
© 1999 by Elsevier Science Inc. 655 Avenue of the Americas, New York, NY 10010
0041-1345/99/$–see front matter PII S0041-1345(99)00148-7
Transplantation Proceedings, 31, 1903–1904 (1999)
1903
1904
damage. It is difficult to draw definite conclusions based on our current series, however, due to the lack of a back-up system for urgent retransplantation in our center, we tend to adopt the revascularization approach for cases with early HAT. Anastomotic complications of the IVC following OLT are very rare.9 They usually present as Budd-Chiari like syndrome and respond to balloon dilatation angioplasty. Some cases of complete anastomotic obstruction may require bypass procedure or retransplantation.2 REFERENCES 1. Lopez Santamaria M, Vazquez J, Gamez M, et al: J Pediatr Surg 31:600, 1996
EID, LYASS, VENTURERO ET AL 2. Eid A, Rhamimov R, Ilan Y, et al: Liver Transplant Surg (in press) 3. Sheiner PA, Varma CV, Guarrera JV, et al: Transplantation 64:1295, 1997 4. Valente JF, Alonso MH, Weber FL, et al: Transplantation 61:61, 1996 5. Pinna AD, Smith CV, Furukawa H, et al: Transplantation 62:1584, 1996 6. Lallier M, St VD, Dubois J, et al: J Pediatr Surg 30:1122, 1995 7. Soin AS, Friend PJ, Rasmussen A, et al: Br J Surg 83:637, 1996 8. Langnas AN, Marujo W, Stratta RP, et al: Transplantation 51:86, 1991 9. Langnas AN, Marujo W, Stratta RP, et al: Am J Surg 161:76, 1991