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Vascular Complications After Pediatric Liver Transplantation From the Living Donors
Technical
Vascular Complications After Pediatric Liver Transplantation From the Living Donors D. Broniszczak, M. Szymczak, A. Kamin´ski, A. Chyz˙yn´ska, H. Ismail, T. Drewniak, P. Nachulewicz, M. Markiewicz, J. Teisseyre, E. Dzik, A. Lembas, and P. Kalicin´ski ABSTRACT Early arterial or portal vein thrombosis is a complications that can lead to graft loss and patient death or need of immediate retransplantation. The aim of the study was to assess the incidence, causes, treatment, and outcome of vascular thrombosis after living related donor liver transplantation (LRdLTx). Between 1999 and 2004 71 LRdLTx were performed in children aged from 6 months to 10 years. Vascular thrombosis was found in 12 recipients. Hepatic artery thrombosis (HAT) occurred in 4 (5.6%), portal vein thrombosis (PVT) in 8 (11.2%) cases. HAT occurred 5 to 8 days, PVT 1 to 22 days after LTx. Diagnosis of vascular thrombosis was confirmed by routine Doppler ultrasound examination. Thrombectomy was successful in one patient with HAT and in three patients with PVT. Venous conduit was performed in one patient with PVT after second thrombosis. Two children developed biliary strictures as a late complication of HAT and required additional surgical interventions. Two children with PVT developed portal hypertension with esophageal bleeding, which required surgical intervention; one another underwent endoscopic variceal ligation for grade III varices. Follow-up ranged from 7 to 60 months. One patient died as a result of HAT after retransplantation due to multiple intrahepatic abscesses 2 months after first transplant. Any risk factors of vascular thrombosis that can be controlled should be avoided after transplantation. Routine posttransplant Doppler examination should be performed at least twice a day within 7 to 14 posttransplant days. Immediate thrombectomy should be always carried out to avoid late complications and even mortality.
V
ASCULAR THROMBOSIS after liver transplantation is the serious complication that can lead to increased morbidity, graft loss, and patient death. Children, especially after living related donor liver transplantation (LRdLTx), have been reported to be at a greater risk of developing vascular thrombosis compared to adult population because of the small diameter of vessels and the recipient’s weight.1–3 The incidence of hepatic artery thrombosis (HAT) and portal vein thrombosis (PVT) in children after liver transplantation from living donors is high, ranging up to 25% and up to 11%, respectively.3–5
The aim of the study was to asses the incidence, cause, treatment, and outcome of arterial and portal thrombosis after LRdLTx in children in our institute.
From the Children’s Memorial Health Institute, Warsaw, Poland. Address reprint requests to Mrs Dorota Broniszczak, MD, Children’s Memorial Health Institute, Department of Pediatric Surgery and Organ Transplantation, Dzieci Polskich 20, Warsaw 04 ⫽ 736, Poland.
0041-1345/06/$–see front matter doi:10.1016/j.transproceed.2006.02.094
© 2006 by Elsevier Inc. All rights reserved. 360 Park Avenue South, New York, NY 10010-1710
1456
Transplantation Proceedings, 38, 1456 –1458 (2006)
VASCULAR COMPLICATIONS POST–PEDIATRIC TRANSPLANTATION
MATERIALS AND METHODS Between 1999 and 2004 71 LRdLTx were performed in Children’s Memorial Health Institute. Recipients age ranged from 6 months to 10 years (70% were younger than 2 years old), and their body mass ranged from 4.5 to 10 kg (50% weighed less than 10 kg). Graft/recipients weight ratio (GRWR) varied from 0.86% to 5.11%. Biliary atresia was the main indication for transplantation (46 children, 66.7%). The others were: acute liver failure in six cases, malignant tumors in five, nonbiliary atresia cholestasis in five, hamartoma in two, mucoviscidiosis in two, cirrhosis in two, large hepatic hemangiomas in two, graft-versus-host disease after bone marrow transplantation in one. Vascular anastomoses were performed with the use of loupe magnification, interrupted 8/0 non absorbable sutures in the hepatic artery and interrupted or continuous 6/0-7/0 absorbable monofilament sutures in the portal vein. Doppler ultrasound and detailed biochemical monitoring of graft function were performed twice daily for 7 to 10 days after transplantation. Every patient received anticoagulants: nadroparine 40 to 50 IU/kg/d for 7 to 10 days, continuous dextran 40,000 infusion for 5 to 7 days and aspirin for 6 months after transplantation. Hematocrit was kept between 27% and 30%. Fresh-frozen plasma was administered only when International Normalized Ratio exceeded 1.7. Dopamine and dobutamine infusions were administered routinely for 5 to 7 days after transplantation.
RESULTS
Vascular thrombosis was found in 12 recipients (16.9%), aged 9 month to 4 years (mean 1 year, 5 months, 11 patients below 2 years old) with body mass 7.2 to 15 kg (mean 9 kg, 10 patients below 10 kg). HAT occurred in 4 (5.6%) and PVT in 8 (11.2%) cases. HAT was diagnosed 5 to 8 days after transplantation and PVT between 1 to 22 days. HAT was associated with sudden increase of liver function tests in two of four children, while PVT did not present specific laboratory findings; in two of eight children bleeding from esphageal varices occurred. Diagnosis of vascular thrombosis was confirmed by routine Doppler ultrasound examination. PVT occurred only in children with biliary atresia and hypoplastic portal vein. In four children compression by liver graft and sudden hypovolemia in one case could play a main role. Technical problems with very tiny arteries (diameter less than 2 mm in two cases) led probably to HAT in all four cases. Two of four patients (50%) with HAT and six of eight patients (75%) with PVT had GRWR ⬎3%. Surgical thrombectomy was performed in three of four patients with HAT and in seven of eight with PVT. Two children with HAT and five with PVT had local infusion of recombinant tissue plasminogen activator after thrombectomy. One child with HAT and two with PVT had systemic infusion after thrombectomy. One patient with HAT had systemic infusion without surgical intervention. Thrombectomy was successful in one patient with HAT and in three patients with PVT. Venous conduit was performed in one patient with PVT after a second thrombosis. Two children developed biliary strictures as a late complication of HAT and required additional surgical interventions. Two children with PVT developed portal hypertension with esophageal bleeding, which required surgical intervention; one
1457
another underwent endoscopic variceal ligation for grade III varices. Despite unsuccessful thrombectomy intrahepatic arterial blood flow is detected in two of 3 children (66.6%) with persistent HAT and intrahepatic portal blood flow in four out of five children (80%) with persistent PVT. None of patients with PVT have any symptoms of portal hypertension at present. Actual follow-up in patients with vascular complications after LRdLTx range from 7 to 60 months. One patient died as a result of HAT after retransplantation due to multiple intrahepatic abscesses 2 months after first transplant. DISCUSSION
The risk of vascular thrombosis is relatively high in pediatric recipients receiving graft from living related donors. The reported rates vary between different centers, but always are higher than in recipients of whole graft and in adult population.1–3 In our material HAT occurred in 4 (5.6%), which is regarded as an acceptable incidence, and PVT in 8 (11.2%) cases, which is regarded as a rather high incidence compared to other centers.1–3 Many factors are considered as predisposing to vascular thrombosis in children after LRdLTx.6 Portal vein hypoplasia, which is common in patients with biliary atresia, is one of the main risk factors of posttransplant thrombosis, and it was present in all children who developed this complication in our series. Particularly small diameter of hepatic artery was seen in 2 patients (50%) from the HAT group. Additional risk factors—namely, age below 2 years and body mass below 10 kg—were present in 11 (91.6%) and 10 patients (83%), respectively, in our series, which are regarded as high percentages. These factors are probably responsible for the relatively high incidence of PVT in our material. The risk of PVT is always significantly higher in groups of small children, reaching as much as 20% in some reports.7,8 All the above-mentioned factors cannot be eliminated in the pediatric population of liver transplant recipients; however, it is very important to avoid the ones that can be controlled, namely, high hematocrit, overcorrection of coagulation, hypovolemia, and compression of the graft.6 Size mismatch between graft and recipient frequently occurs in liver transplantation in children. It is particularly common in small recipients of LRdLTx. Eight of 12 patients with vascular complications had GRWR above 3%, which is considered as large-for-size graft. Graft compression can compromise hepatic vascular flow and lead to thrombotic complications. Large-for-size grafts can also impact increased incidence of vascular complications because of vessel kinking, low portal flow speed, and disproportion of vessels diameter.9,10 Clear differentiation is difficult because these causes occur often simultaneously. Delayed abdominal wound closure or creation of abdominal hernia with closure of the skin only is often performed in these patients. Several surgical techniques are used to prevent vascular complications: performance of all vascular anastomosis
BRONISZCZAK, SZYMCZAK, KAMIN´SKI ET AL
1458
with loupe magnification or microscope, anastomosing of donor portal vein to the confluence of recipient’s superior mesenteric and splenic vein, or the bifurcation of portal vein to donor portal vein. All these technical innovations contributed significantly to reduction of vascular complications in children after LRdLTx in our, as well other, reported series.2,11,12 Patients with HAT are at significant risk for graft loss, increased morbidity, and mortality and our experience confirms these observations.1,2,13,14 One (25%) patient of four with HAT had successful thrombectomy and remains free of late complications. In all three remaining patients we observed biliary complications: one of them developed intrahepatic abscesses, lost the graft 2 months after LRdLTx, and finally died during retransplantation. Two long-term survivors developed biliary strictures and recurrent cholangitis and are actually well after biliary reconstructions. In the treatment of PVT surgical intervention is favored as the first-line approach.11 In our material 3 of 7 (42.8%) portal thrombectomies were successful. However, in the remaining four patients, despite unsuccessful thrombectomy, partial recanalization of portal vein can be seen in the late follow-up. This reappearance of portal flow seems to be responsible for the lack of symptoms of portal hypertension in these children. In two patients after unsuccessful thrombectomy of hepatic artery, intrahepatic arterial flow was also detectable, probably coming from the adhesions to the hepatic capsula. In our material all HAT and the large majority of PVT incidents occurred during the first posttransplant week, but only in two cases of HAT was elevation of liver function tests observed. Therefore, it is highly recommended to assess blood flow of the graft twice a day by color Doppler imaging as the best tool for early detection of vascular thrombosis.15 In conclusion, any risk factors of vascular thrombosis that can be controlled should be avoided after transplantation, particularly hypercoagulation, hypovolemia, and graft compression. Clinical and laboratory symptoms of vascular thrombosis after LRdLTx are not specific in the majority of patients, therefore routine posttransplant Doppler examination should be performed at least twice a day within 7 to 14 posttransplant days. Immediate thrombectomy should be
always carried out to avoid late complications and even mortality. REFERENCES 1. Hashikura Y, Kawasaki S, Okumura N, et al: Prevention of hepatic artery thrombosis in pediatric liver transplantation. Transplantation 60:1109, 1995 2. Hatano E, Terajima H, Yabe S, et al: Hepatic artery thrombosis in living related liver transplantation. Transplantation 64: 1443, 1997 3. Stevens LH, Emond JC, Piper JB, et al: Hepatic artery thrombosis in infants. A comparison of whole livers, reduced-size grafts, and grafts from living-related donors. Transplantation 53: 396, 1992 4. Jurim O, Shackleton CR, McDiarmid SV, et al: Living-donor liver transplantation at UCLA. Am J Surg 169:529, 1995 5. Broelsch CE, Whitington PF, Emond JC, et al: Liver transplantation in children from living related donors. Surgical techniques and results. Ann Surg 214:428, 1991 6. Mazzaferro V, Esquivel CO, Makowka L, et al: Factors responsible for hepatic artery thrombosis after pediatric liver transplantation. Transplant Proc 21:2466, 1989 7. Lin CC, Chuang FR, Wang CC, et al: Early postoperative complications in recipients of living donor liver transplantation. Transplant Proc 36:2338, 2004 8. Wagner C, Beebe DS, Carr RJ, et al: Living related liver transplantation in infants and children: report of anesthetic care and early postoperative morbidity and mortality. J Clin Anesth 12:454, 2000 9. Cheng YF, Chen CL, Huang TL, et al: Risk factors for intraoperative portal vein thrombosis in pediatric living donor liver transplantation. Clin Transplant 18:390, 2004 10. Kiuchi T, Kasahara M, Uryuhara K, et al: Impact of graft size mismatching on graft prognosis in liver transplantation from living donors. Transplantation 67:321, 1999 11. Saad S, Tanaka K, Inomata Y, et al: Portal vein reconstruction in pediatric liver transplantation from living donors. Ann Surg 227:275, 1998 12. Colombani PM, Lau H, Prabhakaran K, et al: Cumulative experience with pediatric living related liver transplantation. J Pediatr Surg 35:9, 2000 13. Sakamoto Y, Harihara Y, Nakatsuka T, et al: Rescue of liver grafts from hepatic artery occlusion in living-related liver transplantation. Br J Surg 86:886, 1999 14. Garcia-Gallont R, Bar-Nathan N, Shaharabani E, et al: Hepatic artery thrombosis in pediatric liver transplantation: graft salvage after thrombectomy. Pediatr Transplant 3:74, 1999 15. Someda H, Moriyasu F, Fujimoto M, et al: Vascular complications in living related liver transplantation detected with intraoperative and postoperative Doppler US. J Hepatol 22:623, 1995
Vascular Complications After Pediatric Liver Transplantation From the Living Donors D. Broniszczak, M. Szymczak, A. Kamin´ski, A. Chyz˙yn´ska, H. Ismail, T. Drewniak, P. Nachulewicz, M. Markiewicz, J. Teisseyre, E. Dzik, A. Lembas, and P. Kalicin´ski ABSTRACT Early arterial or portal vein thrombosis is a complications that can lead to graft loss and patient death or need of immediate retransplantation. The aim of the study was to assess the incidence, causes, treatment, and outcome of vascular thrombosis after living related donor liver transplantation (LRdLTx). Between 1999 and 2004 71 LRdLTx were performed in children aged from 6 months to 10 years. Vascular thrombosis was found in 12 recipients. Hepatic artery thrombosis (HAT) occurred in 4 (5.6%), portal vein thrombosis (PVT) in 8 (11.2%) cases. HAT occurred 5 to 8 days, PVT 1 to 22 days after LTx. Diagnosis of vascular thrombosis was confirmed by routine Doppler ultrasound examination. Thrombectomy was successful in one patient with HAT and in three patients with PVT. Venous conduit was performed in one patient with PVT after second thrombosis. Two children developed biliary strictures as a late complication of HAT and required additional surgical interventions. Two children with PVT developed portal hypertension with esophageal bleeding, which required surgical intervention; one another underwent endoscopic variceal ligation for grade III varices. Follow-up ranged from 7 to 60 months. One patient died as a result of HAT after retransplantation due to multiple intrahepatic abscesses 2 months after first transplant. Any risk factors of vascular thrombosis that can be controlled should be avoided after transplantation. Routine posttransplant Doppler examination should be performed at least twice a day within 7 to 14 posttransplant days. Immediate thrombectomy should be always carried out to avoid late complications and even mortality.
V
ASCULAR THROMBOSIS after liver transplantation is the serious complication that can lead to increased morbidity, graft loss, and patient death. Children, especially after living related donor liver transplantation (LRdLTx), have been reported to be at a greater risk of developing vascular thrombosis compared to adult population because of the small diameter of vessels and the recipient’s weight.1–3 The incidence of hepatic artery thrombosis (HAT) and portal vein thrombosis (PVT) in children after liver transplantation from living donors is high, ranging up to 25% and up to 11%, respectively.3–5
The aim of the study was to asses the incidence, cause, treatment, and outcome of arterial and portal thrombosis after LRdLTx in children in our institute.
From the Children’s Memorial Health Institute, Warsaw, Poland. Address reprint requests to Mrs Dorota Broniszczak, MD, Children’s Memorial Health Institute, Department of Pediatric Surgery and Organ Transplantation, Dzieci Polskich 20, Warsaw 04 ⫽ 736, Poland.
0041-1345/06/$–see front matter doi:10.1016/j.transproceed.2006.02.094
© 2006 by Elsevier Inc. All rights reserved. 360 Park Avenue South, New York, NY 10010-1710
1456
Transplantation Proceedings, 38, 1456 –1458 (2006)
VASCULAR COMPLICATIONS POST–PEDIATRIC TRANSPLANTATION
MATERIALS AND METHODS Between 1999 and 2004 71 LRdLTx were performed in Children’s Memorial Health Institute. Recipients age ranged from 6 months to 10 years (70% were younger than 2 years old), and their body mass ranged from 4.5 to 10 kg (50% weighed less than 10 kg). Graft/recipients weight ratio (GRWR) varied from 0.86% to 5.11%. Biliary atresia was the main indication for transplantation (46 children, 66.7%). The others were: acute liver failure in six cases, malignant tumors in five, nonbiliary atresia cholestasis in five, hamartoma in two, mucoviscidiosis in two, cirrhosis in two, large hepatic hemangiomas in two, graft-versus-host disease after bone marrow transplantation in one. Vascular anastomoses were performed with the use of loupe magnification, interrupted 8/0 non absorbable sutures in the hepatic artery and interrupted or continuous 6/0-7/0 absorbable monofilament sutures in the portal vein. Doppler ultrasound and detailed biochemical monitoring of graft function were performed twice daily for 7 to 10 days after transplantation. Every patient received anticoagulants: nadroparine 40 to 50 IU/kg/d for 7 to 10 days, continuous dextran 40,000 infusion for 5 to 7 days and aspirin for 6 months after transplantation. Hematocrit was kept between 27% and 30%. Fresh-frozen plasma was administered only when International Normalized Ratio exceeded 1.7. Dopamine and dobutamine infusions were administered routinely for 5 to 7 days after transplantation.
RESULTS
Vascular thrombosis was found in 12 recipients (16.9%), aged 9 month to 4 years (mean 1 year, 5 months, 11 patients below 2 years old) with body mass 7.2 to 15 kg (mean 9 kg, 10 patients below 10 kg). HAT occurred in 4 (5.6%) and PVT in 8 (11.2%) cases. HAT was diagnosed 5 to 8 days after transplantation and PVT between 1 to 22 days. HAT was associated with sudden increase of liver function tests in two of four children, while PVT did not present specific laboratory findings; in two of eight children bleeding from esphageal varices occurred. Diagnosis of vascular thrombosis was confirmed by routine Doppler ultrasound examination. PVT occurred only in children with biliary atresia and hypoplastic portal vein. In four children compression by liver graft and sudden hypovolemia in one case could play a main role. Technical problems with very tiny arteries (diameter less than 2 mm in two cases) led probably to HAT in all four cases. Two of four patients (50%) with HAT and six of eight patients (75%) with PVT had GRWR ⬎3%. Surgical thrombectomy was performed in three of four patients with HAT and in seven of eight with PVT. Two children with HAT and five with PVT had local infusion of recombinant tissue plasminogen activator after thrombectomy. One child with HAT and two with PVT had systemic infusion after thrombectomy. One patient with HAT had systemic infusion without surgical intervention. Thrombectomy was successful in one patient with HAT and in three patients with PVT. Venous conduit was performed in one patient with PVT after a second thrombosis. Two children developed biliary strictures as a late complication of HAT and required additional surgical interventions. Two children with PVT developed portal hypertension with esophageal bleeding, which required surgical intervention; one
1457
another underwent endoscopic variceal ligation for grade III varices. Despite unsuccessful thrombectomy intrahepatic arterial blood flow is detected in two of 3 children (66.6%) with persistent HAT and intrahepatic portal blood flow in four out of five children (80%) with persistent PVT. None of patients with PVT have any symptoms of portal hypertension at present. Actual follow-up in patients with vascular complications after LRdLTx range from 7 to 60 months. One patient died as a result of HAT after retransplantation due to multiple intrahepatic abscesses 2 months after first transplant. DISCUSSION
The risk of vascular thrombosis is relatively high in pediatric recipients receiving graft from living related donors. The reported rates vary between different centers, but always are higher than in recipients of whole graft and in adult population.1–3 In our material HAT occurred in 4 (5.6%), which is regarded as an acceptable incidence, and PVT in 8 (11.2%) cases, which is regarded as a rather high incidence compared to other centers.1–3 Many factors are considered as predisposing to vascular thrombosis in children after LRdLTx.6 Portal vein hypoplasia, which is common in patients with biliary atresia, is one of the main risk factors of posttransplant thrombosis, and it was present in all children who developed this complication in our series. Particularly small diameter of hepatic artery was seen in 2 patients (50%) from the HAT group. Additional risk factors—namely, age below 2 years and body mass below 10 kg—were present in 11 (91.6%) and 10 patients (83%), respectively, in our series, which are regarded as high percentages. These factors are probably responsible for the relatively high incidence of PVT in our material. The risk of PVT is always significantly higher in groups of small children, reaching as much as 20% in some reports.7,8 All the above-mentioned factors cannot be eliminated in the pediatric population of liver transplant recipients; however, it is very important to avoid the ones that can be controlled, namely, high hematocrit, overcorrection of coagulation, hypovolemia, and compression of the graft.6 Size mismatch between graft and recipient frequently occurs in liver transplantation in children. It is particularly common in small recipients of LRdLTx. Eight of 12 patients with vascular complications had GRWR above 3%, which is considered as large-for-size graft. Graft compression can compromise hepatic vascular flow and lead to thrombotic complications. Large-for-size grafts can also impact increased incidence of vascular complications because of vessel kinking, low portal flow speed, and disproportion of vessels diameter.9,10 Clear differentiation is difficult because these causes occur often simultaneously. Delayed abdominal wound closure or creation of abdominal hernia with closure of the skin only is often performed in these patients. Several surgical techniques are used to prevent vascular complications: performance of all vascular anastomosis
BRONISZCZAK, SZYMCZAK, KAMIN´SKI ET AL
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with loupe magnification or microscope, anastomosing of donor portal vein to the confluence of recipient’s superior mesenteric and splenic vein, or the bifurcation of portal vein to donor portal vein. All these technical innovations contributed significantly to reduction of vascular complications in children after LRdLTx in our, as well other, reported series.2,11,12 Patients with HAT are at significant risk for graft loss, increased morbidity, and mortality and our experience confirms these observations.1,2,13,14 One (25%) patient of four with HAT had successful thrombectomy and remains free of late complications. In all three remaining patients we observed biliary complications: one of them developed intrahepatic abscesses, lost the graft 2 months after LRdLTx, and finally died during retransplantation. Two long-term survivors developed biliary strictures and recurrent cholangitis and are actually well after biliary reconstructions. In the treatment of PVT surgical intervention is favored as the first-line approach.11 In our material 3 of 7 (42.8%) portal thrombectomies were successful. However, in the remaining four patients, despite unsuccessful thrombectomy, partial recanalization of portal vein can be seen in the late follow-up. This reappearance of portal flow seems to be responsible for the lack of symptoms of portal hypertension in these children. In two patients after unsuccessful thrombectomy of hepatic artery, intrahepatic arterial flow was also detectable, probably coming from the adhesions to the hepatic capsula. In our material all HAT and the large majority of PVT incidents occurred during the first posttransplant week, but only in two cases of HAT was elevation of liver function tests observed. Therefore, it is highly recommended to assess blood flow of the graft twice a day by color Doppler imaging as the best tool for early detection of vascular thrombosis.15 In conclusion, any risk factors of vascular thrombosis that can be controlled should be avoided after transplantation, particularly hypercoagulation, hypovolemia, and graft compression. Clinical and laboratory symptoms of vascular thrombosis after LRdLTx are not specific in the majority of patients, therefore routine posttransplant Doppler examination should be performed at least twice a day within 7 to 14 posttransplant days. Immediate thrombectomy should be
always carried out to avoid late complications and even mortality. REFERENCES 1. Hashikura Y, Kawasaki S, Okumura N, et al: Prevention of hepatic artery thrombosis in pediatric liver transplantation. Transplantation 60:1109, 1995 2. Hatano E, Terajima H, Yabe S, et al: Hepatic artery thrombosis in living related liver transplantation. Transplantation 64: 1443, 1997 3. Stevens LH, Emond JC, Piper JB, et al: Hepatic artery thrombosis in infants. A comparison of whole livers, reduced-size grafts, and grafts from living-related donors. Transplantation 53: 396, 1992 4. Jurim O, Shackleton CR, McDiarmid SV, et al: Living-donor liver transplantation at UCLA. Am J Surg 169:529, 1995 5. Broelsch CE, Whitington PF, Emond JC, et al: Liver transplantation in children from living related donors. Surgical techniques and results. Ann Surg 214:428, 1991 6. Mazzaferro V, Esquivel CO, Makowka L, et al: Factors responsible for hepatic artery thrombosis after pediatric liver transplantation. Transplant Proc 21:2466, 1989 7. Lin CC, Chuang FR, Wang CC, et al: Early postoperative complications in recipients of living donor liver transplantation. Transplant Proc 36:2338, 2004 8. Wagner C, Beebe DS, Carr RJ, et al: Living related liver transplantation in infants and children: report of anesthetic care and early postoperative morbidity and mortality. J Clin Anesth 12:454, 2000 9. Cheng YF, Chen CL, Huang TL, et al: Risk factors for intraoperative portal vein thrombosis in pediatric living donor liver transplantation. Clin Transplant 18:390, 2004 10. Kiuchi T, Kasahara M, Uryuhara K, et al: Impact of graft size mismatching on graft prognosis in liver transplantation from living donors. Transplantation 67:321, 1999 11. Saad S, Tanaka K, Inomata Y, et al: Portal vein reconstruction in pediatric liver transplantation from living donors. Ann Surg 227:275, 1998 12. Colombani PM, Lau H, Prabhakaran K, et al: Cumulative experience with pediatric living related liver transplantation. J Pediatr Surg 35:9, 2000 13. Sakamoto Y, Harihara Y, Nakatsuka T, et al: Rescue of liver grafts from hepatic artery occlusion in living-related liver transplantation. Br J Surg 86:886, 1999 14. Garcia-Gallont R, Bar-Nathan N, Shaharabani E, et al: Hepatic artery thrombosis in pediatric liver transplantation: graft salvage after thrombectomy. Pediatr Transplant 3:74, 1999 15. Someda H, Moriyasu F, Fujimoto M, et al: Vascular complications in living related liver transplantation detected with intraoperative and postoperative Doppler US. J Hepatol 22:623, 1995