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Management of portal vein thrombosis in liver transplantation
ELSEVIER
Management of Portal Vein Thrombosis in Liver Transplantation T. Karatzas, E. Lykaki-Karatzas, A. Demirbas, A. Tsaroucha, J. Phipps, J. Nery, M. Webb, F. Khan, G. Ciancio, R. Reddy, E. Schiff, J. Miller, and A.G. Tzakis
A
MONG the technical difficulties in orthotopic liver transplantation (OLT) that can place in jeopardy the patient and graft outcome is portal vein thrombosis (PVT), which has been one of the most challenging problems to overcome. Considerable progress has been made in the last few years in the evolution of technical adjustments that allowed even the more complex thrombosis to reach excellent resu1ts.l.’ The management of PVT requires an appropriate surgical strategy at the time of surgery. Nowadays, even a very extensive PVT with involvement of its tributaries to portal system may no longer be a contraindication to OLT because almost all patients can be safely and successfully transplanted.le3 In this study, we report our experience with PVI in OLT and we describe the technical approaches to restore portal venous flow to liver allografts. PATIENTS AND SURGICAL TECHNIQUES
From June 1994 through April 1996,343 OLT in 313 patients, 289 adults, and 35 children were performed at the Department of Transplantation, University of Miami. Twenty-six PVT were documented preoperatively by Doppler ultrasound and arteriogram and were confirmed at the time of transplantation. Nine of the 26 cases were associated with extensive fibrosis surrounding the PV tissues. Six cases occurred as a result of previously inserted transjugular intrahepatic portosystemic shunts (TIPS), one was due to a mesocaval dacron shunt, two cases were due to hepatocellular carcinoma, one was due to a posttraumatic injury from a gun shot, and one was due to a very large varix arising from the border of the PV. The surgical techniques involved in PVT depend on the extent of the thrombosis, which may vary from a segment of the PV only to extensive involvement beyond the confluence of the superior mesenteric vein (SMV) and splenic vein (SV). Technically, the PV was skeletonized in a retrograde dissection, at an adequate length that could be encircled and clamped superior to the pancreas. In the cases of segmental thrombosis, an endothrombectomy was enough to recanalize the lumen of the vein and to perform a usual end-to-end anastomosis. In the alternative cases, in which more extensive thrombosis was found to involve the confluence, which could endanger a safe direct anastomosis, the reconstruction was done with a short interposition vein graft from the donor iliac vein. Extensive thrombosis beyond the confluence, associated occasionally with an abnormal vein and calcium-containing wall and/or obliterated by an old thrombus, required a jump graft from the SMV. A free segment of the donor common iliac vein including the external portion was anastomosed end-to-side to the recipient SMV and tunneled through an avascular window anterior to the 0041-1345/97/$17.00
pancreas, beneath the pylorus, and anastomosed to the donor PV. The infrapancreatic route was not used in any of the jump grafts. When a bypass was required, only a single veno-Venus from the saphenous to the axillary vein was used to avoid propagation of the lethal embolus through the bypass system. TREATMENT AND OUTCOME
According to the extent of PVT, we followed three different technical approaches to resolve the problem. The first approach included 14 cases with partial or complete PV occlusion which were treated with thrombectomy followed by extensive dissection of the PV to the conlhrence of the SMV and SV and end-to-end donor-recipient anastomosis. In addition to thrombectomy, four cases required removal of clotted TIPS and one case the removal of a mesocaval dacron shunt. A l-year-old child with an extremely small and hypoplastic PV (0.15 cm diameter) and a large thrombus had thrombectomy and low anastomosis which ended up to be of double size caliber (0.3 cm). The second technical approach included eight cases that required jump grafts from the donor iliac vein. Indications for jump graft involved extensive calcified thrombus to the SMV-SV confluence (n = 2), very small, fibrotic, and thrombosed PV (n = 2) removal of clotted TIPS (n = 2), and hepatocellular carcinoma (n = 1). The dissection usually extended to the SMV beyond the confluence, to find a soft and compressible vessel. In the third approach, four interposition vein grafts from the donor iliac vein or vena cava were used to bridge the recipient PV or SMV to the donor PV. The indications included fibrotic and thrombosed PV (n = 2) post-TIPS procedure with very thin, friable, and thrombosed PV (n = l), and one case of small PV with a large varix arising from its border close to the confluence. All patients in this series with PVT and OLT had no problems with portal flow after transplantation. Routine clinical monitoring in the early posttransplant period indicated no problems related to previous PVT. Follow-up by Doppler From the Department of Surgery, Division of Liver/G1 Transplantation, University of Miami, School of Medicine, Miami, Florida. Address reprint requests to Theodore Karatzas, University of Miami School of Medicine, Department of Surgery, Division of Liver/G1 Transplantation (Mi340), PO Box 015809, Miami, FL, 33101.
PII so041 -1345(97)0071 l-2
0 1997 by Elsevier Science Inc. 655 Avenue of the Americas, New York, NY 10010
2866
Transplantation
Proceedings,
29, 2866-2867
(1997)
MANAGEMENT OF PORTAL VEIN THROMBOSIS
ultrasound demonstrated normal PV patency and excellent vein graft function. None of the interposition or jump grafts failed. The patient survival rate in the PVT group was 61.5% (16 of 26) compared to 81.8% (235 of 287) for all other liver transplant patients. The graft survival rate in the PVT group was 61.2% (19 of 31) compared to 78.9% (262 of 332) in all other liver grafts for the same time period. DISCUSSION
Portal vein thrombosis is no longer a contraindication to liver transplantation. In this study, PVT most likely occurred in patients with postnecrotic cirrhosis, with severely shrunken livers, in posttrauma patients, and in patients with hepatocellular carcinoma. While the insertion of TIPS was very effective to control variceal hemorrhage in our liver transplant candidates, it complicated the transplant in 40% of the cases. Major problems created by TIPS were transposition up or downwards and occlusion, which resulted in PVT. Moreover, patients with a previously performed mesocaval shunt developed a sclerotic PV with a calciumcontaining wall that increased the difficulties for vascular anastomosis. Technically, it is almost always possible to solve the problem of PVT during transplantation. However, it is important to know in advance the precise extension of thrombosis, particularly when the SMV and SV are involved. Special attention should be paid to children with a history of billiard arts because a small and hypoplastic PV is very common.’ In our series of children, in one case in which a very hypoplastic PV was found, the dissection was extended down to the confluence to obtain an adequate caliber vein for a wide and safe anastomosis that could ensure optimal portal flow. In those cases of extensive PVT in which a vein jump
graft was required to bypass the obstruction, this conduit provided excellent recanalization to the liver allograft and perfect portal flow. Technically, we avoided maneuvers on the superior pancreatic area that could create posttransplant pancreatitis. Also, the dissection for the exposure of SMV was limited inferior to the pancreas at the base of the transverse mesocolon, to perform the anastomosis. Although it was used in one case in this series, the SV might also provide an acceptable portal inflow access should the SMV prove inadequate.4 The portal collaterals may exceptionally be used for anastomosis. These collaterals are sometimes dilated enough to allow anastomosis with the donor PV. In our patient with sclerosing cholangitis and complete SMV and SV thrombosis with multiple collaterals, the PV was reestablished with a jump graft which was anastomosed to a good-sized collateral vein located on the mesenteric route. This vein conduit functioned very well and provided an excellent portal flow to the liver allograft. Seven months posttransplant, the patient is doieg well with normal liver function. A total of 30.8% PVT in this series required an extra-anatomical vein jump graft. None of the patients had any complications related to the vein conduit. We feel confident to conclude that, based on our recent experience, the variations used from the standard operative technique for PV reconstruction made it possible for all patients with portal system thrombosis to undergo a successful liver transplantation. REFERENCES 1. Stieber AC, Zetti G, Todo S, et al: Ann Surg 213:199, 1991 2. Lerut J, Tzakis AG, Bron K, et al: Ann Surg 205:404, 1987 3. Shaw BW, Iwatsuki S, Bron K, et al: Surg Gynecol Obstet 161:67, 1985 4. Kirsch JP, Howard TK, Klintmalm GB, et al: Surgery 107:544, 1990
Management of Portal Vein Thrombosis in Liver Transplantation T. Karatzas, E. Lykaki-Karatzas, A. Demirbas, A. Tsaroucha, J. Phipps, J. Nery, M. Webb, F. Khan, G. Ciancio, R. Reddy, E. Schiff, J. Miller, and A.G. Tzakis
A
MONG the technical difficulties in orthotopic liver transplantation (OLT) that can place in jeopardy the patient and graft outcome is portal vein thrombosis (PVT), which has been one of the most challenging problems to overcome. Considerable progress has been made in the last few years in the evolution of technical adjustments that allowed even the more complex thrombosis to reach excellent resu1ts.l.’ The management of PVT requires an appropriate surgical strategy at the time of surgery. Nowadays, even a very extensive PVT with involvement of its tributaries to portal system may no longer be a contraindication to OLT because almost all patients can be safely and successfully transplanted.le3 In this study, we report our experience with PVI in OLT and we describe the technical approaches to restore portal venous flow to liver allografts. PATIENTS AND SURGICAL TECHNIQUES
From June 1994 through April 1996,343 OLT in 313 patients, 289 adults, and 35 children were performed at the Department of Transplantation, University of Miami. Twenty-six PVT were documented preoperatively by Doppler ultrasound and arteriogram and were confirmed at the time of transplantation. Nine of the 26 cases were associated with extensive fibrosis surrounding the PV tissues. Six cases occurred as a result of previously inserted transjugular intrahepatic portosystemic shunts (TIPS), one was due to a mesocaval dacron shunt, two cases were due to hepatocellular carcinoma, one was due to a posttraumatic injury from a gun shot, and one was due to a very large varix arising from the border of the PV. The surgical techniques involved in PVT depend on the extent of the thrombosis, which may vary from a segment of the PV only to extensive involvement beyond the confluence of the superior mesenteric vein (SMV) and splenic vein (SV). Technically, the PV was skeletonized in a retrograde dissection, at an adequate length that could be encircled and clamped superior to the pancreas. In the cases of segmental thrombosis, an endothrombectomy was enough to recanalize the lumen of the vein and to perform a usual end-to-end anastomosis. In the alternative cases, in which more extensive thrombosis was found to involve the confluence, which could endanger a safe direct anastomosis, the reconstruction was done with a short interposition vein graft from the donor iliac vein. Extensive thrombosis beyond the confluence, associated occasionally with an abnormal vein and calcium-containing wall and/or obliterated by an old thrombus, required a jump graft from the SMV. A free segment of the donor common iliac vein including the external portion was anastomosed end-to-side to the recipient SMV and tunneled through an avascular window anterior to the 0041-1345/97/$17.00
pancreas, beneath the pylorus, and anastomosed to the donor PV. The infrapancreatic route was not used in any of the jump grafts. When a bypass was required, only a single veno-Venus from the saphenous to the axillary vein was used to avoid propagation of the lethal embolus through the bypass system. TREATMENT AND OUTCOME
According to the extent of PVT, we followed three different technical approaches to resolve the problem. The first approach included 14 cases with partial or complete PV occlusion which were treated with thrombectomy followed by extensive dissection of the PV to the conlhrence of the SMV and SV and end-to-end donor-recipient anastomosis. In addition to thrombectomy, four cases required removal of clotted TIPS and one case the removal of a mesocaval dacron shunt. A l-year-old child with an extremely small and hypoplastic PV (0.15 cm diameter) and a large thrombus had thrombectomy and low anastomosis which ended up to be of double size caliber (0.3 cm). The second technical approach included eight cases that required jump grafts from the donor iliac vein. Indications for jump graft involved extensive calcified thrombus to the SMV-SV confluence (n = 2), very small, fibrotic, and thrombosed PV (n = 2) removal of clotted TIPS (n = 2), and hepatocellular carcinoma (n = 1). The dissection usually extended to the SMV beyond the confluence, to find a soft and compressible vessel. In the third approach, four interposition vein grafts from the donor iliac vein or vena cava were used to bridge the recipient PV or SMV to the donor PV. The indications included fibrotic and thrombosed PV (n = 2) post-TIPS procedure with very thin, friable, and thrombosed PV (n = l), and one case of small PV with a large varix arising from its border close to the confluence. All patients in this series with PVT and OLT had no problems with portal flow after transplantation. Routine clinical monitoring in the early posttransplant period indicated no problems related to previous PVT. Follow-up by Doppler From the Department of Surgery, Division of Liver/G1 Transplantation, University of Miami, School of Medicine, Miami, Florida. Address reprint requests to Theodore Karatzas, University of Miami School of Medicine, Department of Surgery, Division of Liver/G1 Transplantation (Mi340), PO Box 015809, Miami, FL, 33101.
PII so041 -1345(97)0071 l-2
0 1997 by Elsevier Science Inc. 655 Avenue of the Americas, New York, NY 10010
2866
Transplantation
Proceedings,
29, 2866-2867
(1997)
MANAGEMENT OF PORTAL VEIN THROMBOSIS
ultrasound demonstrated normal PV patency and excellent vein graft function. None of the interposition or jump grafts failed. The patient survival rate in the PVT group was 61.5% (16 of 26) compared to 81.8% (235 of 287) for all other liver transplant patients. The graft survival rate in the PVT group was 61.2% (19 of 31) compared to 78.9% (262 of 332) in all other liver grafts for the same time period. DISCUSSION
Portal vein thrombosis is no longer a contraindication to liver transplantation. In this study, PVT most likely occurred in patients with postnecrotic cirrhosis, with severely shrunken livers, in posttrauma patients, and in patients with hepatocellular carcinoma. While the insertion of TIPS was very effective to control variceal hemorrhage in our liver transplant candidates, it complicated the transplant in 40% of the cases. Major problems created by TIPS were transposition up or downwards and occlusion, which resulted in PVT. Moreover, patients with a previously performed mesocaval shunt developed a sclerotic PV with a calciumcontaining wall that increased the difficulties for vascular anastomosis. Technically, it is almost always possible to solve the problem of PVT during transplantation. However, it is important to know in advance the precise extension of thrombosis, particularly when the SMV and SV are involved. Special attention should be paid to children with a history of billiard arts because a small and hypoplastic PV is very common.’ In our series of children, in one case in which a very hypoplastic PV was found, the dissection was extended down to the confluence to obtain an adequate caliber vein for a wide and safe anastomosis that could ensure optimal portal flow. In those cases of extensive PVT in which a vein jump
graft was required to bypass the obstruction, this conduit provided excellent recanalization to the liver allograft and perfect portal flow. Technically, we avoided maneuvers on the superior pancreatic area that could create posttransplant pancreatitis. Also, the dissection for the exposure of SMV was limited inferior to the pancreas at the base of the transverse mesocolon, to perform the anastomosis. Although it was used in one case in this series, the SV might also provide an acceptable portal inflow access should the SMV prove inadequate.4 The portal collaterals may exceptionally be used for anastomosis. These collaterals are sometimes dilated enough to allow anastomosis with the donor PV. In our patient with sclerosing cholangitis and complete SMV and SV thrombosis with multiple collaterals, the PV was reestablished with a jump graft which was anastomosed to a good-sized collateral vein located on the mesenteric route. This vein conduit functioned very well and provided an excellent portal flow to the liver allograft. Seven months posttransplant, the patient is doieg well with normal liver function. A total of 30.8% PVT in this series required an extra-anatomical vein jump graft. None of the patients had any complications related to the vein conduit. We feel confident to conclude that, based on our recent experience, the variations used from the standard operative technique for PV reconstruction made it possible for all patients with portal system thrombosis to undergo a successful liver transplantation. REFERENCES 1. Stieber AC, Zetti G, Todo S, et al: Ann Surg 213:199, 1991 2. Lerut J, Tzakis AG, Bron K, et al: Ann Surg 205:404, 1987 3. Shaw BW, Iwatsuki S, Bron K, et al: Surg Gynecol Obstet 161:67, 1985 4. Kirsch JP, Howard TK, Klintmalm GB, et al: Surgery 107:544, 1990