Living Donor Liver Transplantation in a Patient With Extensive Portomesenteric Venous Thrombosis: Case Report S. Choi*, K.K. Kim, W.S. Lee, J.M. Kang, and Y.H. Park Department of Surgery, Gil Medical Center, Gachon Medicine and Science, Guwol-dong, Namdong-gu, Incheon, Republic of Korea
ABSTRACT Extensive portomesenteric venous thrombus preventing restoration of adequate portal venous flow used to be considered a contraindication to liver transplantation. The subject was a 49-year-old male with hepatitis B cirrhosis and extensive thrombosis of portal, splenic, and superior mesenteric veins, and two large collateral vessels; one dilated and tortuous inferior to the pancreaticoduodenal vein and relevant to splanchnic venous return and the other a dilated coronary vein relevant to splenic venous return. During operation, the portal vein was anastomosed to these large collateral vessels using cryopreserved iliac vein. In conclusion, portal reconstruction with large collateral vessels in living-donor liver transplantation could be used selectively for patients with extensive portomesenteric venous thrombosis.
P
ORTAL vein thrombosis (PVT) is a common complication of end-stage liver disease and has an incidence rate between 0.6% and 15% [1e3]. PVT used to be an absolute contraindication for liver transplantation, but recent advances in surgical techniques and patient care make it possible to overcome PVT during liver transplantation [4,5]. In fact, innovative surgical techniques, such as thrombectomy and the use of a venous jump graft, mean that chronic PVT is no longer considered a contraindication of liver transplantation. However, in cases of complete thrombosis of the portal vein and of the proximal and distal superior mesenteric vein (SMV), securing mesenteric flow for successful transplantation is challenging. Here, we describe a case of portal reconstruction with large collateral vessels in a living-donor liver transplantation patient with extensive portomesenteric venous thrombosis. CASE REPORT A 49-year-old male with hepatitis B cirrhosis had suffered from repeated esophageal variceal bleeding and massive ascites. Computed tomography failed to visualize the main portal vein, but revealed extensive thrombosis of portal, splenic, and superior mesenteric veins and two large collateral vessels; one dilated and tortuous inferior to the pancreaticoduodenal vein relevant to splanchnic venous return and the other a dilated coronary vein relevant to splenic venous return (Fig 1). The living donor was his 19-year-old son. Modified right lobectomy was performed; graft ª 2016 Elsevier Inc. All rights reserved. 230 Park Avenue, New York, NY 10169
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weight was 636 g, graft to recipient ratio was 1.19, and segment 5 and 8 veins were reconstructed with cryopreserved cadaveric iliac artery. During exploration of the recipient, large collaterals were initially isolated to confirm adequate mesenteric flow, and then the portal vein was anastomosed to two large collateral vessels using cryopreserved iliac vein (Fig 2). Adequate portal venous blood flow was maintained during postoperative hospitalization, but at 3 months postoperatively, Doppler sonography revealed portal vein stenosis. Because of concerns of portal occlusion, a portal vein stent was inserted using a transhepatic approach. Portal vein flow and wave form were maintained over 7 years of follow-up after stent insertion.
DISCUSSION
PVT used to be considered an absolute contraindication to liver transplantation because of its associated technical difficulties and hazards [1,2]. However, several innovative surgical techniques, such as thrombectomy and the usage of a venous jump graft or portal vein tributaries, have been introduced in recent years, and many technical obstacles have been overcome [6e8]. As a result, PVT is no longer
*Address correspondence to Sangtae Choi, MD, Gil Medical Center, Gachon Medicine and Science 1198, Guwol-dong, Namdong-gu, Incheon 405-760, Republic of Korea. E-mail:
[email protected] 0041-1345/16 http://dx.doi.org/10.1016/j.transproceed.2016.03.029
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Fig 1. Computed tomography showed collaterals with extensive portomesenteric venous thrombosis. One collateral was dilated and tortuous inferior to the pancreaticoduodenal vein and relevant to splanchnic venous return and the other was a dilated coronary vein relevant to splenic venous return (A, B), stenotic site in portal vein anastomosis (C), and improved portal vein flow after portal vein stent insertion using a transhepatic approach (D).
regarded a contraindication to liver transplantation and several series have reported encouraging postoperative results in affected patients [7,8]. Nonetheless, despite developments in surgical techniques, morbidity and mortality rates remain high due to compromised mesenteric flow in the presence of a cavernous formation caused by severe PVT [9,10]. The prerequisites for successful liver transplantation in such cases are precise preoperative evaluations of splanchnic vein and portosystemic shunt anatomies.
Fig 2. Intraoperative findings showed the donor portal vein anastomosed to two large collateral vessels using cryopreserved iliac vein.
PVT exhibits varying degrees of thrombus, from partial or segmental thrombosis to total obstruction and cavernous formation of the portal system [11]. Furthermore, PVT severity causes difficulties during transplantation, and thus, is likely to affect graft and patient outcomes. In cases of grade I and II PVT, a thrombus confined to the top of the pancreas can be addressed by simple thrombectomy. However, if organized thrombosis involves the whole portal vein, extends posterior to the pancreas and more peripherally below the SMV, the phlebotic portal vein is often an inadequate conduit after thrombectomy, and the re-establishment of portomesenteric blood flow in the portal vein cannot be performed without more complex vascular reconstructions [12]. Sometimes, we are forced to find another supply of adequate mesenteric flow other than thrombectomy. Collateral vessels of cavernous transformation of the portal vein can be classified as hepatopetal or hepatofugal pathways, where the former provide the liver with nutrients, and the latter constitute hepatofugal shunts accompanying portal hypertension [9,12]. However, it is extremely difficult to differentiate hepatopetal and hepatofugal pathways on axial images. Hepatopetal vessels can be also classified as paracholedochal venous plexus or cystic venous vessels [9,13]. In our case, primary hepatopetal flow probably originated from a paracholedochal venous plexus. The techniques reported for complete PVT in livingdonor liver transplantation include renoportal anastomosis
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interposed external iliac vein connected to the left renal vein [14]. Inferior mesenteric vein can be used to provide portal inflow for venovenous bypass and the same jump graft can be used to perfuse a graft [15]. If organized thrombosis involves the whole portal vein, extends posterior to the pancreas and to the more peripheral portion below the SMV, as in our patient, large collaterals, if patent, can be used for bypass and as a potential source of portal inflow. Summarizing, successful portal reconstruction is an essential component of liver transplantation in patients with extensive PVT and no definite normal enteric flow, and portal reconstruction using large collateral vessels in livingdonor liver transplantation could be used selectively in patients with extensive portomesenteric venous thrombosis. REFERENCES [1] Davidson BR, Gibson M, Dick R, Burroughs A, Rolles K. Incidence, risk factors, management and outcome of portal vein abnormalities at orthotopic liver transplantation. Transplantation 1994;57:1174e7. [2] Lerut JP, Mazza D, van Leeuw V, et al. Adult liver transplantation and abnormalities of splanchnic veins: experience in 53 patients. Transpl Int 1997;10:125e32. [3] Gayowski TJ, Marino IR, Doyle HR, et al. A high incidence of native portal vein thrombosis in veterans undergoing liver transplantation. J Surg Res 1996;60:333e8. [4] Kadry Z, Selzner N, Handschin A, Mullhaupt B, Renner EL, Clavien PA. Living donor liver transplantation in patients with portal vein thrombosis: a survey and review of technical issues. Transplantation 2002;74:696e701.
3155 [5] Nonami T, Yokoyama I, Iwatsuk I. The incidence of portal vein thrombosis at LT. Hepatology 1992;16:1195. [6] Davidson BR, Gibson M, Dick R. Incidence, risk factors, management, and outcome of portal vein abnormalities at orthotopic LT. Transplantation 1994;57:1174. [7] Robles R, Fernandez JA, Hernandez Q. Eversion thromboendovenectomy in organized portal vein thrombosis during LT. Clin Transplant 2004;18:79. [8] Dumortier J, Czyglik O, Poncet G. Eversion thrombectomy for portal vein thrombosis during LT. Am J Transplant 2002;2:934. [9] Stieber AC, Zetti G, Todo S, Tzakis AG, Fung JJ, Marino I. The spectrum of portal vein thrombosis in liver transplantation. Ann Surg 1991;213:199e206. [10] Turrion VS, Mora NP, Cofer JB, Salomon H, Morris CA, Gonwa TA, et al. Retrospective evaluation of liver transplantation for cirrhosis: a comparative study of 100 patients with or without previous porta-systemic shunt. Transplant Proc 1991;23:1570e1. [11] Haddad MC, Clark DC, Sharif HS, Shahed MA, Aideyan O, Sammak BM. MR, CT and ultrasonography of splanchnic venous thrombosis. Gastrointest Radiol 1992;17:34e40. [12] Yerdel MA, Gunson BR, Mirza DA, Karayalcin K, Olliff S, Buckels J. Portal vein thrombosis in adults undergoing liver transplantation: risk factor, screening, management and outcome. Transplantation 2000;69(9):1873e81. [13] Zhang LJ, Yang GF, Jiang B, Wen LQ, Shen W, Qi J. Cavernous transformation of portal vein: 16-slice CT portography and correlation with surgical procedure of orthotopic liver transplantation. Abdom Imaging 2008;33:529e35. [14] Egawa H, Tanaka K, Kasahara M. Single center experience of 39 patients with preoperative portal vein thrombosis among 404 adult living donor liver transplantations. Liver Transpl 2006;12: 1512e8. [15] Iyer SG, Lau CL, Chang KY, Mak SW, Madhavan KK. Am J Transplant 2010;10:1483e5.