Raja Kaiser, Jacob Mathew, Asthana Sonal
Department of Hepatology, Hepatobiliary Surgery & Multiorgan Transplantation, Global Integrated Liver Care Program, BGS Global Hospitals, Bangalore, India.
J Clin Exp Hepatol. 2014 Dec;4(4):320-31. doi: 10.1016/j.jceh.2013.12.003. Epub 2013 Dec 31.
Portal vein thrombosis (PVT) is being increasingly recognized in patients with advanced cirrhosis and in those undergoing liver transplantation. Reduced flow in the portal vein is probably responsible for clotting in the spleno-porto-mesenteric venous system. There is also increasing evidence that hypercoagulability occurs in advanced liver disease and contributes to the risk of PVT. Ultrasound based studies have reported a prevalence of PVT in 10-25% of cirrhotic patients without hepatocellular carcinoma. Partial thrombosis of the portal vein is more common and may not have pathophysiological consequences. However, there is high risk of progression of partial PVT to complete PVT that may cause exacerbation of portal hypertension and progression of liver insufficiency. It is thus, essential to accurately diagnose and stage PVT in patients waiting for transplantation and consider anticoagulation therapy. Therapy with low molecular weight heparin and vitamin K antagonists has been shown to achieve complete and partial recanalization in 33-45% and 15-35% of cases respectively. There are however, no guidelines to help determine the dose and therapeutic efficacy of anticoagulation in patients with cirrhosis. Anticoagulation therapy related bleeding is the most feared complication but it appears that the risk of variceal bleeding is more likely to be dependent on portal pressure rather than solely related to coagulation status. TIPS has also been reported to restore patency of the portal vein. Patients with complete PVT currently do not form an absolute contraindication for liver transplantation. Thrombectomy or thromboendovenectomy is possible in more than 75% of patients followed by anatomical end-to-end portal anastomosis. When patency of the portal vein and/or superior mesenteric vein is not achieved, only non-anatomical techniques (reno-portal anastomosis or cavo-portal hemitransposition) can be performed. These techniques, which do not fully reverse portal hypertension, are associated with higher morbidity and mortality risks in the short term.
门静脉血栓形成（PVT）在晚期肝硬化患者和接受肝移植的患者中越来越受到关注。门静脉血流减少可能是脾-门静脉-肠系膜静脉系统血栓形成的原因。越来越多的证据表明，晚期肝病患者存在高凝状态，这增加了PVT的风险。基于超声的研究报告显示，在无肝细胞癌的肝硬化患者中，PVT的发生率为10%-25%。门静脉部分血栓形成更为常见，可能不会产生病理生理后果。然而，部分PVT进展为完全PVT的风险很高，这可能会导致门静脉高压加剧和肝功能不全进展。因此，准确诊断并对等待移植的患者进行PVT分期，并考虑抗凝治疗至关重要。低分子量肝素和维生素K拮抗剂治疗分别在33%-45%和15%-35%的病例中实现了完全和部分再通。然而，目前尚无指导原则来帮助确定肝硬化患者抗凝治疗的剂量和疗效。抗凝治疗相关出血是最令人担忧的并发症，但似乎静脉曲张出血的风险更可能取决于门静脉压力，而不仅仅与凝血状态有关。也有报道称经颈静脉肝内门体分流术（TIPS）可恢复门静脉通畅。目前，完全PVT患者并非肝移植的绝对禁忌证。超过75%的患者可行血栓切除术或血栓内膜切除术，随后进行解剖性端端门静脉吻合术。当无法实现门静脉和/或肠系膜上静脉通畅时，只能采用非解剖技术（肾门静脉吻合术或腔门静脉半转位术）。这些技术不能完全逆转门静脉高压，在短期内与较高的发病率和死亡率风险相关。
