Abstract

Portal vein thrombosis (PVT) is a common complication among patients with cirrhosis. However, its pathophysiology is not well established and there are currently very few predictive factors, none of which are actually useful, from a clinical perspective. The contribution of each of the vertices of Virchow’s triad, e.g., blood hypercoagulability, blood flow, and portal vein endothelial damage in the development of PVT is not clear. In this review, we aim to recapitulate the latest studies on the field of PVT development in order to understand its mechanisms and discuss some of the future directions in the study of this important complication of cirrhosis.

Highlights

  • Portal vein thrombosis (PVT) is defined as the appearance of a thrombus in the portal vein or its branches, with or without an extension to the superior mesenteric vein or the splenic vein [1]

  • The portal venous system is unique. It is responsible for draining the blood from the gastrointestinal tract to the liver and, it does not drain into the heart but into a capillary system that becomes highly resistant in the setting of cirrhosis

  • These results are in agreement with other recently published studies [11,40], together leading to the conclusion that blood hypercoagulability may not be the culprit of PVT development

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Summary

Introduction

Portal vein thrombosis (PVT) is defined as the appearance of a thrombus in the portal vein or its branches, with or without an extension to the superior mesenteric vein or the splenic vein (the so-called splanchnic territory) [1]. It is responsible for draining the blood from the gastrointestinal tract to the liver and, it does not drain into the heart but into a capillary system (the hepatic sinusoids) that becomes highly resistant in the setting of cirrhosis. We aim to incorporate the latest studies on PVT development in the context of cirrhosis with the existent knowledge, as well as discuss all three vertices of Virchow’s triad in detail and propose future directions for the advancement of this field Both the clinical management of PVT and the invasion of the portal vein due to HCC, which have been reviewed elsewhere [27,28], are out of the scope of this review

Blood Hypercoagulability
Portal Vein Hemodynamics and Blood Flow
Thrombus Composition
Findings
Main Challenges and Future Directions
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