Cirrhosis is a late stage of progressive liver fibrosis characterized by disruption of liver tissue architecture and the formation of regenerative nodules. One of its complications is portal vein thrombosis (PVT), which is defined by the formation of a thrombus within the main portal vein or its branches, with or without spreading to the superior mesenteric or splenic vein. PVT can be evaluated based on its degree into partial and complete, extension regarding the involvement of the surrounding veins and age into acute and chronic. The prevalence of PVT in cirrhosis is known to increase parallely with the severity of liver disease and is around 1% in the compensated phase, around 10% in acute decompensation, and 10-44% in the case of underlying HCC. The pathogenesis of PVT in liver cirrhosis is probably multifactorial and results from changes in various components of the Virchow triad: slow blood flow, hypercoagulability, and endothelial damage. Acute PVT is characterized by a sudden thrombus formation in the portal vein leading to its partial or complete obstruction. The clinical presentation may be asymptomatic or may include abdominal cramps, dyspepsia, or diarrhea if the thrombus has affected the superior mesenteric vein. Involvement of the distal part of the superior mesenteric vein can lead to intestinal ischemia, intestinal infarction and ileus. After 3-5 weeks following an episode of acute PVT, a network of venous collaterals is formed, i.e., cavernoma, which is a feature of chronic PVT. It may be asymptomatic or portal hypertension may develop. Complications of portal hypertension together with portal cholangiopathy represent the main clinical manifestations of chronic PVT. Therapeutic modalities include anticoagulants and transjugular intrahepatic portosystemic shunt (TIPS). Additional prospective studies are needed to better define the prevention and prognosis of PVT.