Although portal vein thrombosis (PVT) is due to hematologic conditions associated with thrombogenic tendencies, the cause of PVT is evident in less than 50 percent of cases. PVT occurs in 10 percent of patients with cirrhosis and frequently accompanies hepatocellular carcinoma. PVT may be associated with systemic or local infection or mesenteric inflammation. PVT can complicate pregnancy, especially eclampsia, and conditions causing portal venous stasis such as hepatic venous obstruction, chronic heart failure, and constrictive pericarditis. Encasement of the portal vein by pancreatic, gastric, and other malignancies can also lead to PVT.

Signs and symptoms of PVT depend on the location and extent of the thrombus, how rapidly PVT develops, and the nature of any underlying liver disease. PVT may lead to segmental atrophy and infarction. It can be acutely fatal when associated with mesenteric vein thrombosis. Collateral channels form and the portal vein recanalizes (cavernous transformation) in 1/3 of patients in whom PVT develops slowly (subacute or chronic). Portal vein thrombosis can cause or exacerbate portal hypertension.

As in this case, the predominant clinical feature is often the underlying disease. However, bleeding from esophageal varices is a frequent presentation. The presence of splenomegaly and absence of ascities are common findings.

CT findings may include (1) increased size of the portal vein, (2) hyperdense thrombus on noncontrast CT or low density, nonenhancing intraluminal thrombus on contrast enhanced CT, (3) low density filling defect on contrast CT/lack of contrast medium enhancement of the portal vein, (4) failure to visualize the portal vein, (5) canvernous transformation (nest of collateral veins in the porta hepatis), and (6) calcification within the thrombus. T1WI reveals hperintense portal vein thrombus and numerous portal flow voids (collaterals). Ultrasound is the best screening imaging modality. Thrombus appears echogenic and collaterals and varices are often seen.