Portal vein thrombosis is the major cause of presinusoidal hypertension in the United States. Common causes include cirrhosis, pancreatitis, ascending cholangitis, propagation of splenic vein thrombus after splenectomy, and neoplasm (hepatic, biliary, pancreatic, or gastric). Less common causes include hypercoagulable states, trauma, intra-abdominal infection, and inflammation.

Postcontrast CT images demonstrate lack of central portal vein enhancement, usually with peripheral rim enhancement that is likely due to flow through dilated vasa vasorum or flow of enhanced blood around an incomplete portal vein thrombus. Streaky enhancement within the obstructed portal vein suggests the presence of tumor thrombus. When thrombosis is acute, the portal vein contents may be high in attenuation on precontrast scans. With chronic portal vein thrombosis, cavernous transformation is often identified.

Alterations in hepatic blood supply result in indirect evidence of portal vein thrombosis. Decreased hepatic lobar attenuation on precontrast scans results from hepatic glycogen depletion and increased hepatocyte fat content related to loss of nutrients and insulin normally supplied by the portal venous circulation. Transiently increased parenchymal enhancement during the hepatic arterial and early portal venous phases due to increased hepatic arterial flow to a segment or lobe in which portal venous flow is diminished may be seen. This is known as transient hepatic attenuation difference (THAD). Diminished portal venous flow due occlusion or extrinsic compression from any cause may result in THAD. Over time the affected area may undergo atrophy.


MRI is also an excellent way to identify both portal vein thrombosis and the resultant differences in hepatic perfusion (THID: Transient Hepatic Intensity Difference).