Hepatobiliary and Pancreatic: Transient hepatic ischemia caused by acute portal vein thrombosis

A 79-year-old man was investigated because of a 10-day history of pain in the right upper quadrant of his abdomen. There was no preceding history of liver disease. Blood tests revealed a mild elevation of bilirubin (66 μmol/l), alanine aminotransferase (168 U/L) and aspartate aminotransferase (78 U/L). The international normalized ratio (INR) was mildly elevated (1.6). A contrast-enhanced computed tomography (CT) scan showed extensive thrombosis in the intrahepatic and extrahepatic portal vein (Figure 1 left). In addition, there were diffuse low-density liver lesions that were best shown in the portal venous phase (Figure 1 right). Subsequently, he was treated with anticoagulants to maintain the INR between 2 and 3. After 2 weeks, his pain resolved and liver function tests returned to normal. A repeat CT scan showed that the portal vein thrombosis was less prominent than previously (Figure 2 left) and that the low-density liver lesions had resolved. He was discharged from hospital on oral anticoagulants and had a further CT scan after 3 months. The scan showed cavernous transformation of the portal vein (Figure 2 right). The portal vein normally supplies approximately two-thirds of the blood supply to the liver. The remainder is provided by the hepatic artery. Although portal vein thrombosis is relatively common in cirrhosis and hepatic tumors, it appears to develop slowly in most patients and is usually asymptomatic without significant changes in liver enzymes. Presumably, the compensation for reduced portal flow is enhanced arterial flow as well as portal to portal collaterals. However, if portal vein thrombosis is acute, at least some patients have abdominal pain as well as changes in liver function tests. Fortunately, death due to hepatic ischemia is very rare. In the above patient, the appearance of low-density ischemic lesions was similar to that of multiple hepatic neoplasms. However, most neoplasms are best visualized in the arterial phase whereas ischemic lesions are more prominent in the portal venous phase. The interval between portal vein thrombosis and imaging features of cavernous transformation is somewhat variable but is usually between 2 and 12 months. In the patient described above, the cause of portal vein thrombosis remained unclear as various investigations for hypercoagulable states were unhelpful.