Objective: Cavernous transformation of the portal vein is defined as the formation of venous channels within or around a previously thrombosed portal vein. The purpose of this work was to study the hemodynamic consequences of cavernous transformation of the portal vein in a group of afflicted patients by use of Doppler sonography. We wished to study the evolution from portal vein thrombosis to the formation of cavernous transformation, the extent of resulting extrahepatic collateral channels, and the patterns of splanchnic collateral circulation.
Materials and methods: Seventy-five patients (48 adults and 27 children) with cavernous transformation of the portal vein were studied with color and/or pulsed Doppler sonography. Blood flow in the extrahepatic portal vein, in its segmental branches, in the hepatic veins and artery, and in the splanchnic veins was examined. Collateral pathways were sought. For nine patients with acute thrombosis of the portal vein, serial examinations were performed during the formation of cavernous transformation.
Results: In nine patients, a fresh thrombus filled and distended the portal vein and became recanalized within a few days. Tortuous vessels appeared at the porta hepatis. These were characterized as veins or arteries with Doppler sonography. Soon the portal vein could no longer be identified within the mass of tortuous vessels. The cavernous transformation developed within 6-20 days of the acute thrombosis. A spongelike mass of collateral vessels around the main portal vein was seen in all but two patients. Intrahepatic extension of the cavernous transformation was seen in 57 patients (76%) and involved one or more intrahepatic portal veins. Two types of collateral circulation were observed: portosystemic, mainly through the left gastric and the perisplenic veins (the caput medusae, i.e., the paraumbilical-to-abdominal venous route, was never seen); and portoportal, from the periportal or pericholecystic venous channels to the intrahepatic portal veins. In nine patients, flow within unaffected intrahepatic branches of the portal vein was reversed as directed toward the cavernous transformation surrounding other, thrombosed intrahepatic segments of the portal vein.
Conclusion: After thrombosis of the portal vein, portoportal venous channels may form not only at the porta hepatis but also within the liver. Intrahepatic blood may be shunted from one segmental portal vein to another. In addition, portosystemic collateral channels are formed, suggesting that, despite extensive hemodynamic adaptations, portal hypertension ensues.