Before discussing the sonographic findings in patients with portal hypertension, it is important to recall the gross and histopathologic changes that occur in patients with cirrhosis. Using alcoholic cirrhosis as a model, classic changes include hepatocyte necrosis, nodular regeneration, and the formation of fibrotic septae. Alcohol can also induce hepatocyte enlargement by stimulating intracellular fat and protein deposition that compresses the sinusoids and obstructs flow. Likewise, collagen deposition occurs in the sinusoids, which also increases resistance to portal venous flow. An abnormal imbalance of vasodilators and vasoconstrictors also contributes to portal hypertension. When resistance to portal venous flow increases beyond a pressure gradient of ≥ 12 mm of Hg, portosystemic collaterals develop, which diverts some of the portal venous blood flow. In an effort to compensate for the decreased portal venous flow, hepatic artery flow increases. In patients with advanced end-stage liver disease, hepatic artery flow may be diverted through the sinusoids to the portal vein producing hepatofugal flow (which is flow retrograde through the portal venous system).
