In alcoholic liver disease vascular distortion by the regenerative nodule may not be a satisfactory explanation for the sinusoidal or postsinusoidal location of the vascular resistance postulated from the findings at hepatic vein catheterization. Diffuse collagen deposition in the central portion of the liver lobule after cellular injury may be a more important mechanism.
Twenty-eight patients were studied with acute alcoholic liver damage, a pathologic diagnosis of acute sclerosing hyaline necrosis, and a clinical syndrome consisting of tender hepatomegaly, jaundice, fever, abdominal pain, leukocytosis, and often ascites. Microscopic features included evidence of cellular damage, alcoholic hyalin, polymorphonuclear infiltration, and collagen deposition, predominantly centrolobularly. Regenerative nodules were not seen microscopically, and in 19 patients the liver surface was smooth when viewed at peritoneoscopy, autopsy, or surgery. All patients had portal hypertension, evidenced by elevated, wedged hepatic vein pressure (range, 6 to 20 mm Hg; mean, 13.6 mm Hg above vena caval pressure). Esophageal varices were seen in 13 patients.