(Passive Hepatic Congestion)
Congestive hepatopathy is diffuse venous congestion within the liver that results from right-sided heart failure (usually due to a cardiomyopathy, tricuspid regurgitation, mitral insufficiency, cor pulmonale, or constrictive pericarditis).
(See also Overview of Vascular Disorders of the Liver.)
Moderate or severe right-sided heart failure increases central venous pressure, which is transmitted to the liver via the inferior vena cava and hepatic veins. Chronic congestion leads to atrophy of hepatocytes, distention of sinusoids, and centrizonal fibrosis, which, if severe, progresses to cirrhosis (cardiac cirrhosis). The basis for liver cell death is probably sinusoidal thrombosis that propagates to the central veins and branches of the portal vein, causing ischemia.
Most patients are asymptomatic. However, moderate congestion causes right upper quadrant discomfort (due to stretching of the liver capsule) and tender hepatomegaly. Severe congestion leads to massive hepatomegaly and jaundice. Ascites may result from the transmitted central venous hypertension; infrequently, splenomegaly results. With transmitted central venous hypertension, the hepatojugular reflex is present, unlike in hepatic congestion due to Budd-Chiari syndrome.
Congestive hepatopathy is suspected in patients who have right-sided heart failure, jaundice, and tender hepatomegaly. Laboratory test results are modestly abnormal: unconjugated hyperbilirubinemia (total bilirubin < 3 mg/dL), elevated (usually < 2- to 3-fold) aminotransferases, and prolonged PT/INR. Ascitic fluid, if present, has a high albumin content (typically > 2.5 g/dL); in contrast, only 10% of patients with cirrhotic ascites have ascitic albumin levels that high.
Because the laboratory abnormalities are nonspecific, recognition of congestive hepatopathy is ultimately clinical. The liver disorder is more important as an index of the severity of heart failure than as a diagnosis by itself.