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Congestive Hepatopathy

(Passive Hepatic Congestion)

By

Whitney E. Jackson

, MD, University of Colorado School of Medicine

Last full review/revision Feb 2020| Content last modified Feb 2020
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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).

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.

Symptoms and Signs

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.

Diagnosis

  • Clinical evaluation

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 [51.31 micromol/L]), elevated (usually < 2- to 3-fold) aminotransferases, and prolonged prothrombin time/international normalized ratio (PT/INR). Ascitic fluid, if present, is characterized by a high serum-to-ascites albumin concentration gradient (the serum albumin concentration minus the ascitic albumin concentration [SAAG]). Gradients ≥ 1.1 g/dL (11 g/L) are relatively specific for ascites due to portal hypertension (1). In addition, a high ascitic total protein content (typically > 2.5 g/dL [25 g/L]) plus a SAAG ≥ 1.1 g/dL (11 g/L) suggests congestive hepatopathy (2) and differentiates portal hypertension from cirrhosis.

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.

Portal Hypertension

  • Patel YA, Muir AJ: Evaluation of new-onset ascites. JAMA 316(3): 340–341, 2016. doi: 10.1001/jama.2016.7600

  • Runyon BA: Cardiac ascites: A characterization. J Clin Gastroenterol 10(4):410-412, 1988.

Treatment

  • Targets underlying heart failure

Treatment is directed at the underlying heart failure.

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