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Ischemic hepatitis, also called ischemic hepatopathy, hypoxic hepatitis, shock liver, or acute cardiogenic liver injury may affect 2.5 of every 100 patients admitted to an intensive care unit and results from an acute fall in cardiac output due to acute myocardial infarction, arrhythmia, or septic or hemorrhagic shock, usually in a patient with passive congestion of the liver. Clinical hypotension may be absent (or unwitnessed). In some cases, the precipitating event is arterial hypoxemia due to respiratory failure, sleep apnea, severe anemia, heat stroke, carbon monoxide poisoning, cocaine use, or bacterial endocarditis. More than one precipitant is common. Statin therapy prior to admission may protect against ischemic hepatitis.

The hallmark of ischemic hepatitis is a rapid and striking elevation of serum aminotransferase levels (often greater than 5000 units/L); an early rapid rise in the serum lactate dehydrogenase (LD) level (with an ALT-to-LD ratio less than 1.5) is also typical. Elevations of serum alkaline phosphatase and bilirubin are usually mild, but jaundice is associated with worse outcomes. The prothrombin time may be prolonged, and encephalopathy or hepatopulmonary syndrome may develop. The mortality rate due to the underlying disease is high (particularly in patients receiving vasopressor therapy or with septic shock, acute kidney disease, or coagulopathy), but in patients who recover, the aminotransferase levels return to normal quickly, usually within 1 week—in contrast to viral hepatitis.

In patients with passive congestion of the liver (“nutmeg liver”) due to right-sided heart failure, the serum bilirubin level may be elevated, occasionally as high as 40 mg/dL (684 mcmol/L), due in part to hypoxia of perivenular hepatocytes, and its level is a predictor of mortality and morbidity. Serum alkaline phosphatase levels are normal or slightly elevated, and, in the absence of superimposed ischemia, aminotransferase levels are only mildly elevated. Hepatojugular reflux is present, and with tricuspid regurgitation the liver may be pulsatile. Ascites may be out of proportion to peripheral edema, with a high serum ascites-albumin gradient (greater than or equal to 1.1) and an ascitic fluid protein level of more than 2.5 g/dL (25 g/L). A markedly elevated serum N-terminal-proBNP or BNP level (greater than 364 pg/mL [364 ng/L]) has been reported to distinguish ascites due to heart failure from ascites due to cirrhosis in the absence of renal insufficiency. In severe cases, signs of encephalopathy may develop. Liver stiffness measurement by elastography is increased even in the absence of fibrosis. Mortality is generally attributable to the underlying heart disease but has also been reported to correlate with a noninvasive measure of liver stiffness. The MELD score excluding the INR (MELD-XI) predicts the clinical outcome.

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Hilscher  M  et al. Congestive hepatopathy. Clin Liver Dis. 2016;8(3):68–71.
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Koehne de Gonzalez  AK  et al. Heart disease and the liver: pathologic evaluation. Gastroenterol Clin North Am. 2017 Jun;46(2):421–35.
[PubMed: 28506373]  
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Lemmer  A  et al. Assessment of advanced liver fibrosis and the risk for hepatic decompensation ...

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