Hypoxic Hepatitis

Abstract

Hypoxic hepatitis (HH), also known as ischemic hepatitis or shock liver, is an acute liver injury caused by liver ischemia. Common underlying conditions that lead to hypoxic hepatitis are cardiac failure, respiratory failure and septic shock. The most significant distinguishing features are a massive, rapid but transient elevation of serum aspartate transaminase (AST) and alanine transaminase (ALT), and the reversal of the original AST/ALT ratio during the declining phase of enzyme changes. Around 50% of patients with HH do not have a documented hypotensive event or shock state and therefore, “shock liver” is not a proper term for these patients. In patients with toxic/septic shock, the oxygen supply to the liver is not decreased, but rather the increased oxygen requirement unbalances the oxygen supply/demand relationship. Thus, the septic liver is not truly “ischemic”. Accordingly, the term “ischemic hepatitis” is not strictly correct either. Hypoxic hepatitis is now the universally preferred term. The incidence of hypoxic hepatitis is 0.2% of total hospital admissions and 1.5–11% in patients in intensive care units. The pathophysiology is multifactorial and includes hepatic congestion due to right heart failure (backward failure) along with decreased hepatic perfusion (forward failure); hypoxemia due to respiratory diseases, reduced oxygen uptake by hepatocytes, and reperfusion injury. The diagnostic criteria include: a compatible clinical setting, such as cardiac, circulatory or respiratory failure; abrupt, significant, but transient rise in serum aminotransferase levels; and exclusion of other causes of hepatocellular necrosis. The therapeutic strategies are mostly supportive including correcting the underlying disease state, avoiding potential complications such as hypoglycemia, hyperglycemia, hyperammonemia and hepatopulmonary syndrome. The mortality rate is more than 50%. High aminotransferases, LDH, PT-INR, arterial ammonia and jaundice are predictors for poor outcomes.