Abstract

Ischemic hepatitis is defined as an acute reversible elevation in either the serum alanine or aspartate aminotransferase level of at least 20 times the upper normal limit, excluding known causes of acute hepatitis or hepatocellular injury (viral or toxic). Histopathologic examination reveals a centrolobular liver cell necrosis. The pathophysiology of ischemic hepatitis is poorly understood. At present, the pathophysiologic hypotheses most often proposed are an ischemic/reperfusion injury of the liver and a selective hypersensitivity of the mesenteric vasculature to the renin–angiotensin axis. In ischemic hepatitis an hepatic venous congestion and a hypoxia hepatitis should be present. An underlying cardiac disease is the factor that often leads to hepatic venous congestion. The hepatic hypoxia is the result of the decrease in systemic blood pressure leading to a reduction in hepatic blood pressure or the result of a severe arterial hypoxemia. The causes of a low cardiac output are more often cardiogenic, but hypovolemia or toxic causes are possible. More rarely, a hypoxemia, without shock, is responsible for ischemic hepatitis. The incidence of ischemic hepatitis in patients admitted to intensive care unit is unknown. The mortality rate, six months after the ischemic hepatitis is 50%. The prognosis is primarily related to cardiac function.

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