Shock liver describes a collecting pool of critically ill patients in whom the elevation of liver function tests or overt hepatic dysfunction is apparent. Different grades of shock liver affect about 50% of all intensive-care patients, varying from a mild elevation of serum aminotransferase and bilirubin levels in septic patients to an acute onset of high serum aminotransferases after haemodynamic shock. Abnormalities can subside within days or progressively deteriorate when persistent hepatic microcirculatory failure is present. Although hepatic injury in critically ill patients influences mortality rates it is underdiagnosed. The underlying pathophysiology involves changes in the portal and arterial blood supply as well as in microcirculation. Cross-talk between hepatocytes, Kupffer cells and endothelial cells, leading to an inflammatory response mediated primarily by tumour necrosis factor-alpha (TNF-alpha), is central to shock liver. The liver is a victim of shock inducers, and can also be the orchestrator of the inflammatory response syndrome (IRS). Hepatic injury by TNF-alpha is modulated by the prevalent pro-inflammatory or anti-inflammatory mediator profile elaborated by Kupffer cells. Kupffer cells additionally participate in the clearance of endotoxin, bacteria and inflammatory mediators and are thereby capable of preventing IRS. The hepatocyte undergoes dramatic alterations in synthetic activity, biliary transport, bile flow and glucose metabolism. Although standard determinations of aminotransferases, coagulation studies, glucose, lactate and bilirubin can detect hepatic injury they only partially reflect the cellular mechanisms driving shock liver. The management of shock liver is focused on the prevention of precipitating causes by controlling sepsis, circulation parameters and metabolism in addition to the cautious monitoring of therapeutic measures that can increase hepatic injury, which include intravenous nutrition, mechanical ventilation and catecholamine administration.