Hypoxic hepatitis (HH), an acute liver injury also known as 'ischaemic hepatitis' or 'shock liver', is frequently observed in intensive care units. HH is heralded by a massive but transient rise in serum aminotransferase activities caused by anoxic necrosis of centrilobular liver cells. Cardiac failure, respiratory failure and toxic-septic shock are the main underlying conditions accounting for more than 90% of cases, but HH may also occur in other circumstances. Until recently, liver ischaemia, i.e. a drop in hepatic blood flow, was considered the leading, and even the sole, hemodynamic mechanism responsible for HH, and it was generally held that a shock state was required. In reality, other hemodynamic mechanisms of hypoxia, such as passive congestion of the liver, arterial hypoxaemia and dysoxia, play an important role while a shock state is observed in only 50% of cases. Accordingly, 'ischaemic hepatitis' and 'shock liver' are misnomers. Therapy of HH depends primarily on the nature of the underlying condition. The prognosis is poor, with more than half of patients dying during the hospital stay.
© 2011 John Wiley & Sons A/S.