PubMed1995
Ischaemic hepatitis, a condition to be distinguished from cardiac liver or stasis cirrhosis, can occur as an acute episode in patients with advanced stage congestive heart failure. The mechanism is massive necrosis in the central lobules resulting from acute hypoxia when low cardiac output reduces oxygen supply further aggravating the underlying condition of congestion due to poor venous outflow. We report 4 cases which illustrate the difficulties in diagnosis and treatment. All four patients (age range 79-86 years) were seen in an emergency situation caused by an acute drop in cardiac output aggravating their underlying heart failure. Clinical signs included jaundice, oligouria, abdominal pain and cardiovascular shock. The first element suggesting the diagnosis of ischaemic hepatitis was a sudden and massive peak in transaminase levels (> 20 times normal) which rapidly returned to normal. Prothrombin and fibrinogen levels fell rapidly and functional renal failure was present in all cases. Viral serology was negative and no hepatotoxic drugs could be incriminated. Despite symptomatic intensive care one patient died on day 15 due to cardiovascular shock. Enzyme movements, together with the lack of evidence for another cause, is the key to diagnosis of acute ischaemic hepatitis which thus is often established after the emergency situation has been controlled. Initially, viral hepatitis or drug-induced hepatotoxicity may be suspected, especially if the episode of low cardiac output goes unrecognized. Cases with signs of encephalopathy may also be difficult to distinguish from fulminating hepatitis and would be the only indication for needle biopsy in this acute situation. Outcome is generally unfavourable with mortality at 6 months estimated at 50%.