Cerebral oedema is well documented as a significant cause of death in patients with fulminant hepatic failure1 2 and in a series from this unit was found in 80% of cases at necropsy.3 The exact relation between cerebral oedema and the metabolic derangements underlying encephalopathy in hepatic failure is uncertain, but in an experimental devascularisation model of acute liver failure in the pig we found a progressive rise in intracranial pressure after surgery which was attenuated by the early administration of methylprednisolone in high doses.4 Since the introduction of continuous monitoring of intracranial pressure in patients with fulminant hepatic failure we have also found that bolus doses of mannitol intravenously can lead to a temporary lowering of intracranial pressure.5In a randomised controlled clinical trial of patients with fulminant hepatic failure and grade IV encephalopathy we have assessed the value of both dexamethasone given prophylactically and mannitol to reverse such cerebral oedema. We have also evaluated the effect on survival of these specific treatments. Methods PATIENTSForty-four patients were studied (17 men and 27

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SUMMARY Cerebral oedema is the commonest immediate cause of death in fulminant hepatic failure and an investigation was carried out to determine the value of monitoring intracranial pressure (ICP) and to examine the effects on ICP of dexamethasone therapy and mannitol administration. ICP values in 10 patients at the time of insertion of a subdural pressure transducer (grade IV encephalopathy) averaged 15.5 ±SD 14-8 mmHg. Despite dexamethansone therapy, which had been started on admission, rises in ICP were subsequently observed in seven of the eight patients who died. In the two patients who survived, the highest readings were 47 and 35 mmHg. Mannitol consistently reversed or arrested ICP rises when pressure was < 60 mmHg. ICP monitoring provides additional information in the management of patients and is essential if mannitol therapy is to be used.

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