Causes of Death in Fulminant Hepatic Failure and Relationship to Quantitative Histological Assessment of Parenchymal Damage

The clinical course and causes of death in 132 consecutive patientswith fulminant hepatic failure and grade III or IV encephalopathyhave been reviewed. 105 patients died and in 96 of these anautopsy examination was performed. In 36 patients there wascerebral oedema and the mean age of this group was significantlyyounger than the other fatal cases. In 28 patients death wasattributed to major haemorrhage which originated in the gastrointestinaltract in 25. The prothrombin time ratio was not significantlygreater in patients with major bleeding than in those withoutbut they did have a significantly lower platelet count. Sepsiscontributed to death in 12 patients. In 25 patients massivehepatic necrosis only was found at autopsy and death was consideredto be due solely to hepatic failure. The degree of hepatocyte loss was assessed in 80 fatal casesby a histological morphometric technique on a needle specimenof liver taken immediately postmortem. The proportion of theliver volume occupied by hepatocytes (hepatocyte volume fraction,HVF) was greatly reduced in all patients (normal 85 ±SD 5 per cent) but the mean value was significantly higher inthe patients dying with sepsis, cerebral oedema or haemorrhagethan in the group in whom death was attributed solely to hepaticfailure. There were ten patients in whom liver function wasimproving at the time of death which was due to cerebral oedema(9) or haemorrhage (1). These observations suggest that manypatients presently dying from fulminant hepatic failure maybe expected to survive, once more effective therapy is availablefor the complications of the illness. ¹Present address: Charing Cross Hospital, London W.C.2