Halothane and the liver: the problem revisited and made obsolete.

The problem ofhalothane and the liver does exist. Experience in Bristol of two bizarre cases of "halothane hepatitis" led Dr Brian Williams to organise a symposium on the subject earlier this year. His survey of anaesthetists in the South Western Region showed a high level (97%) of awareness of the possibility of hepatitis associated with halothane. The reported incidence ranges from one in 10000 to one in 35 000 anaesthetics in adults. The consensus seemed to be that repeated halothane anaesthesia was an important aetiological factor: of those who replied, three quarters let at least an arbitrary three months elapse before choosing to repeat the use of halothane, while two fifths required a minimum interval of six months. The problem may be preventable. Dr Roger Williams described 48 patients (38 of whom died) who had been referred to the liver unit at King's College Hospital, London, from January 1965 to December 1983'; he gave details of a further eight patients admitted since then. Fewer patients might have been seen had note been taken of exposure to halothane within 26 days-and especially when the first anaesthetic had been followed by the non-specific sign of late onset fever.' Other diagnoses such as non-A non-B hepatitis were impossible to exclude completely, but strong evidence that the patients had halothane hepatitis was provided by a relatively specific test based on sensitised rabbit hepatocytes; this was positive in 16 of 24 patients with liver failure associated with halothane.2 The pattern of the problem has also changed.3 Dr Williams referred to five cases among children, one ofwhom had died. It seems that the adult population may be divided into three groups: most may probably be given halothane with impunity -but that has to be a retrospective assessment. Up to one fifth respond on close repeated exposure to halothane with a mild rise in their transaminase activities and some prolongation of the prothrombin time. The remaining few develop jaundice, grossly raised activities of aspartate aminotransferase, encephalopathy in half, and rapidly progressive liver failure. No effective treatment has been found other than the hope of urgent liver transplantation. Whether or not halothane hepatitis can be induced in animals is still not clear. Rats consistently develop a similar syndrome only when they are hypoxic, starved, male, and