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A five-year-old boy was admitted to hospital four days after a minor injury to his eyelid. He had neck rigidity, risus sardonicus and a diagnosis of tetanus was made. He was anaesthetised with nitrous oxide, oxygen and halothane to permit wound toilet. He received anti-tetanic serum and was sedated mainly with pentobarbitone (Nembutal) rectally and diazepam (Valium) via a nasal tube. Twentyfour hours after admission an endotracheal tube was passed under the same anaesthesia as before and twelve hours later a tracheostomy was performed.For the next twenty-one days he was maintained under nitrous oxide, oxygen and halothane anasthesia with intermittent curarisation and IPPV to control the manifestations of a severe attack of tetanus. Anasthesia was maintained for a further three weeks making a total of six weeks in all, during which intensive medical and nursing care and physiotherapy were maintained. Unfortunately, when the disease appeared to be almost cured, he died from a gross haemorrhage following erosion of the innominate artery.During the first three weeks of general anaesthesia, 1,500ml of halothane were utilised. In view of the current interest in the effect of halothane on the liver it is felt that the results of the post-mortem examination would be of particular interest.The liver was enlarged with some opaque swelling and on section showed a completely maintained lobular structure. The liver cells were rather poor in glycogen content at the lobular periphery, particularly around the periportal areas where there were some slight fatty infiltrations. There was moderately copious pigment in the Kuppfer cells reacting positively to a test for iron.In the opinion of the pathologist there was no abnormal pathology or any degenerative liver changes indicative of necrosis. At no time 636