Controlled Prospective Study of the Effect on Liver Function of Multiple Exposures to Halothane

Wright, Ralph; Chisholm, Morag; Lloyd, Barbara; Edwards, John N.; Eade, O E; Hawksley, Margaret; Moles, T. M.; Gardner, M.J.

doi:10.1016/s0140-6736(75)93000-7

Cited by 109 publications

(17 citation statements)

References 5 publications

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“…In the UHFH group bilirubin levels remained less than 85 lsmol/I (5 mg/ 100 ml) in 17 % of patients, although in a further 17 O' of patients levels greater than 425 jtmol/l (25 mg/100 ml) were seen. Jaundice in the 61 surviving patients lasted from under one week (five patients) to over 12 weeks (one patient).…”

Section: Methodsmentioning

confidence: 84%

Unexplained hepatitis following halothane.

Walton¹,

Simpson²,

Strunin³

et al. 1976

BMJ

132

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SummaryFull clinical and laboratory details of 203 patients with postoperative jaundice were submitted to a panel of hepatologists. All patients whose jaundice may have had an identifiable cause were excluded, which left 76 patients with unexplained hepatitis following halothane anaesthesia (UHFH). Hepatitis in 95°o of these cases followed multiple exposure to halothane, with repeated exposure within four weeks in 551)O of cases. Twenty-nine patients were obese, 52 were aged 41-70, and 53 were women. Thirteen patients died in acute hepatic failure. Rapid onset of jaundice after anaesthesia, male sex, and obesity in either sex were poor prognostic signs. Of the clinical stigmata of hypersensitivity, only eosinophilia was impressive. The UHFH group had a much greater incidence of liver kidney microsomal (LKM) and thyroid antibodies and autoimmune complement fixation than those patients whose jaundice related to identifiable factors. Thirteen of the 19 patients with LKM antibodies also had thyroid antibodies. In six patients retested two to three years later LKM antibodies had disappeared, although thyroid antibodies persisted.Rapidly repeated exposure to halothane may cause hepatitis, but such a complication is probably rare. Possibly obese women with a tendency to organ-specific autoimmunity may be more at risk. Nevertheless, the comparative risks of rapidly repeated halothane or non-

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Section: Methodsmentioning

confidence: 84%

Unexplained hepatitis following halothane.

Walton¹,

Simpson²,

Strunin³

et al. 1976

BMJ

132

View full text Add to dashboard Cite

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“…By contrast, several more recent episodes have been much less easy to resolve than these earlier ones. The nature of the relationship between postoperative jaundice and exposure to holothane is hotly disputed (see Inman and Mushin, 1974 and subsequent correspondence); the demonstration that halothane affects liver function, as assessed by changes in serum enzyme levels, (Wright et al, 1975;Trowell, Trowell, Peto, and Crampton Smith, 1975) strengthens, but by no means settles, the case. Whether tolbutamide causes rather than prevents arterial complications in diabetics is another controversial issue (Feinstein, 1971).…”

Section: Wider Implications Of the Smon Conmoversymentioning

confidence: 99%

Subacute myelo-optic neuropathy and clioquinol. An epidemiological case-history for diagnosis.

Meade¹

1975

Journal of Epidemiology & Community Health

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“…6 Abnormalities in liver function were not always apparent until the second postoperative week. Rises of serum amunotransterase activity were also greater in those receiving halothane than with enflurane,8 and obese women were more likely to develop abnormalities.…”

mentioning

confidence: 99%

Halothane anaesthesia and liver damage.

Neuberger¹,

Williams²

1984

BMJ

102

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A recent experience of the senior author when addressing a meeting of anaesthetists prompted this review, since it was apparent that there was still considerable disagreement between hepatologists and anaesthetists over the association between liver cell damage and halothane anaesthesia and the measures by which the risk could be minimised. Although during the 1960s and 1970s the evidence was hotly debated, there has since been increasing acceptance, both clinical and experimental, of a strong prima facie case for an association.'" Two, probably distinct, forms of liver damage have been defined.'2 Serum aminotransferase activities are raised in up to a fifth of patients anaesthetised with halothane during the first and second postoperative weeks (type I). Such minor forms of liver injury are to be distinguished from the rare occurrence of massive liver cell necrosis (type II).Three well controlled studies of minor reactions have been reported from Britain.s 6 8 Significant rises in serum aspartate aminotransferase (AST) activity during the postoperative period were found only in those patients receiving halothane,5 and these activities were significantly higher than in those receiving trichloroethylene.6 Abnormalities in liver function were not always apparent until the second postoperative week. Rises of serum amunotransterase activity were also greater in those receiving halothane than with enflurane,8 and obese women were more likely to develop abnormalities.Most patients who have developed massive necrosis have had a previous and milder reaction to halothane. Nevertheless, the frequency of minor abnormalities (up to 20%) and the very low incidence of massive necrosis make it clear that minor reactions are not necessarily followed by more severe effects. There is no way of predicting which patients will follow this course.We have seen now 48 patients with otherwise unexplained massive liver cell necrosis after halothane anaesthesia referred to the liver unit over the period January 1965 to December 1983. In each of the 48 patients other possible causes of liver damage were excluded, including exposure to hepatotoxic agents, sepsis, hypotension during surgery, and infection with hepatitis A and B, cytomegalovirus, and Epstein-Barr virus. In no case was there evidence of pre-existing liver disease.Thirty one of the 48 patients were women, giving a female to male ratio of 1 8:1. Ages ranged from 21 to 76 years (median 57 years), contrasting appreciably with the much younger age distribution of patients with fulminant viral hepatitis (fig 1). In comparison with the age distribution of patients undergoing anaesthesia in England and Wales, as given in the Hospital Inpatient Enquiry,'3 the patients with halothane hepatotoxicity are in a slightly older age group. Sixty eight per cent of the patients were obese and there was a history of allergy to other drugs in one third of them.The interval between the last exposure to halothane and the onset of jaundice ranged from two to 26 days, with a median of five days, and i...

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Controlled Prospective Study of the Effect on Liver Function of Multiple Exposures to Halothane

Cited by 109 publications

References 5 publications

Unexplained hepatitis following halothane.

Unexplained hepatitis following halothane.

Subacute myelo-optic neuropathy and clioquinol. An epidemiological case-history for diagnosis.

Halothane anaesthesia and liver damage.

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