Although the local anaesthetic prilocaine is less cardio- and neurotoxic than lidocaine, it bears the disadvantage of the formation of methaemoglobin by the metabolite o-toluidine. Prilocaine is often successfully used, especially for the blockade of the brachial plexus, but one problem of this technique is the failure rate of 3-10%, with the consequence that general anaesthesia after administration of prilocaine is frequently necessary. Methaemoglobin formation after prilocaine administration has been thoroughly investigated. Nothing is known, however, about the interactions of prilocaine and the induction of general anaesthesia relative to methaemoglobinaemia. CASE REPORT. Two patients (47 and 52 years old) each received 500 mg prilocaine for the axillary blockade of the brachial plexus. After 100 and 120 min respectively, it was necessary to induce general anaesthesia, for which 350 mg thiopental, 1 mg alfentanil and 45 mg atracurium were used. At 15 min after induction, methaemoglobin levels had increased by 70% and 25%, respectively, from baseline before general anaesthesia. CONCLUSION. It is not possible to explain these findings conclusively with the present method. To check whether displacement of o-toluidine from the plasma protein binding might have been responsible, we provoked methaemoglobinaemia in vitro by adding o-toluidine to heparinised blood. Thiopental was then added to half the specimens. Subsequently, methaemoglobin levels were lower in the samples with thiopental. Three explanations seem plausible: (1) Thiopental blocks the hydroxylase of the endoplasmic reticulum, with the result that o-toluidine cannot be further metabolised, leading to higher o-toluidine and methaemoglobin levels. (2) Isoflurane improves the blood supply of the liver. This results in increased metabolism of prilocaine to o-toluidine. (3) The results were accidental. To clarify which of these explanations is correct, further investigation is necessary.

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