Hepatic Necrosis Associated with Herpesvirus After Anesthesia with Desflurane and Nitrous Oxide

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Abstract
The search for the ideal inhaled anesthetic has lack of toxicity as one goal, particularly an absence of hepatotoxicity or nephrotoxicity. In large part this may translate to a resistance to degradation in vivo and in vitro. Desflurane would seem to approach the ideal. Biodegradation is approximately one-tenth that of isoflurane, previously the least metabolized of all potent inhaled anesthetics (1), and soda lime has little effect on desflurane versus other potent drugs (2). Reports in animals (3–6) and humans (6–10) provide support for an absence of toxicity attributable to desflurane. However, desflurane is a halogenated anesthetic, and the minimal biodegradation of desflurane produces trifluoroacetate (l), a compound incriminated in the hepatotoxicity associated with halothane, with a potential for cross-sensitization to other anesthetics, including enflurane (11) and possibly desflurane. Perhaps only trace amounts of this compound are required to produce the allergic response said to underlie halothane hepatotoxicity. Although trace amounts of trifluoroacetate are produced from the biodegradation of isoflurane, the incidence of unexplained hepatic injury after anesthesia with isoflurane is too small to establish a causal connection (12). The still smaller production of trifluoroacetate from desflurane should further reduce even this minimal potential for risk. Evaluation of hepatotoxicity is confounded by the huge number of anesthetics given annually. Such numbers admit the possibility that hepatitis may develop in association with anesthesia merely by chance. Not all such cases have an obvious explanation, and it may be tempting to attribute the hepatitis to the halogenated anesthetic because the diagnosis of anesthetic-induced hepatitis is one of exclusion. We report one such case.

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