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[Sevoflurane: metabolism and toxicity]

M Nuscheler¹, P Conzen, K Peter

¹Klinik für Anästhesiologie, Ludwig-Maximilians-Universität München.

Der Anaesthesist

|January 20, 1999

Summary

Sevoflurane anesthesia leads to elevated serum fluoride levels, but this is not clinically significant. Studies show sevoflurane and its metabolites do not cause kidney or liver toxicity.

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Area of Science:

Anesthesiology
Clinical Chemistry
Toxicology

Background:

Sevoflurane is a widely used inhalational anesthetic.
Its biotransformation yields fluoride ions, raising concerns about potential nephrotoxicity.
Previous studies have investigated the relationship between anesthetic metabolism and fluoride levels.

Purpose of the Study:

To evaluate the clinical significance of elevated serum fluoride concentrations following sevoflurane anesthesia.
To assess the nephrotoxic and hepatotoxic potential of sevoflurane and its degradation products.

Main Methods:

Review of existing clinical and animal studies on sevoflurane metabolism and fluoride levels.
Analysis of factors influencing serum fluoride concentrations, including hepatic defluorination rate and anesthetic solubility.
Comparison of fluoride levels and toxicity profiles with other volatile anesthetics like enflurane and methoxyflurane.

Main Results:

Sevoflurane is metabolized by approximately 5%, with fluoride levels dependent on hepatic defluorination, anesthetic dose, and blood gas partition coefficient.
Despite elevated fluoride levels post-sevoflurane anesthesia, no fluoride-related toxicity has been observed in clinical or animal studies.
The established threshold for methoxyflurane-induced nephrotoxicity is not applicable to sevoflurane, isoflurane, or enflurane.

Conclusions:

Elevated serum fluoride concentrations after sevoflurane anesthesia are clinically insignificant.
Intrarenal metabolism of volatile anesthetics may explain the absence of observed nephrotoxicity.
Sevoflurane exposure is not associated with hepatic toxicity.

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