Sevoflurane, which has low solubility in blood, facilitates rapid induction and recovery. Sevoflurane is metabolized to hexafluoroisopropanol by cytochrome P450. Hexafluoroisopropanol has significantly less protein binding capability, does not accumulate and rapidly undergoes phase II biotransformation to form Hexafluoroisopropanol glucuronide, which is mostly excreted in the urine within 12 hours. Thus, the hepatotoxic potential of sevoflurane has been considered very low. However, there are many reports about hepatic toxicity after sevoflurane anesthesia. We report a case of a 21-year-old male who had high levels of aspartate transaminase and alanine transaminase with crushing injuries and had low hepatic dysfunction after 29 sevoflurane anesthesia treatments within three months.
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