Renal effects

The proposed metabolic pathway yields two fluoride ions for each isoflurane molecule undergoing metabolism. Plasma inorganic fluoride concentrations above 50 pmol/l have been associated with a reduction in the kidney's ability to concentrate urine.

Isoflurane does not cause any fluoride-induced nephrotoxicity after normal anesthesia, but these findings cannot be extrapolated to more prolonged exposure.

There have been several studies and reports of elevated fluoride concentrations after sedation with isoflurane in the ICU. Despite the high plasma fluoride concentrations seen in some of these ICU patients, there was no effect on renal function as determined by creatinine clearance and urine osmolality. Although there is a relationship between MAC hours and the maximum fluoride concentration seen in each patient, it is not possible to predict how many MAC hours of isoflurane could be administered before a potentially nephrotoxic level of fluoride is reached ( Spencer.,etMa| 1991).

There appears to be a greater mean plasma concentration after isoflurane sedation than would be expected after the equivalent MAC hours of anesthesia. The metabolism of isoflurane in severely ill patients may vary considerably, like that of other sedatives, owing to variations in hepatic blood flow, cellular oxygenation, and concurrent medications which may interact with liver enzyme systems and interfere with isoflurane metabolism. There may be a more complex biotransformation of isoflurane following chronic exposure as prolonged exposure leads to its accumulation in adipose tissue and continuing metabolism.

Isoflurane should be used with caution for sedation lasting for more than 3 to 4 days and renal function should be monitored closely.

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