Desflurane undergoes very little desflurane metabolism because of low blood/gas and low blood/tissue solubility.
However, 0.02% is metabolized during desflurane metabolism with the production of trifluoroacetic acid which may interact with hepatic proteins and induce an immune response in susceptible patients. Previous exposure to halothane may produce antibodies.
In desflurane metabolism , the elimination is almost exclusively by the lungs, metabolism by the liver is less than 0.02%.
Trufluoroacetic acid (TFA), a breakdown product, has been detected in the urine but one-tenth the level seen with isoflurane; increase in serum or urine fluoride levels have not been reported. It is metabolized in the liver by cytochrome P450 (2E1) in traces.
We find the followiing mentioned in Miller’s Anesthesia about desflurane metabolism –
Saturation of the enzymes responsible for the metabolism of anesthetics may limit the ability of metabolism to significantly alter the rate at which the alveolar anesthetic partial pressure rises.
This limitation does not exist on recovery, and metabolism may be an important determinant of the rate at which the alveolar anesthetic partial pressure declines.
However, such metabolism applies significantly only to obsolete anesthetics such as halothane and methoxyflurane.
Sevoflurane is only slightly metabolized and desflurane metabolism and isoflurane undergo so little metabolism that such degradation cannot affect their kinetics.