Which of the following is true concerning sevoflurane use in pediatrics?
A. Sevoflurane is associated with seizures post-operatively
B. Sevoflurane causes more tachycardia than isoflurane
C. MAC-sparing effects of nitrous oxide with sevoflurane are similar to its effects with isoflurane
D. The majority of sevoflurane metabolism is in the liver
The answer is D.
The minimum alveolar concentration (MAC) of sevoflurane decreases from 3.3% in neonates and infants younger than 6 months old to 2.5% in children between 6 months and 5 years old and continues to decrease even further to 2.0% in adults. The MAC-sparing effect of nitrous oxide was significantly less for sevoflurane when compared to some of the other volatile anesthetics.[1] Ok, so I feel like I was lied to...the additive effects of nitrous oxide at 60% (about 0.6 MAC) for halothane is 60% of MAC or 0.6 MAC.[2] Figured that one. But for nitrous oxide at the the same level (60%) combined with isoflurane is only 40%, desflurane its 20% and sevoflurane its 24%.[3][4] What? Nitrous doesn't add the same value for every anesthetic. Crazy, I know. Mind blown.
Sevoflurane causes minimal cardiovascular side effects in children. When compared with desflurane, sevoflurane causes less hypotension. Isoflurane is noted to cause more tachycardia than sevoflurane and halothane causes more less more myocardial depression when compared with sevoflurane. There is a low association with arrhythmias with sevoflurane use. Sevoflurane is, however, an effective bronchodilator.
From a neurologic standpoint, sevoflurane has been associated with cortical epileptiform electroencephalograms, although no lasting clinical sequelae (such as seizures) have been attributed to sevoflurane alone.
As much as 5% of sevoflurane is metabolized, with defluorination producing an inorganic fluoride that has urinary excretion. Peak fluoride concentrations, although higher in sevoflurane than in isoflurane, are still well below the accepted nephrotoxic level of 50 mmol/L. This fluroide is rapid eliminated, and these levels remain below toxic levels even with prolonged anesthetics. In addition, the metabolism of sevoflurane by the P450E1 system is mostly in the liver and not the kidneys. Thus, the concern of nephrogenic diabetes insipidus (DI) by elevated fluoride levels does not appear to be an issue. However, this is the reason that most practitioners tend to use flows at or above 2 LPM when using sevoflurane.