Sofnolime with Different Water Content Causes Different Effects in Two Sevoflurane Inhalational Induction Techniques with Respect to the Output of Compound-A

Abstract

Objective: During sevoflurane anesthesia with Sofnolime for CO2 absorption, the factors affecting the production of compound A (a chemical is nepherotoxic) are still not clear. This study is designed to investigate the effects of different fresh gas flow during induction, the vital capacity induction (VCI) vs. the tidal volume breath induction (TBI) on the compound-A production with a fresh Sofnolime or a dehydrated Sofnolime using a simulated lung model.Method: The experiments were randomly divided into four groups: group one, VCIf, vital capacity fresh gas inflow with fresh Sofnolime; group two, TBIf, tidal volume breath fresh gas inflow with fresh Sofnolime; group three, VCId, vital capacity fresh gas inflow with dehydrated Sofnolime, and group four, TBId, tidal volume breath fresh gas inflow with dehydrated Sofnolime. The inspired sevoflurane was maintained at 8%, the concentrations of compound-A were assayed using Gas-spectrum technique, and Sofnolime temperatures were monitored at 1-min intervals throughout the experiment.Results: The mean and maximum concentrations of compound A were significantly higher in the vital capacity group than the tidal volume breath group (P<0.01). At the beginning of anesthesia maintenance, the compound-A concentration in group VCIf was 36.28±6.13 ppm, which was significantly higher than the 27.32±4.21 ppm observed in group TBIf (P<0.01). However, these values decreased to approximately 2 ppm in the dehydrated Sofnolime groups. Sofnolime temperatures increased rapidly in the dehydrated Sofnolime groups but slowly in the fresh Sofnolime groups.Conclusion: With fresh Sofnolime, vital capacity induction increased compound-A production in the circuit system compared with tidal volume breath induction. However, with dehydrated Sofnolime, the effects of the two inhalation induction techniques on compound-A output were not significantly different.

Hepatotoxicity after Sevoflurane Exposure in a Patient with Chronic Hepatitis C

“…It is important to note that at a low concentration of sevoflurane, compound a toxicity would not affect this patient either through beta lyase pathway or N-acetylation. Even though this patient was at a low flow rate of 2L/min, anesthesia providers should be aware of the accumulation of compound A and its association with sevoflurane in the setting of renal and hepatic toxicity [70].…”