The Myth or Truth of Modern Inhalational Anesthetics Nephrotoxicity

Abstract

A large variety of inhalation anesthetics with the potential for use in humans have been synthesized during the past decades. Fluoride-induced nephrotoxicity is a well-known entity historically associated with methoxyflurane administration and prolonged exposure to enflurane. During the administration of sevoflurane, serum inorganic fluoride levels can exceed 50 μmol/L, the level known to produce nephrotoxicity. Two factors may help explain the differences seen with methoxyflurane and sevoflurane. First, it is not the peak serum fluoride concentration that determines injury but rather the duration of the systemic increase in fluoride . Second, the liver is the primary organ of sevoflurane metabolism, whereas both the liver and kidney metabolize methoxyflurane, and it is thought that the high intrarenal fluoride production from methoxyflurane contributes to its nephrotoxicity. Degradation products from sevoflurane’s interaction with carbon dioxide absorbents, particularly compound A, can produce renal injury. However, injury does not occur below a particular compound A threshold (150-200 ppm–hours, eg, 100 ppm given for 1.5-2 hours), a threshold rarely reached in clinical practice. Compound A doses exceeding threshold produce increasing injury with increasing dose. If injury occurs in humans, it is mild and transient. There are some measures that help in prevention of inhalational anesthetics induced nephrotoxicity: CO2 absorbent shouldn't contain strong base, as they cause more inhalational anesthetic degradation. Also fresh gas flow shouldn't be left on for long time as Co2 absorbent will become desiccated .That leads to the importance of changing co2 absorbent on regular bases.