Toxicity of inhalational anesthesia

Hepatotoxicily has been seen since the introduction of anesthetics. Chloroform and trichloroethylene have been abandoned for toxicity of inhalational anesthesia . The toxicity may be intrinsic as seen with Chloroform or acetaminophen. Halothane exhibits an allergic or hypersensitivity reaction to a drug metabolite protein.

The toxicity of inhalational anesthesia with the incidence of liver injury is Halothane> Isoflurane > Desflurane. Sevoflurane does not produce acetylated protein adducts. Since isoflurane and desflurane are metabolized in very small amounts, toxicity is not seen.

Repeated exposure may result in cross sensitization to different agents. Toxicity of inhalational anaesthesia includes the incidence of halothane hepatitis in the adult population is estimated at 1 in 10,000 and I in 2,00,000 in children.

Halothane is reductively biotransformed to two volatile metabolites, chloro-difluro ethylene and chlorotrifluorethene, which are hepatotoxic. Glutathion-S-transferase is a marker for hepatotoxicity.

Nephrotoxicity: Methoxyflurane with a high metabolism (50—75%) produces high levels of fluoride ions resulting in polyuric renal insufficiency. Phenobarbitone, ethanol and isoniazid enhance the nephrotoxicity.

Carbon dioxide absorbent interactions and toxicity of inhalational anesthesia : Sevoflurane with CO2 absorbents, sodalime and baralyme, produces compound A. Renal injury may result from compound A after several hours of anesthesia.

It is recommended that in pre-existing renal disease it should be avoided or used for a limited period. Halothane also has a degradation product with soda lime but its toxicity is negligible. Trichloroethylene produces phosgene with soda lime, which is neurotoxic.

Carbon monoxide: CO is present up to 1% in all humans, but up to 10% in smokers. Its affinity for binding to Hb is 250 times more than that of oxygen, 50% can cause death due to toxicity of inhalational anesthesia. Desiccated CO2 absorbents and inhaled anesthetic interaction can lead to production of CO toxicity of inhalational anesthesia .

Haematopoietic and neurologic toxicity of inhalational anesthesia : Nitrous oxide is the only agent which on prolonged exposure can produce V megaloblastic anaemia and neurologic effects. This is due V to interaction of nitrous oxide with vitamin B12, due to oxidation of cobalt in the vitamin.

Subacute combined degeneration of the spinal cord is the ultimate result. However, this is possible only after months of daily exposure to N2O. Megaloblastic anemia has been reported in dentists. Numbness, paraesthesia, loss of balance, unsteady gait and muscle weakness are the result.

Occupational hazard and toxicity of inhalational anesthesia : At present, with good scavenging and low level exposure to waste, anaesthetic gases do not appear to be risky. However, high concentration of occupational exposure may be correlated with a greater incidence of abortions and decreased fertility.


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