Halothane Complications

One of the most dreaded Halothane Complications is hepatic injury. There are two types, the first which is a transient sub clinical type with increases in liver enzymes. Halothane Complications may occur due to decreased hepatic blood flow and reductive biotransformation.

Secondly, fatal hepatic necrosis may occur up to one month after exposure. The National Halothane Study (US) describes halothane complications as a rare disease occurring in 1 in 35,000 administrations.

This is likely to be immune mediated due to protein bound trifluoroacetyl halide which may bond to hepatocytes and cause necrosis. It presents as fever, rash, arthralgia followed by jaundice.

The antibodies can be detected by immunoassay or Elisa kits. History of previous multiple exposure, drug allergies, eosinophilia and presence of antibodies are the precipitating factors.

There is marked elevation of ALT, AST, bilirubin and alkaline phosphatase; mortality rate is 50%. Fluoride ions are produced in the minimal reductive pathway of halothane metabolism, clinically this is not nephrotoxic.

To read more about about hepatotoxicity see Halothane Hepatitis .

Another important among halothane complications is its nephrotoxicity. Lets see what Miller’s Anesthesia 7th edition has to say about this –

Halothane is not significantly defluorinated under normal clinical conditions and is not nephrotoxic. In patients who received about 19 MAC-hours of halothane, peak plasma fluoride levels were much higher in the isoflurane group than in the halothane group.

In summary, 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; however, no correlation with sevoflurane and polyuric renal failure has been documented. 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 (the area under the curve for serum fluoride).

In addition, sevoflurane is an order of magnitude less soluble than methoxyflurane and thus is eliminated much more rapidly from the body.

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.


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