Editorials

Hyperbaric oxygen in carbon monoxide poisoning

BMJ 1999; 319 doi: https://doi.org/10.1136/bmj.319.7217.1083 (Published 23 October 1999) Cite this as: BMJ 1999;319:1083

Conflicting evidence that it works

  1. Lindell K Weaver, medical director, hyperbaric medicine
  1. LDS Hospital, University of Utah School of Medicine, Salt Lake City, Utah 84143, USA

    There is little dispute that carbon monoxide poisoning is common: in the United States it produces an estimated 40 000 emergency department visits each year,1 and the accompanying editorial outlines the difficulties in diagnosing poisoning caused by this “silent killer.” There is disagreement, however, about how best to treat carbon monoxide poisoning, and in particular about the role of hyperbaric oxygen.

    Carbon monoxide is produced endogenously in small amounts and as a byproduct of incomplete combustion. It is colourless, odourless, and undetectable by human senses. It binds to haemoglobin, displacing oxygen; causes a leftward shift of the oxyhaemoglobin dissociation curve; binds to many intracellular proteins; and may interfere with ATP production at the cytochrome level.2 It can also activate neutrophils pathologically, leading to a reperfusion injury manifested by lipid peroxidation.3 Low levels of carbon monoxide produce evidence of oxidative stress.4 Recently, apoptosis in brain tissue has been observed after carbon monoxide poisoning.5

    Supplemental oxygen was found helpful in treating carbon monoxide poisoning in 1868,6 and hyperbaric oxygen was first used for clinical poisoning in 1942.7 The theoretical benefits of hyperbaric oxygen include …

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