Controversies in the treatment of acute carbon monoxide intoxication
Paul G. Harch, M.D., Keith Van Meter, M.D.

Acute carbon monoxide (CO) poisoning causes brain lipid peroxidation as well as an hypoxic injury. Traditional therapy has been 1 ATA oxygen but now includes hyperbaric oxygen therapy (HBOT) which hastens dissociation of COHgb, reverses anoxia, inhibits reperfusion injury, and has toxic effects. All of these are dose dependant and time sensitive. The human experience with HBOT is anecdotal cases, uncontrolled and controlled series, which are largely positive, and randomized, prospective e controlled studies with conflicting results. A controversy exists over the pressure and number of HBOTs. What is suggested by the accumulating animal and human data is that high pressure (>2.0 ATA) HBOT may be the drug of choice in the hyper acute period (0-3 hours) after CO exposure but, as time progresses, toxic effects demand lower pressure (<2.0 ATA).

A second controversy involves diagnosis, inclusion criteria, and endpoints of HBOT. Currently, HBOT is indexed to physical exam and functional testing (psychometrics) both of which are crude in acute poisoning. Logistical problems further preclude psychometrics for continuing treatment or establishing endpoints. An alternative functional test is SPECT brain blood flow imaging which is very sensitive and has utility and facility early in treatment, pre- and post= a single treatment, at the conclusion of treatment, in diagnosing delayed neuropsychiatric sequelae, and in long term follow-up. Literature will be discussed and cases presented.