Gas Poisoning

Carbon Monoxide
Hydrogen Sulfide, Cyanide, Carbon tetrachloride, Nitrates and Nitrobenzene



Inhalation of carbon monoxide (CO) block the normal oxygen carrying function of the hemoglobin (HgB) in red blood cells and cause tissue hypoxia which can cause asphyxiation or brain damage. The same is true of the some of the other gases such as Hydrogen Sulfide, cyanide gases and carbon tetrachloride, nitrites and Nitrobenzene. The most common cause of CO poisoning are gasoline and diesel exhausts, smoke inhalation defective gas, coal or charcoal heaters in which the fuel is not burnt efficiently or leaks, or when there is a source of CO and inadequate ventilation.


Symptoms of acute CO poisoning are, flu like symptoms, headache, nausea, vomiting, weakness, and collapse which may lead to coma and death. It has occasionally been mistaken for food poisoning. Chronic sequel may include lack of mental acuity and other neurological problems. Slight CO poisoning over an extended period can lead to chronic tiredness and a lack of mental acuity.

Status of HBOT as a treatment:

Treatment of CO poisoning with Hyperbaric Oxygen, whether or not complicated with cyanide gases, is the first choice treatment. ” The Text Book of Hyperbaric Oxygen” states, Review of all the available evidence indicates HBOT has a definite place in the management of CO poisoning.

Ref: The Book of Hyperbaric Medicine, Vol. 3 pages 179- 182 By K.K. Jain.


Oxygen inhalation to hasten the dissociation of CO from HgB as well as to enhance tissue oxygenation is essential to the treatment of CO poisoning. Most of the sequel damage is done by tissue caused by inhibition of cytochrome A3 oxidase. There are benefits to be derived from Hyperbaric Oxygen which can not be obtained by exposure or breathing oxygen at surface atmosphere. HBOT accelerates the dissociation of the Carboxy-hemoglobin (HbCO) beyond anyrate achievable by breathing 100% oxygen at normal atmospheric pressure. HBOT given within 6 hours of a patient being resusctated greatly reduces mortality and neurological sequel, which may set in from 3days to 3 weeks after apparent recovery from acute CO poisoning. New information seems to implicate that HBOT given at a later stage may help the latent effects of CO exposure.

Test and mechanisms:

CO reacts with HgB 240 times more easily than does oxygen. Tissue oximetry shows a radical drop in PO2. The HbCO level may be between 25% and 40%, Lactate levels will be a shift to the left of oxygen dissociation curve.

Cost Impact:

The cost of HBOT in treating CO poisoning is modest, since it is a primary mode of therapy. Morbidity has been estimated to be between 30% and 40% with out HBOT and Goulin et al demonstrated in a large retrospective study that this was reduced to 20 deaths in 147 acute incidents using HBOT (13.5%)


Cabalane m. and Demling R.H. Early respiratory abnormalities from smoke inhalation Jama 251: 771-773, 1984
Myers R.A.M., Snyder S.K. Emhoff T.A., and others, Subacute Squelae of carbon monoxide poisoning.

Ann Emer. Med. 14:1163-1167, 1985

Kindwall E.P. and Goldmann R.W.

Hyperbaric Medicine Procedures, Milwaukee, Wisconsin. St Luke’s Hospital, 1988

K.K. Jain.

The Text Book of Hyperbaric Medicine, Vol.3

Richard A. Neubauer, Morton Walker.

Hyperbaric Oxygen Therapy.

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