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
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:
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
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
Snyder S.K. Emhoff T.A., and others, Subacute Squelae of carbon
Ann Emer. Med. 14:1163-1167, 1985
Kindwall E.P. and Goldmann R.W.
Hyperbaric Medicine Procedures, Milwaukee, Wisconsin. St
Luke’s Hospital, 1988
The Text Book of Hyperbaric Medicine, Vol.3
Richard A. Neubauer, Morton Walker.
Hyperbaric Oxygen Therapy.