HBOT for Carbon Monoxide Poisoning & Smoke Inhalation
The heart is extremely vulnerable to CO poisoning as heart muscle binds three times more avidly to CO than skeletal muscle. Also, due to formation of COHb, ischemia is also a resultant effect on cardiac function.This may result in arrhythmias and conduction defects.
The main injury to the brain in addition to the effects of general lack of oxygen is damage to the basal ganglia, resulting in Parkinson-like syndrome. Delayed effects may include movement disorders, memory disturbances, personality changes, psychosis, dementia, reduced IQ, cortical blindness and deafness.
Carbon Monoxide & Smoke Inhalation management
The main tissue poisons are:
- Hydrogen sulfide
- Carbon Monoxide
- Carbon tetrachloride
- Nitrites and nitrobenzene causing methemoglobinemia.
The main causes of CO poisoning include:
- Automobile exhaust fumes
- Defective domestic appliances for heating and cooking
- Industrial plant exhausts
- Mining accidents
- Indirectly from poisoning by methylene chloride (a paint stripper)
- Cigarette smoke (active and passive)
The half-life of CO is diminished significantly with administration of HBOT. Adjunctive therapy should include reducing cerebral edema with steroids and Mannitol.Cellular protection with magnesium management consists of oxygen at 1.3 atmospheres for hours until COHb is less than 10% in acute poisoning. In chronic or delayed poisoning, management usually consists of multiple sessions. Normobaric oxygen should not be used between multiple hyperbaric oxygen therapies, as this may contribute to oxygen toxicity. Delayed management is utilized to awaken the idling neurons, and to induce cerebral reparative processes. What is critical to understand that if firefighters are showing even minor neurological findings after a smoke-inhalation episode, a trial of HBOT is warranted.
- George Allibone M.D.