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Hyperbaric Oxygen Therapy and Carbon Monoxide Poisoning
Hyperbaric oxygen therapy (HBOT) is breathing 100% oxygen at pressure greater than one atmosphere absolute (1 ATA). This is usually accomplished by intermittent delivery at 2 to 3 ATA in a monoplace (single occupant) or multiplace (multiple occupants) hyperbaric chamber. Notably, topical oxygen using very low pressures (less than 1.1 ATA) is not considered HBOT, as no oxygen is felt to be absorbed into the wound or through skin by such application.
Even though high oxygen levels cause small (microscopic) arteries (called arterioles) to constrict, the overall hyperoxygenaton results in a gain in delivery of oxygen to the tissues. From an infection-fighting perspective, HBOT causes white blood cells to be better “killers” of germs. In addition, organisms that thrive in an oxygen-deficient environment (anaerobes) are inhibited. These include clostridial organisms, which cause certain forms of gas gangrene. The next effect is clearance of other types of bacteria.
Any situation in which an enhanced presence or higher level of oxygen might be beneficial is improved. While there persist varying opinions about the degree to which these mechanisms are enhanced, they include prevention of ischemic (lack of oxygen) reperfusion (restoration of perfusion) injury and situations in which white blood cells become sticky and cause blood vessel occlusion or needed to fight infection.
HBOT is currently considered acceptable therapy for arterial gas embolism, decompression sickness (the “bends”), carbon monoxide poisoning, exceptional blood loss anemia, crush injuries, compartment syndrome, necrotizing soft tissue infections, severe thermal burns, acute peripheral arterial ischemia, compromised skin grafts and flaps, chronic osteomyelitis, persistent soft tissue or bony radiation injury, certain diabetic foot ulcers, enhancement of wound healing in selected problems, and intracranial abscess.
Of all of these, it’s very much worth mentioning here carbon monoxide (CO) poisoning. CO is an odorless, colorless gas that is the product of incomplete combustion. This gas has an enormous affinity for hemoglobin in human red blood cells, and may rapidly overwhelm a person. Symptoms of CO poisoning include headache, dizziness, fatigue, nausea and vomiting, weakness, fatigue, tiredness, chest pain, shortness of breath, confusion, difficulty with coordination and walking a straight line, fainting, unconsciousness, seizures, and coma. CO poisoning may be fatal. Following a nonfatal episode of CO poisoning, a victim may suffer prolonged neuropsychiatric symptoms, including a delayed neuropsychiatric syndrome (DNS) that may occur days to 8 months after the initial poisoning. This syndrome includes any of the following: abnormal muscle movements, blindness, dementia, depression, disorientation, seizures, gait disturbances, hearing impairment, partial paralysis, mutism, hysteria, parkinsonism, sensory nerve dysfunction, personality changes, speech disturbances, and urinary or fecal incontinence.
The immediate treatment for CO poisoning is elimination of the exposure and treatment with oxygen. The “half life” (time to reduce the amount of CO in the blood by half) of CO breathing room air is 320 minutes; breathing 100% oxygen is 90 minutes; and receiving HBOT at 3 ATA oxygen is 23 minutes. Furthermore, prompt HBOT may decrease the incidence of DNS by mechanisms that are not yet clear.
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