Carbon Monoxide Poisoning
Carbon monoxide (CO) is a colorless, odorless gas produced as a byproduct of combustion. Poisoning occurs by inhalation, either accidentally or intentionally (suicide attempt). CO poisoning is responsible for an estimated 40,000 emergency department visits and 1,000 accidental deaths in the United States annually. Approximately 5-6% of patients evaluated in emergency departments for CO poisoning are treated with hyperbaric oxygen (HBO2).
CO binds to hemoglobin in red blood cells at the sites usually utilized to carry oxygen to tissues. Oxygen, and especially hyperbaric oxygen, accelerates the clearance of CO from the body, thereby restoring oxygen delivery to sensitive tissues such as brain and heart. This has traditionally considered to be the mechanism of benefit of HBO2. However, research published in the past few years has demonstrated a number of other mechanisms of toxicity from CO. Blood vessel (vascular) injury from CO has been demonstrated to result from CO-induced production of nitric oxide-derived oxidants and cellular injury from activated white blood cells (neutrophils). CO also causes direct central nervous system cellular injury through mechanisms that include disturbance of energy metabolism and intracellular production of oxygen free radicals. In animal experiments, hyperbaric oxygen, but not normobaric oxygen (NBO2), has been demonstrated to block each of these mechanisms of toxicity.
Until ten years ago, the benefit of hyperbaric oxygen treatment of CO poisoning was demonstrated by comparing the clinical experience at institutions where HBO2 was used with that at facilities where it was not available. Since 1989, six randomized prospective trials have been reported comparing HBO2 with NBO2 treatment of acute CO poisoning. Of these, three demonstrate improved patient outcomes with hyperbaric oxygen, two report no difference between the two therapies, and one remains blinded with regard to the treatment administered. A full listing of the investigations, as well as a discussion of the study designs and findings, can be found in the UHMS Hyperbaric Oxygen Therapy Committee Report (available for purchase through this web site). The UHMS currently recommends HBO2 treatment of individuals with serious CO poisoning, as manifest by transient or prolonged unconsciousness, abnormal neurologic signs, cardiovascular dysfunction, or severe acidosis.
- Thom SR, Fisher D, Xu YA, Garner S, Ischiropoulos H. Role of nitric oxide-derived oxidants in vascular injury from carbon monoxide in the rat. Am J Physiol 1999;276:H984-992.
- Brown SD, Piantadosi CA. Recovery of energy metabolism in rat brain after carbon monoxide hypoxia. J Clin Invest 1991;89:666-672.
- Hyperbaric Oxygen Therapy Committee. Hyperbaric Oxygen Therapy: 1999 Committee Report. Hampson NB, ed. Kensington, MD: Undersea and Hyperbaric Medical Society; 1999.
- Hampson N, Dunford RG, Kramer CC, Norkool DM. Selection criteria utilized for hyperbaric oxygen treatment of carbon monoxide poisoning. J Emerg Med 1995;13:227-231.
The information above is a synopsis of a more detailed description found on the UHMS website. It is presented here for educational and informative purposes. Always consult a hyperbaric physician for specific recommendations regarding any HBO therapy.