Carbon monoxide (CO) is a colorless, odorless gas produced as a by-product 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 to 6 percent of patients evaluated in emergency departments for CO poisoning are treated with hyperbaric oxygen therapy.

CO binds to the hemoglobin in red blood cells at the sites usually utilized to carry oxygen to the tissues. Oxygen, and especially hyperbaric oxygen, accelerates the clearance of CO from the body, thereby restoring oxygen delivery to sensitive tissues such as the brain and the heart. This has traditionally been considered how CO works in the body and how hyperbaric oxygen helps.. However, research published in the past few years has demonstrated a number of other ways CO can be toxic. Blood vessel (vascular) injury from CO can result from CO-induced production of nitric oxide-derived oxidants and cellular injury can occur from activated white blood cells (neutrophils). CO also causes direct central nervous system cellular injury through disturbance of energy metabolism and intracellular production of oxygen free radicals. In basic research experiments, hyperbaric oxygen has been demonstrated to stop these problems from occurring.

Until ten years ago, the benefit of hyperbaric oxygen treatment of CO poisoning was demonstrated by comparing the use of hyperbaric oxygen therapy with normal oxygen therapy. Since 1989, six of these research trials have been reported. Of these, four demonstrate improved patient outcomes with hyperbaric oxygen and two reported no difference between the two therapies. A full listing of the investigations, as well as a discussion of the study designs and findings, can be found in the Undersea Hyperbaric Medical Society (UHMS) Hyperbaric Oxygen Therapy Committee Report (available for purchase through the Web site: www.uhms.org).

The UHMS currently recommends hyperbaric oxygen treatment for individuals with serious CO poisoning, with symptoms such as transient or prolonged unconsciousness, abnormal neurological signs, cardiovascular dysfunction or severe acidosis.

References:

  1. 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.
  2. Brown SD, Piantadosi CA. Recovery of energy metabolism in rat brain after carbon monoxide hypoxia. J Clin Invest 1991;89:666-672.
  3. Feldmeier JJ, Chairman and Editor. Hyperbaric Oxygen 2003: Indications and Results: The Hyperbaric Oxygen Therapy Committee Report. Kensington, MD: Undersea and Hyperbaric Medical Society; 2003.
  4. 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.

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