The Poison Control Center

Carbon Monoxide

Late in the winter of 1986, the boiler of an apartment building temporarily failed. That night, two women in one of the apartments used their oven to heat the room. Through the evening, each developed a slight headache which progressed to a throbbing frontal headache. One of the women developed vomiting. The headache and vomiting finally forced the two women to their local emergency room. After a short history the physician began to suspect carbon monoxide as the agent involved. A carboxyhemoglobin level confirmed his suspicions. They were treated with oxygen via mask for 4 hours and discharged asymptomatic. Forty-eight hours later, the fatigue, nausea, and persistent headache had returned. There had been no reexposure. They missed two days of work without relief. By coincidence, one woman's niece was a nurse at The Children's Hospital of Philadelphia. Because of her concern, she discussed the case with one of the attending physicians at her workplace. He suspected delayed sequelae from carbon monoxide exposure and referred the two women for treatment with hyperbaric oxygen at the University of Pennsylvania hyperbaric chambers. The symptoms were relieved and a 30 day follow-up showed no return of sequelae.

When the winter heating season is upon us, it brings with it the increased incidence of carbon monoxide poisoning, both frank and occult. The symptoms of the patients arriving in the emergency room may vary widely from a vague flu-like syndrome to chest pain or mental confusion. Published reports of initial misdiagnoses have included gastroenteritis, psychiatric disorders, migraine headaches, heart disease, food poisoning, cerebral vascular accidents and hypoglycemia.1,2,4,6 Treatment involves displacing the carbon monoxide molecule from the heme molecules to which it is bound, using normobaric or hyperbaric oxygen. The pathophysiological mechanism of carbon monoxide poisoning has not been clearly elucidated. Presently, it is believed that carbon monoxide binds to cytochrome oxidase and consequently, disrupts the mitochondrial respiratory enzyme system.5,8-11 Experimental studies seem to indicate that delivery of CO dissolved in the serum to the cells, and not blockage of oxygen transport by the COHb bond, is perhaps more important in the sequence of pathological events of the poisoning.3,14 Although in severe poisonings, all factors may contribute to the outcome of the case.

Most hospitals have the capability to rapidly determine COHb levels in suspected CO poisonings. However, the COHb level may be misleading and of limited predictive value. A COHb level determination will fail to show the important tissue concentrations, as well as the level of dissolved CO and therefore, may not correlate well with symptoms or tissue injury secondary to CO exposure.10 Moreover, due to the short half life of the carboxyhemoglobin bond (5-6 hours on room air, 69-90 minutes on 100 percent oxygen at sea level) the patient's COHb level in the emergency department may be considerably reduced from the level that was present at the time of the exposure. Questionable results might occur if the patient has delayed seeking treatment, if oxygen has been administered before the level was drawn, or if it is a chronic intermittent exposure (i.e., automobile or occupational). The history is important in the diagnosis, as well as the selection of treatment.

Hyperbaric oxygen therapy is recommended in severe poisonings (regardless of carboxyhemoglobin level) with significant neurologic or cardiovascular symptoms including, loss of consciousness (at any time during the exposure), seizures, syncope, hypotension, angina or EKG evidence of myocardial ischemia.5,8-11 Cases with significant neurologic symptoms, including confusion, ataxia, irritability and aggressive behavior and with a COHb level of greater than 30 percent are also recommended for hyperbaric therapy in order to prevent neurologic sequelae.8,9,11,12 Carbon monoxide poisonings with mild symptoms, such as headache, nausea and fatigue, and with COHb levels of less than 30 percent can be treated with 100 percent oxygen via tight fitting mask until a repeat COHb level is normal. Patients should be instructed to return if symptoms reappear, and hyperbaric therapy should be considered for these patients at that time. Reported sequelae have included headache, nausea, fatigue, temporal spacial disorientation, confusion, impaired memory, deterioration of personality, delirium, blindness, stupor and progressive coma. Treatment of the sequelae with hyperbaric oxygen has shown good results in most cases.9

If hyperbaric therapy might be needed you can contact the Poison Control Center 24 hours a day at 800-222-1222 for consultation or assistance in arranging treatment. The hyperbaric chambers at the Institute of Environmental Medicine can be reached during business hours at 215-662-7785. After working hours, emergency calls should be placed through the switchboard at the Hospital of the University of Pennsylvania 215-662-4000, and ask for the hyperbaric therapy on-call physician.



  1. Barret L, Danel V, Faure J. Carbon monoxide poisoning, a diagnosis frequently overlooked. J Toxicol Clin Toxicol. 1985;23(4-6):309-313.
  2. Gemelli F, Cattani R. Carbon monoxide poisoning in childhood. Br Med J (Clin Res Ed) 1985 Oct 26;291(6503):1197.
  3. Goldbaum LR, Ramirez RG, Absalon KB. What is the mechanism of carbon monoxide toxicity? Aviat Space Environ Med 1975;46(10):1289-1291.
  4. Kelley JS, Sophocleus GJ. Retinal hemorraghages in subacute carbon monoxide poisoning. JAMA 1978 Apr 14;239(15):1515-7.
  5. Kindwal EP. Hyperbaric treatment of carbon monoxide poisoning. Ann Emerg Med 1985;14:1233-4.
  6. Kirkpatrick JN. Occult carbon monoxide poisoning. West J Med. 1987 Jan;146(1):52-56.
  7. Lacey DJ. Neurologic sequelae of acute carbon monoxide intoxication. Am J Dis Child 1981 Feb;135(2):145-7.
  8. Mathieu D, Nolf M, Durocher A, Saulnier F, Frimat P, Furon D, Wattel F. Acute carbon monoxide poisoning. Risk of late sequelae and treatment by hyperbaric oxygen. J Toxicol Clin Toxicol. 1985;23(4-6):315-324.
  9. Myers RA, Snyder Sk, Emhoff TA. Subacute sequelae of carbon monoxide poisoning. Ann Emerg Med 1985 Dec;14(12):1163-7.
  10. Myers RA, Snyder SK, Linberg S, Cowley RA. Value of hyperbaric oxygen in suspected carbon monoxide poisoning. JAMA 1981 Nov 27;246(21):2478-80.
  11. Norkool DM, Kirpatrick JN. Treatment of acute carbon monoxide poisoning with hyperbaric oxygen: a review of 115 cases. Ann Emerg Med 1985 Dec;14(12):1168-71.
  12. Poisindex, Vol. 54, Micromedex.
  13. Smith JS, Brandon S. Morbidity from acute carbon monoxide poisoning at three-year follow-up. Br Med J 1973 Feb 10;1:318-21.
  14. Walum E, Varnbo I, Peterson A. Effects of dissolved carbon monoxide on the respiratory activity of perfused neuronal and muscle cell cultures. J Toxicol Clin Toxicol. 1985;23(4-6):299-308.


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