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explain the disparity between maternal and fetal COHb concentrations in our case, it is necessary to postulate that fetal death occurred at the time that the fetal circulation reached its maximal COHb saturation. According to available research information, the fetal COHb concentration is not expected to change after death in utero. CO is not produced by decomposition, nor is it absorbed in significant amounts by a body when exposed to an environment rich in CO. Indeed, COHb persists for weeks in the human body and may be accurately quantified even after embalming and burial [7].

In chronic or nonfatal CO poisoning, degenerative changes can often be seen involving the basal ganglia, kidneys, liver, and heart. These lesions are indicative of severe tissue hypoxia and are not pathognomonic of CO poisoning [9]. In acute asphyxia due to CO, death occurs before these lesions can develop. The fetal autopsy suggested COHb poisoning by the cherry red discoloration of the skin and visceral organs.

The carboxyhemoglobin concentration that causes fetal death in humans has not yet been defined. The clinician’s ability to predict fetal survival is poor because the fetal COHb concentration cannot be estimated from a single determination of maternal concentration without knowledge of the maternal exposure pattern. At the present time, the best predictive index of fetal morbidity and mortality appears to be the severity of maternal symptoms at the site of exposure.

The authors hope that this account of fetal death associated with nonfatal maternal exposure to CO, which is only the second report to include measurement of both maternal and fetal COHb saturations, will alert both death investigators and clinicians to the fragile relationship that exists between mother and fetus under circumstances of CO exposure.


Since the completion of this report, an additional recent case of nonlethal maternal CO poisoning with fetal death has come to the authors’ attention.4


The authors wish to thank Kevin Fallon, Ph.D., of Instrumentation Laboratory, Inc., for his technical advice regarding blood gas analysis of fetal blood.


[1] Centers for Disease Control, “Carbon Monoxide Intoxication—A Preventable Environmental Health Hazard,” Morbidity and Mortality Weekly Report, Vol. 31, 1982, pp. 529–531.

[2] Finck, P.A., “Exposure to Carbon Monoxide,” Forensic Medicine: A Study in Trauma and Environmental Hazards, C.G.Tedeschi, W.G.Eckert, and L.G.Tedeschi, Eds., W.B. Saunders Co., Philadelphia, PA, 1977.

[3] Cramer, C.R., “Fetal Death Due to Accidental Maternal Carbon Monoxide Poisoning,” Journal of Toxicology: Clinical Toxicology, Vol. 19, No. 3, 1982, pp. 297–301.

[4] Cornellison, P.J.H., Van Woensel, C.L.M., Van Oel, W.C., and de Jong, P.A., “Correction Factors for Hemoglobin Derivatives in Fetal Blood, as Measured with the IL-282 CO-Oximeter,” Clinical Chemistry, Vol. 29, No. 8, 1983, pp. 1555–1556.

[5] Winter, P.M. and Miller, J.N., “Carbon Monoxide Poisoning,” Journal of the American Medical Association, Vol. 236, No. 13, 27 Sept. 1976, pp. 1502–1504.

[6] Myers, R.A.M., Linberg, S.E., and Cowley, R.A., “Carbon Monoxide Poisoning: The Injury and Its Treatment,” Journal of the American College of Emergency Physicians, Vol. 8, No. 11, Nov. 1979, pp. 479–484.

[7] Spitz, W.V. and Fisher, R.S., Medicolegal Investigation of Death: Guidelines for the Application of Pathology to Crime Investigation, 2nd ed., Charles C Thomas, Springfield, IL, 1980.


Walker, F.B., M.D., deputy chief medical examiner, Phoenix, AZ, 1989, personal communication.

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