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Fetal brain injury after maternal carbon monoxide intoxication

Clinical and neuropathologic aspects

From the Laboratory of Perinatal Physiology, National Institute of Neurological and Communicative Disorders and Stroke, National Institutes of Health, United States Public Health Service, Department of Health, Education, and Welfare.

In a model of brain damage in the rhesus monkey fetus, carbon monoxide inhalation by the mother was used to produce graded fetal hypoxia. Four fetuses with arterial oxygen contents of 2.1 to 2.4 ml per 100 ml during the most severe insult hour appeared neurologically normal, and their brains contained no lesions. A single animal with an intermediate degree of hypoxia was moderately abnormal; its brain showed extensive necrosis of the basal ganglia. Four fetuses with arterial oxygen contents of 1.6 to 1.8 ml per 100 ml during the most severe insult hour showed profound clinical deficits, and on postmortem examination the brains were markedly swollen and showed an extensive hemorrhagic necrosis. The fetal brain exhibits a high threshold to the effects of sustained hypoxia, but once a critical level of deoxygenation is exceeded, extensive brain damage with early death results.

Dr. Ginsberg's address is Department of Neurology, Hospital of the University of Pennsylvania, 3400 Spruce Street, Philadelphia, Pennsylvania 19104.

Dr. Ginsberg was recipient of NINDS Special Traineeship No. 1 F11 SN 2582-01 NSRB.

Received for publication June 20, 1975.

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