The syndrome of acute near-total intrauterine asphyxia in the term infant.

Eleven term infants sustained an acute, near-total intrauterine asphyxia at the end of labor. Imaging studies documented a consistent pattern of injury in subcortical brain nuclei, including thalamus, basal ganglia, and brainstem; in contrast the cerebral cortex and white matter were completely or relatively spared. This pattern of injury correlated with the acute and long-term neurologic syndromes in these patients. Four patients had a severe neonatal encephalopathy that included prominent signs of brainstem dysfunction. The other seven patients had a moderate neonatal encephalopathy. Three of these patients had dystonia consistent with basal ganglia injury; all seven remained normocephalic and had good cognitive outcomes consistent with sparing of cerebral cortex and white matter. Finally, in all 11 patients, injury to organs other than the brain was usually subtle. The distribution of injury in these patients reflects the hierarchy of metabolic needs that are unmet after a severe, sudden disruption of substrate supply as occurs in an acute, severe asphyxia. Thus, the higher metabolic rate of the brain compared with other organs explains the significant neonatal encephalopathy with relative sparing of nonbrain organs. Similarly, the higher metabolic rate of subcortical nuclei compared with cerebral hemispheres explains the preponderance of subcortical damage. This clinical and imaging syndrome is in contrast with that seen in more prolonged but less severe intrauterine asphyxia, in which shunting of blood flow from nonbrain organs to the brain and from cerebral hemispheres to the thalamus and brainstem renders nonbrain organs and cerebral hemispheres most vulnerable.