Perinatal Asphyxia: Pathophysiology and an Approach Towards Therapy

Abstract

Perinatal asphyxia is an all too common phenomenon in the newborn nursery. Approximately 20% of all neonates weighing greater than 2500 grams receive Apgar scores under 7 at 1 minute and 2–3% receive Apgar scores under 7 at 5 minutes. In addition, if the Apgar score is below 3 at 1 minute or under 5 at 5 minutes and there are neurologic manifestations of asphyxia, approximately 20% of these infants die, 30% sustain marked and 15% minimal neurologic sequelae while only 35% are normal. In order to understand the full scope of this problem we must consider the amount of neurologic damage and loss of potential occurring secondary to asphyxia that cannot be measured. Windle noted that newborn monkeys who were subjected to sublethal asphyxia and who evidenced gross neurologic dysfunction which cleared within a few days or weeks had pathologic evidence of nerve cell loss and bilateral cerebral lesions at autopsy.(1) It is possible to extrapolate from these findings and postulate that even short asphyxial episodes, to which the human newborn is thought to be resistant, may blunt his potential and produce neurologic and developmental deficits that are difficult to detect clinically.(2)