The relationship between intermittent hypoxemia events and neural outcomes in neonates.

This brief review examines 1) patterns of intermittent hypoxemia in extremely preterm infants during early postnatal life, 2) the relationship between neonatal intermittent hypoxemia exposure and outcomes in both human and animal models, 3) potential mechanistic pathways, and 4) future alterations in clinical care that may reduce morbidity. Intermittent hypoxemia events are pervasive in extremely preterm infants (<28 weeks gestation at birth) during early postnatal life. An increased frequency of intermittent hypoxemia events has been associated with a range of poor neural outcomes including language and cognitive delays, motor impairment, retinopathy of prematurity, impaired control of breathing, and intraventricular hemorrhage. Neonatal rodent models have shown that exposure to short repetitive cycles of hypoxia induce a pathophysiological cascade. However, not all patterns of intermittent hypoxia are deleterious and some may even improve neurodevelopmental outcomes. Therapeutic interventions include supplemental oxygen, pressure support and pharmacologic drugs but prolonged hyperoxia and pressure exposure have been associated with cardiopulmonary morbidity. Therefore, it becomes imperative to distinguish high risk from neutral and/or even beneficial patterns of intermittent hypoxemia during early postnatal life. Identification of such patterns could improve clinical care with targeted interventions for high-risk patterns and minimal or no exposure to treatment modalities for low-risk patterns.