The Etiology and Pharmacologic Approach to Hypoxic-Ischemic Encephalopathy in the Newborn

Introduction Perinatal hypoxia-ischemia affects approximately 2 to 4 per 1,000 term infants and a much greater proportion of preterm infants. Despite improved methods of intrapartum monitoring and advances in neonatal care and treatment, neonatal hypoxic-ischemic injury produces significant morbidity and mortality, often leading to long-term neurologic consequences. Neurologic sequelae of hypoxic-ischemic encephalopathy include delayed motor development, mental retardation, learning disabilities, seizure disorders, and cerebral palsy. The mechanisms underlying this injury are complex and are the focus of both current and future investigation. This article examines some of the major biochemical pathways fundamental to the development of hypoxic-ischemic brain injury and describes approaches that are being investigated to reduce or prevent neuronal injury and death.