Hypoxic Ischemic Encephalopathy in the Full-Term Neonate

Hypoxic-ischemic encephalopathy (HIE) in the full-term neonate is a clinical diagnosis defined by impaired neurological function at birth, or in the first few days of life, in an infant born at or beyond 35 weeks of gestation. Several neonatal signs indicate that an acute hypoxic or ischemic event may have occurred either in the immediate peripartum or intrapartum period. These signs include characteristic findings of encephalopathy, an Apgar Score of less than 5 at the 5- and 10-min evaluations, fetal umbilical artery acidemia (pH < 7), evidence of acute brain injury on neuroimaging, and the presence of multisystem organ failure [1]. Thirty-seven percent of infants with HIE develop long-term neurological sequelae [27], with cerebral palsy reported in 10–13% of infants following a moderate to severe HIE event [1]. Brain Magnetic Resonance Imaging within 24–96 h, with or without Magnetic Resonance Spectroscopy (MRS), is the preferred imaging technique to assess cerebral injury in neonates [1]. Decreased N-acetyl aspartate, increased choline, lactate peak, and a glutamine-glutamate peak on MRS are also consistent with HIE [36]. Therapeutic hypothermia is considered standard of care in the treatment of infants with moderate to severe encephalopathy. Its use does not affect the prognostic value of neonatal MRI [50].