Introduction

Hypoxic–ischemic encephalopathy (HIE) is a well-recognized clinical syndrome and the most common cause of acute neurological impairment and seizures in the neonatal period. Neonatal encephalopathy is a term used to describe newborns with acute neurological syndromes and encephalopathy that may be caused by diverse processes including hypoxia–ischemia, infections, inflammation, trauma, and metabolic disorders. Neonatal encephalopathy due to perinatal asphyxia can lead to neurological sequelae and cerebral palsy, but recent literature has shown that only a small percentage of children with cerebral palsy had intrapartum asphyxia as a possible etiology. More emphasis has been placed on antenatal events as having a greater association with cerebral palsy. Although newborns with neonatal encephalopathy may have antenatal risk factors associated with other findings, such as delayed onset of respiration, arterial cord blood pH less than 7.1, and multiorgan failure, the MRI most often shows signs of acute perinatal insult. Therefore, hypoxic–ischemic injury during the perinatal period can lead to a neurological syndrome in the newborn period, i.e., HIE, and subsequent neurological sequelae in the survivors. Recognizing and understanding hypoxic–ischemic encephalopathy are therefore important.