Hypoxic-Ischemic Encephalopathy

Hypoxic-ischemic encephalopathy (HIE) following severe perinatal asphyxia (also described in the literature as perinatal hypoxia-ischemia or asphyxia neonatorum) has an incidence of 1 to 2 per 1000 live births in the Western world and is far more common in developing countries. Although metabolic disorders may mimic perinatal asphyxia, and genetic and placental factors may contribute to the clinical picture, brain imaging techniques have demonstrated acute changes in the term neonatal brain following perinatal asphyxia. The risk for of irreversible damage or death following severe perinatal asphyxia is high, up to 65% of patients enrolled in trials of neuroprotective strategies. Therapeutic hypothermia is neuroprotective as has been demonstrated in several trials and is standard therapy for (near-) term neonates with severe perinatal asphyxia and encephalopathy in high income countries. Ongoing studies will aim at additive strategies to augment the neuroprotection of hypothermia. Experiments in animals have demonstrated that the immature brain is more resistant to hypoxia-ischemia than the brain of the term neonate. The several reasons to explain this difference are a lower cerebral metabolic rate; lower sensitivity to neurotransmitters with potential neurotoxicity; and the greater plasticity of the immature central nervous system. Nevertheless, in the fetus and preterm neonate, cerebral hypoxia-ischemia is a major cause of acute mortality and morbidity in survivors. However, the neuropathology will be different from that of the full-term neonate.