Hypoxic-ischemic encephalopathy (HIE) is an important cause of acute neurologic injury at birth, affecting approximately two to three cases per 1000 full-term live births. Despite advancements in many aspects of neonatal intensive care, the outcome for infants with HIE remains poor. Interventions to improve outcomes in this population have been disappointing. The treatment of infants who have HIE is generally supportive and includes fluid and electrolytes homeostasis, correction of hypotension, and treatment of seizures. It is now known that severe hypoxia-ischemia may not necessarily cause immediate cell death, but can precipitate a complex biochemical cascade leading to the delayed neuronal loss. The key phases of injury include a latent phase after reperfusion, with initial recovery of cerebral energy metabolism, followed by a secondary phase characterized by accumulation of cytotoxins, seizures, cytotoxic edema, and failure of cerebral oxidative metabolism starting 6 to 15 h post insult. Studies designed around this conceptual framework have shown that moderate cerebral hypothermia initiated as early as possible before the onset of secondary deterioration, and continued for a sufficient duration has been associated with long-lasting neuroprotection. Three large controlled trials have demonstrated that post resuscitation cooling is generally safe and reduces death or disability at 18 months of age after neonatal encephalopathy. Hypothermia is now widely recommended as a standard of care for infants with HIE. However, national guidelines concerning regional organization and supportive care are necessary. A developmental follow-up must be organized. Neonatologists involved in this procedure must be encouraged joining a national data collection and registry.
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