Neonatal HIE

Hypoxic-ischaemic encephalopathy (HIE) is brain dysfunction caused by impaired cerebral oxygen delivery and perfusion around birth. The initial insult may follow placental abruption, uterine rupture, cord prolapse, profound maternal hypotension, shoulder dystocia, or a difficult resuscitation. Not every infant with a low Apgar score has HIE, and not every infant with HIE has an obvious sentinel event. Brain injury does not end when circulation is restored. During the initial hypoxic-ischaemic period, depleted ATP disables membrane ion pumps. Sodium and water enter neurons, calcium accumulates intracellularly, and glutamate-driven excitotoxicity amplifies cell injury. After resuscitation, there is often a latent phase of partial metabolic recovery. This interval, roughly the first 6 hours after birth, is the opportunity to prevent part of the next wave of injury. Secondary energy failure develops over hours to days through mitochondrial dysfunction, oxidative injury, inflammation, and programmed cell death. Therapeutic hypothermia slows these damaging processes. It does not reverse dead tissue or replace effective resuscitation; it reduces the extension of injury that would otherwise occur after the original event. The clinical implication is urgent: an infant can...