Hypoxic-ischaemic brain injury: Viva

Branch 1: Classification and the principle of secondary injury

The candidate should classify hypoxic-ischaemic brain injury in the infant and child beyond the neonatal period as global brain injury from a cardiorespiratory arrest or asphyxial event, and should separate it from neonatal hypoxic-ischaemic encephalopathy. A strong candidate states that the injury divides into a primary injury, the neuronal death at the moment of arrest that is already fixed, and a secondary injury, the reperfusion cascade over hours to days that intensive care targets, and that this temporal classification drives the entire management because every intervention aims at a specific element of the secondary cascade. ^[7]

If the examiner presses on the biology, the candidate should describe the energy-failure cascade: ATP depletion, pump failure, cytotoxic oedema, glutamate release, and calcium influx producing rapid neuronal death, followed after reperfusion by mitochondrial dysfunction, oxidative stress, inflammation, and apoptosis. The candidate should explain that this is why cooling works, because it reduces metabolic demand, suppresses excitotoxicity, dampens inflammation, and limits apoptotic cascades. ^[1][7]