Perinatal hypoxic-ischaemic encephalopathy: Clinical and etiopathogenetic classification

Hypoxic-ischaemic encephalopathy is one of the clinical expressions of hypoxic-ischaemic damage in which concomitant hypoxia and ischaemia are responsible for the death of the foetus or neonate, or result in organ impairment with possible long-term sequelae. Neurological deficits are among the most common and severe sequelae, leading to hypoxic-ischaemic encephalopathy whose incidence is between 0.6 and 0.9 per thousand live births in Anglosaxon countries. The following four major and two minor criteria must be present to establish the link between intrapartum hypoxic-ischaemic injury and neurological deficit: metabolic acidosis on umbilical cord sampling, persistent Apgar score of < 5 after the fifth minute, neonatal neurological symptoms, multiorgan involvement, abnormal cardiotocographic tracing, passage of meconium. None of the six criteria alone is diagnostic: the more criteria are present, the more likely the presence of asphyxia. Early electroencephalographic recording may yield useful information for the diagnosis of hypoxic-ischaemic injury to determine the neurological outcome and the diagnosis of convulsions. Neuroradiological investigations will identify and define the extent of cerebral lesions, confirming intrapartum hypoxic-ischaemic damage suspected clinically and yielding additional prognostic information on the basis of the anatomical structures involved.