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Published on: November 20, 2015
Hypoxic-ischemic encephalopathy in preterm infants: antecedent factors, brain imaging, and outcome
Pavithra Logitharajah1, Mary A Rutherford, Frances M Cowan
1Division of Clinical Sciences, Imperial College London and MRC Clinical Sciences Centre, London W12 0HS, United Kingdom.
Insights
Hypoxic-ischemic encephalopathy (HIE) in preterm infants often results from placental abruption. Early brain MRI accurately predicts neurodevelopmental outcomes, including cerebral palsy, in these vulnerable newborns.
Area of Science:
- Neonatal Neurology
- Neuroimaging
- Perinatal Medicine
Background:
- Hypoxic-ischemic encephalopathy (HIE) affects preterm infants, posing significant risks for long-term neurological impairment.
- Identifying antecedent factors and injury patterns is crucial for understanding HIE prognosis.
Purpose of the Study:
- To establish antecedent factors and brain injury patterns in preterm infants with HIE.
- To determine the prognostic value of these findings for neurodevelopmental outcomes.
Main Methods:
- Retrospective analysis of 55 preterm infants (gestation ≤36 wk) with HIE.
- Inclusion criteria: low Apgar scores, resuscitation, brain MRI <6 weeks postnatal, and additional clinical factors.
- Assessment of antenatal/perinatal data and neurodevelopmental outcomes at ≥2 years.
Main Results:
- Placental abruption was the most common antecedent event; infection was not prominent.
- Main injury sites: basal ganglia (75%), white matter (89%), brainstem (44%), and cortex (58%).
- Brainstem injury correlated with severe injury in other brain regions. Outcomes included death (32%), cerebral palsy (26%), mild impairment (10%), and normal (32%).
Conclusions:
- Preterm infants with HIE frequently exhibit significant central gray matter and brainstem injury.
- Neonatal MRI findings are valuable predictors of long-term neurodevelopmental outcomes.
- Early MRI is a feasible and important tool for managing this patient group.
Abstract:
Our objectives were to establish antecedent factors and patterns of brain injury and their prognostic value in preterm infants with hypoxic-ischemic encephalopathy (HIE). Essential inclusion criteria were gestation (GA) < or =36 wk, Apgar scores <5/<7 at 1/5 min, major resuscitation at birth, and a brain MRI <6 postnatal wk. At least one additional criterion was required of the following: abnormal intrapartum CTG, sentinel event, meconium, cord pH <7.0, neonatal seizures, and multiorgan failure. Antenatal and perinatal data and > or =2 y neurodevelopmental outcome were documented. Fifty-five infants (GA 26-36; median, 35 wk) were eligible; all had 1-6 (median, 3) additional criteria. Placental abruption was the commonest identifiable antecedent event. Evidence of infection was not prominent. Main sites of injury were basal ganglia (BG, 75%), mostly severe, white matter (WM, 89%), mostly mild, brainstem (44%), and cortex (58%). Brainstem injury was associated with severe BG, WM, and cortical injury. Two-year outcome: death (32%), cerebral palsy (26%, mostly severe quadriplegia), mild impairment (10%), and normal (32%). Significant central gray matter and brainstem injury was found in many preterm infants with HIE. Neonatal MRI findings allowed accurate prediction of neurodevelopmental outcome. Early MRI is feasible and a valuable tool in this poorly reported group of infants.
