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Hypoxic-Ischemic Encephalopathy in Preterm Infants
Hypoxic-Ischemic Encephalopathy in Preterm Infants: Antecedent Factors, Brain Imaging, and Outcome PAVITHRA LOGITHARAJAH, MARY A. RUTHERFORD, AND FRANCES M. COWAN Division of Clinical Sciences [P.L., M.A.R., F.M.C.], Imperial College London and MRC Clinical Sciences Centre, London W12 0HS, United Kingdom; Division of Neonatology [P.L., F.M.C.], Imperial College Comprehensive Biomedical Research Centre, London W12 0HS, United Kingdom 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 in- clusion criteria were gestation (GA) 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 peri- natal data and 2 y neurodevelopmental outcome were documented. Fifty-five infants (GA 26–366; 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 im- pairment (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 neurodevel- opmental outcome. Early MRI is feasible and a valuable tool in this poorly reported group of infants. (Pediatr Res 66: 222–229, 2009) Hypoxic-ischemic encephalopathy (HIE), and subsequentmorbidity and mortality, is seldom reported in preterm infants. Criter
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