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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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