Original ArticlePlacental Pathology in Full-Term Infants with Hypoxic-Ischemic Neonatal Encephalopathy and Association with Magnetic Resonance Imaging Pattern of Brain Injury
Section snippets
Methods
Full-term infants (36-43 weeks gestational age [GA]) with neonatal encephalopathy subsequent to HI admitted to the neonatal intensive care unit of the Wilhelmina Children's Hospital, Utrecht between January 2005 and July 2012 were eligible for this study if they had the placenta available for histopathological investigation and had undergone neonatal MRI performed within 15 days of birth. This tertiary hospital is a referral center for a geographical area in the central region of The
Results
A total of 181 infants with neonatal encephalopathy secondary to presumed HI underwent neonatal MRI. Three infants with trisomy 21, 3 infants with an inborn error of metabolism, 1 infant with antenatal cerebral injury due to intraventricular hemorrhage and a periventricular cyst at birth, and 3 infants with postnatal collapse were excluded from the analysis. Placentas were available for histopathological examination in 95 of the remaining 171 infants (56%). There were no significant differences
Discussion
Based on extensive experiments in animals without previous placental pathology, BGT injury secondary to neonatal encephalopathy has been assumed to be related to profound acute HI, although prolonged chronic hypoxia is more often associated with a watershed pattern of injury.4 However, in the human neonate, the timing and severity of HI, and thereby the spectrum of brain injury following HI, is much more heterogeneous. In addition, in infants with neonatal encephalopathy presenting with
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The authors declare no conflicts of interest.