Elsevier

The Journal of Pediatrics

Volume 163, Issue 4, October 2013, Pages 968-975.e2
The Journal of Pediatrics

Original Article
Placental Pathology in Full-Term Infants with Hypoxic-Ischemic Neonatal Encephalopathy and Association with Magnetic Resonance Imaging Pattern of Brain Injury

https://doi.org/10.1016/j.jpeds.2013.06.010Get rights and content

Objective

To investigate the relationship between placental pathology and pattern of brain injury in full-term infants with neonatal encephalopathy after a presumed hypoxic-ischemic insult.

Study design

The study group comprised full-term infants with neonatal encephalopathy subsequent to presumed hypoxia-ischemia with available placenta for analysis who underwent cerebral magnetic resonance imaging (MRI) within the first 15 days after birth. Macroscopic and microscopic characteristics of the placenta were assessed. The infants were classified according to the predominant pattern of brain injury detected on MRI: no injury, predominant white matter/watershed injury, predominant basal ganglia and thalami (BGT) injury, or white matter/watershed injury with BGT involvement. Maternal and perinatal clinical factors were recorded.

Results

Placental tissue was available for analysis in 95 of 171 infants evaluated (56%). Among these 95 infants, 34 had no cerebral abnormalities on MRI, 27 had white matter/watershed injury, 18 had BGT injury, and 16 had white matter/watershed injury with BGT involvement. Chorioamnionitis was a common placental finding in both the infants without injury (59%) and those with white matter/BGT injury (56%). On multinomial logistic regression analysis, white matter/watershed injury with and without BGT involvement was associated with decreased placental maturation. Hypoglycemia was associated with an increased risk of the white matter/BGT injury pattern (OR, 5.4; 95% CI, 1.4-21.4). The BGT injury pattern was associated with chronic villitis (OR, 12.7; 95% CI, 2.4-68.7). A placental weight <10th percentile appeared to be protective against brain injury, especially for the BGT pattern (OR, 0.1; 95% CI, 0.01-0.7).

Conclusion

Placental weight <10th percentile was mainly associated with normal cerebral MRI findings. Decreased placental maturation and hypoglycemia <2.0 mmol/L were associated with increased risk of white matter/watershed injury with or without BGT involvement. Chronic villitis was associated with BGT injury irrespective of white matter 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

References (43)

  • D.S. Gardner et al.

    The effect of a reversible period of adverse intrauterine conditions during late gestation on fetal and placental weight and placentome distribution in sheep

    Placenta

    (2002)
  • X. Fan et al.

    The role and regulation of hypoxia-inducible factor-1α expression in brain development and neonatal hypoxic-ischemic brain injury

    Brain Res Rev

    (2009)
  • J.C. Harteman et al.

    Patterns of placental pathology in preterm infants with a periventricular haemorrhagic infarction: association with time of onset and clinical presentation

    Placenta

    (2012)
  • C.V. Ananth et al.

    Evidence of placental abruption as a chronic process: associations with vaginal bleeding early in pregnancy and placental lesions

    Eur J Obstet Gynecol Reprod Biol

    (2006)
  • N. Linduska et al.

    Placental pathologies in fetal MRI with pathohistological correlation

    Placenta

    (2009)
  • N. Badawi et al.

    Intrapartum risk factors for newborn encephalopathy: the Western Australian case-control study

    BMJ

    (1998)
  • K.B. Nelson et al.

    Antecedents of neonatal encephalopathy in the vermont oxford network encephalopathy registry

    Pediatrics

    (2012)
  • T. Alderliesten et al.

    Antemortem cranial MRI compared with postmortem histopathological examination of the brain in term infants with neonatal encephalopathy following perinatal asphyxia

    Arch Dis Child Fetal Neonatal Ed

    (2013)
  • R.E. Myers

    Four patterns of perinatal brain damage and their conditions of occurrence in primates

    Adv Neurol

    (1975)
  • A.M. Li et al.

    White matter injury in term newborns with neonatal encephalopathy

    Pediatr Res

    (2009)
  • M.J. Barrett et al.

    Isolated acute non-cystic white matter injury in term infants presenting with neonatal encephalopathy

    Arch Dis Child Fetal Neonatal Ed

    (2013)
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    The authors declare no conflicts of interest.

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