Studies of preterm neonates suggest that infection may potentiate hypoxic-ischemic (HI) brain injury. In term neonates, infection is a risk factor for encephalopathy and cerebral palsy. Whether it potentiates the risk of brain injury and adverse outcome in the setting of hypoxic-ischemic encephalopathy (HIE) is not clear.
The charts of 257 term newborns with HIE were reviewed for signs of maternal and infant infection, including chorioamnionitis and proven or suspected sepsis. Multivariate logistic regression was used to assess the effect of infection on severity of brain injury as seen on a neonatal MRI (normal-mild vs. moderate-severe), and on risk of adverse neurodevelopment at 30 months in a subset of subjects (neuromotor score, NMS >2, or Bayley Scales of Infant Development II or III MDI < 70 or cognitive score < 85).
Chorioamnionitis (42 subjects) was associated with a lower risk of moderate-severe brain injury (OR 0.3; 95%CI 0.1–0.7; p=0.003), and trended toward lower risk of adverse neurodevelopment. Infant infection (32 subjects) trended toward association with moderate-severe injury (OR 1.6; 95%CI 0.8–3.5; p=0.2), and was significantly associated with an abnormal NMS (OR 3.4; 95%CI 1.2–10.2; p=0.03) but not cognitive outcome. After adjusting for hypothermia and severity of encephalopathy, maternal infection remained associated with a lower risk of brain injury, whereas the association between infant infection and NMS was no longer significant.
These preliminary results are in keeping with animal studies that suggest that the timing of an inflammatory signal may determine whether infection is injurious or protective.
Acknowledgements NIH UL1 RR024131&P50NS035902.
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