Abstract
BackgroundNeurodevelopmental disabilities persist in survivors of neonatal hypoxic-ischemic encephalopathy (HIE) despite treatment with therapeutic hypothermia. Cerebrovascular autoregulation, the mechanism that maintains cerebral perfusion during changes in blood pressure, may influence outcomes. Our objective was to describe the relationship between acute autoregulatory vasoreactivity during treatment and neurodevelopmental outcomes at 2 years of age.MethodsIn a pilot study of 28 neonates with HIE, we measured cerebral autoregulatory vasoreactivity with the hemoglobin volume index (HVx) during therapeutic hypothermia, rewarming, and the first 6 h of normothermia. The HVx, which is derived from near-infrared spectroscopy, was used to identify the individual optimal mean arterial blood pressure (MAPOPT) at which autoregulatory vasoreactivity is greatest. Cognitive and motor neurodevelopmental evaluations were completed in 19 children at 21–32 months of age. MAPOPT, blood pressure in relation to MAPOPT, blood pressure below gestational age + 5 (ga + 5), and regional cerebral oximetry (rSO2) were compared to the neurodevelopmental outcomes.ResultsNineteen children who had HIE and were treated with therapeutic hypothermia performed in the average range on cognitive and motor evaluations at 21–32 months of age, although the mean performance was lower than that of published normative samples. Children with impairments at the 2-year evaluation had higher MAPOPT values, spent more time with blood pressure below MAPOPT, and had greater blood pressure deviation below MAPOPT during rewarming in the neonatal period than those without impairments. Greater blood pressure deviation above MAPOPT during rewarming was associated with less disability and higher cognitive scores. No association was observed between rSO2 or blood pressure below ga + 5 and neurodevelopmental outcomes.ConclusionIn this pilot cohort, motor and cognitive impairments at 21–32 months of age were associated with greater blood pressure deviation below MAPOPT during rewarming following therapeutic hypothermia, but not with rSO2 or blood pressure below ga + 5. This suggests that identifying individual neonates’ MAPOPT is superior to using hemodynamic goals based on gestational age or rSO2 in the acute management of neonatal HIE.Electronic supplementary materialThe online version of this article (doi:10.1186/s12883-015-0464-4) contains supplementary material, which is available to authorized users.
Highlights
Neurodevelopmental disabilities persist in survivors of neonatal hypoxic-ischemic encephalopathy (HIE) despite treatment with therapeutic hypothermia
We previously reported that blood pressure deviation below MAPOPT during rewarming is associated with greater brain injury on Magnetic resonance imaging (MRI) in pilot studies of autoregulation during HIE [9, 10]
All neonates who were admitted to the neonatal intensive care unit (NICU) between September 2010 and October 2012 were screened for study eligibility, which was based on the diagnosis of HIE according to criteria used by the NICHD Neonatal Research Network’s clinical trial of hypothermia in neonatal HIE [12]
Summary
Neurodevelopmental disabilities persist in survivors of neonatal hypoxic-ischemic encephalopathy (HIE) despite treatment with therapeutic hypothermia. Long-term severe sequelae of neonatal HIE include intellectual disability and cerebral palsy. In children who received therapeutic hypothermia for HIE, the incidence of cerebral palsy is approximately 17 % and the incidence of IQ < 70 is 27 % [3]. In the Total Body Hypothermia for Neonatal Encephalopathy Trial, 55 % of HIE survivors who received hypothermia had persistent neurologic abnormalities at age 6–7 years, including % with cerebral palsy and % with moderate or severe disabilities [6]. The National Institute of Child Health and Human Development (NICHD) Neonatal Research Network trial of therapeutic hypothermia in HIE found that 35 % of survivors who received hypothermia had moderate or severe disabilities at 6–7 years of age [3]. Additional modifiable factors and potential adjuvant therapies to hypothermia must be identified to improve neurologic outcomes
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