Loss of CO2 reactivity of cerebral blood flow is associated with severe brain damage in mechanically ventilated very low birth weight infants.

Abstract Background: Early detection of pathophysiological factors associated with permanent and severe brain damage in preterm infants requiring intensive care is a major issue in neonatal neurology. The aim of this study was to investigate if an abnormal CO 2 reactivity of cerebral blood flow in high risk very low birth weight infants is associated with severe brain injury demonstrated at autopsy or by neurodevelopment examination at 18 months. Methods: The CO 2 reactivity of cerebral blood flow (xenon-133) was measured in 18 mechanically ventilated, severely ill, very low birthweight infants (gestational age 26–32 weeks, birthweight: 630–1360g) during the first 36 hours of life. Cerebral outcome was assessed on autopsy findings (n = 8) or at the age of 18 months using Bayley developmental scales (n = 10) Results: Eight infants with normal development at 18 months (within mean ± 2.5 SD of reference group) and two infants with normal cerebral autopsy findings had a median CO 2 reactivity of 24.4%/kPa CO 2 (interquartile range 14.7–41.2). Two infants with abnormal development (> 2.5 SD below mean) and six infants with hypoxic-ischaemic encephalopathy at autopsy had a median CO 2 reactivity of 3.4%/kPa CO 2 (interquartile range 8.0–11.7). Conclusion: In mechanically ventilated very low birthweight infants low CO 2 reactivity of cerebral blood flow (below 10%/kPa CO 2 ) during the first 36 hours of life was associated with poor neurodevelopmental outcome or hypoxicischaemic encephalopathy at autopsy. Loss of CO 2 reactivity may play a role in the pathogenesis of hypoxic ischaemic encephalopathy. It is a candidate for predicting early severe brain damage in preterm infants requiring intensive care and for controlling the effect of early interventions.