title: 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 CO2 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 CO2 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: 630-1360 g) 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 CO2 reactivity of 24.4%/kPa CO2 (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 has a median CO2 reactivity of 3.4%/kPa CO2 (interquartile range 8.0-11.7).
  
  
  CONCLUSIONS
  In mechanically ventilated very low birthweight infants low CO2 reactivity of cerebral blood flow (below 10%/kPa CO2) during the first 36 hours of life was associated with poor neurodevelopmental outcome or hypoxic-ischaemic encephalopathy at autopsy. Loss of CO2 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.
authors.affiliation: Department of Obstetrics and Gynecology, University of Zurich, Switzerland.
authors.forename: A M
authors.initials: AM
authors.lastname: Müller
authors.forename: C
authors.initials: C
authors.lastname: Morales
authors.forename: J
authors.initials: J
authors.lastname: Briner
authors.forename: O
authors.initials: O
authors.lastname: Baenziger
authors.forename: G
authors.initials: G
authors.lastname: Duc
authors.forename: H U
authors.initials: HU
authors.lastname: Bucher
mesh_terms: D001921:Brain / Q000098:blood supply* / Q000473:pathology; D001925:Brain Damage, Chronic / Q000175:diagnosis* / Q000473:pathology / Q000503:physiopathology; D002245:Carbon Dioxide / Q000502:physiology; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D020925:Hypoxia-Ischemia, Brain / Q000175:diagnosis / Q000473:pathology / Q000503:physiopathology; D007223:Infant; D007231:Infant, Newborn; D007235:Infant, Premature, Diseases / Q000175:diagnosis* / Q000473:pathology / Q000503:physiopathology; D019102:Infant, Very Low Birth Weight; D008297:Male; D012039:Regional Blood Flow / Q000502:physiology; D012121:Respiration, Artificial; D014655:Vascular Resistance / Q000502:physiology*
chemical_list: D002245:Carbon Dioxide