As neuroprotection may become reality, this prospective study was conducted
in order to identify, during the first hour of life, the term neonates who
experience severe birth asphyxia.
Methods We studied patients born at term with birth asphyxia defined by at
least two of the following criteria: fetal distress, depression at birth an
d metabolic acidosis (arterial base deficit > 10 mEq/l at 30 min of life).
Nine indicators were prospectively recorded: fetal monitoring, aspect of am
niotic fluid, delay in establishing respiration, Apgar scores, early neurol
ogical score, arterial pH and base deficit at 30 min (BD30). We followed th
e evolution of each patient according to Finer's classification and defined
severe birth asphyxia as birth asphyxia further followed by moderate or se
vere postasphyxial encephalopathy. Using multilogistic regression, we analy
zed the significance of the indicators in order to identify neonates with s
evere birth asphyxia.
Results Among the 221 patients included in the study, severe birth asphyxia
occurred in 50 (42 moderate and eight severe post-asphyxial encephalopathy
). Except for fetal monitoring and amniotic fluid, all indicators were sign
ificantly different between neonates with severe birth asphyxia and the oth
ers. Multilogistic analysis identified BD30 and early neurological score as
better predictors of severe birth asphyxia than Apgar scores and delay in
establishing respiration. BD30 and early neurological score were associated
in a single logistic model (logistic score = 0.33 x BD30 - 1.06 x early ne
urological score). A logistic score greater than -0.33 identified severe bi
rth asphyxia with both sensitivity and specificity of more than 80%.
Conclusion The association of high base deficit and low neurological status
at 30 min of life is predictive of moderate to severe neurological complic
ations after birth asphyxia and may serve to select the high-risk candidate
s for future treatment of birth asphyxia.