TY - JOUR

T1 - Early cerebral hypoxia in extremely preterm infants and neurodevelopmental impairment at 2 year of age

T2 - A post hoc analysis of the SafeBoosC II trial

AU - Plomgaard, Nne Mette

AU - Schwarz, Christoph E.

AU - Claris, Olivier

AU - Dempsey, Eugene M.

AU - Fumagalli, Monica

AU - Hyttel-Sorensen, Simon

AU - Lemmers, Petra

AU - Pellicer, Adelina

AU - Pichler, Gerhard

AU - Greisen, Gorm

PY - 2022/1/24

Y1 - 2022/1/24

N2 - BackgroundThe SafeBoosC II, randomised clinical trial, showed that the burden of cerebral hypoxia was reduced with the combination of near infrared spectroscopy and a treatment guideline in extremely preterm infants during the first 72 hours after birth. We have previously reported that a high burden of cerebral hypoxia was associated with cerebral haemorrhage and EEG suppression towards the end of the 72-hour intervention period, regardless of allocation. In this study we describe the associations between the burden of cerebral hypoxia and the 2-year outcome.MethodsCerebral oxygenation was continuously monitored from 3 to 72 hours after birth in 166 extremely preterm infants. At 2 years of age 114 of 133 surviving children participated in the follow-up program: medical examination, Bayley II or III test and the parental Ages and Stages Questionnaire. The infants were classified according to the burden of hypoxia: within the first three quartiles (n = 86, low burden) or within in the 4(th) quartile (n = 28, high burden). All analyses were conducted post hoc.ResultsThere were no statistically significant differences between the quantitative assessments of neurodevelopment in the groups of infants with the low burden of cerebral hypoxia versus the group of infants with the high burden of cerebral hypoxia. The infants in the high hypoxia burden group had a higher-though again not statistically significant-rate of cerebral palsy (OR 2.14 (0.33-13.78)) and severe developmental impairment (OR 4.74 (0.74-30.49).ConclusionsThe burden of cerebral hypoxia was not significantly associated with impaired 2-year neurodevelopmental outcome in this post-hoc analysis of a feasibility trial.

AB - BackgroundThe SafeBoosC II, randomised clinical trial, showed that the burden of cerebral hypoxia was reduced with the combination of near infrared spectroscopy and a treatment guideline in extremely preterm infants during the first 72 hours after birth. We have previously reported that a high burden of cerebral hypoxia was associated with cerebral haemorrhage and EEG suppression towards the end of the 72-hour intervention period, regardless of allocation. In this study we describe the associations between the burden of cerebral hypoxia and the 2-year outcome.MethodsCerebral oxygenation was continuously monitored from 3 to 72 hours after birth in 166 extremely preterm infants. At 2 years of age 114 of 133 surviving children participated in the follow-up program: medical examination, Bayley II or III test and the parental Ages and Stages Questionnaire. The infants were classified according to the burden of hypoxia: within the first three quartiles (n = 86, low burden) or within in the 4(th) quartile (n = 28, high burden). All analyses were conducted post hoc.ResultsThere were no statistically significant differences between the quantitative assessments of neurodevelopment in the groups of infants with the low burden of cerebral hypoxia versus the group of infants with the high burden of cerebral hypoxia. The infants in the high hypoxia burden group had a higher-though again not statistically significant-rate of cerebral palsy (OR 2.14 (0.33-13.78)) and severe developmental impairment (OR 4.74 (0.74-30.49).ConclusionsThe burden of cerebral hypoxia was not significantly associated with impaired 2-year neurodevelopmental outcome in this post-hoc analysis of a feasibility trial.

KW - TISSUE OXYGENATION

KW - IMMEDIATE TRANSITION

KW - SATURATION

KW - ASSOCIATION

KW - HYPOXEMIA

U2 - 10.1371/journal.pone.0262640

DO - 10.1371/journal.pone.0262640

M3 - Journal article

C2 - 35073354

VL - 17

JO - PLoS ONE

JF - PLoS ONE

SN - 1932-6203

IS - 1

M1 - 0262640

ER -