Background: Episodes of hyperoxaemia and hypocapnia, which may contribute to brain injury, occur unintentionally in severely asphyxiated neonates in the first postnatal hours.
Objective: To determine whether hyperoxaemia and/or hypocapnia during the first 2 hours of life add to the risk of brain injury after intrapartum asphyxia.
Methods: Retrospective cohort study in term infants with post-asphyxial hypoxic ischaemic encephalopathy (HIE) born between 1985 and 1995. Severe and moderate hyperoxaemia were defined as Pao2 >26.6 and Pao2 >13.3 kPa (200 and 100 mm Hg). Severe and moderate hypocapnia were defined as Paco2 <2.6 and Paco2 <3.3 kPa (20 and 25 mm Hg). Adverse outcome ascertained by age 24 months was defined as death, severe cerebral palsy, or any cerebral palsy with blindness, deafness, or developmental delay. With outcome as the dependent variable, multivariate analyses were performed including hyperoxaemic and hypocapnic variables, and factors adjusted for initial disease severity.
Results: Of 244 infants, 218 had known outcomes, 127 of which were adverse (64 deaths, 63 neurodevelopmental deficits). Multivariate analyses showed an association between adverse outcome and episodes of severe hyperoxaemia (odds ratio (OR) 3.85, 95% confidence interval (CI) 1.67 to 8.88, p = 0.002), and severe hypocapnia (OR 2.34, 95% CI 1.02 to 5.37, p = 0.044). The risk of adverse outcome was highest in infants who had both severe hyperoxaemia and severe hypocapnia (OR 4.56, 95% CI 1.4 to 14.9, p = 0.012).
Conclusions: Severe hyperoxaemia and severe hypocapnia were associated with adverse outcome in infants with post-asphyxial HIE. During the first hours of life, oxygen supplementation and ventilation should be rigorously controlled.
- CI, confidence interval
- Fio2, fraction of inspired oxygen
- HIE, hypoxic ischaemic encephalopathy
- NICU, neonatal intensive care unit
- OR, odds ratio
- Pao2, partial arterial oxygen pressure
- Paco2, partial arterial carbon dioxide pressure
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Competing interests: MP acts as a consultant and provides expert written and oral testimony on behalf of plaintiffs, physicians, and hospitals related to medical malpractice claims for compensation. The claims are made by children with brain injuries associated with intrapartum asphyxia. He has not provided evidence, and does not intend to testify, that hyperoxia and/or hypocarbia contributed to the cause of brain and other injuries of term infants with post-intrapartum asphyxial encephalopathy and cerebral palsy.
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