Why are we still using oxygen to resuscitate term infants?

Abstract

This article summarizes the historical background for the use of oxygen during newborn resuscitation and describes some of the research and the process of changing the previous practice from a high-to a low-oxygen approach. Findings of a recent Cochrane review suggest that more than 100 000 newborn lives might be saved globally each year by changing from 100 to 21% oxygen for newborn resuscitation. This estimate represents one of the largest yields for a simple therapeutic approach to decrease neonatal mortality in the history of pediatric research. Available data also suggest that, for the very low birth weight infant, use of the low-oxygen approach should be considered with the understanding that some of the smallest and sickest preterm neonates will need some level of oxygen supplementation during the first minutes of postnatal life. As more data are needed for the very preterm population, creation of strict guidelines for these infants would be premature at present. However, it can be stated that term and late preterm infants in need of resuscitation should, in general, be started on 21% oxygen, and if resuscitation is not started with 21% oxygen, a blender should be available, enabling the administration of the lowest FiO 2 possible to keep heart rate and SaO 2 within the target range. For extremely low birth weight infants, initial FiO 2 could be between 0.21 and 0.30 and adjusted according to the response in SaO 2 and heart rate.

A Review of Oxygen Physiology and Appropriate Management of Oxygen Levels in Premature Neonates

“…Use of 100% oxygen was previously recommended for resuscitation because of the known detrimental effects of hypoxia 35 and the positive effects of oxygen in promoting pulmonary vascularization. 7 However, over the past 20 to 30 years, research has determined that overexposure to oxygen immediately following hypoxia can lead to accumulation of oxygen free radicals and ischemia–reperfusion injury.…”

“… 7 However, over the past 20 to 30 years, research has determined that overexposure to oxygen immediately following hypoxia can lead to accumulation of oxygen free radicals and ischemia–reperfusion injury. 35 In preclinical studies, toxicity associated with 100% oxygen resuscitation included increased pulmonary artery contractility and accumulation of ROS. 36 – 38 Given these findings, preclinical and clinical studies evaluated the efficacy and safety of room air (21% oxygen) for neonatal resuscitation.…”

The developing human preterm neonatal immune system: A case for more research in this area

“…According to recent data in human infants, brief periods of oxygen administered at birth may generate sufficient inflammation and oxidative injury to cause sustained organ damage [71]. This oxidative stress is likely exacerbated by a profound immaturity of anti-oxidant defenses [73], which continues to drive a controversy in neonatal care about the amount of supplemental oxygen that is safe to administer to preterm newborns [74]. These data clearly mandate a proper understanding of the impact of therapeutically altering the normal preterm homeostatic innate immune balance in infants exposed to intensive care, before responses can be safely manipulated for the purpose of preventing infection.…”

Short‐ and long‐term behavioral effects of exposure to 21%, 40% and 100% oxygen after perinatal hypoxia–ischemia in the rat

“…We found contradictory effects of exposure to 40% or 100% oxygen compared to 21% oxygen after perinatal H/I in this model, thus the results of this study do not provide strong support for a specific treatment regimen. While experimental data are not conclusive, there are a number of clinical studies that have shown that resuscitation of newborns with room air may be more beneficial than resuscitation with 100% oxygen, and clinical practice is gradually changing towards the use of lower concentrations of oxygen, often titrated to targeted oxygen saturations measured by pulse oximetry (Van Den Dungen et al, 2010; Vento and Saugstad, 2010; Saugstad, 2010; Sweet et al, 2010; Davis et al, 2004).…”