Many premature infants experience respiratory failure and receive supplemental oxygen for prolonged periods. While this therapy is crucial for their survival, it can be associated with complications such as retinopathy of prematurity (ROP), bronchopulmonary dysplasia (BPD), and central nervous system damage. In recent years, to minimize these complications clinicians have targeted progressively lower arterial oxygen saturation (SpO2) levels in these infants. This occurred despite little evidence for the efficacy and safety of this approach. Several randomized controlled trials have been conducted to test if targeting oxygen saturations in the lower (85%-89%) vs the upper (91%-95%) part of the recommended range confer advantages in regard to neurodevelopmental outcome and severe ROP in extremely premature infants.1
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