Hylke Salverda

16 Chapter 1 hypoxia, hyperoxia and fluctuation in oxygenation all increase the rate of ROP in preterm infants.11-13 Oxygen and other improvements in neonatal care throughout the last century have led to increased survival, but have also increased the incidence of retinopathy of prematurity.14 Globally for the year 2010, it was estimated that ROP led to 20,000 blind infants, and left another 12,300 visually impaired.15 Bronchopulmonary dysplasia (BPD), a chronic disease of the lungs, is a major cause of respiratory illness in preterm infants leading to significant morbidity and mortality after discharge from the neonatal intensive care unit (NICU). The aetiology is multifactorial and involves disruption of the later phases of lung development and injury to the lung. Specifically for oxygen toxicity, high concentrations of free radicals are thought to cause chronic inflammation to the lung.16 This chronic inflammation in turn leads to changes in lung tissue: decreased alveolarization leading to less surface area for gas exchange; vascular remodelling leading to an increase in pulmonary resistance which in turn may lead to pulmonary hypertension;17 and changed lung elasticity.18 The incidence of BPD differs depending on the definition applied. When defined as supplemental oxygen requirement at 36 weeks postmenstrual age the overall incidence was estimated at 42% of infants born between 22-28 weeks gestational age, where a higher gestational age at birth reduced the change of having BPD.19 Titration of supplemental oxygen Mindful of the effects of supplemental oxygen on morbidity, its level must be carefully balanced within safe limits. Continuous monitoring using pulse oximetry (SpO2, the percentage of peripheral oxyhaemoglobin over total haemoglobin) is currently the most appropriate tool to guide the fraction of inspiratory oxygen (FiO2) delivered to the patient. In contrast to repeated arterial blood sampling, SpO2 is non-invasive and continuous. The ideal range for SpO2 in a given subject has been the subject of considerable debate,20 and remains unsolved to date. The accepted target in preterm infants has recently undergone refinement as a result of a series of randomised controlled trials comparing two SpO2 target ranges (SpO2 85-89% vs 91-95%). 21-23 These trials once again highlighted the impact of hypoxaemia and hyperoxaemia on preterm infants, with the lower target range associated with an increase in mortality and necrotizing enterocolitis, and higher target range with ROP. The need for supplemental oxygen is more common and prolonged in very preterm infants. These infants often present with respiratory instability and fluctuation in oxygenation. Whilst the need to target an SpO2 range is widely accepted, data from