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Chronic respiratory sequelae are still a major health problem in surviving premature infants. These complications are less severe today than those originally described by Northway and collaborators in the 1960s,1 but occur more frequently now as the survival of extremely low birth weight infants has increased. The underlying alteration in lungs with bronchopulmonary dysplasia (BPD) is an arrest of alveolar and capillary development. The more severe cases are frequently associated with airway and vascular remodelling, leading to airway obstruction and pulmonary hypertension. These alterations, which may be accompanied by interstitial oedema and fibrous tissue proliferation, are responsible for the abnormalities in lung function observed in these infants.
The findings reported by Hjalmarson et al2 are in agreement with previous publications that have shown that extreme preterm infants frequently have abnormal lung function later in life, independent of their initial respiratory course compared with infants born at term.3 ,4 These abnormalities are characterised by lower specific lung compliance and lung volume, combined with airway obstruction that can lead to impaired gas distribution in the distal lung. These alterations are present in …
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