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Bronchopulmonary dysplasia (BPD) is a leading cause of mortality and morbidity in premature infants with significant lifelong respiratory and neurodevelopmental sequelae into adulthood.1 Since it was first described in 1967, the pathophysiological understanding of BPD has evolved with advances in neonatal practice, such as the use of surfactant and maternal antenatal steroids. As the care of extremely premature infants improves, more immature infants born during the late canalicular and early saccular phases of lung development are surviving, altering the pathophysiology of BPD and diagnostic criteria.2
There is an ongoing debate on the optimal method of diagnosing and classifying BPD. The current 2018 National Institute of Child Health and Human Development BPD definition3 adopts a treatment-based, semiquantitative approach. Very premature infants with abnormal chest X-ray findings are classified into three grades of BPD depending on oxygen requirement and type of respiratory support required over three consecutive days around 36 weeks of corrected gestational age (CGA). Hence, differences in oxygen and ventilation strategies among clinicians and centres may lead to inconsistencies in BPD definition and classification.
Impaired pulmonary gas exchange is a cardinal feature of BPD. A pathophysiological-based approach in defining BPD by measuring pulmonary gas exchange in very preterm infants may offer a physiological assessment of BPD severity at the parenchymal level.2 The rightward shift of the oxyhaemoglobin dissociation curve …
Contributors Both authors drafted and approved the final manuscript.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Provenance and peer review Commissioned; externally peer reviewed.
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