The pattern of postnatal corticosteroid (PNC) use for bronchopulmonary dysplasia (BPD) follows a pendulum swinging from overt optimism 30 years ago over PNC’s benefits to the current pessimism over PNC’s apparent risks. Bronchopulmonary dysplasia affects 30% to 45% of extremely low-gestational-age newborns (born <28 weeks’ gestational age) and remains among the most common and intractable sequelae of preterm birth. This chronic lung disease results from a variety of antenatal and postnatal exposures, including infection and inflammation. Such insults, when combined with the immature lungs’ aberrant reparative processes, are associated with reduced alveolar surface area and long-term functional morbidities. Bronchopulmonary dysplasia is also associated with delayed brain maturation and diffuse white matter abnormality that increase the risk of neurodevelopmental impairment (NDI). Rates of BPD have remained stable or even increased in some populations over the past 2 to 3 decades. Population-based studies from Australia and Europe since the late-1990s have demonstrated a decrease in the frequency, dose, and timing of PNC use, particularly for systemic dexamethasone. This use pattern is a key factor in the increased incidence of BPD.
Clinical Practice Guidelines