BPD: Complication of prematurity
Despite advances in perinatal care and a steady decline in mortality among preterm infants, preventing bronchopulmonary dysplasia is still a challenge to care for children born prematurely.
Bronchopulmonary dysplasia (BPD) is a chronic lung disease usually following mechanical ventilation and oxygen therapy in premature infants requiring treatment for acute respiratory distress. Despite improvements in obstetric and neonatal care leading to increased survival of premature infants, little progress has been made in the prevention of BPD. Pediatricians need to be aware of changing definitions, risk factors, prevention, and long-term health outcomes of this disease in their premature patients.
Definition of BPD
The definition of BPD has undergone multiple changes since Northway’s1 original description in 1967. A 2001 workshop sponsored by the National Institute of Child Health and Human Development (NICHD) proposed to define BPD in the following manner based on severity:2-5
The NICHD definition was shown to better predict pulmonary outcomes (eg, requirement for pulmonary medication, rehospitalization) and neurodevelopment outcomes at age 18 to 22 months (eg, lower development index scores, cerebral palsy, hearing loss, blindness) compared with previous definitions.6 The definition is still under significant debate and research. More recent investigations found that significant respiratory morbidity is best predicted by oxygen use and respiratory support at 40 weeks PMA. Also, more recent studies find the prediction of neurosensory impairment to be less strong.5
In terms of pathology of the lung disease, airway injury, inflammation, and fibrosis were seen prior to development of surfactant as a treatment in the 1980s. In the “new” postsurfactant BPD, the more prominent pathology is reduced surface area availability for gas exchange from alveolar hypoplasia and fewer and larger alveoli. Dysregulation of the pulmonary vasculature also contributes.7-9
Bronchopulmonary dysplasia is a multifactorial disease, including both antenatal and postnatal factors, leading to a disruption in pulmonary development, inflammation, and damage to the lungs.10
Higher levels of inflammatory markers are noted in infants that develop BPD. However, whether this inflammation is attributed to another disease process such as chorioamnionitis, the exact role of inflammation in the pathogenesis remains a significant area of study.20 Likewise, whether there is a genetic predisposition to BPD remains controversial as recent research has demonstrated mixed results.21-23