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Bronchopulmonary Dysplasia (BPD) is a chronic lung disease primarily seen in preterm infants who have required prolonged oxygen therapy and/or mechanical ventilation. It represents impaired alveolar development and lung injury, typically evolving from conditions like respiratory distress syndrome (RDS).
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Revised Definition (NICHD 2018)
BPD is defined in infants <32 weeks gestation, who require supplemental oxygen for ≥28 days with severity assessed at 36 weeks postmenstrual age (PMA):
| Severity | Description |
|---|---|
| Grade 1 | Nasal cannula ≤2 L/min |
| Grade 2 | >2 L/min nasal cannula or non-invasive positive pressure |
| Grade 3 | Invasive mechanical ventilation |
| Contributors | Mechanism |
|---|---|
| Prematurity | Immature lungs with fewer and larger alveoli |
| Oxygen toxicity | Free radical injury to alveolar epithelium |
| Volutrauma/barotrauma | Mechanical ventilation → alveolar overdistension |
| Inflammation | Infection/sepsis → cytokine-mediated lung injury |
| Nutritional deficiency | Impairs postnatal lung growth |

Timeline and stages of BPD: The timeline indicates variables that may modulate lung development from preconception through fetal development before preterm birth. Acute injury (on the timescale of days and weeks) resulting from neonatal care that is required to ensure survival then progresses to chronic lung injury and, ultimately, repair and remodelling over months and years. The unique aspect of bronchopulmonary dysplasia (BPD) is that it is an injury process that occurs as the premature lung is being injured and must repair as the lung continues to develop and mature. Remodelling of the lungs can occur over years.
Thébaud, B., Goss, K.N., Laughon, M. et al. Bronchopulmonary dysplasia. Nat Rev Dis Primers 5, 78 (2019). https://doi.org/10.1038/s41572-019-0127-7

Human lung morphogenesis: Schematic of the stages of lung formation from the embryonic stage to alveolarization. Changes in lung structure with advancing gestation are shown. In the embryonic period of lung bud formation, the tracheal primordium forms from the ventral region of the anterior foregut endoderm and separates from the oesophagus. During the pseudoglandular period, the lung buds proliferate and invade the splanchnic mesenchyme in the process of branching morphogenesis to form the airways and peripheral acinar buds, the latter forming the alveoli later in development. During the saccular stage, epithelial cells lining conducting airways differentiate, producing basal, goblet, ciliated and other secretory cells, which are distinct from the epithelial cells lining the peripheral saccules, namely the cuboidal pre-alveolar type 2 (AT2) cells and squamous AT1 cells. In the saccular–alveolar transition, the peripheral saccules further dilate and the surface is increasingly covered by AT1 cells as the gas exchange region expands. AT2 cells differentiate and produce increasing amounts of surfactant lipid and proteins, which are stored in lamellar bodies. Lung growth continues until adolescence.
Adapted from Whitsett, J. A., Wert, S. E. & Trapnell, B. C. Genetic disorders influencing lung formation and function at birth. Hum. Mol. Genet. 13, R207–R215 (2004), Oxford University Press. Thébaud, B., Goss, K.N., Laughon, M. et al. Bronchopulmonary dysplasia. Nat Rev Dis Primers 5, 78 (2019). https://doi.org/10.1038/s41572-019-0127-7
| Presentation | Description |
|---|---|
| Persistent oxygen dependency | Beyond 28 days of life in preterm neonate |
| Tachypnea, retractions, wheezing | Chronic respiratory distress |
| Recurrent infections | Bronchiolitis, pneumonia |
| Poor weight gain (failure to thrive) | Increased work of breathing |

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Clinical + Radiologic + Oxygen dependency criteria
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