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Bronchopulmonary dysplasia (BPD) was described by Northway and colleagues1 in 1967 as a syndrome of severe lung injury in preterm infants who had received mechanical ventilation and high levels of supplemental oxygen. This initial description of BPD occurred in the era when mechanical ventilation was just beginning to be used for preterm infants and the mean birth weight of the infants who survived mechanical ventilation to develop BPD was 2.3 kg. The pathology was characterized by prominent airway injury, epithelial metaplasia, smooth muscle hypertrophy, and parenchymal fibrosis alternating with emphysema. The experimental work during that era demonstrated that the causes of BPD were primarily mechanical ventilation of and oxygen exposure to the developing lung.2

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Neonatal care practices have changed over the last 30 years with the use of antenatal corticosteroids, continuous positive airway pressure, surfactant, improved ventilation strategies, improvements in nutrition, and other care practices. Many extremely low-birth-weight infants (< 1 kg) with gestational ages under 28 weeks now survive, and these more immature infants are at higher risk for BPD.3 The epidemiology of BPD has changed because factors other than mechanical ventilation and oxygen exposure contribute to the occurrence of BPD in extremely low-birth-weight infants. Major associations are postnatal sepsis, patent ductus arteriosus, and antenatal chorioamnionitis.4 Some extremely low-birth-weight infants now develop BPD without initially having severe respiratory distress syndrome or initially requiring much supplemental oxygen or mechanical ventilation.5

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The diagnosis of BPD is confounded by a series of definitions that have changed over the years as the patients at risk have become increasingly premature.6 Many recent reports define BPD as the need for supplemental oxygen at 36 weeks postconceptional age. However, because clinicians use supplemental oxygen inconsistently, oxygen use and target saturations vary widely in clinical practice. A National Institutes of Health workshop in 2000 recommended a graded diagnosis for BPD to better describe the clinical status of infants with BPD6 (see eTable 59.1). More recently, Walsh and colleagues7 developed an oxygen-need test to make the diagnosis of BPD more uniform. Neonates on positive pressure support or receiving >30% supplemental oxygen with saturations between 90% and 96% were diagnosed with BPD and not tested further. Those receiving <30% oxygen or effective oxygen >30% with saturations >96% underwent a room-air challenge with continuous observation and oxygen-saturation monitoring. Those that could not maintain saturations >90% during weaning and in room air for 30 minutes were also diagnosed with BPD. With the use of the oxygen-need test, the diagnosis of BPD decreased from 35% to 25% of the infants with birth weights below 1250 grams. The diagnostic definition of BPD as oxygen need at 36 weeks does not require antecedent exposures (eg, respiratory distress syndrome, mechanical ventilation), abnormalities on a chest radiograph, or any laboratory test. This is not a precise diagnosis relative to most diagnoses in medicine, which generally include specific clinical associations and laboratory findings. While the diagnosis of BPD is made at 36 weeks, efforts to prevent BPD need to begin with antenatal exposures and to focus on the known associations with BPD in the minutes ...

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