title: Bronchopulmonary dysplasia: then and now.
abstract: When bronchopulmonary dysplasia (BPD) was first described in 1967, the use of assisted ventilation in neonates was in its infancy. High concentrations of oxygen were implicated, and BPD was equated with 'pulmonary oxygen toxicity'. The etiologic role of not only oxygen but also peak inspiratory pressures and the duration of exposure to both was emphasized in the 1970s, but BPD remained a dreaded complication of managing respiratory distress syndrome in the 1980s. It was only after exogenous surfactant became commercially available for endotracheal administration that 'classical' BPD began to disappear and was replaced by the 'new' BPD. 'Classical' BPD was seen in more mature preterm infants (>28 weeks' gestational age) and in its severe form was characterized radiographically by micro- and macrocysts of the lung, lung hyperinflation and flattening of the diaphragms. In contrast, 'new' BPD is seen in less mature infants (<28 weeks' gestational age), has comparatively mild radiographic abnormalities and has been defined as continued oxygen requirement at 36 weeks' postmenstrual age. Pathologically, 'classical' BPD frequently revealed obstructive bronchiolitis and fibrosis of lung parenchyma, whereas 'new' BPD demonstrates minimal fibrosis but uniform arrest of development. Herein, factors which may contribute to the etiology of BPD are described, as well as possible preventative and therapeutic strategies.
authors.affiliation: Division of Neonatal and Developmental Medicine, Stanford University School of Medicine, Palo Alto, CA 94304, USA. aphilip@stanford.edu
authors.forename: Alistair G S
authors.initials: AG
authors.lastname: Philip
mesh_terms: D001997:Bronchopulmonary Dysplasia / Q000503:physiopathology* / Q000628:therapy*; D006801:Humans; D007231:Infant, Newborn; D007234:Infant, Premature; D010100:Oxygen / Q000627:therapeutic use; D012121:Respiration, Artificial / Q000009:adverse effects
chemical_list: D010100:Oxygen