ABSTRACT
When bronchopulmonary dysplasia (BPD) was first described in premature infants in 1967, Northway et al. speculated that its pathogenesis was a prolongation of the healing phase of severe hyaline membrane disease (HMD) combined with generalized pulmonary oxygen toxicity. They recognized that endotracheal intubation and mechanical ventilation might have contributed to the development of the disease (1). The concept that BPD is primarily a disease that results from an arrest in alveolar development has only emerged over the last two decades. As better oxygenation and ventilatory strategies were developed and utilized, the classically described lung lesions of bronchial squamous metaplasia, alternating sites of emphysema (overinflation) and severe fibrosis, and the consequences of pulmonary vascular hypertension largely disappeared. These were replaced as the result of newer studies with descriptious of what were termed simplified lung (2); a ‘‘premature lung pattern (3); an interstitial form of BPD, characterized by arrested development of terminal air spaces (4); or acinar arrest’’ (5). Classic, or what is termed old BPD, pathological findings reflected primarily the consequences of elevated oxygen and ventilator-induced injury on a relatively immature and
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surfactant deficient lung. For example, Northway et al.’s study group had an average gestational age and birthweight of 32 weeks and 1893 gr, respectively. Even before the introduction of exogenous surfactant therapy, the better clinical management and technological advances had resulted in BPD occurring primarily in infants who were born <28 weeks’ gestation and weighed <1200 g. The more widespread use of prenatal steroids and postnatal exogenous surfactant has further influenced the incidence of BPD; infants now at most risk are 24-28 weeks’ gestation, and weigh 500-1000 g (6). It is not surprising that new descriptions of a simplified lung or acinar arrest reflect
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Figure 1 A. A lung tissue section during the canalicular phase of lung development from an infant stillborn at 24 weeks’ gestation. The immersion-fixed lung specimen shows a terminal bronchiole (b) and its branches in the respiratory portion of the lung. The distal air spaces [Dq] are rounded separated by intervening mesenchyme (ln) and little evidence of secondary crest formation. B.A lung tissue section during the alveolar phase of lung development from an infant stillborn at 38 week’s shows the remarkable maturation and differentiation the lung undergoes during prenatal development.
Considerable thinning of the secondary crests (arrows) and a more thinned interstitium are evident throughout the lung. V, vessel (Hematoxylin & eosin, original magnification X110 and X106, respectively).
