Pathophysiology and Prevention of Bronchopulmonary Dysplasia

Jonathan   W.   Davis; David   G.   Sweet

Abstract

BPD is the major respiratory complication of preterm delivery and is typified by chronic oxygen dependency and respiratory insufficiency beyond 36 weeks postconceptional age. It is caused by a combination of insults on the developing lung precipitated by preterm birth and its subsequent respiratory management. The common pathway linking the various causative factors is inflammation, which may be initiated prior to birth in the setting of maternal chorioamnionitis, or after birth by mechanical ventilation, infection or oxidative stress. Inflammation in the developing lung induces airways remodeling which adversely affects lung function. Multiple inflammatory mediators are implicated in this process and modifying the course of the disease has proven difficult. The emphasis of management should be directed towards prevention with strategies aimed at minimizing early lung injury and oxidative stress. These include delivery room stabilization and mechanical ventilation techniques that aim to avoid volutrauma and atelectotrauma. Drugs may also influence BPD progression and can broadly be divided into three categories; those administered prenatally to accelerate lung maturation, those administered postnatally to reduce initiation of inflammatory stimuli and those to modify any established inflammatory response. In this review we have examined recent evidence for each of these ventilatory and therapeutic strategies to prevent BPD. A better understanding of the pathophysiology of airways remodeling in BPD could have significant implications for future potential targeted interventions.

Keywords: Vascular endothelial growth factor, Matrix metalloproteinases, Oxidative Stress, Continuous Positive Airway Pressure, Permissive Hypercapnia

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