Pathogenesis of bronchopulmonary dysplasia

被引:122
作者
Chess, Patricia R. [1 ]
D'Angio, Carl T. [1 ]
Pryhuber, Gloria S. [1 ]
Maniscalco, William M. [1 ]
机构
[1] Univ Rochester, Dept Pediat, Rochester, NY 14642 USA
关键词
bronchopulmonary dysplasia; respiratory distress syndrome; surfactant deficiency; arrested pulmonary development; inflammation; patent ductus arteriosus;
D O I
10.1053/j.semperi.2006.05.003
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
Bronchopulmonary dysplasia (BPD), initially described 40 years ago, is a dynamic clinical entity that continues to affect tens of thousands of premature infants each year. BPD was first characterized as a fibrotic pulmonary endpoint following severe Respiratory Distress Syndrome (RDS). It was the result of pulmonary healing after RDS, high oxygen exposure, positive pressure ventilation, and poor bronchial drainage secondary to endotracheal intubation in premature infants. With improved treatment for RDS, including surfactant replacement, oxygen saturation monitoring, improved modes of mechanical ventilation, antibiotic therapies, nutritional support, and infants surviving at younger gestations, the clinical picture of BPD has changed. In the following pages, we will summarize the multifaceted pathophysiologic factors leading to the pulmonary changes in "new" BPD, which is primarily characterized by disordered or delayed development. The contribution of hyperoxia and hypoxia, mechanical forces, vascular maldevelopment, inflammation, fluid management, patent ductus arteriosus (PDA), nutrition, and genetics will be discussed. © 2006 Elsevier Inc. All rights reserved.
引用
收藏
页码:171 / 178
页数:8
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