新发支气管肺发育不良的病理分析

Jacqueline J. Coalson
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引用次数: 514

摘要

技术进步,改进的通气策略和更好的护理技术,加上产前类固醇和产后表面活性剂的使用,导致了更小和更不成熟的婴儿的生存。在24-26周的肺小管发育阶段出生的早产儿有可能患上支气管肺发育不良(BPD),此时肺泡和远端血管开始发育。“旧”BPD中严重气道损伤的组织病理学病变和交替的过度充气和纤维化部位已被“新”BPD所取代,病理改变为大而简化的肺泡结构、畸形的毛细血管配置和可变的间质细胞和/或纤维增生。当出现气道和血管病变时,往往发生在婴儿身上,随着时间的推移,他们会发展成更严重的疾病。新发BPD的肺泡和毛细血管发育不全需要开发特异性治疗方法,但避免肺泡损伤、氧化损伤和炎症/感染将改善肺形态。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Pathology of new bronchopulmonary dysplasia

Technological advances, improved ventilatory strategies and better nursing techniques, coupled with the use of prenatal steroids and postnatal surfactant, have resulted in the survival of smaller and more immature infants. Preterm infants likely to develop bronchopulmonary dysplasia (BPD) are born during the canalicular phase of lung development at 24–26 weeks, a time when alveolar and distal vascular development commences. The histopathologic lesions of severe airway injury and alternating sites of overinflation and fibrosis in ‘old’ BPD have been replaced in ‘new’ BPD with the pathologic changes of large, simplified alveolar structures, a dysmorphic capillary configuration and variable interstitial cellularity and/or fibroproliferation. Airway and vascular lesions, when present, tend to occur in infants who over time develop more severe disease. The alveolar and capillary hypoplasia of new BPD will require the development of specific therapies, but avoiding volutrauma, oxidant injury and inflammation/infection will improve lung morphology.

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