Coalson Jacqueline J
University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA.
Semin Perinatol. 2006 Aug;30(4):179-84. doi: 10.1053/j.semperi.2006.05.004.
Over the past three decades, advances in prenatal and neonatal intensive care have contributed to marked improvements in survival rates for extremely immature infants born during the canalicular phase of lung development at 24 to 26 weeks, a time when alveolar and distal vascular development is rapidly occurring. The histopathological 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 be present in infants, who over time develop more severe disease. The concept that "new" BPD results in an arrest in alveolization should be modified to that of an impairment in alveolization as evidence shows that short ventilatory times and/or the use of nCPAP allow continued alveolar formation.
在过去三十年中,产前和新生儿重症监护技术的进步显著提高了在肺发育小管期24至26周出生的极不成熟婴儿的存活率,这一时期肺泡和远端血管发育迅速。“旧”型支气管肺发育不良(BPD)中严重气道损伤以及过度充气和纤维化交替出现部位的组织病理学病变,在“新”型BPD中已被大的、简化的肺泡结构、畸形的毛细血管构型以及不同程度的间质细胞增多和/或纤维增生等病理变化所取代。气道和血管病变(若存在)往往出现在随着时间推移会发展为更严重疾病的婴儿身上。“新”型BPD导致肺泡化停滞的概念应修正为肺泡化受损,因为有证据表明短时间通气和/或使用鼻塞持续气道正压通气(nCPAP)可使肺泡持续形成。