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早产儿慢性肺疾病:简史。

Chronic lung disease of prematurity: a short history.

机构信息

Stanford University School of Medicine, Division of Neonatal and Developmental Medicine, 750 Welch Road, Palo Alto, CA 94304, USA.

出版信息

Semin Fetal Neonatal Med. 2009 Dec;14(6):333-8. doi: 10.1016/j.siny.2009.07.013. Epub 2009 Aug 20.

Abstract

Chronic lung disease of prematurity (CLD) is commonly considered to be a consequence of assisted ventilation. However, prior to the description in 1967 of bronchopulmonary dysplasia (BPD), following ventilator therapy for respiratory distress syndrome, Wilson-Mikity syndrome (WMS) had been described in very preterm infants on minimal oxygen supplementation. In the 1970s and 1980s, many infants treated with assisted ventilation required prolonged mechanical ventilation after developing radiographic features of coarse infiltrates, severe hyperinflation, and microcystic changes, associated with hypercarbemia and the need for increased inspired oxygen concentrations. Some infants died and showed evidence of pulmonary fibrosis, obstructive bronchiolitis, and dysplastic change. The role of supplemental oxygen, positive pressure ventilation, and the immaturity of the lung have long been considered important in the etiology of CLD/BPD. More recently, the role of inflammation (particularly antenatal exposure to cytokines) and individual susceptibility (genetic predisposition) have assumed greater etiologic importance. The historical setting into which corticosteroid treatment for BPD was introduced is also discussed. After the licensing of exogenous surfactant to treat RDS in the early 1990s and more widespread use of prenatal corticosteroids in the mid-1990s, severe BPD became an unusual event. Gradually, the diagnosis of CLD, still often referred to as BPD, was based on an oxygen requirement at 36 weeks postmenstrual age. However, it is not clear that this 'new BPD' is substantially different from WMS. It is difficult to make prognostications about long-term lung function of these infants based on oxygen 'requirement' at 36 weeks, since supplemental oxygen is frequently used unnecessarily.

摘要

早产儿慢性肺病(CLD)通常被认为是辅助通气的结果。然而,在 1967 年描述支气管肺发育不良(BPD)之前,在呼吸机治疗呼吸窘迫综合征之后,极低出生体重儿在最低氧补充的情况下已经出现了威尔逊-米基蒂综合征(WMS)。在 20 世纪 70 年代和 80 年代,许多接受辅助通气治疗的婴儿在出现粗浸润、严重过度充气和微囊变化的放射学特征后需要长时间的机械通气,同时伴有高碳酸血症和需要增加吸入氧浓度。一些婴儿死亡,并显示出肺纤维化、阻塞性细支气管炎和发育不良改变的证据。补充氧、正压通气和肺不成熟在 CLD/BPD 的病因中一直被认为很重要。最近,炎症(特别是产前暴露于细胞因子)和个体易感性(遗传易感性)在病因学中的作用变得更加重要。本文还讨论了 BPD 皮质类固醇治疗引入的历史背景。在 20 世纪 90 年代初外源性表面活性剂获准用于治疗 RDS 以及 20 世纪 90 年代中期更广泛地使用产前皮质类固醇后,严重 BPD 成为一种罕见事件。逐渐地,CLD 的诊断,仍常称为 BPD,基于出生后 36 周的氧需求。然而,尚不清楚这种“新型 BPD”与 WMS 有很大不同。根据出生后 36 周的氧“需求”来预测这些婴儿的长期肺功能是困难的,因为补充氧经常被不必要地使用。

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