Division of Pediatric Pulmonology, Miller School of Medicine, University of Miami, Miami, FL 33136, USA.
Pediatrics. 2010 Jul;126(1):115-28. doi: 10.1542/peds.2009-1381. Epub 2010 Jun 7.
Normal lung development follows a series of orchestrated events. Premature birth interrupts normal in utero lung development, which results in significant alterations in lung function and physiology. Increasingly, there are reports documenting the broad range of complications experienced by infants aged 34 to 36 weeks' gestational age (GA). Our objective was to summarize the evidence demonstrating respiratory system vulnerability in infants aged 34 to 36 weeks' GA and to review the developmental and physiologic principles that underlie this vulnerability. A comprehensive search for studies that reported epidemiologic data and respiratory morbidity was conducted on the PubMed, Medline, Ovid Biosis, and Embase databases from 2000 to 2009 by using medical subject headings "morbidity in late preterm infants," "preterm infants and lung development," "prematurity and morbidity," and "prematurity and lung development." Because the number of studies exclusive to infants aged 34 to 36 weeks' GA was limited, selected studies also included infants aged 32 to 36 weeks' GA. Of the 24 studies identified, 16 were retrospective population-based cohort studies; 8 studies were observational. These studies consistently revealed that infants born at 32 to 36 weeks' GA, including infants of 34 to 36 weeks' GA, experience substantial respiratory morbidity compared with term infants. Levels of morbidity were, at times, comparable to those observed in very preterm infants. The developmental and physiologic mechanisms that underlie the increased morbidity rate and alterations in respiratory function are discussed. We also present evidence to demonstrate that the immaturity of the respiratory system of infants 34 to 36 weeks' GA at birth results in increased morbidity in infancy and leads to deficits in lung function that may persist into adulthood.
正常的肺部发育遵循一系列协调的事件。早产打断了子宫内正常的肺部发育,导致肺功能和生理学发生显著改变。越来越多的报告记录了 34 至 36 周胎龄(GA)的婴儿经历的广泛并发症。我们的目的是总结证明 34 至 36 周 GA 婴儿呼吸系统脆弱性的证据,并回顾构成这种脆弱性的发育和生理原理。通过使用医学主题词“晚期早产儿发病率”、“早产儿和肺发育”、“早产和发病率”以及“早产和肺发育”,在 2000 年至 2009 年期间,在 PubMed、Medline、Ovid Biosis 和 Embase 数据库中对报告流行病学数据和呼吸道发病率的研究进行了全面搜索。由于专门针对 34 至 36 周 GA 婴儿的研究数量有限,因此还选择了一些包括 32 至 36 周 GA 婴儿的研究。在确定的 24 项研究中,有 16 项是回顾性基于人群的队列研究;8 项是观察性研究。这些研究一致表明,与足月婴儿相比,32 至 36 周 GA 出生的婴儿,包括 34 至 36 周 GA 的婴儿,经历了大量的呼吸道发病率。有时,发病率水平与观察到的极早产儿相似。讨论了导致发病率增加和呼吸功能改变的发育和生理机制。我们还提供了证据表明,出生时 34 至 36 周 GA 婴儿呼吸系统的不成熟导致婴儿期发病率增加,并导致肺功能缺陷,这些缺陷可能持续到成年期。