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The online version of this article, along with updated information and services, is
located on the World Wide Web at:
http://www.pediatrics.org/cgi/content/full/123/6/1562
aDivision of Pediatric Pulmonology, Connecticut Children’s Medical Center, Hartford, Connecticut; bDivision of Perinatal Medicine, Yale University School of Medicine,
New Haven, Connecticut
The authors have indicated they have no financial relationships relevant to this article to disclose.
ABSTRACT
Bronchopulmonary dysplasia is a chronic lung disease associated with premature
birth and characterized by early lung injury. In this review we discuss some pitfalls,
problems, and progress in this condition over the last decade, focusing mainly on www.pediatrics.org/cgi/doi/10.1542/
peds.2008-1962
the last 5 years, limited to studies in human neonates. Changes in the definition,
pathogenesis, genetic susceptibility, and recent biomarkers associated with broncho- doi:10.1542/peds.2008-1962
pulmonary dysplasia will be discussed. Progress in current management strategies, Key Words
chronic lung disease, prematurity,
along with novel approaches/therapies, will be critically appraised. Finally, recent pulmonary sequelae, noninvasive
data on long-term pulmonary and neurodevelopmental outcomes of infants with ventilation
bronchopulmonary dysplasia will be summarized. Pediatrics 2009;123:1562–1573 Abbreviations
BPD— bronchopulmonary dysplasia
GA— gestational age
PATHOGENESIS
Although an immature lung on which a variety of “environmental” factors (infection, hyperoxia, barotrauma/
volutrauma) act to cause injury has been the cornerstone of the pathogenesis of BPD, an improved understanding
of this process has occurred over the last 5 years. Antenatal/postnatal factors contribute to the release of “proin-
flammatory and antiinflammatory” cytokines. An imbalance in these mediators leads to activation of the cellular
death pathways in the lung, which is followed by healing (resolution of injury to a normal lung architecture) or
repair.17,18 The latter is characterized by impaired alveolarization and dysregulated angiogenesis, which lead to fewer,
larger simplified alveoli and a dysmorphic pulmonary vasculature (Fig 1): the pathologic hallmarks of BPD.1
Proinflammatory Antiinflammatory
(eg, IL-1) (eg, IL-10)
Immature lung
FIGURE 1
Pathogenesis of new BPD. Cell death
Bronchopulmonary dysplasia
to prevent the development of BPD,98 although achiev- BPD was reported in 2 trials and was found to be signif-
ing intended targets may be difficult.99,100 Identification icantly reduced.101
of the optimal target oxygen-saturation ranges is an area
of intense research.
Other drugs studied include the following: Macrolide Antibiotics
Erythromycin has not been shown to decrease BPD in
Inositol infants when treated prophylactically or after known
In a meta-analysis of RCTs using inositol supplemen- Ureaplasma colonization.102 In a pilot study, azithromycin
tation in premature infants, the outcome of death or did not reduce the incidence of BPD.103