Ventilatory management and bronchopulmonary dysplasia in preterm infants
Introduction
Classic bronchopulmonary dysplasia (BPD) described by Northway et al. in 1967 was seen in relatively mature babies, who were ventilated at high pressures, with high fractional concentration of inspired oxygen, resulting in lung overinflation, cystic emphysema, and fibrosis.1 By contrast, BPD is now seen primarily in very preterm newborns weighing <1000 g, who are born at 24–26 weeks of gestation. The histopathologic lesions of the ‘old’ BPD have now been replaced by a ‘new’ BPD with the large, simplified alveolar structures, variable interstitial cellularity and/or fibroproliferation.2 The clinical picture is also different. Today's premature babies developing BPD may initially have modest ventilatory and oxygen needs and demonstrate a different radiographic picture, which shows diffuse haziness and a fine, lacy pattern (Fig. 1). These differences can be better understood with the realisation that the lungs of infants born at 24–26 weeks of gestation are in the early phases of lung development (canalicular and saccular stages), and that alveolar and capillary development are inhibited following exposure to the noxious effects of mechanical ventilation, oxygen exposure, and inflammation. These differences become important in planning ventilatory strategies to prevent or treat BPD in preterm infants.
Section snippets
Can ventilatory strategies prevent BPD?
BPD is multifactorial and an understanding of the pulmonary injury sequence may enable the development of strategies to circumvent this cascade. There are two prominent pathways leading to BPD (Fig. 2). The first is intrinsic and is related to a developmental ‘arrest’ of the lung resulting in diminished alveolarisation. This results in inadequate surface area for gas exchange and impaired lung function, requiring the initiation of chronic ventilation and subsequent ventilator-induced lung
Ventilatory strategies for infants with established BPD
The management of infants with established BPD has not been studied adequately, and the role of various ventilatory strategies for infants with the disorder is not clear. A suggested guideline for dealing with different lung issues is shown in Table 1. A number of other strategies can also be employed to reduce the duration of mechanical ventilation with a hope that earlier extubation might ameliorate the pulmonary injury sequence and thus reduce the severity of BPD. The scientific evidence in
Conclusion
BPD is a recognised sequel of preterm birth. With improving survival of infants at lower gestational ages, the prevalence is on the rise. Pathological features of BPD include alveolar maldevelopment, with or without areas of pulmonary fibrosis. Assisted ventilation, infection/inflammation, oxygen administration, and fluid overload are major identified risk factors in the evolution of BPD. The prevention of BPD needs a multifocal approach by decreasing VILI through utilisation of newer
Conflict of interest statement
None declared.
Funding sources
None.
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2021, Early Human DevelopmentCitation Excerpt :Extensive research has been done regarding the prevention of bronchopulmonary dysplasia (BPD); including the use of antenatal steroids, preferencing non-invasive respiratory support and if intubated, using minimally invasive ventilation strategies. Despite ongoing best-efforts, BPD remains one of the most frequent complications of prematurity, with more babies born extremely preterm and extreme low birth weight (ELBW) in the earlier phases of lung development (canalicular and sacular stages) [1]. Following exposure to mechanical ventilation, oxygen and subsequent inflammation, the alveolar and capillary development are inhibited leading to large simplified alveolar structures, variable interstitial cellularity and/or fibroproliferation [2].
Prenatal administration of the cytochrome P4501A inducer, Β-naphthoflavone (BNF), attenuates hyperoxic lung injury in newborn mice: Implications for bronchopulmonary dysplasia (BPD) in premature infants
2011, Toxicology and Applied PharmacologyCitation Excerpt :In fact, the prolonged exposure of newborn mice to hyperoxia creates pulmonary lesions that are very similar to human BPD (Warner et al., 1998; Ohki et al., 2009). Mechanical ventilation, which is almost always used in conjunction with supplemental oxygen in premature infants suffering from pulmonary insufficiency, also contributes to BPD in these patients (Gagliardi et al., 2011; Gupta et al., 2009). In utero viral infection may also contribute to BPD pathogenesis (Sawyer et al., 1987; Couroucli et al., 2000).
Myth: Mechanical ventilation is a therapeutic relic
2011, Seminars in Fetal and Neonatal MedicineCurrent methods of non-invasive ventilatory support for neonates
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