Ventilatory management and bronchopulmonary dysplasia in preterm infants

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Summary

Improvements in antenatal and neonatal care have resulted in increased survival of very preterm infants. However, the incidence of bronchopulmonary dysplasia (BPD) has not changed, probably as a consequence of a demographic shift. The underlying pathophysiology of BPD appears to differ for the current population of preterm infants compared to that described by Northway et al., and management strategies should be targeted to limit ventilator-induced lung injury. Non-invasive respiratory support techniques are currently under evaluation, but results of the trials have thus far failed to show a reduction in BPD. This review will focus upon various ventilation modalities for preventing and managing bronchopulmonary dysplasia.

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 The histopathologic lesions of the ‘old’ BPD have now been replaced by a ‘new’ BPD with the large, simplified alveolar structures, variable interstitial cellularity and/or fibroproliferation.2 The clinical picture is also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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