Non-Invasive Ventilatory Strategies to Decrease Bronchopulmonary Dysplasia—Where Are We in 2021?

Abstract

Recent advances in neonatology have led to the increased survival of extremely low-birth weight infants. However, the incidence of bronchopulmonary dysplasia (BPD) has not improved proportionally, partly due to increased survival of extremely premature infants born at the late-canalicular stage of lung development. Due to minimal surfactant production at this stage, these infants are at risk for severe respiratory distress syndrome, needing prolonged ventilation. While the etiology of BPD is multifactorial with antenatal, postnatal, and genetic factors playing a role, ventilator-induced lung injury is a major, potentially modifiable, risk factor implicated in its causation. Infants with BPD are at a higher risk of developing complications including sepsis, pulmonary arterial hypertension, respiratory failure, and death. Long-term problems include increased risk of hospital readmissions, respiratory infections, and asthma-like symptoms during infancy and childhood. Survivors who have BPD are also at increased risk of poor neurodevelopmental outcomes. While the ultimate solution for avoiding BPD lies in the prevention of preterm births, strategies to decrease its incidence are the need of the hour. It is time to focus on gentler modes of ventilation and the use of less invasive surfactant administration techniques to mitigate lung injury, thereby potentially decreasing the burden of BPD. In this article, we discuss the use of non-invasive ventilation in premature infants, with an emphasis on studies showing an effect on BPD with different modes of non-invasive ventilation. Practical considerations in the use of nasal intermittent positive pressure ventilation are also discussed, considering the significant heterogeneity in clinical practices and management strategies in its use.

Simvastatin Inhibits NLRP3 Inflammasome Activation and Ameliorates Lung Injury in Hyperoxia-Induced Bronchopulmonary Dysplasia via the KLF2-Mediated Mechanism

“…Bronchopulmonary dysplasia (BPD) is a common complication of premature birth [ 38 ]. Exposure to high-oxygen concentrations has been demonstrated to cause simplified lung development, leading to BPD [ 39 ].…”

Establishment and efficiency analysis of the risk prediction model predicting the likelihood of bronchopulmonary dysplasia in preterm infants: A retrospective observational study

“…Also, previous research [23] indicated that infants on endotracheal tube for 4-7 days are likely to have BPD or death compared with NIPPV (p < 0.02) and NCPAP (p < 0.01) groups. Researchers also suggested that prematurity should wean from NIPPV to NCPAP after the acute phase to minimize lung injury and promote lung growth [24].…”

Research Progress in Bronchopulmonary Dysplasia: A Narrative Review by Etiology

“…In many infants, the lung injury that leads to BPD begins with abnormal lung development before birth (for example, when the lungs are tiny for their gestational period, chorioamnionitis, and tobacco exposure) [22]. When combined with other risk factors such as surfactant inadequacy, ventilation-associated lung injury, nutritional deficiency, oxygen radical's toxicity, perinatal and postnatal infections, and inflammatory conditions, the vicious circle of lung injury hinders pulmonary vasculature development, eventually leading to BPD [23]. This section examines the key etiology and how they lead to BPD development.…”