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High-frequency oscillatory ventilation (HFOV) is an established mode of respiratory support in the neonatal intensive care unit. Large clinical trial data is based on first intention use in preterm infants with acute respiratory distress syndrome. Clinical practice has evolved from this narrow population. HFOV is most often reserved for term and preterm infants with severe, and often complex, respiratory failure not responding to conventional modalities of respiratory support.
To examine follow-up outcomes at corrected postnatal age (cPNA) 2 years of preterm infants previously enrolled in an RCT and treated with IN-REC-SUR-E or IN-SUR-E in 35 tertiary neonatal intensive care units.
Instability of peripheral oxyhemoglobin saturation (SpO2) in preterm infants is correlated with late disability and is poorly understood. We hypothesised that a reduced ventilation to perfusion ratio (VA/Q) is the key predisposing factor for SpO2 instability.
Data on static compliance of the chest wall (Ccw) in preterm infants are scarce. We characterized the static compliance of the lung and Ccw to determine their relative contribution to static compliance of the respiratory system in very preterm infants at 36 wk postmenstrual age. We also aimed to investigate how these compliances were influenced by the presence of bronchopulmonary dysplasia and impacted breathing variables.
Preterm infants are often vitamin A deficient, and vitamin A has functions that could mitigate the processes that lead to bronchopulmonary dysplasia. Therefore, supplementation of preterm infants with vitamin A to reduce the risk of bronchopulmonary dysplasia makes inherent sense.
Lung inflammation and impaired alveolarization precede bronchopulmonary dysplasia (BPD). Glucocorticoids are anti-inflammatory and reduce ventilator requirements in preterm infants. However, high-dose glucocorticoids inhibit alveolarization. The effect of glucocorticoids on lung function and structure in preterm newborns exposed to antenatal inflammation is unknown. We hypothesise that postnatal low-dose dexamethasone reduces ventilator requirements, prevents inflammation and BPD-like lung pathology, following antenatal inflammation.
Perinatal inflammation increases the risk for bronchopulmonary dysplasia in preterm neonates, but the underlying pathophysiological mechanisms remain largely unknown. Given their anti-inflammatory and regenerative capacity, multipotent adult progenitor cells (MAPC) are a promising cell-based therapy to prevent and/or treat the negative pulmonary consequences of perinatal inflammation in the preterm neonate.
Inflammation and oxidative stress play a key role in the development of bronchopulmonary dysplasia (BPD), possibly contributing to persistent respiratory morbidity after preterm birth. We aimed to assess if inflammatory markers were elevated in exhaled breath condensate (EBC) of infants born very prematurely (< 32 weeks gestation) at 12-16 corrected months of age, and if increased levels were associated with BPD diagnosis and respiratory morbidity.
Surfactant is a well-established therapy for preterm neonates affected by respiratory distress syndrome (RDS). The goals of different methods of surfactant administration are to reduce the duration of mechanical ventilation and the severity of bronchopulmonary dysplasia (BPD); however, the optimal administration method remains unknown.
Preterm infants have immature control of breathing and impaired pulmonary gas exchange. We hypothesized that infants with bronchopulmonary dysplasia (BPD) have a blunted ventilatory response and peripheral oxygen saturation (SpO2 ) instability during a hypoxic challenge.