Articles: respiratory-distress-syndrome.
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We aimed to discuss term infants who are given surfactant due to respiratory disorder according to the underlying etiology, the dose of surfactant administration, and the need for repeated surfactant administration. ⋯ Despite the difference on administration time and repeat dose interval due to etiology, surfactant treatment is improving the respiratory distress of term infants.
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Randomized Controlled Trial
Adaptive Support Ventilation and Lung-Protective Ventilation in ARDS.
Adaptive support ventilation (ASV) is a partially closed-loop ventilation mode that adjusts tidal volume (VT) and breathing frequency (f) to minimize mechanical work and driving pressure. ASV is routinely used but has not been widely studied in ARDS. ⋯ ASV targeted similar settings as standard of care consistent with lung-protective ventilation strategies in mostly passive subjects with ARDS. ASV delivered VT based upon respiratory mechanics, with lower VT and mechanical power in subjects with stiffer lungs.
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Extracorporeal carbon dioxide removal (ECCO2R) uses mechanical systems to treat hypercapnic respiratory failure. Its utility has been investigated in acute respiratory distress syndrome (ARDS), acute exacerbations of chronic obstructive pulmonary disease (COPD), and status asthmaticus, and as a bridge to lung transplant. In this review, we discuss how it works, why it should help, and current evidence supporting its use.
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Identify the metabolites that are increased in the plasma of severely injured patients that developed ARDS versus severely injured patients that did not, and assay if these increased metabolites prime pulmonary sequestration of neutrophils (PMNs) and induce pulmonary sequestration in an animal model of ARDS. We hypothesize that metabolic derangement due to advanced shock in critically injured patients leads to the PMNs, which serves as the first event in the ARDS. Summary of Background Data: Intracellular metabolites accumulate in the plasma of severely injured patients. ⋯ After controlling for confounders, 4 metabolites significantly increased: creatine, dehydroascorbate, fumarate, and succinate in trauma patients who developed ARDS ( P < 0.05). Succinate alone primed the PMN oxidase in vitro at physiologically relevant levels. Intravenous succinate-induced PMN sequestration in the lung, a first event, and followed by intravenous lipopolysaccharide, a second event, resulted in ARDS in vivo requiring PMNs. SUCNR1 inhibition abrogated PMN priming, PMN sequestration, and ARDS. Conclusion: Significant increases in plasma succinate post-injury may serve as the first event in ARDS. Targeted inhibition of the SUCNR1 may decrease ARDS development from other disease states to prevent ARDS globally.