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Pathobiology of Pediatric Acute Respiratory Distress Syndrome

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Pediatric Acute Respiratory Distress Syndrome

Abstract

Acute respiratory distress syndrome (ARDS) is a restrictive lung disease with severe hypoxemia and often hypercarbia. ARDS is caused by direct (alveolar epithelial) and indirect (endothelial) injuries and is conceptually divided into three phases: acute, fibroproliferative, and repair. Diffuse disruption of the alveolar epithelial-endothelial barrier (diffuse alveolar damage) resulting in noncardiogenic pulmonary edema is the main pathologic finding. The primary pathobiological mechanisms are reduction in alveolar fluid clearance, decreased production and inactivation of surfactant, inflammation, apoptosis, and coagulopathy. With multiple causes and pathobiologic mechanisms, resolving the initial injury and restoring normal lung architecture and function are complex processes that have been difficult to model experimentally. Furthermore, regulation of normal postnatal lung development overlaps with many of the pathways of the acute and repair phases of ARDS, making extrapolation of knowledge gained from adult clinical and laboratory models to children challenging.

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Smith, L.S. (2020). Pathobiology of Pediatric Acute Respiratory Distress Syndrome. In: Shein, S., Rotta, A. (eds) Pediatric Acute Respiratory Distress Syndrome. Springer, Cham. https://doi.org/10.1007/978-3-030-21840-9_3

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