Acute respiratory distress syndrome (ARDS) is an illness of great interest and importance in pediatric critical care. Children who suffer from ARDS are often among the sickest and most challenging patients in the PICU. In addition, an even greater proportion of the patients in pediatric critical care present with respiratory illnesses that have substantial mechanistic overlap with ARDS, even without cleanly fitting the clinical case definition of that condition. Understanding the cellular and molecular mechanisms that underlie ARDS, then, is important for understanding current and future approaches to treatment of many serious respiratory illnesses in the PICU.

The central derangement in ARDS is the disruption of the alveolar-capillary barrier, which allows proteinrich plasma components to cross into the airspaces. Once alveoli are flooded, surfactant is inactivated and a cycle of inflammation and local hypoxia leads to injury progression, augmented by mechanical forces from the use of artificial mechanical ventilation and oxidant stress from high inspired O₂ concentrations. These changes comprise the early, acute phase of ARDS, characterized by pulmonary edema, hypoxemic respiratory failure, poor lung compliance, and, often, some degree of pulmonary hypertension (Fig. 44.1). As the illness progresses, the disease enters a fibroproliferative phase, in which lung compliance improves but lung function remains poor as a result of progressive scarring and thickening of the lung interstitium. Ultimately, many patients recover lung function completely or nearly so, but substantial numbers of survivors have long-lasting pulmonary function deficits. These themes of injury, inflammation, fibroproliferation, and repair appear in almost every respiratory disease seen in the PICU

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