Since its initial description, the acute respiratory distress syndrome (ARDS) has been the target of many therapeutic interventions, but with only modest success.1 Improved understanding of the complex pathogenesis responsible for ARDS has led to several promising pharmacologic therapies aimed at reducing the morbidity and mortality associated with ARDS in critically ill patients. However, the majority of clinical trials of pharmacologic interventions have shown no beneficial effects, leaving ARDS mortality and morbidity unacceptably high. One possible explanation for the inefficacy of ARDS therapies is timing of delivery. Conventional ARDS clinical trials have been designed to enroll patients within 48 hours of ARDS onset, sometimes well into the critical illness phase. In rodent models, several potential therapies are effective at preventing lung injury if administered prior to insult but are less effective at rescuing the animals once the injury is substantial.2,3 These findings suggest that some therapies may be better at interrupting the initial cascade of events leading to ARDS (eg, leukocyte recruitment, platelet activation, and microvascular coagulation) than reversing lung injury once the alveolar-capillary barrier has broken down.
Reilly JP, Christie JD. Is It Possible to Prevent ARDS? JAMA. 2016;315(22):2403–2405. doi:10.1001/jama.2016.5988
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