The pulmonary capillary endothelium is also disrupted causing an influx of proteinacious fluid and white blood cells into the alveolus resulting in diffuse pulmonary inflammation and coagulation. In the case of direct injury to the lung epithelium by pneumonia, for example, there is an increase in epithelial permeability, and normal clearance of fluid from the alveolus is disrupted. Since the first description of ARDS in 1967, investigation into the pathophysiology of ARDS has focused on the interaction between the underlying cause, the lung endothelium, vasculature, and epithelium, and circulating white blood cells and platelets. The lack of targeted pharmacologic therapies may be a result of an incomplete understanding of the underlying pathophysiology of ARDS. Although processes of care interventions such as lung protective ventilation, prone positioning, and neuromuscular blockade may be beneficial, there are no specific pharmacologic interventions to improve outcomes in this patient population. This syndrome of acute lung inflammation and non-cardiogenic pulmonary edema is associated with significant morbidity and mortality during the acute hospitalization along with poor long-term outcomes including reduced functional status and increased mortality even beyond the initial hospitalization.
The acute respiratory distress syndrome (ARDS) frequently complicates critical illness from a variety of underlying causes.