The acute respiratory distress syndrome.

The acute respiratory distress syndrome (ARDS) is defined by noncardiogenic pulmonary edema and respiratory failure in the seriously ill patient. The diagnosis is clinical, established by the development of new bilateral pulmonary infiltrates and severe hypoxemia without congestive heart failure (1). The risk for ARDS also depends on both host and etiologic factors. The most common causes are sepsis, pneumonia, aspiration, trauma, pancreatitis, several blood transfusions, smoke or toxic gas inhalation, and certain types of drug toxicity (2, 3). Several etiologic factors often are present, and this increases the probability of developing the syndrome. The acute respiratory distress syndrome is a major cause of morbidity, death, and cost in intensive care units. Our review describes the clinical, etiologic, and physiologic basis of ARDS and summarizes our understanding of how its molecular pathogenesis leads to the physiologic alterations of respiratory failure, emphasizing factors known to be involved in the formation and resolution of permeability pulmonary edema. It also provides a physiologic basis for understanding and implementing modern strategies for the respiratory management of patients with ARDS. In 1967, Ashbaugh and colleagues (4) defined ARDS as an acute lung injury syndrome associated with trauma, sepsis, or aspiration. The syndrome’s similarities to shock lung and neonatal respiratory distress led to its original name, the adult respiratory distress syndrome, now the acute respiratory distress syndrome. Over the years, ARDS became associated with clinical risk factors that may cause lung injury either by direct involvement or by secondary processes that activate systemic inflammation and coincidentally damage the lung.