This article provides a description of the clinical disorders associated with the development of acute noncardiogenic pulmonary edema, better known as clinical acute lung injury (ALI) or the acute respiratory distress syndrome (ARDS). Much has been learned about the mechanisms by which the lung is injured in patients with sepsis, pneumonia, aspiration of gastric contents, and following major trauma. In the last 5 years, major progress has been made in the treatment of patients with ALI/ARDS. A lung protective ventilatory strategy with a low tidal volume (6 mL/kg/predicted body weight) in conjunction with a plateau pressure limit of 30 cm H(2)0 attenuated the severity of clinical lung injury and reduced mortality by 22%. Ironically, after years of searching for anti-inflammatory treatments for ALI/ARDS, it turns out that a lung protective ventilatory strategy has proven to be the most efficacious anti-inflammatory treatment ever discovered for ALI/ARDS. However, it is still possible that pharmacologic treatments also may enhance survival. For example, a recent report that activated protein C reduces mortality in patients with sepsis raises hope that the incidence and severity of sepsis-induced ALI/ARDS may be reduced by treatment with this agent that has both anti-inflammatory and anticoagulant properties. Also, therapy directed at hastening the resolution of lung injury by increasing the functional recovery of the alveolar epithelium may be of value, both in diminishing the fibroproliferative phase of ALI/ARDS as well as accelerating the resolution of alveolar edema.