Abstract
The acute respiratory distress syndrome (ARDS) and acute lung injury (ALI) are part of a devastating syndrome characterized by acute onset, hypoxemia and bilateral infiltrates on chest radiography. ALI/ARDS is the response of the lung to a local or systemic insult, resulting in local inflammation and coagulation disorders, which lead to increased inflammatory pulmonary edema. ARDS is a major cause of morbidity, death, and expense in intensive care units. ALI and ARDS are associated with increased procoagulant and reduced fibrinolytic activities, mainly in alveoli and in interstitial spaces in the lung. Fibrin deposition, which is the hallmark of early-phase ALI, stimulates fibroblast aggregation and collagen secretion, participating in the constitution of pulmonary fibrosis. Despite the significant progress in the understanding of the disease made over the past 10 years, the only clinical intervention found to have a significant impact on mortality in ARDS is the use of low tidal volume ventilation. In severe sepsis, only recombinant human activated protein C administration has demonstrated a mortality reduction, together with a faster improvement in respiratory dysfunction and a shorter duration of mechanical ventilation. Future clinical trials in ALI/ARDS should evaluate the potential benefits of anticoagulants administered systemically or locally in the lungs.