Acute lung injury or its more severe form—acute respiratory distress syndrome (ARDS)—are common and important intensive care syndromes affecting many patients. Acute lung injury is characterised by damage to the alveolar-capillary membrane resulting in alveolar flooding, pulmonary inflammation and alveolar coagulopathy, and changes in surfactant properties with severe impairment of oxygenation and respiratory failure mandating mechanical ventilation. It is rarely present at the time of hospital admission but develops over a period of hours to days in subsets of patients with predisposing conditions such as trauma, shock or sepsis, and accompanying interventions including mechanical ventilation and transfusion.1 Acute lung injury may therefore be viewed as a potentially preventable complication. Indeed, implementation of acute lung injury prevention strategies such as lung-protective mechanical ventilation using normal-sized tidal volumes and restrictive blood transfusion leads to a significant decrease in acute lung injury and mortality of mechanically ventilated patients.2 Pharmacotherapies targeting progression to acute lung injury may also benefit patients at risk of this complication. One such preventive strategy might be attenuation of pulmonary coagulopathy.

COAGULOPATHY IN ACUTE LUNG INJURY

Recent studies have shown that prominent changes in alveolar fibrin turnover are intrinsic to acute lung injury.3 The profile and extent of these changes vary with the severity of the injury.4 The mechanisms that contribute to pulmonary coagulopathy in acute lung injury are supposed to be similar to those found in the intravascular spaces in severe systemic inflammation (eg, sepsis or septic shock).5^–7 Indeed, in acute lung injury, alveolar thrombin generation seems to be mediated, at least in part, by the tissue factor (TF)–factor VIIa (FVIIa) pathway, as the alveolar epithelium has been found to initiate TF-dependent intra-alveolar coagulation in response to inflammation.8 Patients with ARDS …