Acquired antithrombin deficiency following severe traumatic injury: rationale for study of antithrombin supplementation.

Hemorrhage, head injury, and multiple organ dysfunction are the most frequent causes of mortality in patients who experience severe injury. Acceleration of the coagulation cascade is known to result in hemorrhage secondary to disseminated intravascular coagulation (DIC) and end-organ dysfunction, as manifest by pulmonary and renal failure. Few studies have been conducted to evaluate the effects of injury on the endogenous anticoagulants that inhibit excessive coagulation activation. We evaluated a group of patients following severe injury and found that procoagulant markers (prothrombin fragment 1.2, thrombin antithrombin complexes, and D dimers) were significantly elevated for the population as a whole. Levels of circulating endogenous anticoagulants [antithrombin (AT) and protein C] were relatively unchanged for the total population. However, patients with adverse outcomes [DIC and adult respiratory distress syndrome (ARDS)] had significant reductions in AT and protein C activities. Decreased levels of AT and protein C 8 hours after admission served as independent predictors of both DIC and ARDS. Prospective, randomized studies should be conducted to evaluate the effect of supplementation of these factors after severe injury has occurred.