• J T Owings, M Bagley, R Gosselin, D Romac, and E Disbrow.
• University of California, Davis, Medical Center, Sacramento 95817-2282, USA.
• J Trauma. 1996 Sep 1;41(3):396-405; discussion 405-6.

ObjectiveDetermine whether severe injury results in decreased plasma antithrombin (AT) activity and whether this decreased AT activity is associated with thromboembolic complications.DesignProspective observational.SubjectsA total of 157 critically injured trauma patients.MethodsEach patient underwent laboratory analysis on arrival to the emergency room at hours 8, 16, 24, and 48, and days 3, 4, 5, and 6. Laboratory analyses included AT, tissue factor pathway inhibitor, protein C, prothrombin fragment 1.2, thrombin-antithrombin complex, and D-dimer. Patients were followed for thromboembolic complications including: deep venous thrombosis (DVT), pulmonary embolus, disseminated intravascular coagulation (DIC) and adult respiratory distress syndrome (ARDS).ResultsMean Injury Severity Score was 23 (+/-11). AT activity fell below normal in 95 (61%) patients; AT activity rose to greater than normal in 51 (32%) patients. Nine (6%) patients developed DVT, two (1%) pulmonary embolus, 13 (8%) DIC and 26 (17%) ARDS. Using logistic regression analysis, low AT levels were a significant predictor of DVT, DIC, and ARDS (p < 0.05). Supranormal At levels were associated with closed head injury (p < 0.05). D-dimer levels were inversely correlated with AT (p < 0.05).ConclusionsAT activity was depressed in critically injured patients. Patients with head injury developed supranormal AT activity. The risk factors for AT deficiency mimicked those for thromboembolism. Patients with decreased AT activity were at increased risk for thromboembolic complications. Given heparin's dependence on AT, these data call into question the use of unmonitored heparin thromboembolism prophylaxis.

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