Effect of critical injury on plasma antithrombin activity

Low antithrombin levels are associated with thromboembolic complications

John T Owings, Margaret Bagley, Robert Gosselin, Diane Romac, Elizabeth Disbrow

Research output: Contribution to journalArticle

74 Citations (Scopus)

Abstract

Objective: Determine whether severe injury results in decreased plasma antithrombin (AT) activity and whether this decreased AT activity is associated with thromboembolic complications. Design: Prospective observational. Subjects: A total of 157 critically injured trauma patients. Methods: Each 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). Resulted: Mean 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). Conclusions: AT 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.

Original languageEnglish (US)
Pages (from-to)396-406
Number of pages11
JournalJournal of Trauma - Injury, Infection and Critical Care
Volume41
Issue number3
StatePublished - Sep 1996

Fingerprint

Antithrombins
Wounds and Injuries
Disseminated Intravascular Coagulation
Adult Respiratory Distress Syndrome
Venous Thrombosis
Thromboembolism
Embolism
Heparin
Closed Head Injuries
Lung
Injury Severity Score
Protein C
Craniocerebral Trauma
Hospital Emergency Service

Keywords

  • Adult respiratory distress syndrome
  • Antithrombin
  • Deep venous thrombosis
  • Disseminated intravascular coagulation
  • Heparin
  • Thromboembolism prophylaxis
  • Trauma

ASJC Scopus subject areas

  • Surgery

Cite this

Effect of critical injury on plasma antithrombin activity : Low antithrombin levels are associated with thromboembolic complications. / Owings, John T; Bagley, Margaret; Gosselin, Robert; Romac, Diane; Disbrow, Elizabeth.

In: Journal of Trauma - Injury, Infection and Critical Care, Vol. 41, No. 3, 09.1996, p. 396-406.

Research output: Contribution to journalArticle

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abstract = "Objective: Determine whether severe injury results in decreased plasma antithrombin (AT) activity and whether this decreased AT activity is associated with thromboembolic complications. Design: Prospective observational. Subjects: A total of 157 critically injured trauma patients. Methods: Each 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). Resulted: Mean 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). Conclusions: AT 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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N2 - Objective: Determine whether severe injury results in decreased plasma antithrombin (AT) activity and whether this decreased AT activity is associated with thromboembolic complications. Design: Prospective observational. Subjects: A total of 157 critically injured trauma patients. Methods: Each 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). Resulted: Mean 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). Conclusions: AT 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.

AB - Objective: Determine whether severe injury results in decreased plasma antithrombin (AT) activity and whether this decreased AT activity is associated with thromboembolic complications. Design: Prospective observational. Subjects: A total of 157 critically injured trauma patients. Methods: Each 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). Resulted: Mean 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). Conclusions: AT 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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KW - Disseminated intravascular coagulation

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KW - Thromboembolism prophylaxis

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