Elsevier

Surgery

Volume 149, Issue 2, February 2011, Pages 221-230
Surgery

Original Communication
Disseminated intravascular coagulation at an early phase of trauma is associated with consumption coagulopathy and excessive fibrinolysis both by plasmin and neutrophil elastase

https://doi.org/10.1016/j.surg.2010.06.010Get rights and content

Background

The aims of the present study were to confirm the consumption coagulopathy of disseminated intravascular coagulation with the fibrinolytic phenotype at an early phase of trauma and to test the hypothesis that thrombin-activatable fibrinolysis inhibitor, neutrophil elastase, and plasmin contribute to the increased fibrinolysis of this type of disseminated intravascular coagulation. Furthermore, we hypothesized that disseminated intravascular coagulation at an early phase of trauma progresses dependently to disseminated intravascular coagulation with a thorombotic phenotype from 3 to 5 days after injury.

Methods

Fifty-seven trauma patients, including 30 patients with disseminated intravascular coagulation and 27 patients without disseminated intravascular coagulation, were studied prospectively. Levels of thrombin-activatable fibrinolysis inhibitor, tissue-type plasminogen activator plasminogen activator inhibitor-1 complex, plasmin alpha2 plasmin inhibitor complex, D-dimer, neutrophil elastase, and fibrin degradation product by neutrophil elastase were measured on days 1, 3, and 5 after trauma. The prothrombin time, fibrinogen, fibrin/fibrinogen degradation product, antithrombin, and lactate also were measured.

Results

Independent of the lactate levels, disseminated intravascular coagulation patients showed a prolonged prothrombin time, lesser fibrinogen and antithrombin levels, and increased levels of fibrin/fibrinogen degradation product on day 1. Disseminated intravascular coagulation diagnosed on day 1 continued to late-phase disseminated intravascular coagulation on days 3 and 5 after trauma. Increased levels of tissue-type plasminogen activator plasminogen activator inhibitor-1 complex, plasmin alpha2 plasmin inhibitor complex, D-dimer, neutrophil elastase, and fibrin degradation product by neutrophil elastase but not thrombin-activatable fibrinolysis inhibitor were observed in the disseminated intravascular coagulation patients. No correlation was observed between plasmin alpha2 plasmin inhibitor complex and fibrin degradation product by neutrophil elastase in disseminated intravascular coagulation patients. Multiple regression analysis showed the disseminated intravascular coagulation score and the tissue-type plasminogen activator plasminogen activator inhibitor-1 complex levels on day 1 to correlate with the total volume of transfused blood. Patient prognosis deteriorated in accordance with the increasing disseminated intravascular coagulation severity.

Conclusion

Disseminated intravascular coagulation at an early phase of trauma is associated with consumption coagulopathy and excessive fibrinolysis both by plasmin and neutrophil elastase independent of hypoperfusion and continues to disseminated intravascular coagulation at a late phase of trauma. Increased fibrinolysis requires more blood transfusions, contributing to a poor patient outcome.

Section snippets

Patient selection

With the approval of the Institutional Review Board and after written informed consent was obtained from either the patients or their next of kin, 57 severe trauma patients defined as having an Injury Severity Score (ISS) ≥9 (at 1 abbreviated injury scale ≥3) were enrolled in the present study. Trauma patients under 12 yeas of age or older than 90 years of age, those with cardiac arrest or who had been resuscitated from cardiac arrest, and individuals receiving anticoagulant therapy and having

Baseline patient characteristics

Table III indicates that although the ISS and APACHE II scores are identical between the 2 groups, DIC patients demonstrate a severe degree of SIRS and organ dysfunction (SOFA) and were transfused with more blood products. Increased lactate levels in DIC patients suggest tissue hypoperfusion in this group. The prevalence of sepsis during the study period was 7% (4/57) and was distributed identically between the groups.

Serial changes in the DIC scores, platelet counts, coagulation, and fibrinolysis variables

Significant differences were observed in the JAAM and ISTH overt DIC scores

Discussion

The members of the Educational Initiative on Critical Bleeding in Trauma (EICBT) announced the new disease entities of acute coagulopathy of trauma shock and coagulopathy of trauma.22 They did not, however, propose clear definitions or diagnostic criteria, and a rebuttal has been made to these concepts.23 The acute coagulopathy of trauma has not been defined by the EICBT, but the EICBT has reconfirmed the presence of trauma-related DIC.1, 24, 25 Although traumatic coagulopathy is

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    Supported by Grants-in-Aid for Scientific Research from the Ministry of Education, Science, Sports, and Culture in Japan (Grants 2007-19390456 and 2009-21249086).

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