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Clinical Trial
. 2011 Nov;71(5 Suppl 1):S427-34.
doi: 10.1097/TA.0b013e318232e5ab.

Clotting factor deficiency in early trauma-associated coagulopathy

Sandro B Rizoli  1 , Sandro Scarpelini, Jeannie Callum, Bartolomeu Nascimento, Kenneth G Mann, Ruxandra Pinto, Jan Jansen, Homer C Tien
Affiliations
Clinical Trial

Clotting factor deficiency in early trauma-associated coagulopathy

Sandro B Rizoli et al. J Trauma. 2011 Nov.

Abstract

Background: Coagulopathic bleeding is a leading cause of in-hospital death after injury. A recently proposed transfusion strategy calls for early and aggressive frozen plasma transfusion to bleeding trauma patients, thus addressing trauma-associated coagulopathy (TAC) by transfusing clotting factors (CFs). This strategy may dramatically improve survival of bleeding trauma patients. However, other studies suggest that early TAC occurs by protein C activation and is independent of CF deficiency. This study investigated whether CF deficiency is associated with early TAC.

Methods: This is a prospective observational cohort study of severely traumatized patients (Injury Severity Score ≥ 16) admitted shortly after injury, receiving minimal fluids and no prehospital blood. Blood was assayed for CF levels, thromboelastography, and routine coagulation tests. Critical CF deficiency was defined as ≤ 30% activity of any CF.

Results: Of 110 patients, 22 (20%) had critical CF deficiency: critically low factor V level was evident in all these patients. International normalized ratio, activated prothrombin time, and, thromboelastography were abnormal in 32%, 36%, and 35%, respectively, of patients with any critically low CF. Patients with critical CF deficiency suffered more severe injuries, were more acidotic, received more blood transfusions, and showed a trend toward higher mortality (32% vs. 18%, p = 0.23). Computational modeling showed coagulopathic patients had pronounced delays and quantitative deficits in generating thrombin.

Conclusions: Twenty percent of all severely injured patients had critical CF deficiency on admission, particularly of factor V. The observed factor V deficit aligns with current understanding of the mechanisms underlying early TAC. Critical deficiency of factor V impairs thrombin generation and profoundly affects hemostasis.

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Figures

Figure 1
Figure 1
Patient enrolment ISS = injury severity score; L = litre; IV = intravenous; min = minutes
Figure 2
Figure 2
Computational model with concentration of thrombin as a function of time in a reaction initiated by tissue factor . A = coagulopathic patients. B = non coagulopathic patients with all clotting factor levels >30%
See this image and copyright information in PMC

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