Coagulopathy in Trauma

Many of our patients arrive to us with a coagulopathy -

 

Clotting Factor Deficiency in Early Trauma-Associated Coagulopathy

Rizoli, Sandro B. MD, PhD, FRCSC, FACS; Scarpelini, Sandro MD, PhD; Callum, Jeannie MD, FRCPC; Nascimento, Bartolomeu MD; Mann, Kenneth G. PhD; Pinto, Ruxandra PhD; Jansen, Jan MBBS, PhD, FRCS; Tien, Homer C. MD, MSc, FRCSC, FACS

 

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.

Journal of Trauma-Injury Infection & Critical Care:

November 2011 - Volume 71 - Issue 5 - pp S427-S434