Background: Trauma patients present with a coagulopathy, termed early trauma-induced coagulopathy (ETIC), that is associated with increased mortality. This study investigated hemostatic changes responsible for ETIC.
Methods: Case-control study of trauma patients with and without ETIC, defined as prolonged prothrombin time (PT), was performed from prospective cohort of consecutive trauma patients who presented to Level I trauma center. Univariate and multivariate analyses were performed.
Results: The case-control study group (n = 91) was 80% male, with mean age of 37 years, 17% penetrating trauma and 7% mortality rate. Patients with ETIC demonstrated decreased common and extrinsic pathway factor activities (factors V and VII) and decreased inhibition of the coagulation cascade (antithrombin and protein C activities) when compared with the matched control patients without ETIC. Both cohorts had evidence of increased thrombin and fibrin generation (prothrombin fragment 1.2 levels, thrombin-antithrombin complexes, and soluble fibrin monomer), increased fibrinolysis (d-dimer levels), and increased inhibition of fibrinolysis (plasminogen activator inhibitor-1 activity) above normal reference values. Patients with versus without ETIC had increased mortality and received increased amount of blood products.
Conclusion: ETIC following injury is associated with decreased factor activities without significant differences in thrombin and fibrin generation, suggesting that despite these perturbations in the coagulation cascade, patients displayed a balanced hemostatic response to injury. The lower factor activities are likely secondary to increased hemodilution and coagulation factor depletion. Thus, decreasing the amount of crystalloid infused in the early phases following trauma and administration of coagulation factors may prevent the development.
From the New York Blood Center (B.H.S., C.D.H.), New York, New York; Department of Pathology and Laboratory Medicine (B.H.S., A.M.W., A.B.J.), Emory University School of Medicine, Atlanta, Georgia; and Department of Surgery (J.B.M.), Faculty of Health Sciences College, Aga Khan University Hospital, Nairobi, Kenya.
Submitted for publication November 15, 2010.
Accepted for publication January 25, 2011.
Supported, in part, by PHS Grant (UL1 RR025008) from the Clinical and Translational Science Award Program, National Institutes of Health, National Center for Research Resource, and Emory Medical Care Foundation.
Address for reprints: Beth H. Shaz, MD, New York Blood Center, New York, NY 10065; email: email@example.com.