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KEY POINTS
The pathogenesis of trauma-induced coagulopathy is multifactorial and includes impaired thrombin generation, defective fibrinogen, platelet dysfunction, and dysregulated fibrinolysis.
Metabolic acidosis has a more significant effect on trauma-induced coagulopathy than hypothermia at clinically relevant levels.
Fibrinolysis is the active degradation of polymerized fibrin through the co-localization of tissue plasminogen activator or urine-type plasminogen activator with the lysine avid binding plasminogen and subsequent conversion to plasmin.
Systemic hyperfibrinolysis occurs in 10% to 15% of those requiring a massive transfusion.
Impaired fibrinolysis (shutdown) is present in the majority of severely injured patients and may result in microvascular occlusion and organ dysfunction.
Tranexamic acid should be used selectively and only in patients with active bleeding and severe shock (systolic blood pressure <75 mm Hg or base deficit >6) and optimally with documented hyperfibrinolysis.
Prehospital plasma improves survival in patients with transport times that are anticipated to exceed 20 minutes.
Goal-directed hemostatic strategies employing viscoelastic assays improve survival.
Cryoprecipitate contains fibrinogen, factor VIII, von Willebrand factor, fibronectin, factor XIII, and platelet microparticles.
Weight-based low molecular weight heparin and antifactor Xa–guided dosing are advantageous in the prevention of venous thromboembolism.
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Despite advances in emergency medical systems (EMS) and trauma care, deaths from injury have increased in the United States over the past decade.1 In both the civilian2 and military3 settings, uncontrolled hemorrhage is the leading cause of preventable death after injury. In civilian studies, more than 95% of deaths from hemorrhage occur within the first 24 hours at a median time of less than 3 hours.2 Consequently, there is intense interest worldwide in the pathogenesis of trauma-induced coagulopathy (TIC) and its early management. Although there have been substantial insights, the words of Mario Stefanini in his address to the New York Academy of Medicine in 19544 remain applicable today:
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The ponderous literature on the subject of hemostasis could perhaps be considered a classical example of the infinite ability of the human mind for abstract speculation. For several years, the number of working theories of the hemostatic mechanism greatly exceeded and not always respected the confirmed experimental facts. In recent years, however, the revived interest in this field has led to an accumulation of new findings which has been almost too rapid for their orderly incorporation into a logical working pattern. As a result, we have rapidly gone from a state of orderly ignorance to one of confused enlightenment.
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Although transfusion medicine has undergone enormous development over the past 60 years since the challenge issued by Stefanini, important gaps in scientific knowledge persist, and several fundamental issues involving the diagnosis and management of TIC remain unclear. The more we learn about TIC, the more we appreciate the contributions of surgical scientists from the past century who had the insight to form the basis of our current understanding of trauma-related bleeding. This chapter will review important ...