www.aana.com/aanajournalonline.aspx AANA Journal ß February 2010 ß Vol. 78, No. 1 35 Nearly one-fourth of all trauma admissions present in varying degrees of coagulopathy. According to a US study, 40% of trauma fatalities are due to hemorrhage and hemorrhagic shock, and nearly all patients who are alive when they reach the hospital are coagulopathic when they die. Once coagulopathy develops, patient morbidity drastically increases. Because of the clinical significance of trauma-induced coagulopathy, manage- ment strategies to reduce the morbidity and mortality have recently become of interest. This article will review the pathology of trauma-induced coagulopathy and current trends in management, as well as closely exam- ine the data surrounding the use of recombinant factor VII for the treatment of trauma-induced coagulopathy. Keywords: Coagulopathy, trauma. Management of Trauma-Induced Coagulopathy: Trends and Practices Matthew R. D’Angelo, CRNA, DNP Richard P. Dutton, MD, MBA T raumatic injury is a common and growing phe- nomenon. Globally, 1 in 7 deaths is attributed to traumatic injury, exceeding the combined mortality of stroke, cardiovascular disease, and HIV. 1,2 Nearly 25% of all trauma admissions present in varying degrees of coagulopathy. 3 According to a US study, 40% of trauma fatalities are due to hemorrhage and hemorrhagic shock, and most patients who reach the hospital alive are coagulopathic when they die. 4 In other- wise healthy patients, an elevated prothrombin time (PT) at admission indicates rapid hemorrhage, massive injury, and a steadily worsening perfusion state. 5 As such, man- agement strategies to reduce the morbidity and mortality of trauma-induced coagulopathy have recently become of particular interest. This article will review the pathology of trauma- induced coagulopathy and current trends in manage- ment, as well as closely examine the data surrounding the use of recombinant factor VII for the treatment of trauma-induced coagulopathy. Clot Formation Coagulation is a complicated physiologic process involving multiple proteins and other blood components in a series of reactions intended to produce the fibrin and platelet network. Clot formation begins with a vascular insult. Vascular injury causes blood vessels to vasoconstrict and release collagen, von Willebrand factor, and tissue factor from the damaged vascular endothelium. Vascular spasm assists platelets’ migration from the vascular lumen toward the vessel wall and injury. Platelet aggregation at the site of an injury produces a plug, with the intent to reduce blood loss. Unfortunately, the tensile strength of platelets alone is inadequate to maintain hemostasis. 6 In addition to attracting platelets to the site of injury, tissue factor accelerates the activation of factor VII, which, in turn, activates factor IX. 6 The cascade continues with the activation of factors VIII and X that ultimately begins the conversion of prothrombin (II) to activated thrombin (IIa). resulting in a “thrombin burst” on the surface of the platelet converting fibrinogen to fibrin (Ia). 5 Fibrin poly- merizes, forming a strong matrix over the platelet plug. The clot is stabilized when fibrin is cross-linked to factor XIIIa. Under normal conditions, activation of fibrinolytic pathways maintains appropriate clot size and location, minimizing thrombosis and embolic events. These nega- tive feedback mechanisms can become deranged as a result of traumatic injury, further exacerbating coagulopa- thy. Figure 1 illustrates the normal coagulation process. Trauma-Induced Coagulopathy Clot formation is an intricate process that requires multi- ple events and variables to produce a stable clot. Under normal conditions, clot formation reduces blood loss and assists with the return of hemostasis. Massive injury can disrupt the clotting cascade at several points in the process, resulting in life-threatening consequences. Four mechanisms have been identified as primary causes of trauma-induced coagulopathy. 3 These mecha- nisms are: (1) hypothermia/acidosis, (2) dilution of factors, (3) severe traumatic brain injury (TBI), and (4) hemor- rhagic shock. • Hypothermia and Acidosis. Less than 9% of trauma admissions are hypothermic on presentation. 7,8 Although core temperatures below 34°C can significantly increase morbidity and mortality, hypothermia is actually an un- common event. 1,9,10 Despite this, hypothermia remains an issue. Hospital-acquired hypothermia can be detri- mental to coagulation. 10 Removal of clothing, muscle re- laxation, cold intravenous fluid administration (resusci- tation), and frequent examination (removal of blankets) contribute to rapid heat loss. Nearly 65% of patient hy-