• Marc Maegele, Herbert Schöchl, and Mitchell J Cohen.
• *Department of Traumatology, Orthopedic Surgery and Sportsmedicine, Cologne-Merheim Medical Center, and †Institute for Research in Operative Medicine, University of Witten/Herdecke, Cologne, Germany; ‡Ludwig Boltzmann Institute for Experimental and Clinical Traumatology, Vienna; and §Department of Anaesthesiology and Intensive Care, AUVA Trauma Hospital, Salzburg, Austria; and ∥Department of Surgery, University of California San Francisco, San Francisco, California.
• Shock. 2014 May 1; 41 Suppl 1: 21-5.

AbstractTrauma remains the leading cause of death with bleeding as the primary cause of preventable mortality during the first 24 h following trauma. When death occurs, it happens quickly, typically within the first 6 h after injury. One of four patients to arrive in the emergency department after trauma is already in the state of acute traumatic coagulopathy and shock. The principal drivers of acute traumatic coagulopathy have been characterized by tissue hypoperfusion, inflammation, and the acute activation of the neurohumoral system. Hypoperfusion leads to an activation of protein C with cleavage of activated factors V and VIII and the inhibition of plasminogen activator inhibitor 1 with subsequent hyperfibrinolysis. Endothelial damage and activation result in Weibel-Palade body degradation and glycocalyx shedding associated with autoheparinization. In contrast, there is an iatrogenic coagulopathy that occurs secondary to uncritical volume therapy leading to acidosis, hypothermia, and hemodilution. This coagulopathy then may be an integral part of the "vicious cycle" when combined with acidosis and hypothermia. The present article summarizes an update on the principal mechanisms and triggers of the coagulopathy of trauma including traumatic brain injury.

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