Pathogenesis of acute traumatic coagulopathy

Authors

  • Ross Davenport

    Corresponding author
    • Trauma Sciences, Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary, University of London, London, UK
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Address reprint requests to: Ross Davenport, PhD, MRCS, Trauma Sciences, Barts Health NHS Trust, Trauma Research Office - Ward 12D, The Royal London Hospital, Whitechapel, London E1 1BB, UK; e-mail: ross.davenport@qmul.ac.uk.

Abstract

Acute traumatic coagulopathy (ATC) is an early endogenous process, driven by the combination of tissue injury and shock that is associated with increased mortality and worse outcomes in the polytrauma patient. This review summarizes our current understanding of the pathophysiology of ATC and the role of rapid diagnostics in the management of severe trauma hemorrhage. In particular we consider diagnostic and therapeutic strategies for bleeding trauma patients with short versus long prehospital times and the concept of remote damage control resuscitation. Endothelial activation of Protein C is a central mechanism of ATC, which produces rapid anticoagulation and fibrinolysis following severe trauma. Continued blood loss, hypothermia, acidosis, and hemodilution potentiate ATC and lead to a global derangement in all components of hemostasis. The contribution and interplay between platelet activity, fibrinogen utilization, endothelial dysfunction, and neurohormonal pathways remain to be defined in ATC pathogenesis but may offer novel therapeutic targets. Conventional laboratory-based tests of coagulation have a limited role in the early management of major trauma hemorrhage. TEG and ROTEM provide a rapid evaluation of clot dynamics in whole blood and are of greater value than coagulation screens in diagnosing and managing trauma hemorrhage.

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