Acute traumatic coagulopathy

Recent therapeutic and observational studies have demonstrated improved survival with better management of haemostasis early after injury. This review delineates our current understanding of the clinical importance, aetiology and pathophysiology of acute traumatic coagulopathy (ATC).

Trauma causes an acute disruption of the equilibrium between all components of haemostasis (coagulation, anticoagulation, fibrinolysis, platelets and endothelium). In patients with a combination of severe tissue damage and systemic hypoperfusion, this will progress rapidly to an endogenous coagulopathy that is independently associated with worse outcomes. New discoveries of the interactions between neurohormonal, vascular, and coagulation systems are beginning to explain how this haemostatic impairment develops and offer novel targets for therapeutic manipulation. Routine coagulation screening tests are ineffective for diagnosing ATC and guiding resuscitation in real-time. Viscoelastic coagulation tests (such as ROTEM or TEG) have emerged as practical, rapid and sensitive diagnostic modalities. Their role in therapeutic targeting requires further validation.

Conventional concepts of traumatic coagulopathy as a late occurring condition in response to iatrogenic haemodilution are redundant. ATC is an endogenous impairment of haemostasis that begins at the moment of injury. Further outcome improvements are possible with better understanding of the process by which this coagulopathy develops and how it may be inhibited.