- new terms that are in vogue are trauma-induced coagulopathy (TIC) and acute traumatic coagulopathy (ATC)
- not simply a ‘dilutional coagulopathy’ or ‘consumptive coagulopathy’!
- TIC was conventionally construed simply as depletion, dysfunction or dilution of procoagulant factors
- actually an imbalance of the dynamic equilibrium between procoagulant factors, anticoagulant factors, platelets, endothelium and fibrinolysis
- characterized by isolated factor V inhibition, dysfibrinogenemia, systemic anticoagulation, impaired platelet function and hyperfibrinolysis
- exacerbated by hypothermia, acidosis (together with coagulopathy they form ‘the lethal triad’) and resuscitation with hypocoagulable fluids
- early detection (ROTEM /TEG holds promise for this)
- early activation of massive transfusion protocols
- aggressive proactive blood product administration (PRBCs, FFP, platelets, cryoprecipitate)
- prevent and treat hypothermia and acidosis
- early use of tranexamic acid
- give calcium if hypocalcaemic
- consider Factor VII if non-surgical bleeding and all the other parameters have been corrected
References and Links
- Frith D, Brohi K. The pathophysiology of trauma-induced coagulopathy. Curr Opin Crit Care. 2012 Dec;18(6):631-6. PMID: 23010636.
- Frith D, Davenport R, Brohi K. Acute traumatic coagulopathy. Curr Opin Anaesthesiol. 2012 Apr;25(2):229-34. PMID: 22270921.