Trauma-induced coagulopathy (TIC) is a multifactorial, global failure of the coagulation system to sustain adequate haemostasis after trauma haemorrhage. Damage control resuscitation is associated with improved outcomes although the mechanisms of how it corrects TIC have yet to be fully characterized. Identification of predominant pathophysiological pathways in TIC is required to develop effective treatment algorithms for trauma haemorrhage.
TIC is described by varying degrees of dysfibrinogenaemia, hyperfibrinolysis, endothelial dysfunction and impaired platelet activity, dependent on the magnitude of trauma, and severity of haemorrhagic shock. Acute traumatic coagulopathy is the early endogenous process mediated by the protein C pathway in response to tissue injury and hypoperfusion. Thrombin generation appears maintained with altered fibrinogen utilization and activation of fibrinolytic pathways representing key components of TIC. Shedding of the endothelial glycocalyx appears capable of triggering systemic thrombin generation, protein C activation and hyperfibrinolysis and may itself represent a therapeutic target.
Further advances in TIC treatment require an enhanced understanding of the dynamic changes in the equilibrium between pro and anticoagulant factors, downstream effectors, and the host response. Delineating the interaction between fibrinolysis, fibrinogen utilization, platelet activity, and thrombin generation may provide opportunity for targeted intervention.
Centre for Trauma Sciences, Blizard Institute, Queen Mary University of London, London UK
Correspondence to Ross A. Davenport, FRCS, PhD, Centre for Trauma Sciences, Blizard Institute, Queen Mary University of London, 4 Newark Street, London E1 2AT, UK. Tel: +44 020 737 40723; e-mail: firstname.lastname@example.org