Figure 2.

Association between assessment time-point, trauma hit and type of coagulopathy in trauma patients. Association between assessment time-point (blood sampling), trauma hit (tissue injury, shock) and trauma-induced coagulopathy (TIC), acute coagulopathy of trauma shock (ACoTS), non-ACoTS, disseminated intravascular coagulation (DIC) and non-DIC. We infer that TIC represents an early (minutes) progressive endogenous response to the trauma hit (tissue injury, shock) ranging from and covering both non-ACoTS and ACoTS (defined as moderately increased plasma based coagulation tests), with a biomarker profile indicative of endothelial and glycocalyx damage, factor consumption, hyperfibrinolysis and inflammation. The immediate hemostatic response to trauma is probably evolutionarily adapted to improve the chance of survival by, for example, inducing local hemostasis while preserving perfusion and oxygen delivery [16] with ACoTS representing an exaggerated non-adapted response in patients that without immediate life support would have succumbed. Progression to overt DIC does not appear to be part of the early response to trauma but may occur later (hours or days) post-injury, probably driven by a combination of the tissue injury exerted by the initial trauma hit, systemic endothelial dysfunction/damage, exhaustion of the natural anticoagulant pathways and/or excessive inflammation. Whether early TIC progresses to DIC may be determined by a combination of exogenous factors (the early trauma hit and later hits) [30] and endogenous factors (genetically determined response to the hits).

Johansson et al. Critical Care 2011 15:R272   doi:10.1186/cc10553
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