Johansson PI, Sorensen AM, Perner A, Welling KL, Wanscher M, Larsen CF, Ostrowski SR.; Crit Care. 2011 Nov 17;15(6):R272. [Epub ahead of print]
INTRODUCTION: It is debated whether the early trauma induced coagulopathy (TIC) in severely injured patients reflects disseminated intravascular coagulation (DIC) with a fibrinolytic phenotype, acute coagulopathy of trauma shock (ACoTS) or yet other entities. This study investigated the prevalence of overt DIC and ACoTS in trauma patients and characterized these conditions based on their biomarker profiles.
METHODS: Observational study at a single Level I Trauma Centre. Inclusion of 80 adult trauma patients ([greater than or equal to]18 years) who met criteria for full trauma team activation and had an arterial cannula inserted. Blood was sampled a median of 68 min (IQR 48-88) post-injury. Data on demography, biochemistry, injury severity score (ISS) and mortality were recorded. Plasma/serum was analyzed for biomarkers reflecting tissue/endothelial cell/glycocalyx damage (histone-complexed DNA fragments, Annexin V, thrombomodulin, syndecan-1), coagulation activation/inhibition (prothrombinfragment 1+2, thrombin/antithrombin-complexes, antithrombin, protein C, activated protein C, endothelial protein C receptor, protein S, tissue factor pathway inhibitor, vWF), factor consumption (fibrinogen, FXIII), fibrinolysis (D-dimer, tissue-type plasminogen activator, plasminogen activator inhibitor-1) and inflammation (interleukin (IL)-6, terminal complement complex (sC5b-9)). Comparison of patients stratified according to presence or absence of overt DIC (ISTH criteria) or ACoTS (activated partial thromboplastin time (APTT) and/or international normalized ratio (INR) above normal reference).
RESULTS: No patients had overt DIC whereas 15% had ACoTS. ACoTS patients had higher injury severity score (ISS), transfusion requirements and mortality (all P<0.01) and a biomarker profile suggestive of enhanced tissue, endothelial cell and glycocalyx damage and consumption coagulopathy with low protein C, antithrombin, fibrinogen and FXIII levels, hyperfibrinolysis and inflammation (all P<0.05). Importantly, in non-ACoTS patients, apart from APTT/INR, higher ISS correlated with biomarkers of enhanced tissue, endothelial cell and glycocalyx damage, protein C activation, coagulation factor consumption, hyperfibrinolysis and inflammation, i.e., resembling that observed in patients with ACoTS.
CONCLUSIONS: ACoTS and non-ACoTS may represent a continuum of coagulopathy reflecting a progressive early evolutionary adapted hemostatic response to the trauma hit and both are parts of TIC whereas DIC does not appear to be part of this early response.
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