Abstract
IntroductionIt is debated whether 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.MethodsAn observational study was carried out at a single Level I Trauma Center. Eighty adult trauma patients (≥18 years) who met criteria for full trauma team activation and had an arterial cannula inserted were included. Blood was sampled a median of 68 minutes (IQR 48 to 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 the presence or absence of overt DIC (International Society of Thrombosis and Hemostasis (ISTH) criteria) or ACoTS (activated partial thromboplastin time (APTT) and/or international normalized ratio (INR) above normal reference).ResultsNo patients had overt DIC whereas 15% had ACoTS. ACoTS patients had higher 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, that is, resembling that observed in patients with ACoTS.ConclusionsACoTS and non-ACoTS may represent a continuum of coagulopathy reflecting a progressive early evolutionarily 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.
Highlights
It is debated whether 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
We report that no trauma patients with blood sampled approximately one hour post-injury had overt DIC, whereas 15% had ACoTS defined as moderately increased activated partial thromboplastin time (APTT) and/or international normalized ratio (INR)
In non-ACoTS patients, higher injury severity score (ISS) was associated with a biomarker profile indicative of enhanced tissue, endothelial cell and glycocalyx damage as well as an early hemostatic response/coagulopathy characterized by protein C activation, coagulation factor consumption, hyperfibrinolysis and inflammation suggesting that TIC represents a continuum of hemostatic response/coagulopathy dependent on the trauma hit and its downstream effects
Summary
It is debated whether 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. Different drivers of trauma-induced coagulopathy (TIC) have been proposed by different groups of researchers [9]: Some advocate that TIC reflects disseminated intravascular coagulation (DIC) with a fibrinolytic (hemorrhagic) phenotype based on the observation that trauma DIC patients display prolonged prothrombin time (PT), have low fibrinogen and antithrombin (AT) levels early after injury and have high fibrin/fibrinogen degradation products (FDP) and D-dimer levels indicating massive (uncontrolled) thrombin generation and activation (through the tissue-factor dependent coagulation pathway) followed by extensive fibrin(ogen)olysis and consumption coagulopathy [8,10,11] They infer that the higher FDP/D-dimer ratio and low fibrinogen levels result from fibrin(ogen)olysis caused by excessive plasmin and neutrophil elastase production and release, independent of hypoperfusion [11,12]. They emphasize that microvascular thrombosis does not occur in trauma hemorrhage and that there is a relative sparing of platelets and fibrinogen, thereby making ACoTS a distinct clinical entity from the DIC observed in, for example, sepsis and other disease conditions classically associated with DIC [4]
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