Background: Uncontrolled bleeding accounts for the majority of preventable deaths in the severely injured in both the civilian and military settings. Trauma induced coagulopathy (TIC) is now widely accepted as a major contributing factor to worsening bleeding in these patients. A quarter of severe trauma patients present with coagulopathy on admission and remain a group with high morbidity and mortality. Objectives: To describe the spectrum of coagulation profiles amongst severely injured patients presenting to an urban level-one trauma centre at Groote Schuur Hospital and to correlate these with blood product requirements, morbidity and mortality. Method: This is a retrospective study of all patients with complete baseline TEG coagulation parameters collected prior to randomization in the FIRST (Fluids In Resuscitation of Severe Trauma) trial between January 2007 and December 2009. Parameters recorded for this study included patient demographics, mechanism of injury, admission vital signs, lactate, base excess, coagulation studies PT, INR, TEG parameters, volume and type of fluids administered, volume of blood products administered, length of ICU stay, and major outcomes. Injury severity was categorized according to the Injury Severity Score (ISS) and New Injury Severity Score (NISS). Results: A total of 87 patients were included in this study, with a median ISS of 20 and 57.5% had a penetrating injury mechanism. Coagulopathy was highly prevalent in this cohort, of which a majority (69%) was diagnosed with hypercoagulopathy and 24% had a hypocoagulopathy status on admission. There was no difference in age, gender and amount 9 of pre-hospital fluids administered across the three groups (normal v/s hyper v/s hypo). Median volume of blood products was higher in the hypocoagulopathy group, although not statistically significant. Overall, 30-day mortality rate was 13%, with case fatalities occurring in only coagulopathic patients; hypercoagulopathy (15%) and hypocoagulopathy (10%). Conclusion: Trauma induced coagulopathy is not an infrequent diagnosis and remains a challenging clinical entity to manage in severely injured patients resulting in increased morbidity and mortality. Determining the coagulation profile using TEG at presentation in this group of patients may guide appropriate management guidelines in order to improve outcome. Hypercoagulable patients need to be recognised amongst the TIC patients as it results in different sequelae and impacts on clinical decision in the use of antifibrinolytic agents as compared to hypocoagulopathy.

Haemorrhage is a leading cause of trauma morbidity and mortality, with many deaths potentially preventable. Hyperfibrinolysis is a central characteristic of trauma-induced coagulopathy (TIC) which develops rapidly and is associated with poor outcomes. Tranexamic acid (TXA) improves survival in trauma haemorrhage but its uptake worldwide remains variable, in part because its effects on the coagulation system during trauma haemorrhage have not been described. Further uncertainty regarding patient selection for TXA therapy has emerged following the description of an early viscoelastic haemostatic assay (VHA) diagnosed hypofibrinolytic phenotype in whom TXA may potentiate thrombotic complications. The patient characteristics and mechanisms leading to this apparent hypofibrinolytic phenotype are poorly understood. Over 900 trauma patients prospectively recruited to a multicentre observational cohort study had blood drawn within 2-hours of injury for VHA and fibrinolysis plasma protein analysis. Patients were categorised according to VHA maximum lysis (ML) and D-dimer (DD) levels. Patients with MLLOW exhibited heterogeneity in clinical and injury characteristics and outcomes. Those who died were severely injured, with a high incidence of traumatic brain injury and a 7-fold higher D-dimer. Patients with MLLOW+DDHIGH had a hyperfibrinolytic biomarker profile, with the fibrinolytic mediator S100A10 identified as a potential driver of fibrinolysis, which can ex-vivo artificially reduce ML. Empiric TXA could benefit this occult hyperfibrinolytic phenotype. Over two subsequent observational studies, the effects of TXA on the coagulation system during trauma haemorrhage and the effect of TXA infusion and timing of treatment on thrombotic events were investigated. Early empiric TXA avoided VHA-hyperfibrinolysis and provided a degree of protection from TIC. Whilst univariate analysis suggested increased thromboses with later TXA treatment in patients receiving TXA bolus+infusion, neither the TXA infusion nor time to bolus were associated with thrombotic events after multivariate analysis. A single TXA bolus may provide a lower effective therapeutic dose with reduced complications.

Trauma continues to be a major cause of death across the globe. While the exact causes of trauma differ greatly between the military and civilian lifestyles, the ability to stop bleeding after trauma is paramount for survival. Over the past decade coagulation research has transitioned from a classical understanding of plasma based protein coagulation to the current cell focused research. As part of this shift, platelets have become a central player in hemostasis. Unfortunately little is currently understood about how platelet function is affected by trauma. In an effort to better define platelet function during trauma and the resulting shock from exsanguination, a multipronged approach was developed. The hypothesis that the introduction of a state of clinical shock in a controlled environment would allow for an in-depth assessment of trauma-induced coagulopathy led to the development of a swine based model of hemorrhagic shock. In this model a composite injury consisting of soft tissue damage, long bone fracture, and controlled hemorrhage was used to induce a moderate state of hypovolemic shock. As a result of this injury the animals showed both the beginning of a plasma protein consumption coagulopathy as well as kinetic quickening in the clotting process. These surprising results show competing up-regulation and down-regulation of the coagulation system in response to trauma induced shock. To better define the effect of polytrauma on platelet function in a human population a clinical study was conducted. The hypothesis behind the development of this study was that the examination of platelet function during polytrauma would lead to a more complete understanding of the effects of trauma on hemostasis. This study resulted in the identification of two separate but not mutually exclusive coagulopathies in response to trauma. The first was the traditional consumption based coagulopathies recently suggested to be varying degrees of disseminated intravascular coagulopathy. The second was a development a hypercoagulable state that may be attributed to increased platelet function. The identification of these two competing coagulopathies in separate models highlights the inadequacies of the current plasma based clinical testing, and the need for increased whole blood testing in the trauma treatment environment.

Trauma-induced coagulopathy (TIC) is a recently described condition which traditionally has been diagnosed by the common coagulation tests (CCTs) such as prothrombin time/international normalized ratio (PT/INR), activated partial thromboplastin time (aPTT), platelet count, and fibrinogen levels. The varying sensitivity and specificity of these CCTs have led trauma coagulation researchers and clinicians to use Viscoelastic Tests (VET) such as Thromboelastography (TEG) to provide Targeted Thromboelastographic Hemostatic and Adjunctive Therapy (TTHAT) in a goal directed fashion to those trauma patients in need of hemostatic resuscitation. This review describes the utility of VETs, in particular, TEG, to provide TTHAT in trauma and acquired non-trauma-induced coagulopathy.

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