Defining the clinical syndrome of TIC has been hampered by the wide variations in patient presentation. Severely injured patients manifest diverse phenotypes of TIC spanning hypo‐ and hypercoagulability and may rapidly progress between phenotypes. The presentation is chiefly thought to be a result of the variability of the magnitude and timing of the interaction between tissue injury and shock as well as resuscitation practices. Variations in experimental measurements such as timing of patient presentation, prior therapy, and timing to blood sampling complicate the definition of TIC.3-5
As a result of the difficulty in defining clinical TIC, the underlying biochemical mechanisms of TIC are unclear. Factors contributing to a hypocoaguable state include impaired thrombin generation, impaired platelet function, deficient or defective fibrinogen, increased fibrinolysis, and endothelial dysfunction, while those contributing to hypercoagulability include excessive thrombin generation, endothelial injury, platelet hyperactivity and exhaustion, hyperfibrinogenemia, and impaired fibrinolysis.6-16
In recent years, multiple definitions of the hemostatic disturbances in trauma have been published.17-20 The unstandardized nomenclature and definitions (ATC, acute traumatic coagulopathy; TIC, trauma‐induced coagulopathy; ACoTS, acute coagulopathy of trauma‐shock; CoT, coagulopathy of trauma; DIC, disseminated intravascular coagulation; endotheliopathy of trauma and hemorrhagic blood failure;21 SHINE, shock‐induced endotheliopathy5, 6) used to describe these derangements in trauma has led to a considerable degree of confusion within the field.22-25
This communication, from the International Society on Thrombosis and Haemostasis (ISTH) Scientific and Standardization Committee (SSC) on fibrinolysis, DIC, and perioperative and critical care thrombosis and hemostasis, builds on a previous consideration26 and (a) provides an overview of the current leading theories of the mechanism of TIC, (b) compares and contrasts the major overlapping lessons from coagulopathies related to other critical illnesses such as sepsis‐induced coagulopathy (SIC), (c) addresses the critical knowledge gaps in our understanding of the pathophysiology of TIC, and (d) defines a new categorization scheme for patient groups to better stratify the likely coagulopathic phenotypes and pathophysiology based on the patient’s arrival characteristics. Together, addressing these knowledge gaps may provide a roadmap for the development of clinical and point‐of‐care diagnostic strategies for rapidly and pre‐emptively identifying the patient with TIC in order to optimize transfusion and resuscitation.
- DISSEMINATED INTRAVASCULAR COAGULATION
- ENDOTHELIAL GLYCOCALYX DEGRADATION
- INCREASED MORTALITY
- TRANEXAMIC ACID