Goal-directed hemostatic resuscitation for trauma induced coagulopathy: Maintaining homeostasis

Defining trauma‐induced coagulopathy with respect to future implications for patient management: Communication from the SSC of the ISTH

“…Trauma‐induced coagulopathy is driven by two distinct and synergistic insults: hypovolemic shock due to blood loss and extensive tissue disruption (Figure ) . The variables that modify the TIC phenotype and course include (a) trauma: injury extent and severity, tissue type injured (head, orthopaedic), degree of hemorrhagic shock, mechanism of injury (blunt, penetrating/hemorrhagic), and time from injury; (b) patient factors: age, sex, medical comorbidities (cardiovascular disease), concomitant anticoagulant use, presence of other toxins including alcohol, heritable differences in baseline coagulation; and (c) resuscitation strategies: types of fluids used, the impact of blood components, adjuncts such as TXA, and timing of surgical intervention .…”

“…Proposed mechanisms include the generation of activated protein C with subsequent deactivation of factors Va and VIIIa, and the release of heparan sulfate from the endothelial glycocalyx. Adapted from Moore et al…”

“…Impaired clot formation is driven by both hypoxia and tissue injury (Figure ) . Proposed mechanisms include the activation of protein C with subsequent deactivation of factor (F) V and FVIII, and the release of heparan sulfate and syndecan‐1 from the endothelial glycocalyx .…”

“…Systemic hyperfibrinolysis is stimulated by hypoxia with endothelial release of t‐PA, and thrombin generated by activation of coagulation that also stimulates t‐PA release. Fibrinolysis can be inhibited via the byproducts of tissue injury and activation of platelets releasing antifibrinolytic agents such as PAI‐1 …”

“…On the other hand, fibrinolysis is inhibited via the by‐products of tissue injury and activation of platelets releasing antifibrinolytic agents. Adapted from Moore et al…”