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Background: The majority of potentially preventable deaths in trauma are due to uncontrolled hemorrhage and occur early after injury. How major bleeding is defined is integral to early identification and treatment of this group of high-risk patients. However, there is no consensus on a definition of major bleeding in trauma. The aim of this Delphi study was to develop a consensus definition for research, with transfusion used as a surrogate marker of bleeding.Study Design and Methods: Trauma experts from three international groups were invited to take part in an online Delphi survey. Over the course of four rounds, the group developed a number of definitions of major bleeding and reached consensus on a new definition.Results: Forty-four trauma experts agreed to become members of the Delphi panel, and 30 of 44 (68%) completed all four rounds. The panel agreed to exclude the historical massive transfusion definition (≥10 units of red blood cells within 24 hours). Consensus was reached on a new definition for use in clinical research: 4 or more units of any blood component within 2 hours of injury.Conclusion: This Delphi process has yielded a pragmatic transfusion-based definition of major bleeding. The consensus definition differs from historical definitions: a shorter time frame to reflect the acuity of bleeding, and multiple blood components in keeping with a balanced approach to resuscitation. The definition developed may be best suited to mature trauma systems (reflecting the demographics of the expert panel), and could be used to guide registry data recording and to characterize patients at risk of major bleeding. [ABSTRACT FROM AUTHOR]

Summary: Trauma is a leading cause of death worldwide in persons under 44 years of age, and uncontrolled haemorrhage is the most common preventable cause of death in this patient group. The transfusion management of trauma haemorrhage is unrecognisable from 20 years ago. Changes in clinical practice have been driven primarily by an increased understanding of the pathophysiology of trauma‐induced coagulopathy (TIC), which is associated with poor clinical outcomes, including a 3‐ to 4‐fold increased risk of death. Targeting this coagulopathy alongside changes to surgical and anaesthetic practices (an overarching strategy known as damage control surgery/damage control resuscitation) has led to a significant reduction in mortality rates over the last two decades. This narrative review will discuss the transfusion practices that are currently used for trauma haemorrhage and the evidence that supports these practices. [ABSTRACT FROM AUTHOR]

The article focuses on use of viscoelastic haemostatic assays in the management of major bleeding and blood loss is one of the main causes of morbidity following liver transplantation. It mentions British Society for Haematology (BSH) guidelines recommend the use of serial standard laboratory tests (SLTs) to predict major bleeding. It also mentions viscoelastic haemostatic assays (VHA) are increasingly being used during the management of major bleeding.

Trauma-induced coagulopathy describes a complex set of coagulation changes affecting severely injured patients. The thrombomodulin-protein C axis is believed to be central to the evolution of trauma-induced coagulopathy. Soluble thrombomodulin (sTM) levels are elevated after injury. Our objectives were to explore whether sTM (at concentrations found in patients after injury) plays an important role in trauma-induced coagulopathy, and specifically to evaluate the effects of sTM and activated protein C (APC) on thrombin generation (TG) and clot lysis time (CLT). Plasma from healthy volunteers was spiked with rising concentrations of sTM and APC and the effects on TG and CLT were analyzed. Plasma samples from a cohort of trauma patients were evaluated using TG and CLT, and results correlated to clinical parameters and factor VIII, factor V, APC, sTM and fibrinolytic measures. Increasing sTM concentrations in volunteer plasma led to reductions in endogenous thrombin potential and prolongation of 50% CLT, in a dose-dependent manner. No effect on TG or CLT was seen with rising APC concentrations. In 91 trauma patients, higher sTM values were associated with greater, rather than reduced, endogenous thrombin potential (median 1,483 vs. 1,681 nM/min) and longer 50% CLT (41.9 vs. 54.0 mins). In conclusion, sTM concentrations, across ranges found after trauma, affect both TG and 50% CLT, unlike APC. Despite increased circulating sTM levels, the overriding dynamic coagulation effects seen after injury are: (i) accelerated TG and (ii) increased rates of fibrinolysis. We found no evidence for sTM as the major determinant of the coagulation changes seen in early trauma-induced coagulopathy.

Competing Interests: Conflict of Interest None declared.