Pathophysiology of Early Trauma-Induced Coagulopathy: Emerging Evidence for Hemodilution and Coagulation Factor Depletion

Shaz, Beth H.; Winkler, Anne; James, Adelbert B.; Hillyer, Christopher D.; Macleod, Jana

doi:10.1097/ta.0b013e31821266e0

Cited by 102 publications

(90 citation statements)

References 15 publications

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“…An INR-based ATC definition offers advantages over definitions using the PT or PT ratio since (1) INR is directly reported by the laboratory and (2) INR corrects for variability in the prothrombin time ratio over time and between laboratories (52). While we were unable to evaluate definitions employing PTT, platelet count, or fibrinogen level, these parameters alone are insensitive for clinically significant coagulopathy and unlikely to markedly improve an INR-based definition (9, 26, 53-55). Viscoelastic assays' speed, ability to simulate in vivo clotting, and utility for mechanistic studies of acute coagulopathy make them attractive (14), but data linking specific functional abnormalities detected by these tests to trauma outcomes are too limited to base ATC diagnosis on this technology (56-58).…”

Section: Discussionmentioning

confidence: 98%

An International Normalized Ratio–Based Definition of Acute Traumatic Coagulopathy Is Associated With Mortality, Venous Thromboembolism, and Multiple Organ Failure After Injury

Peltan

Vusse

Maier

et al. 2015

Critical Care Medicine

113

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Objective Acute traumatic coagulopathy (ATC) is associated with adverse outcomes including death. Previous studies examining ATC's relationship with mortality are limited by inconsistent criteria for syndrome diagnosis, inadequate control of confounding and single-center designs. In this study, we validated the admission international normalized ratio (INR) as an independent risk factor for death and other adverse outcomes after trauma and compared two common INR-based definitions for ATC. Design Multicenter prospective observational study. Setting Nine level I trauma centers in the United States. Patients 1,031 blunt trauma patients with hemorrhagic shock. Interventions None. Measurements and Main Results INR exhibited a positive adjusted association with all-cause in-hospital mortality, hemorrhagic shock-associated in-hospital mortality, venous thromboembolism, and multiple organ failure. ATC affected 50% of subjects if defined as an INR >1.2 and 21% of subjects if defined by INR >1.5. After adjustment for potential confounders, ATC defined as an INR >1.5 was significantly associated with all-cause death (OR 1.88, p<0.001), hemorrhagic shock-associated death (OR 2.44, p=0.001), venous thromboembolism (1.73, p<0.001), and multiple organ failure (OR 1.38, p=0.02). ATC defined as an INR >1.2 was not associated with an increased risk for the studied outcomes. Conclusions Elevated INR on hospital admission is a risk factor for mortality and morbidity after severe trauma. Our results confirm this association in a prospectively-assembled multicenter cohort of severely injured patients. Defining ATC using an INR >1.5 but not an INR >1.2 identified a clinically-meaningful subset of trauma patients who, adjusting for confounding factors, suffered more adverse outcomes. Targeting future therapies for ATC to patients with an INR >1.5 may yield greater returns than using a lower INR threshold.

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Section: Discussionmentioning

confidence: 98%

An International Normalized Ratio–Based Definition of Acute Traumatic Coagulopathy Is Associated With Mortality, Venous Thromboembolism, and Multiple Organ Failure After Injury

Peltan

Vusse

Maier

et al. 2015

Critical Care Medicine

113

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“…Activated platelets adhere to damaged tissues and serve as catalysts for amplification of thrombin generation. These processes are reflected in the findings of observational clinical studies that show reduced clotting factor and physiological anticoagulant levels [21][22][23], high thrombin generating capacity [3,4,21,[24][25][26] and reduced platelet counts [27,28] Overall, these data indicate a consumptive coagulopathy. The most depleted coagulation factors are fibrinogen and factor V [22,28], which are likely consumed in part by activated Protein C or free plasmin [29,30], although the relative importance of these proteases in reducing factor levels remains unknown.…”

Section: Pathophysiologymentioning

confidence: 98%

The pathogenesis of traumatic coagulopathy

2014

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SummaryOver the last 10 years, the management of major haemorrhage in trauma patients has changed radically. This is mainly due to the recognition that many patients who are bleeding when they come in to the emergency department have an established coagulopathy before the haemodilution effects of fluid resuscitation. This has led to the use of new terminology: acute traumatic coagulopathy, acute coagulopathy of trauma shock or trauma‐induced coagulopathy. The recognition of acute traumatic coagulopathy is important, because we now understand that its presence is a prognostic indicator, as it is associated with poor clinical outcome. This has driven a change in clinical management, so that the previous approach of maintaining an adequate circulating volume and oxygen carrying capacity before, as a secondary event, dealing with coagulopathy, has changed to haemostatic resuscitation as early as possible. While there is as yet no universally accepted assay or definition, many experts use prolongation of the prothrombin time to indicate that there is, indeed, a coagulopathy. Hypoxia, acidosis and hypothermia and hormonal, immunological and cytokine production, alongside consumption and blood loss, and the dilutional effects of resuscitation may occur to varying extents depending on the type of tissue damaged, the type and extent of injury, predisposing to, or amplifying, activation of coagulation, platelets, fibrinolysis. These are discussed in detail within the article.

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“…Obviously, dilution contributes to coagulopathy in trauma and several studies have shown the close relationship in patients with trauma. 1,61 In the early stage, fluid administration is often small or limited in some countries, 12 thus the critical role of hemodilution in the early stage is questioned.…”

Section: Classic Triad Theorymentioning

confidence: 99%

The Pathophysiology and Management of Acute Traumatic Coagulopathy

Duan

2013

Clin Appl Thromb Hemost

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Acute traumatic coagulopathy (ATC) is commonly seen among patients with severe injury and will lead to uncontrolled bleeding diathesis, which is an important contributor to trauma death. During the past 10 years, the understanding of the mechanism causing ATC has changed rapidly. The mechanisms for ATC are complicated. To date, the possible mechanisms include activation of protein C, shedding of endothelial glycocalyx, catecholamine release, platelet dysfunction, primary, and secondary fibrinolysis, with tissue injury and hypoperfusion as the triggers. Classic factors such as dilution, acidosis, and hypothermia can further aggravate the coagulopathy. Inflammation may have a potential effect on the onset and prognosis of ATC. With the aid of diagnostic device, the outcome can be improved through early and customized treatment. Antifibrinolytics such as tranexamic acid has some benefits in patients with bleeding trauma, especially in the early time. This review presents the current understanding of ATC mechanisms and management.

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Pathophysiology of Early Trauma-Induced Coagulopathy: Emerging Evidence for Hemodilution and Coagulation Factor Depletion

Abstract: Background-Trauma patients present with a coagulopathy, termed early trauma induced coagulopathy (ETIC), which is associated with increased mortality. This study investigated hemostatic changes responsible for ETIC.

Cited by 102 publications

References 15 publications

An International Normalized Ratio–Based Definition of Acute Traumatic Coagulopathy Is Associated With Mortality, Venous Thromboembolism, and Multiple Organ Failure After Injury

An International Normalized Ratio–Based Definition of Acute Traumatic Coagulopathy Is Associated With Mortality, Venous Thromboembolism, and Multiple Organ Failure After Injury

The pathogenesis of traumatic coagulopathy

The Pathophysiology and Management of Acute Traumatic Coagulopathy

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