Early coagulopathy in trauma patients: An on-scene and hospital admission study

Floccard, Bernard; Rugeri, Lucia; Faure, Alexandre; Denis, Marc Saint; Boyle, Eileen M.; Peguet, Olivier; Levrat, Albrice; Guillaume, C.; Marcotte, Guillaume; Vulliez, Alexandre; Hautin, Etienne; David, Jean; Négrier, Claude; Allaouchiche, Bernard

doi:10.1016/j.injury.2010.11.003

Cited by 293 publications

(233 citation statements)

References 33 publications

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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: 97%

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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Section: Pathophysiologymentioning

confidence: 97%

The pathogenesis of traumatic coagulopathy

2014

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“…1 Later, several studies corroborated this assumption by showing TIC to be present at the scene of injury before onset of resuscitative treatment. 2,3 From these data, the thrombin-thrombomodulin-protein C anticoagulant system was implicated as a potential primary mechanism of anticoagulation. 4,5 Brohi et al found increased circulating thrombomodulin that correlated with decreased plasma protein C levels and attributed the decrease in protein C to its activation (activated protein C [aPC]) by thrombin bound to thrombomodulin.…”

Section: Anticoagulationmentioning

confidence: 99%

Mechanisms of trauma-induced coagulopathy

White

2013

Hematology

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The identification and management of coagulopathy is a critical component of caring for the severely injured patient. Notions of the mechanisms of coagulopathy in trauma patients have been supplanted by new insights resulting from close examination of the biochemical and cellular changes associated with acute tissue injury and hemorrhagic shock. Acute intrinsic coagulopathy arising in severely injured trauma patients is now termed trauma-induced coagulopathy (TIC) and is an emergent property of tissue injury combined with hypoperfusion. Mechanisms contributing to TIC include anticoagulation, consumption, platelet dysfunction, and hyperfibrinolysis. This review discusses current understanding of TIC mechanisms and their relative contributions to coagulopathy in the face of increasingly severe injury and highlights how they interact to produce coagulation system dysfunction.

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“…Fibrinogen is the first factor to fall below reference values during bleeding and in trauma reaches critically low levels earlier than any other coagulation factors (23). This has been demonstrated in both the pre-hospital environment and early after arrival in the trauma unit prior to large volume fluid resuscitation (24) (25). In a number of studies the degree of hypofibrinogenaemia is strongly associated with injury severity (22) (26).…”

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confidence: 98%

Fibrinogen in traumatic haemorrhage: A narrative review

Winearls

Campbell

Hurn

et al. 2017

Injury

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Abstract:Haemorrhage in the setting of severe trauma is associated with significant morbidity and mortality. There is increasing awareness of the important role fibrinogen plays in traumatic haemorrhage. Fibrinogen levels fall precipitously in severe trauma and the resultant hypofibrinogenaemia is associated with poor outcomes. Hence, it has been postulated that early fibrinogen replacement in severe traumatic haemorrhage may improve outcomes, although, to date there is a paucity of high quality evidence to support this hypothesis. In addition there is controversy regarding the optimal method for fibrinogen supplementation. We review the current evidence regarding the role of fibrinogen in trauma, the rationale behind fibrinogen supplementation and discuss current research.

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Early coagulopathy in trauma patients: An on-scene and hospital admission study

Cited by 293 publications

References 33 publications

The pathogenesis of traumatic coagulopathy

The pathogenesis of traumatic coagulopathy

Mechanisms of trauma-induced coagulopathy

Fibrinogen in traumatic haemorrhage: A narrative review

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