Acute Coagulopathy of Trauma: Hypoperfusion Induces Systemic Anticoagulation and Hyperfibrinolysis

Brohi, Karim; Cohen, Mitchell J.; Ganter, Michael T.; Schultz, Marcus J.; Levi, Marcel; Mackersie, Robert C.; Pittet, Jean–François

doi:10.1097/ta.0b013e318169cd3c

Cited by 622 publications

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“…Brohi and colleagues 8 showed that D-dimer concentrations are raised in trauma patients at the time of hospital admission (median prehospital time 28 min), with the highest concentrations measured in the most severely injured patients. 8 Similar results were recorded in a 2009 study from Japan that measured fi brin degradation product and D-dimers in 314 severe trauma patients. 10 If this early increased fi brinolysis exacerbates bleeding and increases the risk of death, then we might expect that an antifi brinolytic drug such as tranexamic acid would be most eff ective in this period.…”

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confidence: 99%

“…Acute severe trauma is associated with increased fi brinolysis that contributes to an early coagulopathy and increased mortality. 8,9 Fibrinolysis can be assessed by measurement of fi brin degradation products, which include small protein fragments called D-dimers. Brohi and colleagues 8 showed that D-dimer concentrations are raised in trauma patients at the time of hospital admission (median prehospital time 28 min), with the highest concentrations measured in the most severely injured patients.…”

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confidence: 99%

“…8,9 Fibrinolysis can be assessed by measurement of fi brin degradation products, which include small protein fragments called D-dimers. Brohi and colleagues 8 showed that D-dimer concentrations are raised in trauma patients at the time of hospital admission (median prehospital time 28 min), with the highest concentrations measured in the most severely injured patients. 8 Similar results were recorded in a 2009 study from Japan that measured fi brin degradation product and D-dimers in 314 severe trauma patients.…”

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The importance of early treatment with tranexamic acid in bleeding trauma patients: an exploratory analysis of the CRASH-2 randomised controlled trial

et al. 2011

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The importance of early treatment with tranexamic acid in bleeding trauma patients: an exploratory analysis of the CRASH-2 randomised controlled trialThe CRASH-2 collaborators* SummaryBackground The aim of the CRASH-2 trial was to assess the eff ects of early administration of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with signifi cant haemorrhage. Tranexamic acid signifi cantly reduced all-cause mortality. Because tranexamic acid is thought to exert its eff ect through inhibition of fi brinolysis, we undertook exploratory analyses of its eff ect on death due to bleeding.Methods The CRASH-2 trial was undertaken in 274 hospitals in 40 countries. 20 211 adult trauma patients with, or at risk of, signifi cant bleeding were randomly assigned within 8 h of injury to either tranexamic acid (loading dose 1 g over 10 min followed by infusion of 1 g over 8 h) or placebo. Patients were randomly assigned by selection of the lowest numbered treatment pack from a box containing eight numbered packs that were identical apart from the pack number. Both participants and study staff (site investigators and trial coordinating centre staff ) were masked to treatment allocation. We examined the eff ect of tranexamic acid on death due to bleeding according to time to treatment, severity of haemorrhage as assessed by systolic blood pressure, Glasgow coma score (GCS), and type of injury. All analyses were by intention to treat. The trial is registered as ISRCTN86750102, ClinicalTrials.gov NCT00375258, and South African Clinical Trial Register/Department of Health DOH-27-0607-1919.Findings 10 096 patients were allocated to tranexamic acid and 10 115 to placebo, of whom 10 060 and 10 067, respectively, were analysed. 1063 deaths (35%) were due to bleeding. We recorded strong evidence that the eff ect of tranexamic acid on death due to bleeding varied according to the time from injury to treatment (test for interaction p<0·0001). Early treatment (≤1 h from injury) signifi cantly reduced the risk of death due to bleeding (198 Interpretation Tranexamic acid should be given as early as possible to bleeding trauma patients. For trauma patients admitted late after injury, tranexamic acid is less eff ective and could be harmful.Funding UK NIHR Health Technology Assessment programme, Pfi zer, BUPA Foundation, and J P Moulton Charitable Foundation. IntroductionThe CRASH-2 trial showed that administration of tranexamic acid to adult trauma patients with, or at risk of, signifi cant haemorrhage, within 8 h of injury, signi fi cantly reduces all-cause mortality (relative risk [RR] 0·91, 95% CI 0·85-0·97; p=0·0035) with no apparent increase in vascular occlusive events.1 As a consequence of this trial, tranexamic acid has been incorporated into trauma treatment protocols worldwide.Results from the CRASH-2 trial raise some important questions. The trial was motivated by the evidence that tranexamic acid reduces bleeding in patients undergoing elective surgery, and the hypothesised mechanism was inhi...

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The importance of early treatment with tranexamic acid in bleeding trauma patients: an exploratory analysis of the CRASH-2 randomised controlled trial

et al. 2011

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“…The tissue factor pathway stimulates the release of thrombin normally, but when injury to the vasculature occurs the clotting cascade commences causing a hyper-coagulation state. In addition, coagulopathy is present in 25% of trauma patients and is linked with a 5-times increase in mortality [6].…”

Section: Resultsmentioning

confidence: 99%

Does Deep Vein Thrombosis Usually Precede a Pulmonary Embolism

BA¹

2013

J Trauma Treat

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BackgroundHistorically, traumatic brain injury, pelvic and lower extremity fractures, paralysis or any condition associated with prolonged immobilization were considered risk factors for Deep Vein Thrombosis [DVT] [1] which can predispose to a potentially life threatening pulmonary embolism [PE], a process known as Venous Thromboembolism [VTE] [2]. There is no disputing that the incidence of VTE depends on a patient's risk factors along with the modalities used to prevent and detect DVT and PE. However, there is some dispute as to whether a PE is usually preceded by a DVT, detected or undetected, and whether the prophylactic use of inferior vena cava filters is appropriate in these patients. Some recent studies suggest PEs are not always from a DVT but instead may originate from thrombi formed within the pulmonary vasculature following severe chest trauma [3]. In past years common knowledge presumed that a PE invariably resulted from a DVT within the deep veins of the lower extremities or within the pelvic iliac veins. Since not all DVTs are detected on ultrasound studies, the iliac veins were usually considered as the originating site when a PE was diagnosed without a positive ultrasound study for DVT. However, recent studies showed that in some patients who had experienced PE had a negative ultrasound and Computed Topography [CT] of the pelvis failed to reveal DVTs within the iliac veins as previously suspected [3][4][5]. These studies support the fact that PE may potentially develop de novo in the pulmonary circulation and not deep within the iliac veins as originally suspected [5]. In addition, the American College of Surgeons found the incidence of PE to be 42% higher in patients who sustained serious chest injury, defined as an Abbreviated Injury Scale score of 3 or higher, compared to those without serious chest injury [3]. In summary, these referenced studies provide data suggesting that patients with chest trauma are more at risk for PEs that originate from the pulmonary vasculature than originally thought. This twelve-year retrospective study was performed for the purpose of comparing the correlation of DVT and subsequent PE in the trauma population with and without severe chest trauma. PathophysiologyThree factors predispose to thrombus formation: endothelial injury, stasis or turbulence in blood flow, and hypercoagulability. These three factors are known as Virchow's triad. Endothelial injury occurs any time the collagen within the vasculature is damaged and the clotting cascade is initiated. Examples of injury to the endothelium can be damage to the vein from trauma or hypertension. With vessel injury, an alteration in blood flow occurs, causing turbulence and stasis within the vessel. Blood hypercoagulability is a result of a complex mechanism known as the clotting cascade. The clotting cascade involves several components, including platelets and numerous clotting factors used to maintain blood homeostasis. The clotting factors are composed of enzymes and proteins. In addition, there are three mai...

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“…Even more that, neck laceration of Zone II is very hard to approach in emergency department (ED). If the condition of patient is in hypovolemic shock by massive bleeding, it makes worse causing coagulopathy with hypothermia and acidosis [1]. In this situation, bleeding control and patient management are very hard.…”

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confidence: 99%

Common Carotid Artery Laceration Managed by Clamping at Emergency Department

Choi

Kim

et al. 2017

Journal of Trauma and Injury

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Common carotid artery laceration is a life-threatening injury by causing hypovolemic shock. Nevertheless the initial management is very difficult until definitive surgery at operation room. Before neck exploration at operation room, arterial bleeding control by compressing the bleeding point is not always effective. We experienced one case with externally penetrating injuries in zone II neck, which was operated after clamping of common carotid artery in the emergency department. Here we report this case.

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Acute Coagulopathy of Trauma: Hypoperfusion Induces Systemic Anticoagulation and Hyperfibrinolysis

Cited by 622 publications

References 25 publications

The importance of early treatment with tranexamic acid in bleeding trauma patients: an exploratory analysis of the CRASH-2 randomised controlled trial

The importance of early treatment with tranexamic acid in bleeding trauma patients: an exploratory analysis of the CRASH-2 randomised controlled trial

Does Deep Vein Thrombosis Usually Precede a Pulmonary Embolism

Common Carotid Artery Laceration Managed by Clamping at Emergency Department

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