Traumatic brain injury is not associated with coagulopathy out of proportion to injury in other body regions

Lee, Tim H.; Hampton, David A.; Diggs, Brian S.; McCully, Sean P.; Kutcher, Matthew; Redick, Britt J.; Podbielski, Jeannette; Cotton, Bryan A.; Cohen, Mitchell J.; Schreiber, Martin A.

doi:10.1097/ta.0000000000000255

Cited by 30 publications

(25 citation statements)

References 17 publications

(16 reference statements)

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“…2 Four of five studies reported rates between 0.4 and 0.9, which is well in accordance with the present UK data. 1 In addition, UK fatal accident rate was within the previously published ranges. In this context, it would be more accurate to use exact flying times and to access even more specific mission-associated parameters (e.g., helicopter model, 3 location, flying conditions, and accident circumstances 4 ) to calculate specific rates and risks.…”

Section: Problems In Analyzing Helicopter Emergency Medical Service Asupporting

confidence: 69%

“…To the Editor: I t is with great interest that we have read the article by Chesters et al 1 on a 26-year comparative review of UK helicopter emergency medical service (HEMS) crashes. We do appreciate this work, since research in this area is scarce and of extraordinary importance to improve flight safety in HEMS operations.…”

Section: Problems In Analyzing Helicopter Emergency Medical Service Amentioning

confidence: 99%

“…I t is with great interest that we read the recently published article by Lee et al 1 The question of what role traumatic brain injury (TBI) plays on the coagulopathy of severely injured trauma patients is very pertinent and has an immediate impact on treating the two leading causes of mortality. We applaud the authors of this multiinstitutional study for adding to the existing literature these disease processes and for bringing a counterpoint to the view that TBI causes a unique coagulopathic state.…”

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confidence: 99%

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Traumatic brain injury is not associated with coagulopathy out of proportion to injury in other body regions

Edavettal

Vellucci

Rogers

2014

Journal of Trauma and Acute Care Surgery

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Section: Problems In Analyzing Helicopter Emergency Medical Service Asupporting

confidence: 69%

Section: Problems In Analyzing Helicopter Emergency Medical Service Amentioning

confidence: 99%

mentioning

confidence: 99%

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Traumatic brain injury is not associated with coagulopathy out of proportion to injury in other body regions

Edavettal

Vellucci

Rogers

2014

Journal of Trauma and Acute Care Surgery

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“…However, this translation to the human scenario remains a challenge as most patients have variable combinations of tissue injury and shock. TEG detected coagulopathy in a heterogeneous mix of trauma patients does not appear to correlate with anatomic injury severity score(30). Our study also failed to identify a specific injury pattern associated with any of the fibrinolytic phenotypes.…”

Section: Discussionmentioning

confidence: 99%

Acute Fibrinolysis Shutdown after Injury Occurs Frequently and Increases Mortality: A Multicenter Evaluation of 2,540 Severely Injured Patients

Moore

Liras

et al. 2016

Journal of the American College of Surgeons

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254

262

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Background Fibrinolysis is a physiologic process to maintain microvascular patency by breaking down excessive fibrin clot. Hyperfibrinolysis (HF) is associated with a doubling of mortality. Fibrinolysis shutdown (SD), an acute impairment of fibrinolysis, has been recognized as a risk factor for increased mortality. The purpose of this study was to assess the incidence and outcomes of fibrinolysis phenotypes in two urban trauma centers. Study Design Injured patients admitted 2010-2013, who were ≥18 years of age, had an injury severity score (ISS) >15 were included in the analysis. Admission fibrinolysis phenotypes were determined by the clot lysis at 30 minutes (LY30): SD ≤0.8%, physiologic 0.9-2.9%, HF ≥3%. Logistic regression was used to adjust for age, arrival blood pressure, ISS, mechanism, and facility. Results 2540 patients met inclusion. Median age was 39(IQR 26-55) and median ISS was 25(IQR 20-33) with a mortality rate of 21%. Fibrinolysis shutdown was the most common phenotype (46%) followed by physiologic (36%) and hyperfibrinolysis(18%). HF was associated with the highest death rate (34%), followed by SD(22%), and physiologic (14%, p<0.001). The risk of mortality remained increased for HF(OR=3.3, 95%C: 2.4-4.6, p<0.0001) and SD(OR 1.6 95%CI 1.3-2.1, p=0.0003) compared to physiologic when adjusting for age, ISS, mechanism, head injury, and blood pressure (AUROC=0.82, 95% CI 0.80-0.84). Conclusions Fibrinolysis SD is the most common phenotype upon admission and is associated with increased mortality. Moreover, these data provide additional evidence of distinct phenotypes of coagulation impairment and that individualized hemostatic therapy may be required.

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“…5,6 Retrospective and observational studies have consistently shown that coagulopathy is common in patients with traumatic brain injury (TBI). [7][8][9][10][11] However, isolated TBI lacks 2 key causal factors for coagulopathy associated with injury to the trunk and limbs, heavy blood loss and a large volume of fluid resuscitation, suggesting that it follows a distinct pathogenic pathway. The finding that coagulopathy is common in patients with penetrating brain injury 10 further indicates that damage to cerebral tissue plays a role in developing the coagulopathy.…”

Section: Introductionmentioning

confidence: 99%

Brain-derived microparticles induce systemic coagulation in a murine model of traumatic brain injury

Tian

Salsbery

Wang

et al. 2015

Blood

133

182

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• Brain-derived cellular microparticles induce systemic coagulopathy in traumatic brain injury.• Platelets facilitate the transmigration of brain microparticles through the endothelial barrier into the circulation.Traumatic brain injury (TBI) is associated with coagulopathy, although it often lacks 2 key risk factors: severe bleeding and significant fluid resuscitation associated with hemorrhagic shock. The pathogenesis of TBI-associated coagulopathy remains poorly understood. We tested the hypothesis that brain-derived microparticles (BDMPs) released from an injured brain induce a hypercoagulable state that rapidly turns into consumptive coagulopathy. Here, we report that mice subjected to fluid percussion injury (1.9 6 0.1 atm) developed a BDMP-dependent hypercoagulable state, with peak levels of plasma glial cell and neuronal BDMPs reaching 17 496 6 4833/mL and 18 388 6 3657/mL 3 hours after TBI, respectively. Uninjured mice injected with BDMPs developed a dosedependent hyper-turned hypocoagulable state measured by a progressively prolonged clotting time, fibrinogen depletion, and microvascular fibrin deposition in multiple organs. The BDMPs were 50 to 300 nm with intact membranes, expressing neuronal or glial cell markers and procoagulant phosphatidylserine and tissue factor. Their procoagulant activity was greater than platelet microparticles and was dose-dependently blocked by lactadherin. Microparticles were produced from injured hippocampal cells, transmigrated through the disrupted endothelial barrier in a platelet-dependent manner, and activated platelets. These data define a novel mechanism of TBI-associated coagulopathy in mice, identify early predictive markers, and provide alternative therapeutic targets. (Blood. 2015;125(13):2151-2159

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Traumatic brain injury is not associated with coagulopathy out of proportion to injury in other body regions

Abstract: Epidemiologic study, level III.

Cited by 30 publications

References 17 publications

Traumatic brain injury is not associated with coagulopathy out of proportion to injury in other body regions

Traumatic brain injury is not associated with coagulopathy out of proportion to injury in other body regions

Acute Fibrinolysis Shutdown after Injury Occurs Frequently and Increases Mortality: A Multicenter Evaluation of 2,540 Severely Injured Patients

Brain-derived microparticles induce systemic coagulation in a murine model of traumatic brain injury

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