Traumatic Brain Injury Associated Coagulopathy

Manoel, Airton Leonardo de Oliveira; Neto, Antônio Capone; Veigas, Precilla; Rizoli, Sandro

doi:10.1007/s12028-014-0026-4

Cited by 78 publications

(61 citation statements)

References 31 publications

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“…8 Prolonged prothrombin and partial thromboplastin times usually occurred late, indicating a transition from a hyper-to a hypocoagulable state. 8,9 Despite strong clinical and laboratory evidence of its presence and association with poor clinical outcomes, 12 the pathogenesis of TBI-associated coagulopathy remains poorly understood. Current clinical tests detect the coagulopathy, but are insufficient to determine its causes or to predict its occurrence, making clinical management of TBI-associated coagulopathy difficult and costly.…”

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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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

View full text Add to dashboard Cite

show abstract

“…20 It seems that potassium plays a role in pathophysiology of brain injury.The relation between coagulopathy and TBI was evaluated in previous studies and they reported that coagulopathy can occur frequently in patients with poor outcome. 30,31 This study also showed higher mortality rate among patients presented with higher levels of PTT but no statistically significant relation between coagulation factors and long-term GOSE was observed.…”

Section: Discussionmentioning

confidence: 57%

Initial GCS and laboratory findings of patients with TBI are associated with the GOSE and mortality rate at one year

Paydar¹,

Bordbar²,

Taghipour³

et al. 2017

Int J Res Med Sci

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Background: To evaluate the relationship between presenting Glasgow Coma Scale (GCS) or laboratory data of patients with TBI and Extended Glasgow Outcome Scale (GOSE) and final outcome (deceased, survived) at one year.Methods: 74 patients (59 males and 15 females; mean age ±SD of 40±19years) who presented with TBI were entered into the study, and their GCS and laboratory data were recorded. After one year, GOSE level and final outcome were evaluated with 11 yes/no questions obtained from the patients or their first-degree relatives.Results: The patients with lower GCS on admission or day six, significantly had lower GOSE. Moreover, the lower the GCS in the first week of admission, the poorer the final outcome. Among laboratory data, the base deficit (BD) level of -6 or worse on admission was an indicator of mortality at one year. Hypernatremia was the only laboratory factor which predicted poor GOSE after a year. Furthermore, patients with serum hypernatremia, hyperkalemia, or high PTT levels on the first week of admission had poor final outcome.Conclusions: Presenting GCS and metabolic derangements are reliable indicators of long-term outcome and GOSE at one year.

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“…63 Coagulopathy can occur in isolated head injury, and the development of coagulopathy after brain injury is associated with a worse outcome. 64 The release of tissue factor from injured cortical parenchyma may contribute to, or even be responsible for, the development of coagulopathy and, when severe, subsequent disseminated intravascular coagulation. 64 The release of cerebral gangliosides and plasminogen-rich substrates from damaged brain tissue is also thought to contribute to coagulopathy in patients with severe head injury.…”

Section: Hematologicmentioning

confidence: 99%

“…64 The release of tissue factor from injured cortical parenchyma may contribute to, or even be responsible for, the development of coagulopathy and, when severe, subsequent disseminated intravascular coagulation. 64 The release of cerebral gangliosides and plasminogen-rich substrates from damaged brain tissue is also thought to contribute to coagulopathy in patients with severe head injury. 65 On the other hand, in a recent prospective observational study of 345 patients with isolated severe traumatic brain injury, no association with the development of coagulopathy was found.…”

Section: Hematologicmentioning

confidence: 99%

“…65 On the other hand, in a recent prospective observational study of 345 patients with isolated severe traumatic brain injury, no association with the development of coagulopathy was found. 64 In Canada, recommendations for organ donor patient management in the ICU include targeting a hemoglobin concentration of 9-10 gÁdL -1 and no less than 7 gÁdL -137 in order to optimize oxygen delivery to organs. Platelets and plasma should be given when clinically significant bleeding is evident, but not to target a specific coagulation test level or platelet count.…”

Section: Hematologicmentioning

confidence: 99%

See 1 more Smart Citation

Anesthetic considerations in organ procurement surgery: a narrative review

Anderson

Bekker

Vagefi

2015

Can J Anesth/J Can Anesth

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Traumatic Brain Injury Associated Coagulopathy

Abstract: Isolated severe TBI is not an independent risk factor for the development of coagulopathy. However, severe TBI patients who develop coagulopathy have extremely high mortality rates.

Cited by 78 publications

References 31 publications

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

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

Initial GCS and laboratory findings of patients with TBI are associated with the GOSE and mortality rate at one year

Anesthetic considerations in organ procurement surgery: a narrative review

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