Isolated traumatic brain injury and venous thromboembolism

Gent, Jan-Michael Van; Bandle, Jesse; Calvo, Richard Y.; Zander, Ashley L.; Olson, Erik J.; Shackford, Steven R.; Peck, Kimberly A.; Sise, C. Beth; Sise, Michael J.

doi:10.1097/ta.0000000000000294

Cited by 32 publications

(23 citation statements)

References 10 publications

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“…Still, other studies which used surveillance methods and larger national studies that used an aggregate of TBI patients across many centers both demonstrated an association between TBI and VTE events. 12,41,42 Given the intrinsic risk of TBI for VTE, further inhibition of clot degradation via an antifibrinolytic is likely to enhance the risk and with little benefit given the lack of an association between TBI and hyperfibrinolysis.…”

Section: Discussionmentioning

confidence: 99%

“…8–10 On the other hand, TBI has been linked to a higher rate of venous thromboembolic (VTE) events, with some studies finding that over 50% of TBI patients develop a deep venous thrombosis (DVT). 11,12 Moreover, studies have shown that the brain tissue is rich in procoagulants, namely tissue factor, 13,14 and that upon systemic release, these procoagulants trigger a hypercoagulable state. 15–17…”

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confidence: 99%

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Severe traumatic brain injury is associated with a unique coagulopathy phenotype

Samuels

Moore

Silliman

et al. 2019

J Trauma Acute Care Surg

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BACKGROUND: Traumatic brain injury (TBI) patients present on a spectrum from hypocoagulability to hypercoagulability, depending on the injury complexity, severity, and time since injury. Prior studies have found a unique coagulopathy associated with TBI using conventional coagulation assays such as INR; however, few studies have assessed the association of TBI and coagulopathy using viscoelastic assays that comprehensively evaluate the coagulation in whole blood. This study aims to reevaluate the TBI-specific trauma- induced coagulopathy using arrival thrombelastography. Because brain tissue is high in key procoagulant molecules, we hypothesize that isolated TBI is associated with procoagulant and hypofibrinolytic profiles compared with injuries of the torso, extremities, and polytrauma, including TBI. METHODS: Data are from the prospective Trauma Activation Protocol study. Activated clotting time (ACT), angle, maximum amplitude (MA), 30-minute percent lysis after MA (LY30), and functional fibrinogen levels (FFLEV) were recorded. Patients were categorized into isolated severe TBI (I-TBI), severe TBI with torso and extremity injuries (TBI + TORSO/EXTREMITIES), and isolated torso and extremity injuries (I-TORSO/EXTREMITIES). Poisson regression was used to adjust for multiple confounders. RESULTS: Overall, 572 patients (48 I-TBI, 45 TBI + TORSO/EXTREMITIES, 479 1-TORSO/EXTREMITIES) were included in this analysis. The groups differed in INR, ACT, angle, MA, and FFLEV but not in 30-minute percent lysis. When compared with I-Torso/Extremities, after adjustment for confounders, severe I-TBI was independently associated with ACT less than 128 seconds (relative risk [RR], 1.5; 95% confidence interval [CI], 1.1–2.2), angle less than 65 degrees (RR, 2.2; 95% CI, 1.4–3.6), FFLEV less than 356 (RR, 1.7; 95% CI, 1.2–2.4) but not MA less than 55 mm, hyperfibrinolysis, fibrinolysis shutdown, or partial thromboplastin time (PTT) greater than 30. CONCLUSION: Severe I-TBI was independently associated with a distinct coagulopathy with delayed clot formation but did not appear to be associated with fibrinolysis abnormalities. Low fibrinogen and longer ACT values associated with I-TBI suggest that early coagulation factor replacement may be indicated in I-TBI patients over empiric antifibrinolytic therapy. Mechanisms triggering coagulopathy in TBI are unique and warrant further investigation.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Severe traumatic brain injury is associated with a unique coagulopathy phenotype

Samuels

Moore

Silliman

et al. 2019

J Trauma Acute Care Surg

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“…Although tissue factor and protein C pathways have long been implicated in TBI‐induced TIC, recent translational and animal‐based studies have identified that vWF may be a potential key mediator of TBI‐induced impairments, including in vitro platelet aggregation, increased microvascular thrombosis, leukocyte recruitment, and endothelial permeability . In a prospective study of TBI patients, the platelet‐vWF‐factor VIII axis was examined using assays of in vitro platelet aggregation and coagulation factor activity.…”

Section: The Role Of Vwf In Coagulopathy and Inflammation After Tbimentioning

confidence: 99%

Von Willebrand factor as a thrombotic and inflammatory mediator in critical illness

et al. 2020

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The endothelial exocytosis of high‐molecular‐weight multimeric von Willebrand factor (vWF) may occur in critical illness states, including trauma and sepsis, leading to the sustained elevation and altered composition of plasma vWF. These critical illnesses involve the common process of sympathoadrenal activation and loss of the endothelial glycocalyx. As a prothrombotic and proinflammatory molecule that interacts with the endothelium, the alterations exhibited by vWF in critical illness have been implicated in the development and damaging effects of downstream pathologies, such as disseminated intravascular coagulation and systemic inflammatory response syndrome. Given the role of vWF in these pathologies, there has been a recent push to further understand how the molecule may be involved in the pathophysiology of related diseases, such as trauma‐induced coagulopathy and acute renal injury, which are also known to develop secondarily to critical illness states. Elucidation of the role of vWF across the broader spectrum of generalized pathologies may provide a basis for the development of novel preventative and restorative measures, while also bolstering the scaffold of more widely used treatments, such as the administration of plasma‐containing blood products.

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“…A substantial part of our analyses investigated the effects of these TBI subtypes in isolation; studying isolated injuries is an effective model for analyzing the impact of particular forms of brain injury individually. 6,10,18,33,34,40,41 Our methods of excluding patients with major extracranial injuries and studying injuries in isolation are important elements of our study that distinguish it from previous work. The aim of our study was not only to provide evi-…”

Section: Discussionmentioning

confidence: 99%

Subdural hematoma as a major determinant of short-term outcomes in traumatic brain injury

Lee

Segar

Morrison

et al. 2018

Journal of Neurosurgery

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OBJECTIVE Early radiographic findings in patients with traumatic brain injury (TBI) have been studied in hopes of better predicting injury severity and outcome. However, prior attempts have generally not considered the various types of intracranial hemorrhage in isolation and have typically not excluded patients with potentially confounding extracranial injuries. Therefore, the authors examined the associations of various radiographic findings with short-term outcome to assess the potential utility of these findings in future prognostic models. METHODS The authors retrospectively identified 1716 patients who had experienced TBI without major extracranial injuries, and categorized them into the following TBI subtypes: subdural hematoma (SDH), traumatic subarachnoid hemorrhage, intraparenchymal hemorrhage (which included intraventricular hemorrhage), and epidural hematoma. They specifically considered isolated forms of hemorrhage, in which only 1 subtype was present. RESULTS In general, the presence of an isolated SDH was more likely to result in worse outcomes than the presence of other isolated forms of traumatic intracranial hemorrhage. Discharge to home was less likely and perihospital mortality rates were generally higher in patients with SDH. These findings were not simply related to age and were not fully captured by the admission Glasgow Coma Scale (GCS) score. The presence of SDH had a much higher sensitivity for poor outcome than the presence of other TBI subtypes, and was more sensitive for these poor outcomes than having a low GCS score (3-8). CONCLUSIONS In these ways, SDH was the most important finding associated with poor outcome, and the authors show that consideration of SDH, specifically, can augment age and GCS score in classification and prognostic models for TBI.

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Isolated traumatic brain injury and venous thromboembolism

Abstract: Epidemiologic/prognostic study, level III.

Cited by 32 publications

References 10 publications

Severe traumatic brain injury is associated with a unique coagulopathy phenotype

Severe traumatic brain injury is associated with a unique coagulopathy phenotype

Von Willebrand factor as a thrombotic and inflammatory mediator in critical illness

Subdural hematoma as a major determinant of short-term outcomes in traumatic brain injury

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