Relationship of Coagulopathy and Platelet Dysfunction to Transfusion Needs After Traumatic Brain Injury

Martin, Grace E.; Shah, Dhavan V.; Elson, Nora C.; Boudreau, Ryan M.; Hanseman, Dennis J.; Pritts, Timothy A.; Makley, Amy T.; Foreman, Brandon; Goodman, Michael D.

doi:10.1007/s12028-017-0485-5

Cited by 31 publications

(18 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Patients with penetrating TBI were more hypocoagulable than patients with blunt TBI demonstrating a longer K-time and an abnormally low MA—findings consistent with clinical observations ( Fig. 2 E ) ( 38 , 40 ). Alpha angle was also lower in penetrating TBI patients but was still well above normal indicating normal clot propagation.…”

Section: Resultssupporting

confidence: 85%

Use of Thromboelastography in the Evaluation and Management of Patients With Traumatic Brain Injury: A Systematic Review and Meta-Analysis

Cannon¹,

Dias

Kumar

et al. 2021

Critical Care Explorations

View full text Add to dashboard Cite

show abstract

Section: Resultssupporting

confidence: 85%

Use of Thromboelastography in the Evaluation and Management of Patients With Traumatic Brain Injury: A Systematic Review and Meta-Analysis

Cannon¹,

Dias

Kumar

et al. 2021

Critical Care Explorations

View full text Add to dashboard Cite

show abstract

“…Previous studies have demonstrated a lack of correlation between the TEG parameter for platelet contribution to clot (MA or MCF) and VerifyNow testing. 31 Viscoelastic tests tend to utilize agonists other than ADP and AA, such as tissue factor and thromboplastin, and therefore compensate for isolation platelet dysfunction via other pathways. In this study, though a difference was observed in the ability of ADP to induce platelet aggregability when MVs from TBI blood were added to normal blood, the percent of platelet contribution to maximum clot firmness was not impacted.…”

Section: Discussionmentioning

confidence: 99%

Microvesicles generated following traumatic brain injury induce platelet dysfunction via adenosine diphosphate receptor

Martin

Pugh²,

Moran³

et al. 2019

J Trauma Acute Care Surg

Self Cite

View full text Add to dashboard Cite

Introduction: Traumatic brain injury (TBI) can result in an acute coagulopathy including platelet dysfunction that can contribute to ongoing intracranial hemorrhage. Previous studies have shown ADP-induced platelet aggregation to be reduced after TBI. In addition, circulating microvesicles (MVs) are increased following TBI and have been shown to play a role in post-TBI coagulopathy and platelet function. We hypothesized that post-TBI MVs would affect platelet aggregation in a murine head injury model. Methods: Moderate TBI was performed using a weight-drop method in male C57BL6 mice. Whole blood, plasma, MVs, and MV-poor plasma were isolated from blood collected 10 minutes following TBI and were mixed separately with whole blood from uninjured mice. Platelet aggregation was measured with Multiplate impedance platelet aggregometry in response to adenosine diphosphate (ADP). The ADP P2Y 12 receptor inhibitor, R-138727, was incubated with plasma and MVs from TBI mice, and platelet inhibition was again measured.Results: Whole blood taken from 10 minute post-TBI mice demonstrated diminished ADPinduced platelet aggregation compared to sham mice. When mixed with normal donor blood, post-TBI plasma and MVs induced diminished ADP-induced platelet aggregation compared to sham plasma and sham MVs. By contrast, the addition of post-TBI MV-poor plasma to normal blood did not change ADP-induced platelet aggregation. The observed dysfunction in post-TBI ADP platelet aggregation was prevented by the pretreatment of post-TBI plasma with R-138727. Treatment of post-TBI MVs with R-138727 resulted in similar findings of improved ADP-induced platelet aggregation compared to non-treated post-TBI MVs.

show abstract

“…For example, because of the nature of ex vivo aggregometry assays (lack of endothelium, lack of flow, and exogenous agonist stimulation of platelets), it remains unclear where impaired postinjury platelet aggregation lies on the spectrum of adaptive to maladaptive responses to injury. It should not be ignored that the majority of investigations in this area have relied on point‐of‐care platelet function assays that were intended to assess the effects of antiplatelet medication on platelet inhibition, and it is of concern that viscoelastic assays do not always correlate well with point‐of‐care assessment of platelet function in trauma patients . In fact, unpublished work by the authors of this review, using multiple electrode aggregometry, has shown identified that platelets may be endogenously activated by injury, diminishing their aggregation response to exogenous agonists.…”

Section: Mechanisms and Mediatorsmentioning

confidence: 99%

Trauma‐induced coagulopathy: The past, present, and future

Kornblith

Moore

Cohen

2019

Journal of Thrombosis and Haemostasis

204

179

View full text Add to dashboard Cite

Trauma remains a leading cause of death worldwide, and most early preventable deaths in both the civilian and military settings are due to uncontrolled hemorrhage, despite paradigm advances in modern trauma care. Combined tissue injury and shock result in hemostatic failure, which has been identified as a multidimensional molecular, physiologic and clinical disorder termed trauma-induced coagulopathy (TIC).Understanding the biology of TIC is of utmost importance, as it is often responsible for uncontrolled bleeding, organ failure, thromboembolic complications, and death.Investigations have shown that TIC is characterized by multiple phenotypes of impaired hemostasis due to altered biology in clot formation and breakdown. These coagulopathies are attributable to tissue injury and shock, and encompass underlying endothelial, immune and inflammatory perturbations. Despite the recognition and identification of multiple mechanisms and mediators of TIC, and the development of targeted treatments, the mortality rates and associated morbidities due to hemorrhage after injury remain high. The purpose of this review is to examine the past and present understanding of the multiple distinct but highly integrated pathways implicated in TIC, in order to highlight the current knowledge gaps and future needs in this evolving field, with the aim of reducing morbidity and mortality after injury. K E Y W O R D Sblood coagulation disorders, exsanguination, hemorrhagic shock, hemostasis, trauma | 853 KORNBLITH eT aL.

show abstract

Relationship of Coagulopathy and Platelet Dysfunction to Transfusion Needs After Traumatic Brain Injury

Abstract: Patients presenting with penetrating TBI demonstrated increased coagulopathy compared to those with blunt TBI as measured by TEG and need for transfusion. PFA results did not correlate with TEG findings in this population.

Cited by 31 publications

References 28 publications

Use of Thromboelastography in the Evaluation and Management of Patients With Traumatic Brain Injury: A Systematic Review and Meta-Analysis

Use of Thromboelastography in the Evaluation and Management of Patients With Traumatic Brain Injury: A Systematic Review and Meta-Analysis

Microvesicles generated following traumatic brain injury induce platelet dysfunction via adenosine diphosphate receptor

Trauma‐induced coagulopathy: The past, present, and future

Contact Info

Product

Resources

About