Effects of platelet dysfunction and platelet transfusion on outcomes in traumatic brain injury patients

Guillotte, Andrew R.; Herbert, Joseph P.; Madsen, Richard; Hammer, Richard; Litofsky, N. Scott

doi:10.1080/02699052.2018.1536805

Cited by 33 publications

(53 citation statements)

References 28 publications

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“…The methods used were TEG, Multiplate® (Roche Diagnostics, Basel, Switzerland) and spectrophotometry. All studies found that platelet function decreased after injury [ 22 , 24 , 29 , 36 – 38 ]. This appeared to be independent of platelet transfusion and pre-injury antithrombic therapy [ 36 , 37 ].…”

Section: Resultsmentioning

confidence: 99%

“…All studies found that platelet function decreased after injury [22,24,29,[36][37][38]. This appeared to be independent of platelet transfusion and pre-injury antithrombic therapy [36,37]. In the largest prospective study of 153 adults with TBI, mean adenosine diphosphate (ADP)-induced aggregation was below-normal on admission and continued to decrease during the first 24 h after injury [36].…”

Section: Platelet Functionmentioning

confidence: 99%

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Time Course of Hemostatic Disruptions After Traumatic Brain Injury: A Systematic Review of the Literature

et al. 2020

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Almost two-thirds of patients with severe traumatic brain injury (TBI) develop some form of hemostatic disturbance, which contributes to poor outcome. While the initial head injury often leads to impaired clot formation, TBI is also associated with an increased risk of thrombosis. Most likely there is a progression from early bleeding to a later prothrombotic state. In this paper, we systematically review the literature on the time course of hemostatic disruptions following TBI. A MEDLINE search was performed for TBI studies reporting the trajectory of hemostatic assays over time. The search yielded 5,049 articles, of which 4,910 were excluded following duplicate removal as well as title and abstract review. Full-text assessment of the remaining articles yielded 33 studies that were included in the final review. We found that the first hours after TBI are characterized by coagulation cascade dysfunction and hyperfibrinolysis, both of which likely contribute to lesion progression. This is then followed by platelet dysfunction and decreased platelet count, the clinical implication of which remains unclear. Later, a poorly defined prothrombotic state emerges, partly due to fibrinolysis shutdown and hyperactive platelets. In the clinical setting, early administration of the antifibrinolytic agent tranexamic acid has proved effective in reducing head-injury-related mortality in a subgroup of TBI patients. Further studies evaluating the time course of hemostatic disruptions after TBI are warranted in order to identify windows of opportunity for potential treatment options.

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Section: Resultsmentioning

confidence: 99%

Section: Platelet Functionmentioning

confidence: 99%

Time Course of Hemostatic Disruptions After Traumatic Brain Injury: A Systematic Review of the Literature

et al. 2020

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“…Of the studies identified and analyzed in this systematic review, none showed a statistically significant benefit of platelet transfusion on mortality, although the included studies were all small in size, with cohorts ranging from 66 to 328 patients. Notably, three studies showed significant evidence of harm . The present meta‐analysis shows an insignificant trend toward increased mortality among TBI patients who received platelet transfusions, although further studies are needed.…”

Section: Discussionmentioning

confidence: 56%

“…A total of 10 manuscripts were identified that met the defined inclusion criteria . Figure shows the process of inclusion and exclusion of the study.…”

Section: Resultsmentioning

confidence: 99%

The effect of platelet transfusion in patients with traumatic brain injury and concomitant antiplatelet use: a systematic review and meta‐analysis

et al. 2019

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Fig. 1. Study inclusion and exclusion process. Diagram demonstrating the inclusion and exclusion process for this systematic review. Articles written in languages other than English (non-English), articles involving animal models (nonhuman), and articles not pertaining to the review question (not relevant) were excluded during title/abstract screening. Articles that investigated an exposure other than platelet transfusion (wrong exposure) or an outcome other than mortality (wrong outcome), or studies that used a study design other than randomized controlled trial or cohort study (wrong study design), were excluded during full-text screening.

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“…Platelet dysfunction, characterized by inhibition of platelet arachidonic acid (AA) and ADP receptors leading to lower levels of AA/ADP-induced platelet activation, occurs early after severe TBI without major systemic trauma [13,14]. This inhibition appears to be dependent on TBI severity, with mild TBI demonstrating lower levels of platelet receptor inhibition [15]. TBI, by itself, results in increased bleeding time, or hypocoagulation, early after injury, which is indicative of deficits in coagulation pathways or platelets' ability to activate [14].…”

Section: Introductionmentioning

confidence: 99%

Differential Leukocyte and Platelet Profiles in Distinct Models of Traumatic Brain Injury

Hubbard

Banerjee

Vekaria

et al. 2021

Cells

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Traumatic brain injury (TBI) affects over 3 million individuals every year in the U.S. There is growing appreciation that TBI can produce systemic modifications, which are in part propagated through blood–brain barrier (BBB) dysfunction and blood–brain cell interactions. As such, platelets and leukocytes contribute to mechanisms of thromboinflammation after TBI. While these mechanisms have been investigated in experimental models of contusion brain injury, less is known regarding acute alterations following mild closed head injury. To investigate the role of platelet dynamics and bioenergetics after TBI, we employed two distinct, well-established models of TBI in mice: the controlled cortical impact (CCI) model of contusion brain injury and the closed head injury (CHI) model of mild diffuse brain injury. Hematology parameters, platelet-neutrophil aggregation, and platelet respirometry were assessed acutely after injury. CCI resulted in an early drop in blood leukocyte counts, while CHI increased blood leukocyte counts early after injury. Platelet-neutrophil aggregation was altered acutely after CCI compared to sham. Furthermore, platelet bioenergetic coupling efficiency was transiently reduced at 6 h and increased at 24 h post-CCI. After CHI, oxidative phosphorylation in intact platelets was reduced at 6 h and increased at 24 h compared to sham. Taken together, these data demonstrate that brain trauma initiates alterations in platelet-leukocyte dynamics and platelet metabolism, which may be time- and injury-dependent, providing evidence that platelets carry a peripheral signature of brain injury. The unique trend of platelet bioenergetics after two distinct types of TBI suggests the potential for utilization in prognosis.

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Effects of platelet dysfunction and platelet transfusion on outcomes in traumatic brain injury patients

Cited by 33 publications

References 28 publications

Time Course of Hemostatic Disruptions After Traumatic Brain Injury: A Systematic Review of the Literature

Time Course of Hemostatic Disruptions After Traumatic Brain Injury: A Systematic Review of the Literature

The effect of platelet transfusion in patients with traumatic brain injury and concomitant antiplatelet use: a systematic review and meta‐analysis

Differential Leukocyte and Platelet Profiles in Distinct Models of Traumatic Brain Injury

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