Platelets and Fibrinogen: Emerging Complexity in Trauma-Induced Coagulopathy

John, Alexander E. St.; White, Nathan J.

doi:10.1055/s-0039-1701017

Cited by 14 publications

(5 citation statements)

References 120 publications

(136 reference statements)

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“…However, we also found reduced platelet counts in nonsurviving patients from day 0 to 10 after injury as compared with those in surviving patients but these differences were not stated as signi cant. These ndings are in line with previously published studies that reported increased mortality in patients with reduced platelet counts at admission [44][45][46][47] .…”

Section: Discussionsupporting

confidence: 93%

Elevation of neutrophil-derived factors in patients after multiple trauma

Lingitz

Wollner

Bauer

et al. 2022

Preprint

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Trauma represents one of the leading causes of death worldwide. Traumatic injuries elicit a dynamic inflammatory response with systemic release of inflammatory cytokines. Disbalance of this response can lead to systemic inflammatory response syndrome or compensatory anti-inflammatory response syndrome. As neutrophils play a major role in innate immune defense and are crucial in the injury-induced immunological response, we aimed to investigate systemic neutrophil-derived immunomodulators in trauma patients. Therefore, serum levels of neutrophil elastase (NE), myeloperoxidase (MPO), and citrullinated histone H3 (CitH3) were quantified in patients with injury severity scores above 15. Additionally, leukocyte, platelet, fibrinogen, and CRP levels were assessed. Lastly, we analyzed the association of neutrophil-derived factors with clinical severity scoring systems. Although the release of MPO, NE, and CitH3 was not predictive of mortality, we found a remarkable increase in MPO and NE in trauma patients as compared with healthy controls. We also found significantly increased levels of MPO and NE on days 1 and 5 after initial trauma in critically injured patients. Taken together, our data suggest a role for neutrophil activation and NETosis in trauma. Targeting exacerbated neutrophil activation might represent a new therapeutic option for critically injured patients.

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Section: Discussionsupporting

confidence: 93%

Elevation of neutrophil-derived factors in patients after multiple trauma

Lingitz

Wollner

Bauer

et al. 2022

Preprint

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“…Studies have found impairment of different and sometimes conflicting agonist pathways, though the degranulation mechanism appears to remain intact 12 . The platelet dysfunction phenotype may be induced by ligand alteration, surface receptor inhibition, receptor shedding, and/or cellular metabolic dysfunction 8,13 . While much of the research in this area focuses on the platelet behaviors, a great deal can also be learned from the plasma environment after injury, which may directly alter platelet function.…”

Section: Introductionmentioning

confidence: 99%

Plasma proteomic profile associated with platelet dysfunction after trauma

John

Wang

Chen

et al. 2021

Journal of Thrombosis and Haemostasis

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Background Coagulopathic bleeding is a major cause of mortality after trauma, and platelet dysfunction contributes to this problem. The causes of platelet dysfunction are relatively unknown, but a great deal can be learned from the plasma environment about the possible pathways involved. Objective Describe the changes in plasma proteomic profile associated with platelet dysfunction after trauma. Methods Citrated blood was collected from severely injured trauma patients at the time of their arrival to the Emergency Department. Samples were collected from 110 patients, and a subset of twenty‐four patients was identified by a preserved (n = 12) or severely impaired (n = 12) platelet aggregation response to five different agonists. Untargeted proteomics was performed by nanoflow liquid chromatography tandem mass spectrometry. Protein abundance levels for each patient were normalized to total protein concentration to control for hemodilution by crystalloid fluid infusion prior to blood draw. Results Patients with platelet dysfunction were more severely injured but otherwise demographically similar to those with retained platelet function. Of 232 proteins detected, twelve were significantly different between groups. These proteins fall into several broad categories related to platelet function, including microvascular obstruction with platelet activation, immune activation, and protease activation. Conclusions This observational study provides a description of the change in proteomic profile associated with platelet dysfunction after trauma and identifies twelve proteins with the most profound changes. The pathways involving these proteins are salient targets for immediate investigation to better understand platelet dysfunction after trauma and identify targets for intervention.

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“…24 In addition, increased proteolysis after trauma can degrade both fibrinogen and fibrin, reducing their function and creating products of degradation that can alter hemostasis. 25…”

Section: Fibrinogenmentioning

confidence: 99%

“…There are many proposed causes for decreased fibrinogen following major trauma, including blood loss, dilution, consumption, hyperfibrinolysis, hypothermia, and acidosis 24 . In addition, increased proteolysis after trauma can degrade both fibrinogen and fibrin, reducing their function and creating products of degradation that can alter hemostasis 25 …”

Section: Mechanismsmentioning

confidence: 99%

Trauma-Induced Coagulopathy: What You Need to Know

Buzzard,

Schreiber

2023

J Trauma Acute Care Surg

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SUMMARY Trauma-induced coagulopathy (TIC) is a global inflammatory state accompanied by coagulation derangements, acidemia, and hypothermia, that occurs after traumatic injury. It occurs in approximately 25% of severely-injured patients, and its incidence is directly related to injury severity. The mechanism of TIC is multi-faceted; proposed contributing factors include dysregulation of activated protein C, increased tPA, systemic endothelial activation, decreased fibrinogen, clotting factor consumption, and platelet dysfunction. Effects of TIC include systemic inflammation, coagulation derangements, acidemia, and hypothermia. TIC may be diagnosed by conventional coagulation tests including platelet count, Clauss assay, INR, thrombin time, PT, and aPTT; viscoelastic hemostatic assays such as thrombelastography (TEG) and rotational thrombelastography (ROTEM), or by a clinical scoring system known as the Trauma Induced Coagulopathy Clinical Score (TICCS). Preventing TIC begins in the prehospital phase with early hemorrhage control, blood product resuscitation, and TXA therapy. Early administration of prothrombin complex concentrate (PCC) is also being studied in the prehospital environment. The mainstays of TIC treatment include hemorrhage control, blood and component transfusions, and correction of abnormalities such as hypocalcemia, acidosis, and hypothermia.

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Platelets and Fibrinogen: Emerging Complexity in Trauma-Induced Coagulopathy

Cited by 14 publications

References 120 publications

Elevation of neutrophil-derived factors in patients after multiple trauma

Elevation of neutrophil-derived factors in patients after multiple trauma

Plasma proteomic profile associated with platelet dysfunction after trauma

Trauma-Induced Coagulopathy: What You Need to Know

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