Pathophysiology of Trauma-Induced Coagulopathy

Duque, Patricia; Calvo, Alberto Martinez; Lockie, Christopher; Schöchl, Herbert

doi:10.1016/j.tmrv.2021.07.004

Cited by 34 publications

(28 citation statements)

References 65 publications

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“…Even in the modern era of MT protocols, half of trauma patients receiving UMT receive an unbalanced transfusion ≥1.5:1 PRBC/FFP or PRBC/PLT 32 . Patients receiving transfusion are likely to experience trauma-induced coagulopathy, leading to increased requirement of blood products 33 . Maintaining a balanced 1:1 ratio of PRBC/FFP improves survival in both combat and civilian trauma patients 34,35 .…”

Section: Discussionmentioning

confidence: 99%

When is enough enough? Odds of survival by unit transfused

Loudon

Rushing

Hue

et al. 2022

J Trauma Acute Care Surg

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Section: Discussionmentioning

confidence: 99%

When is enough enough? Odds of survival by unit transfused

Loudon

Rushing

Hue

et al. 2022

J Trauma Acute Care Surg

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“…Recent statistics show that approximately two-thirds of severe TBI patients have abnormal coagulation function on admission (2), and we previously show that coagulopathy and initial head computer tomography (CT) signs could be independent risk factors for progressive hemorrhagic injury (PHI) including epidural, subdural hematoma, brain contusion, subarachnoid hemorrhage, cranial fracture, and plasma D-dimer level (3,4). The mechanisms of PTC include platelet dysfunction, endogenous anticoagulation, endothelial activation, abnormal fibrinogen (Fg), neuroinflammation, and hyperfibrinolysis (2,(5)(6)(7); however, up to now, the exact mechanism is unclear.…”

Section: Introductionmentioning

confidence: 99%

Integrated single-cell multiomics reveals novel immune candidate markers for post-traumatic coagulopathy

Zheng

Zhang²,

Ren

et al. 2023

Front. Immunol.

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IntroductionPost-traumatic coagulopathy (PTC) is a critical pathology in traumatic brain injury (TBI), however, its potential mechanism is not clear. To explore this in peripheral samples, we integrated single cell RNA-sequencing and T cell repertoire (TCR)-sequencing across a cohort of patients with TBI.MethodsClinical samples from patients with more brain severity demonstrated overexpression of T cell receptor–encoding genes and less TCR diversity.ResultsBy mapping TCR clonality, we found patients with PTC have less TCR clones, and the TCR clones are mainly distributed in cytotoxic effector CD8+T cell. In addition, the counts of CD8+ T cell and natural killer (NK) cells are associated with the coagulation parameter by WGCNA, and the granzyme and lectin-like receptor profiles are also decreased in the peripheral blood from TBI patients, suggesting that reduced peripheral CD8+ clonality and cytotoxic profiles may be involved in PTC after TBI.ConclusionOur work systematically revealed the critical immune status in PTC patients at the single-cell level.

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“…Trauma-related haemostatic dysfunction, also termed trauma-induced coagulopathy (TIC), can be detected in approximately 25-35% of severely injured patients upon emergency room admission [1,2]. Early endogenous TIC is associated with an increased bleeding tendency, a higher rate of red blood cell (RBC) transfusion requirements, and an elevated incidence of secondary complications such as multi organ dysfunction syndrome or thromboembolism [3]. Despite enormous progress in the global understanding of TIC, the exact mechanisms behind this phenomenon are still not fully understood [4].…”

Section: Introductionmentioning

confidence: 99%

Multiplate Platelet Function Testing upon Emergency Room Admission Fails to Provide Useful Information in Major Trauma Patients Not on Platelet Inhibitors

Pommer

Oberladstätter

Schlimp

et al. 2022

JCM

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Platelet dysfunction is a suggested driver of trauma-induced coagulopathy. However, there is still a paucity of data regarding the impact of injury pattern on platelet function and the association of platelet dysfunction on transfusion requirements and mortality. In this retrospective cohort study, patients were grouped into those with isolated severe traumatic brain injury (TBI group), those with major trauma without TBI (MT group), and a combination of both major trauma and traumatic brain injury (MT + TBI group). Platelet function was assessed by whole blood impedance aggregometry (Multiplate®, MP). Three different platelet activators were used: adenosine-diphosphate (ADP test), arachidonic acid (ASPI test), and thrombin activated peptide-6 (TRAP test). Blood transfusion requirements within 6 h and 24 h and the association of platelet dysfunction on mortality was investigated. A total of 328 predominantly male patients (75.3%) with a median age of 53 (37–68) years and a median ISS of 29 (22–38) were included. No significant difference between the TBI group, the MT group, and the MT + TBI group was detected for any of the investigated platelet function tests. Unadjusted and adjusted for platelet count, the investigated MP assays revealed no significant group differences upon ER admission and were not able to sufficiently predict massive transfusion, neither within the first 6 h nor for the first 24 h after hospital admission. No association between platelet dysfunction measured by MP upon ER admission and mortality was observed. Conclusion: Injury pattern did not specifically impact platelet function measurable by MP. Platelet dysfunction upon ER admission measurable by MP was not associated with transfusion requirements and mortality. The clinical relevance of platelet function testing by MP in trauma patients not on platelet inhibitors is questionable.

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Pathophysiology of Trauma-Induced Coagulopathy

Cited by 34 publications

References 65 publications

When is enough enough? Odds of survival by unit transfused

When is enough enough? Odds of survival by unit transfused

Integrated single-cell multiomics reveals novel immune candidate markers for post-traumatic coagulopathy

Multiplate Platelet Function Testing upon Emergency Room Admission Fails to Provide Useful Information in Major Trauma Patients Not on Platelet Inhibitors

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