ArticleShock (Augusta, Ga.)2016
Sympathoadrenal Activation is Associated with Acute Traumatic Coagulopathy and Endotheliopathy in Isolated Brain Injury.
Article in Shock (Augusta, Ga.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
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Who cites it
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.
- Preclinical Studies on Mechanisms Underlying the Protective Effects of Propranolol in Traumatic Brain Injury: A Systematic Review.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024Pooled it
- Early Intravenous Beta-Blockade with Esmolol in Adults with Severe Traumatic Brain Injury: A Phase 2a Intervention Design Study.Neurocritical care · 2024Trial
- Maintenance of prehospital anaesthesia using an intermittent bolus regime in blunt trauma patients with a high GCS and hemodynamic reserve: a retrospective cohort study.Scandinavian journal of trauma, resuscitation and emergency medicine · 2026Observational
- Integrated analysis of WGCNA and machine learning identified diagnostic biomarkers in trauma-induced coagulopathy.Scientific reports · 2025Article
- Group-Based Trajectory Modeling Identifies Distinct Patterns of Sympathetic Hyperactivity Following Traumatic Brain Injury.Neurocritical care · 2025Observational
- Metabolically aberrant extracellular mitochondria induce oxidative endotheliopathy in traumatic brain injury.Blood advances · 2025Article
- Earlier onset of cerebral vasospasm in ruptured infectious intracranial aneurysms.Neurosurgical review · 2025Article
- Maintenance of prehospital anaesthesia in trauma patients: inconsistencies and variability in practice.BJA open · 2025Article
- Repetitive Low-Level Blast Exposure Alters Circulating Myeloperoxidase, Matrix Metalloproteinases, and Neurovascular Endothelial Molecules in Experienced Military Breachers.International journal of molecular sciences · 2025Article
- Concomitant Traumatic Brain Injury Exacerbates Endotheliopathy in Patients with Spinal Cord Injury.Neurotrauma reports · 2025Article
- Group based trajectory modeling identifies distinct patterns of sympathetic hyperactivity following traumatic brain injury.Research square · 2024Article
- Early Intravenous Beta-Blockade with Esmolol in Adults with Severe Traumatic Brain Injury (EBB-TBI): Protocol for a Phase 2a Intervention Design Study.Neurocritical care · 2024Article
- Blood failure: traumatic hemorrhage and the interconnections between oxygen debt, endotheliopathy, and coagulopathy.Clinical and experimental emergency medicine · 2024Article
- Shear Stress and Endothelial Mechanotransduction in Trauma Patients with Hemorrhagic Shock: Hidden Coagulopathy Pathways and Novel Therapeutic Strategies.International journal of molecular sciences · 2023Review
- Coagulopathy in Isolated Traumatic Brain Injury: Myth or Reality.Neurocritical care · 2023Review
- SHock-INduced Endotheliopathy (SHINE): A mechanistic justification for viscoelastography-guided resuscitation of traumatic and non-traumatic shock.Frontiers in physiology · 2023Review
- Traumatic brain injury and risk of heart failure and coronary heart disease: A nationwide population-based cohort study.PloS one · 2023Article
- Beta1-receptor blockade attenuates atherosclerosis progression following traumatic brain injury in apolipoprotein E deficient mice.PloS one · 2023Article
- Importance of catecholamine signaling in the development of platelet exhaustion after traumatic injury.Journal of thrombosis and haemostasis : JTH · 2022Article
- Exploratory Investigation of the Plasma Proteome Associated with the Endotheliopathy of Trauma.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcute coagulopathy after traumatic brain injury (TBI) involves a complex multifactorial hemostatic response that is poorly characterized.
objectivesTo examine early posttraumatic alterations in coagulofibrinolytic, endothelial, and inflammatory blood biomarkers in relation to sympathetic nervous system (SNS) activation and 6-month patient outcomes, using multivariate partial least-squares (PLS) analysis. PATIENTS AND
methodsA multicenter observational study of 159 adult isolated TBI patients admitted to the emergency department at an urban level I trauma center, was performed. Plasma concentrations of 6 coagulofibrinolytic, 10 vascular endothelial, 19 inflammatory, and 2 catecholamine biomarkers were measured by immunoassay on admission and 24 h postinjury. Neurological outcome at 6 months was assessed using the Extended Glasgow Outcome Scale. PLS-discriminant analysis was used to identify salient biomarker contributions to unfavorable outcome, whereas PLS regression analysis was used to evaluate the covariance between SNS correlates (catecholamines) and biomarkers of coagulopathy, endotheliopathy, and inflammation.
resultsBiomarker profiles in patients with an unfavorable outcome displayed procoagulation, hyperfibrinolysis, glycocalyx and endothelial damage, vasculature activation, and inflammation. A strong covariant relationship was evident between catecholamines and biomarkers of coagulopathy, endotheliopathy, and inflammation at both admission and 24 h postinjury.
conclusionsBiomarkers of coagulopathy and endotheliopathy are associated with poor outcome after TBI. Catecholamine levels were highly correlated with endotheliopathy and coagulopathy markers within the first 24 h after injury. Further research is warranted to characterize the pathogenic role of SNS-mediated hemostatic alterations in isolated TBI.
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