Sympathoadrenal Activation is Associated with Acute Traumatic Coagulopathy and Endotheliopathy in Isolated Brain Injury. (September 2016)
- Record Type:
- Journal Article
- Title:
- Sympathoadrenal Activation is Associated with Acute Traumatic Coagulopathy and Endotheliopathy in Isolated Brain Injury. (September 2016)
- Main Title:
- Sympathoadrenal Activation is Associated with Acute Traumatic Coagulopathy and Endotheliopathy in Isolated Brain Injury
- Authors:
- Di Battista, Alex P.
Rizoli, Sandro B.
Lejnieks, Brandon
Min, Arimie
Shiu, Maria Y.
Peng, Henry T.
Baker, Andrew J.
Hutchison, Michael G.
Churchill, Nathan
Inaba, Kenji
Nascimento, Bartolomeu B.
de Oliveira Manoel, Airton Leonardo
Beckett, Andrew
Rhind, Shawn G. - Abstract:
- Abstract : Supplemental Digital Content is available in the text ABSTRACT: Background: Acute coagulopathy after traumatic brain injury (TBI) involves a complex multifactorial hemostatic response that is poorly characterized. Objectives: To 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 Methods: A 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. Results: Biomarker 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 ofAbstract : Supplemental Digital Content is available in the text ABSTRACT: Background: Acute coagulopathy after traumatic brain injury (TBI) involves a complex multifactorial hemostatic response that is poorly characterized. Objectives: To 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 Methods: A 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. Results: Biomarker 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. Conclusions: Biomarkers 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. … (more)
- Is Part Of:
- Shock. Volume 46(2016)Supplement 1 3S
- Journal:
- Shock
- Issue:
- Volume 46(2016)Supplement 1 3S
- Issue Display:
- Volume 46, Issue 3S (2017)
- Year:
- 2017
- Volume:
- 46
- Issue:
- 3S
- Issue Sort Value:
- 2017-0046-NaN-0000
- Page Start:
- 96
- Page End:
- 103
- Publication Date:
- 2016-09
- Subjects:
- Catecholamines -- D-dimer -- hemostasis -- norepinephrine -- syndecan-1 -- thrombin-activatable fibrinolysis inhibitor -- thrombomodulin -- tissue factor pathway inhibitor -- tissue plasminogen activator -- vascular adhesion protein-1
Shock -- Periodicals
Shock -- Periodicals
Choc (Pathologie) -- Périodiques
Shock
Periodicals
616.0475 - Journal URLs:
- http://www.shockjournal.com ↗
http://ovidsp.ovid.com/ovidweb.cgi?T=JS&NEWS=n&CSC=Y&PAGE=toc&D=yrovft&AN=00024382-000000000-00000 ↗
http://journals.lww.com ↗ - DOI:
- 10.1097/SHK.0000000000000642 ↗
- Languages:
- English
- ISSNs:
- 1073-2322
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 8267.443000
British Library DSC - BLDSS-3PM
British Library HMNTS - ELD Digital store - Ingest File:
- 1029.xml