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Citation
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White NJ, Contaifer D, Martin EJ, Newton JC, Mohammed BM, Bostic JL, Brophy GM, Spiess BD, Pusateri AE, Ward KR, Brophy DF. J. Thromb. Haemost. 2015; 13(6): 978-988. |
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Affiliation
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Department of Medicine/Division of Emergency Medicine, University of Washington, Puget Sound Blood Center Research Institute, Seattle, WA. |
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Abstract
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BACKGROUND: Trauma-induced coagulopathy is a complex multifactorial hemostatic response that is poorly understood.
OBJECTIVES: Identify distinct hemostatic responses to trauma and identify key components of the hemostatic system that vary between responses. PATIENTS/METHODS: Cross-sectional observational study of adult trauma patients at an urban Level I trauma center Emergency Department. Hierarchical clustering analysis was used to identify distinct clusters of similar subjects using vital signs, injury/shock severity, and by comprehensive assessment of coagulation, clot formation, platelet function, and thrombin generation.
RESULTS: Of 84 total trauma patients included in the model, three distinct trauma clusters were identified. Cluster 1 (N=57) displayed platelet activation, preserved peak thrombin generation, plasma coagulation dysfunction, moderately decreased fibrinogen concentration, and normal clot formation relative to healthy controls. Cluster 2 (N=18) displayed platelet activation, preserved peak thrombin generation, and preserved fibrinogen concentration with normal clot formation. Cluster 3 (N=9) was the most severely injured and shocked and displayed a strong inflammatory and bleeding phenotype. Platelet dysfunction, thrombin inhibition, plasma coagulation dysfunction, and decreased fibrinogen concentration were present in this cluster. Fibrinolytic activation was present in all clusters, but increased more so in Cluster 3. Trauma clusters were different most noticeably in their relative fibrinogen concentration, peak thrombin generation, and platelet-induced clot contraction.
CONCLUSIONS: Hierarchical clustering analysis identified 3 distinct hemostatic responses to trauma. Further insight into the underlying hemostatic mechanisms responsible for these responses is needed. This article is protected by copyright. All rights reserved.
Language: en |