Trauma-Induced Coagulopathy: Standard Coagulation Tests, Biomarkers of Coagulopathy, and Endothelial Damage in Patients with Traumatic Brain Injury

被引:67
作者
Genet, Gustav Folmer [1 ]
Johansson, Par Ingemar [1 ,5 ]
Meyer, Martin Abild Stengaard [1 ]
Solbeck, Sacha [1 ]
Sorensen, Anne Marie [2 ,3 ]
Larsen, Claus Falck [3 ]
Welling, Karen Lise [4 ]
Windelov, Nis Agerlin [1 ,2 ]
Rasmussen, Lars S. [2 ]
Ostrowski, Sisse Rye [1 ]
机构
[1] Univ Copenhagen, Rigshosp, Copenhagen Univ Hosp, Transfus Med Sect,Capital Reg Blood Bank, DK-2100 Copenhagen, Denmark
[2] Univ Copenhagen, Rigshosp, Copenhagen Univ Hosp, Dept Anaesthesia, DK-2100 Copenhagen, Denmark
[3] Univ Copenhagen, Rigshosp, Copenhagen Univ Hosp, Ctr Trauma,Ctr Head & Orthopaed, DK-2100 Copenhagen, Denmark
[4] Univ Copenhagen, Rigshosp, Copenhagen Univ Hosp, Dept Neurointens Care, DK-2100 Copenhagen, Denmark
[5] Univ Texas Houston, Sch Med, Dept Surg, Ctr Translat Injury Res, Houston, TX USA
关键词
coagulopathy; pathogenesis; TBI; trauma; DISSEMINATED INTRAVASCULAR COAGULATION; SYMPATHOADRENAL ACTIVATION; GLYCOCALYX DEGRADATION; EARLY RELEASE; HYPOPERFUSION; MORTALITY; SHOCK; INFLAMMATION; SEVERITY; RECEPTOR;
D O I
10.1089/neu.2012.2612
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
It remains to be debated whether traumatic brain injury (TBI) induces a different coagulopathy than does non-TBI. This study investigated traditional coagulation tests, biomarkers of coagulopathy, and endothelial damage in trauma patients with and without TBI. Blood from 80 adult trauma patients was sampled (median of 68 min [IQR 48-88] post-injury) upon admission to our trauma center. Plasma/serum were retrospectively analyzed for biomarkers reflecting sympathoadrenal activation (adrenaline, noradrenaline), coagulation activation/inhibition and fibrinolysis (protein C, activated protein C, tissue factor pathway inhibitor, antithrombin, prothrombin fragment 1 + 2, thrombin/antithrombin complex, von Willebrand factor, factor XIII, d-dimer, tissue-type plasminogen activator, plasminogen activator inhibitor-1), immunology (interleukin [IL]6), endothelial cell/glycocalyx damage (soluble thrombomodulin, syndecan-1), and vasculogenesis (angiopoietin-1, -2). Patients were stratified according to: 1) isolated severe head/neck injuries (Abbreviated Injury Score [AIS]-head/neck >= 3, AIS-other < 3) (isoTBI); 2) severe head/neck and extracranial injuries (AIS-head/neck >= 3, AIS-other > 3) (sTBI + other); and 3) injuries without significant head/neck injuries (AIS-head/neck < 3, including all AIS-other scores) (non-TBI). Twenty-three patients presented with isoTBI, 15 with sTBI + other and 42 with non-TBI. Acute coagulopathy of trauma shock, defined as activated partial thromboplastin time (APTT) and/or international normalized ratio (INR) > 35 sec and > 1.2, was found in 13%, 47%, and 5%, respectively (p = 0.000). sTBI + other had significantly higher plasma levels of adrenaline, noradrenaline, annexin V, d-dimer, IL-6, syndecan-1, soluble thrombomodulin, and reduced protein C and factor XIII levels (all p < 0.05). No significant biomarker differences were found between isoTBI and non-TBI patients. Injury Severity Scale (ISS) rather than the presence or absence of head/neck injuries determined the hemostatic and biomarker response to the injury. The coagulopathy identified thus reflected the severity of injury rather than its localization.
引用
收藏
页码:301 / 306
页数:6
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