Global Characterisation of Coagulopathy in Isolated Traumatic Brain Injury (iTBI): A CENTER-TBI Analysis
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ORIGINAL WORK
Global Characterisation of Coagulopathy in Isolated Traumatic Brain Injury (iTBI): A CENTER‑TBI Analysis Julia K. Böhm1, Helge Güting1, Sophie Thorn2, Nadine Schäfer1, Victoria Rambach1, Herbert Schöchl4,5, Oliver Grottke6, Rolf Rossaint6, Simon Stanworth7, Nicola Curry7, Rolf Lefering1, Marc Maegele1,3* and CENTERTBI Participants and Investigators © 2020 The Author(s)
Abstract Background: Trauma-induced coagulopathy in patients with traumatic brain injury (TBI) is associated with high rates of complications, unfavourable outcomes and mortality. The mechanism of the development of TBI-associated coagulopathy is poorly understood. Methods: This analysis, embedded in the prospective, multi-centred,observational Collaborative European NeuroTrauma Effectiveness Research in Traumatic Brain Injury (CENTER-TBI) study, aimed to characterise the coagulopathy of TBI. Emphasis was placed on the acute phase following TBI, primary on subgroups of patients with abnormal coagulation profile within 4 h of admission, and the impact of pre-injury anticoagulant and/or antiplatelet therapy. In order to minimise confounding factors, patients with isolated TBI (iTBI) (n = 598) were selected for this analysis. Results: Haemostatic disorders were observed in approximately 20% of iTBI patients. In a subgroup analysis, patients with pre-injury anticoagulant and/or antiplatelet therapy had a twice exacerbated coagulation profile as likely as those without premedication. This was in turn associated with increased rates of mortality and unfavourable outcome post-injury. A multivariate analysis of iTBI patients without pre-injury anticoagulant therapy identified several independent risk factors for coagulopathy which were present at hospital admission. Glasgow Coma Scale (GCS) less than or equal to 8, base excess (BE) less than or equal to − 6, hypothermia and hypotension increased risk significantly. Conclusion: Consideration of these factors enables early prediction and risk stratification of acute coagulopathy after TBI, thus guiding clinical management. Keywords: CENTER-TBI, Traumatic brain injury, Coagulopathy, Risk factors Introduction Traumatic brain injury (TBI) remains a leading cause of death and disability worldwide [1]. The initial insult often results in disruptions of the cerebral vasculature and pathological alterations of the blood–brain barrier (BBB) *Correspondence: Marc.Maegele@t‑online.de 1 Department of Medicine, Faculty of Health, Institute for Research in Operative Medicine, Witten/Herdecke University, Ostmerheimer Str. 200, Building 38, 51109 Cologne, Germany Full list of author information is available at the end of the article
which may evolve into haemorrhagic lesions. In addition, TBI-associated factors may disturb the body’s haemocoagulative capacity and alter the delicate balance between bleeding and thrombus formation leading to a substantial exacerbation of the initial injury sustained [2–5]. Recent evidence suggests that the acute phase after TBI is rather characterised by dysfunction of t
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