Global Characterisation of Coagulopathy in Isolated Traumatic Brain Injury (iTBI): A CENTER-TBI Analysis

Neurocritical Care - Tập 35 - Trang 184-196 - 2020
Julia K. Böhm1, Helge Güting1, Sophie Thorn2, Nadine Schäfer1, Victoria Rambach1, Herbert Schöchl3,4, Oliver Grottke5, Rolf Rossaint5, Simon Stanworth6, Nicola Curry6, Rolf Lefering1, Marc Maegele1,7
1Department of Medicine, Faculty of Health, Institute for Research in Operative Medicine, Witten/Herdecke University, Cologne, Germany
2Emergency and Trauma Centre, Melbourne, Australia
3Department of Anaesthesiology and Intensive Care, AUVA Trauma Hospital, Academic Teaching Hospital of the Paracelsus Medical University, Salzburg, Austria
4Ludwig Boltzmann Institute for Experimental and Clinical Traumatology, AUVA Research Centre, Vienna, Austria
5Department of Anaesthesiology, RWTH Aachen University Hospital, Aachen, Germany
6NHS Blood and Transplant, Oxford University Hospital NHS Foundation Trust, Oxford, UK
7Department of Traumatology, Orthopaedic Surgery and Sports Traumatology, Cologne-Merheim Medical Centre (CMMC), Witten/Herdecke University, Cologne, Germany

Tóm tắt

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. 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. 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. Consideration of these factors enables early prediction and risk stratification of acute coagulopathy after TBI, thus guiding clinical management.

Tài liệu tham khảo

Hyder AA, Wunderlich CA, Puvanachandra P, Gururaj G, Kobusingye OC. The impact of traumatic brain injuries: a global perspective. NeuroRehabilitation. 2007;22(5):341–53. Harhangi BS, Kompanje EJO, Leebeek FWG, Maas AIR. Coagulation disorders after traumatic brain injury. Acta Neurochir (Wien). 2008;150(2):165–75. Hoyt DB. A clinical review of bleeding dilemmas in trauma. In: Seminars in hematology;2004, p. 40–3. Zhang J, Jiang R, Liu L, Watkins T, Zhang F, Dong JF. Traumatic brain injury-associated coagulopathy. J Neurotrauma. 2012;29(17):2597–605. Maegele M, Schöchl H, Menovsky T, et al. Coagulopathy and haemorrhagic progression in traumatic brain injury: advances in mechanisms, diagnosis, and management. Lancet Neurol. 2017;16(8):630–47. Laroche M, Kutcher ME, Huang MC, Cohen MJ, Manley GT. Coagulopathy after traumatic brain injury. Neurosurgery. 2012;70(6):1334–45. Chen H, Xue LX, Guo Y, et al. The influence of hemocoagulation disorders on the development of posttraumatic cerebral infarction and outcome in patients with moderate or severe head trauma. Biomed Res Int. 2013. https://doi.org/10.1155/2013/685174. Sun Y, Wang J, Wu X, et al. Validating the incidence of coagulopathy and disseminated intravascular coagulation in patients with traumatic brain injury—analysis of 242 cases. Br J Neurosurg. 2011;25(3):363–8. Talving P, Benfield R, Hadjizacharia P, Inaba K, Chan LS, Demetriades D. Coagulopathy in severe traumatic brain injury: a prospective study. J Trauma Inj Infect Crit Care. 2009;66(1):55–61. Yuan Q, Sun YR, Wu X, et al. Coagulopathy in traumatic brain injury and its correlation with progressive hemorrhagic injury: a systematic review and meta-analysis. J Neurotrauma. 2016;33(14):1279–91. Zhang D, Gong S, Jin H, et al. Coagulation parameters and risk of progressive hemorrhagic injury after traumatic brain injury: a systematic review and meta-analysis. Biomed Res Int. 2015. https://doi.org/10.1155/2015/261825. Steyerberg EW, Wiegers E, Sewalt C, et al. Case-mix, care pathways, and outcomes in patients with traumatic brain injury in CENTER-TBI: a European prospective, multicentre, longitudinal, cohort study. Lancet Neurol. 2019;18(10):923–34. Chhabra G, Rangarajan K, Subramanian A, Agrawal D, Sharma S, Mukhopadhayay AK. Hypofibrinogenemia in isolated traumatic brain injury in Indian patients. Neurol India. 2010;58(5):756–7. Shehata M, Afify I, El-Shafie M, Khaled M. Prevalence and clinical implications of coagulopathy in patients with isolated head trauma. Med J Cairo Univ. 2011;79(2):131–7. Stein SC, Smith DH. Coagulopathy in traumatic brain injury. Neurocrit Care. 2004;1(4):479–88. Zehtabchi S, Soghoian S, Liu Y, et al. The association of coagulopathy and traumatic brain injury in patients with isolated head injury. Resuscitation. 2008;76(1):52–6. Chandler WL, Dunbar NM. Thrombin generation in trauma patients. Transfusion. 2009;49(12):2652–60. Schöchl H, Solomon C, Traintinger S, et al. Thromboelastometric (ROTEM) findings in patients suffering from isolated severe traumatic brain injury. J Neurotrauma. 2011;28(10):2033–41. Lustenberger T, Talving P, Kobayashi L, et al. Early coagulopathy after isolated severe traumatic brain injury: relationship with hypoperfusion challenged. J Trauma Inj Infect Crit Care. 2010;69(6):1410–4. Wafaisade A, Lefering R, Tjardes T, et al. Acute coagulopathy in isolated blunt traumatic brain injury. Neurocrit Care. 2010;12(2):211–9. Shoeb M, Fang MC. Assessing bleeding risk in patients taking anticoagulants. J Thromb Thrombolysis. 2013;35:312–9. Gardner RC, Dams-O’Connor K, Morrissey MR, Manley GT. Geriatric traumatic brain injury: epidemiology, outcomes, knowledge gaps, and future directions. J Neurotrauma. 2018;35(7):889–906. Harvey LA, Close JCT. Traumatic brain injury in older adults: characteristics, causes and consequences. Injury. 2012;43:1821–6. Haring RS, Narang K, Canner JK, et al. Traumatic brain injury in the elderly: morbidity and mortality trends and risk factors. J Surg Res. 2015;195(1):1–9. Tauber M, Koller H, Moroder P, Hitzl W, Resch H. Secondary intracranial hemorrhage after mild head injury in patients with low-dose acetylsalicylate acid prophylaxis. J Trauma Inj Infect Crit Care. 2009;67(3):521–5. Nishijima DK, Offerman SR, Ballard DW, et al. Risk of traumatic intracranial hemorrhage in patients with head injury and preinjury warfarin or clopidogrel use. Acad Emerg Med. 2013;20(2):140–5. Nishijima DK, Zehtabchi S, Berrong J, Legome E. Utility of platelet transfusion in adult patients with traumatic intracranial hemorrhage and preinjury antiplatelet use: a systematic review. J Trauma Acute Care Surg. 2012;72(6):1658–63. Nishijima DK, Shahlaie K, Sarkar K, Rudisill N, Holmes JF. Risk of unfavorable long-term outcome in older adults with traumatic intracranial hemorrhage and anticoagulant or antiplatelet use. Am J Emerg Med. 2013;31(8):1244–7. Joseph B, Pandit V, Aziz H, et al. Clinical outcomes in traumatic brain injury patients on preinjury clopidogrel: a prospective analysis. J Trauma Acute Care Surg. 2014;76(3):817–20. Prexl O, Bruckbauer M, Voelckel W, et al. The impact of direct oral anticoagulants in traumatic brain injury patients greater than 60-years-old. Scand J Trauma Resusc Emerg Med. 2018;26(1):20. Grandhi R, Harrison G, Voronovich Z, et al. Preinjury warfarin, but not antiplatelet medications, increases mortality in elderly traumatic brain injury patients. J Trauma Acute Care Surg. 2015;78:614–21. Dossett LA, Riesel JN, Griffin MR, Cotton BA. Prevalence and implications of preinjury warfarin use: an analysis of the National Trauma Databank. Arch Surg. 2011;146(5):565–70. Epstein DS, Mitra B, O’Reilly G, Rosenfeld JV, Cameron PA. Acute traumatic coagulopathy in the setting of isolated traumatic brain injury: a systematic review and meta-analysis. Injury. 2014;45(5):819–24. Epstein DS, Mitra B, Cameron PA, Fitzgerald M, Rosenfeld JV. Acute traumatic coagulopathy in the setting of isolated traumatic brain injury: definition, incidence and outcomes. Br J Neurosurg. 2015;29(1):118–22. Cohen MJ, Brohi K, Ganter MT, Manley GT, Mackersie RC, Pittet JF. Early coagulopathy after traumatic brain injury: the role of hypoperfusion and the protein c pathway. J Trauma. 2007;63(6):1254–62. Waibel BH, Schlitzkus LL, Newell MA, Durham CA, Sagraves SG, Rotondo MF. Impact of hypothermia (below 36°C) in the rural trauma patient. J Am Coll Surg. 2009;209(5):580–8. Lapostolle F, Couvreur J, Koch FX, et al. Hypothermia in trauma victims at first arrival of ambulance personnel: an observational study with assessment of risk factors. Scand J Trauma Resusc Emerg Med. 2017;25(1):43. Perlman R, Callum J, Laflamme C, et al. A recommended early goal-directed management guideline for the prevention of hypothermia-related transfusion, morbidity, and mortality in severely injured trauma patients. Crit Care. 2016;20(1):107. Hess JR, Brohi K, Dutton RP, et al. The coagulopathy of trauma: a review of mechanisms. J Trauma Inj Infect Crit Care. 2008;65(4):748–54. Kaafarani HMA, Velmahos GC. Damage control resuscitation in trauma. Scand J Surg. 2014;103(2):81–8. Yan EB, Satgunaseelan L, Paul E, et al. Post-traumatic hypoxia is associated with prolonged cerebral cytokine production, higher serum biomarker levels, and poor outcome in patients with severe traumatic brain injury. J Neurotrauma. 2014;31(7):618–29. Davis DP, Meade W, Sise MJ, et al. Both hypoxemia and extreme hyperoxemia may be detrimental in patients with severe traumatic brain injury. J Neurotrauma. 2009;26(12):2217–23. Scherer RU, Spangenberg P. Procoagulant activity in patients with isolated severe head trauma. Crit Care Med. 1998;26(1):149–56.