Traumatic Brain Injury Associated Coagulopathy

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1 DOI /s ORIGINAL ARTICLE Traumatic Brain Injury Associated Coagulopathy Airton Leonardo de Oliveira Manoel Antonio Capone Neto Precilla V. Veigas Sandro Rizoli Ó Springer Science+Business Media New York 2014 Electronic supplementary material The online version of this article (doi: /s ) contains supplementary material, which is available to authorized users. A. L. de Oliveira Manoel (&) S. Rizoli Trauma & Neurosurgical Intensive Care Unit, St. Michael s Hospital-University of Toronto, 30 Bond Street Donnelly Wing, Room 3-074B, Toronto, ON M4N 3M5, Canada airtonleo.manoel@gmail.com A. L. de Oliveira Manoel Department of Medical Imaging, Interventional Neuroradiology, St. Michael s Hospital-University of Toronto, Toronto, ON, Canada A. C. Neto Adult Intensive Care Unit, Hospital Israelita Albert Einstein, São Paulo, Brazil P. V. Veigas Sunnybrook Health Sciences Centre, Toronto, Canada S. Rizoli St. Michael s Hospital-University of Toronto Endowed Chair in Trauma Research, Toronto, Canada Abstract Background The presence of coagulopathy is common after severe trauma. The aim of this study was to identify whether isolated severe traumatic brain injury (TBI) is an independent risk factor for coagulopathy. Methods Prospective observational cohort of adult patients admitted to a Level I Trauma Center within 6 h of injury. Patients were categorized according to the abbreviated injury scale (AIS): Group 1-isolated severe TBI (AIS head C 3 + AIS non-head < 3); Group 2-severe multisystem trauma associated with severe TBI (AIS head C 3 + AIS non-head C 3); Group 3-severe multisystem trauma without TBI (AIS head < 3 + AIS nonhead C 3). Primary outcome was the development of coagulopathy. Secondary outcome was in-hospital mortality. Results Three hundred and forty five patients were included (Group 1 = 48 patients, Group 2 = 137, and Group 3 = 160). Group 1 patients had the lowest incidence of coagulopathy and disseminated intravascular coagulopathy, and in general presented with better coagulation profile measured by either classic coagulation tests, thromboelastography or clotting factors. Isolated severe TBI was not an independent risk factor for the development of coagulopathy (OR 1.06; CI, p = 0.92), however, isolated severe TBI patients who developed coagulopathy had higher mortality rates than isolated severe TBI patients without coagulopathy (66 vs %, p < 0.05). The presence of coagulopathy (OR 5.61; CI, p < ) and isolated severe TBI (OR 11.51; CI, p < ) were independent risk factors for in-hospital mortality. Conclusion Isolated severe TBI is not an independent risk factor for the development of coagulopathy. However, severe TBI patients who develop coagulopathy have extremely high mortality rates. Keywords Traumatic brain injury Abbreviated injury scale score Trauma-coagulopathy DIC Introduction Traumatic brain injury (TBI) remains the leading cause of death and long-term disability in young adults [1], and the majority of deaths occur in the first day after trauma [2]. The presence of coagulopathy is relatively common early

2 in the course of isolated blunt and penetrating severe TBI [3], although the incidence of these derangements remains not clearly defined, with a broad range reported from 10 to 97.3 % [4]. Despite of the controversy on the incidence of TBI-induced coagulopathy, the presence of coagulopathy in a setting of acute brain injury is associated with progression of hemorrhagic lesions [5 7] and with increased rates of disability and mortality [4, 8, 9]. The mechanisms involved in pathophysiology of TBIinduced coagulopathy remain not fully understood, but is thought to be mediated by the increased release of tissue factor (TF) [10 12], the development of disseminated intravascular coagulation (DIC) [13 15], thrombocytopenia or platelets dysfunction [16 19], and the activation of protein C pathways in a setting of tissue hypoperfusion (i.e., increased base deficit [BD]), recently called acute coagulopathy of trauma-shock (ACoTS) [20, 21]. Although some studies demonstrated higher levels of TF in patients with isolated severe blunt TBI when compared to patients with severe multisystem trauma without head injury [11], others showed that TBI-induced coagulopathy is not different from trauma coagulopathy [20, 22]. The question remains whether isolated blunt severe TBI is an independent risk factor for the development of coagulopathy, including DIC. Therefore, the aim of the present study was to examine the coagulation reaction to isolated blunt severe TBI when compared to severe multisystem trauma with or without head injury, assessed by classic coagulation tests, thromboelastography (TEG), and advanced coagulation assays (e.g., coagulation factors). Methods Study Design We conducted a post hoc analysis of a large prospective observational cohort study of coagulation profile in adult trauma patients. The original cohort was conducted between February and October 2007 at a Level I Trauma Center of the University of Toronto in Canada. Patient Selection Adult trauma patients (age C 16) admitted within 6 h of injury, with an Injury severity score (ISS) C 16 were considered eligible and included in the study. Patients with penetrating head trauma, known history of coagulation disorder, or on anticoagulants were excluded. Patients were divided into three different groups according to the abbreviated injury scale (AIS-Table S1 supplement). The Group 1 consisted of patients with isolated blunt severe TBI (AIS head > 3 + AIS non-head < 3). Group 2 compromised of patients with severe multisystem trauma associated with severe TBI (AIS head > 3 + AIS nonhead > 3). Group 3 included patients with severe multisystem trauma without head injury (AIS head < 3 + AIS non-head > 3). Outcomes The primary outcome was the development of coagulopathy or DIC. Secondary outcome included coagulation derangements assessed by TEG or clotting factors assay, and in-hospital mortality. Sample Analysis Study blood samples were collected for special coagulation assays, and for TEG along with routine coagulation blood work including international normalized ratio (INR), activated partial thromboplastin time (aptt), platelets, and fibrinogen. The extra study blood tubes were drawn with every routine coagulation blood work over the first 48 h of hospital admission. The analysis considered the most abnormal results which were blinded to all professionals involved in patient s care. Coagulopathy Coagulopathy was defined as an INR > 1.5, and/or aptt > 60 s and/or platelet count < /mm 3. Additional coagulation tests were considered abnormal as following: fibrinogen < 1.0 g/l, any clotting factor < 0.5 (<50 % activity). Abnormal TEG Ò parameters: R > 8, K > 3, alpha < 55, MA < 51. Thromboelastography Thromboelastography blood samples were collected on tubes containing citrate, which was added to improve the precision of the TEG Ò -R measurement. Without anticoagulation, the clotting process would start immediately after collection and any delays in transferring the sample to the TEG machine would affect the precision of the R parameter measurement. TEG Ò 5000 Hemostasis Analyzer (Haemoscope Corporation, Illinois USA) was used for this assay. Briefly, citrated blood samples were kept at room temperature for 40 min from the time of collection as recommended [19]. Five hundred micro liters of the citrated whole blood was transferred to a vial containing buffered stabilizers and phospholipids (Kaolin Ò ); 340 ll was then transferred to a 37 C pre-warmed disposable cup containing 20 ll of calcium chloride and the measurement

3 continued for no less than 40 min to complete the whole TEG exam. Clotting Factors (CF) Assay Clotting factors (CF) assay blood samples were centrifuged (1,700g for 15 min at 4 C); plasma separated and centrifuged for another 5 min to ensures platelet free plasma (< /L). Double spun plasma was frozen at -70 C until analysis by the Hemostasis Reference Laboratory of the McMaster University in Hamilton, Canada. Extrinsic CF activity assays were performed by mixing plasma with controls deficient in extrinsic factors (Precision BioLogics). The degree of correction of the PT (Dade- Behring Innovin) is proportional to the level of the factor in the plasma. The intrinsic factor assays were done in a similar way using plasma deficient in intrinsic factors and aptt degree of correction. Clotting factors were considered critically low if their activity was B50 % as previously described [25]. Lastly, overt disseminated intravascular coagulopathy (DIC) was defined according to the International Society for Thrombosis and Hemostasis (ISTH) (Table S2 supplement). Data Collection Prospective data were collected on patient demographics, including age, gender, the time interval between injury and hospital arrival (i.e., elapse time), Glasgow coma scale (GCS), and the severity of tissue injury (ISS). Hemoglobin and platelets levels, arterial blood gases, INR, aptt, and fibrinogen were drawn along with the research sample as part of the standard of care. A BD greater than 6 at hospital admission was used as a measure of tissue hypoperfusion [23, 24], because it has been recognized as prognostic marker after major trauma [25]. Patients were followed until death or hospital discharge, and were considered alive for mortality analysis if alive at hospital discharge. Statistical Analysis Continuous variables were reported as means and standard deviations, and compared using t test or Wilcoxon ranksum test. Discrete variables were summarized using frequencies and percentages, and the differences were tested by X 2 or Fisher s exact test. The study was approved by the Hospital Research Ethics Board and informed consent was obtained from all patients or substitute decision makers for participation in the original study. All p-values are twotailed, and p-values <0.05 were considered statistically significant. Logistic regression models using coagulopathy, DIC and in-hospital mortality as outcome measures were designed, including age, severity of trauma (ISS), and the presence or absence of tissue hypoperfusion. The first model used coagulopathy as outcome and was calculated excluding the patients without tissue hypoperfusion data. The same model was also calculated imputing those patients as normal (absence of hypoperfusion). The second model used DIC as outcome and managed the missing data in the same way. The last model was calculated using in-hospital mortality as outcome. This last model had no missing data. Results Baseline Characteristics In total, 345 patients fulfilled the inclusion criteria to the present study (Table 1). Forty-eight patients presented with isolated severe TBI (Group 1), 137 with severe TBI associated with multisystem trauma (Group 2), and 160 with multisystem trauma without head injury (Group 3). There was no difference across the groups in terms of age or time from injury to hospital admission (elapsed time). Group 1 patients had the highest percentage of alcohol intoxication and the highest hemoglobin level at admission. Group 2 had the lowest percentage of male adults and the highest ISS score. Group 1 and 2 patients had the lowest GCS at hospital admission, the highest Abbreviated Injury Score (AIS) head, which was translated into the highest in-hospital mortality when compared to Group 3 patients. Additionally, Group 1 patients had less signs of tissue hypoperfusion, as illustrated by the highest ph and the lowest BD levels. However, the three groups had similar lactate levels (Table 1). Coagulation Profile and Disseminated Intravascular Coagulation (DIC) Eighty-four patients developed coagulopathy, present at admission or evolved within 48 h of arrival. Of those patients, six were in Group 1, 42 in Group 2, and 36 in Group 3. Group 1 patients had the lowest incidence of coagulopathy and DIC (Table 1). In general, the Group 1 patients presented with better coagulation profile measured by either classic coagulation tests, clotting factors or TEG (Table 2). The coagulation results will be presented from a classic point of view, followed by the TEG and finally the results of advanced coagulation tests following the modern approach to the coagulation cascade (Fig. 1): initiation, amplification, propagation, and fibrinolysis.

4 Table 1 Baseline characteristics Group 1 (n = 48) Group 2 (n = 137) Group 3 (n = 160) p value Age 39 ± ± ± 17.4 NS Male gender 79 % 63.5 % 72.5 % p < 0.05 a Elapsed time 2.32 ± ± ± 1.63 NS ISS 21.2 ± ± ± 7 p < 0.05 a,b AIS head 4.2 ± ± ± 0.98 p < 0.05 b,c GCS 7 ± 4 8 ± 5 14 ± 3 p < 0.05 b,c Alcohol 42 % 12 % 25 % p < 0.05 a,b,c Hemoglobin ± ± ± 28.2 p < 0.05 a,c ph 7.31 ± ± ± 0.14 p < 0.05 a,c BD 5.24 ± ± ± 5.6 p < 0.05 a Lactate 3.80 ± ± ± 3.1 NS Mortality 11 (22.9) 29 (21.2) 10 (6.25) p < 0.05 b,c Coagulolpathy 6 (12.5) 42 (30.5) 36 (22.5) p < 0.05 a DIC 3 (6.25) 19 (13.9) 18 (11.2) p < 0.05 a Baseline characteristics of the patients who developed coagulopathy, defined as an INR > 1.5, and/or aptt > 60s and/or platelet count < 100 x 103/mm3 Group 1 (n = 6) Group 2 (n = 42) Group 3 (n = 36) p-value Age 59.6 ± ± ± 18.2 p < 0.05 b,c Male sex 50 % 66 % 83 % p < 0.05 b,c Elapsed time 2 ± ± ± 1.2 NS ISS 25.8 ± ± ± 9 p < 0.05 a,b AIS head 4.6 ± ± ± 1 p < 0.05 b,c GCS 5.5 ± ± ± 5 p < 0.05 b,c Hemoglobin 82.5 ± ± ± 22.3 NS ph 7.30 ± ± ± 0.18 p < 0.05 c BD 9.4 ± ± ± 7.2 NS Lactate 5.1 ± ± ± 3.66 p < 0.05 b Mortality 4 (66) 20 (47.6) 7 (19.4) p < 0.05 b,c Continuous variables were reported as means ± standard deviations, and compared using t test or Wilcoxon rank-sum test. Discrete variables were summarized using percentages [n (%)] and the differences were tested by X 2 or Fisher s exact test. All p-values are two-tailed, and p-values <0.05 were considered statistically significant Elapsed time (in hours) time from trauma to admission a Group 1 versus Group 2, p < 0.05 b Group 2 versus Group 3, p < 0.05 c Group 1 versus Group 3, p < 0.05 Classic Coagulation Tests Group 1 patients presented overall with better coagulation profile by classic coagulation tests including INR, aptt, platelets, and fibrinogen levels. This Group had the lowest INR and aptt level, as well as the highest platelet count. More importantly, in the subgroup of patients who developed coagulopathy (Table 3), coagulopathic Group 1 patients displayed the lowest INR and aptt levels. Although, thrombocytopenia was not common among Group 1 patients, six patients in this group had low platelet levels, with a mean value of 99,000/mm 3. Group 3 patients had the worst derangements in the coagulation profile by classic tests followed by Group 2 patients, as shown in Table 3. Thromboelastography (TEG) From a TEG stand point of view, the three groups looked alike. Except from the difference in the TEG-R between Group 1 and 2, all the other TEG parameters did not differ statistically among the three groups. Interestingly, in the overall group of patients (Table 2), no abnormalities in the mean values were detected. In the subgroup of patients who developed coagulopathy (Table 3), we noticed abnormalities

5 Table 2 Coagulation profile of the entire cohort Group 1 (n = 48) Group 2 (n = 137) Group 3 (n = 160) p-value Classic coagulation tests INR (normal: <1.5) 1.17 ± ± ± 2.4 p < 0.05 a,c aptt (normal: <60 s) 34.3 ± ± ± 29.9 NS Platelets (normal: >100) 207 ± ± ± 96 p < 0.05 a Fibrinogen (normal: >1.0) 2.33 ± ± ± 0.95 NS Thromboelastography TEG-R (min) (normal: 3 8) 5.57 ± ± ± 11.9 p < 0.05 a TEG-K (min) (normal: 1 3) 3.87 ± ± ± 2.35 NS TEG-Alpha (degree) (Normal: 55 78) 57 ± ± ± 16.3 NS TEG-MA (mm) (normal: 51 69) 55.6 ± ± ± 14.1 NS TEG-Lys30 (%) (normal: 0 8) 2.72 ± ± ± 10.1 NS Coagulation Initiation Tissue factor (pg/ml) 0.13 ± ± ± 0.34 NS TFPI (ng/ml) (normal: ) 90.1 ± ± ± 26 p < 0.05 a,c Clotting factors F II 0.76 ± ± ± 0.23 p < 0.05 a F V 0.57 ± ± ± 0.33 p < 0.05 a,b F VII 0.89 ± ± ± 0.62 NS F VIII 1.23 ± ± ± 0.98 p < 0.05 b,c F IX 1.09 ± ± ± 0.39 NS F X 0.92 ± ± ± 0.29 p < 0.05 a,b F XI 0.80 ± ± ± 0.4 NS F XII 0.83 ± ± ± 0.4 NS Suppression of fibrinolysis PAI-1 (ng/ml) (normal: 4 40) 63.5 ± ± ± 47.1 NS TAFI (%) 6.76 ± ± ± 2.15 p < 0.05 b Fibrinolysis Plasminogen 0.78 ± ± 0.26* 0.75 ± 0.25 p < 0.05 a,b tpa Ag (ng/ml) (normal: ) 10.7 ± ± ± 11 NS Fibrinolysis biomarkers D-Dimer (ng/ml) (normal: 0 400) 5,998 ± 2,339 6,951 ± 1,547 5,283 ± 2,644 p < 0.05 b Prothrombin fragment ,788 ± 765 1,720 ± 685 1,370 ± 769 p < 0.05 b,c Continuous variables were reported as means ± standard deviations, and compared using t test or Wilcoxon rank-sum test. Discrete variables were summarized using percentages and the differences were tested by X 2 or Fisher s exact test. All p-values are two-tailed, and p-values <0.05 were considered statistically significant R time to initial fibrin formation, K time to clot formation, a alpha angle, rate of clot formation, MA maximum amplitude, absolute clot strength, LY30 fibrinolysis at 30 min after MA a Group 1 versus Group 2, p < 0.05 b Group 2 versus Group 3, p < 0.05 c Group 1 versus Group 3, p < 0.05 across all the TEG parameters in all three groups, from fibrin formation (R) to the fibrinolysis phase. However, the mean values did not differ statistically among the groups. Clotting Factors (Fig. 1) Initiation phase (TFPI, TF, FII, FVII, FV, FX, FIX)-TF pathway inhibitor (TFPI) was overall high in all three groups, including the subgroup of coagulopathic patients. Group 1 had statistically highest levels of TFPI. Interestingly, apart from FV, no other clotting factors were found to be below 0.5 (<50 % activity) taking the entire cohort into account. Group 2 patients were the only group to present with FV activity below 50 %. Among the patients who developed coagulopathy, FV was the only factor found to be below critical levels (<30 % activity) in all

6 Fig. 1 Modern view of coagulation cascade. a) Initiation phase: the presentation of tissue factor (TF) in an injured vessel wall by TFbearing cells (e.g., monocytes and fibroblasts) is the main step to initiate coagulation. TF is a receptor and cofactor for FVII. By binding to TF, FVII is rapidly activated. This first step from TF presentation to the formation of FVIIa/TF complex is known as the initiation phase. The FVIIa/TF complex is responsible for the activation of FX and FIX. Activated FX along with activated FV are responsible for a small conversion of prothrombin into thrombin three groups (Table 3). Amplification phase (FV, FVIII, FXI)-the levels of FVIII were above 100 % in all groups. Group 3 had higher levels, including in the subgroup of coagulopathic patients. No difference in FXI levels was found. Propagation phase (FIX, FX)-coagulation factors responsible for the propagation of coagulation cascade were in normal range. Fibrinolysis/Anti-fibrinolysis (PAI-1, TAFI)-levels of plasminogen activator inhibitor (PAI-1) were increased across the three groups, including the subgroup of coagulopathic patients. However, the Group 1 of coagulopathic patients had the lowest levels of PAI-1, but in the normal range. Thrombin activatable fibrinolytic inhibitor (TAFI) was overall decreased in all three groups. Fibrinolysis (tpa Ag and plasminogen)-tissue plasminogen activator (tpa) and plasminogen levels were similar across the three groups, and in the normal ranges. However, tpa levels were high in all three groups of patients with coagulopathy. Markers of fibrinolysis: The mean D-dimer on the TF-bearing cells surface in this initial phase. b) Amplification phase: this second phase consists on the activation of platelets and coagulation factors on platelets surface. c) Propagation phase: by activating platelets and their surface coagulation factors, the coagulation process moves to its last step when the largest amount of prothombin will be converted to thrombin on the platelets surface, process known as propagation. Those three steps are fundamental to achieve the ultimate goal of hemostasis, which consist on the formation of a fibrin and platelet clot. d) Fibrinolysis levels were extremely elevated in the overall groups, including the subgroup of coagulopathic patients. Group 2 patients displayed the highest values. Group 3 patients had the lowest PF levels, while Group 1 patients who developed coagulopathy had the highest levels. Logistic Regression Models (Table 4) In the logistic regression model including age, ISS, and the presence or absence of tissue hypoperfusion, isolated severe TBI was not an independent factor for the development of either coagulopathy (OR 1.06; CI, p = 0.92) or DIC (p = 0.32). In this model, the ISS and the presence of hypoperfusion were both independent factors for the development of coagulopathy, while coagulopathy and ISS were independent factors for the development of DIC, but not hypoperfusion. The development of coagulopathy was associated with the increased

7 Table 3 Coagulation profile of the patients who developed coagulopathy, defined as an INR >1.5, and/or aptt >60 s, and/or platelet count < /mm 3 Group 1 (n = 6) Group 2 (n = 42) Group 3 (n = 36) p-value Classic coagulation tests INR (normal: <1.5) 1.5 ± ± ± 4.6 p < 0.05 a,c aptt (normal: <60 s) 56.3 ± ± ± 47.7 p < 0.05 c Platelets (normal: >100) 99 ± ± ± 47 p < 0.05 b Fibrinogen (normal: >1.0) 1.37 ± ± ± 0.7 NS Thromboelastography TEG-R (min) (Normal: 3 8) 7.9 ± ± ± 24.6 NS TEG-K (min) (Normal: 1 3) 10.3 ± 9,8 5.4 ± ± 4.1 NS TEG-Alpha (degree) (Normal: 55 78) 35.9 ± ± ± 21.9 NS TEG-MA (mm) (Normal: 51 69) 33.1 ± ± ± 18.8 NS TEG-Lys30 (%) (Normal: 0 8) 14.5 ± ± ± 21.4 NS Coagulation initiation Tissue factor (pg/ml) 0.18 ± ± ± 0.4 NS TFPI (ng/ml) (Normal: ) 98.8 ± ± ± 41.8 NS Clotting factors F II 0.47 ± ± ± 0.25 NS F V 0.16 ± ± ± 0.27 NS F VII 0.91 ± ± ± 0.23 NS F VIII 0.55 ± ± ± 1.3 NS F IX 0.99 ± ± ± 0.45 NS F X 0.64 ± ± ± 0.27 NS F XI 0.59 ± ± ± 0.58 NS F XII 0.55 ± ± ± 0.38 NS Suppression of fibrinolysis PAI-1 (ng/ml) (Normal: 4 40) 49.7 ± ± ± 60.4 p < 0.05 a,c TAFI (%) 4.7 ± ± ± 2 NS Fibrinolysis Plasminogen 0.35 ± ± ± 0.23 NS tpa Ag (ng/ml) (Normal: ) 23.8 ± ± ± 14.6 NS Fibrinolysis biomarkers D-Dimer (ng/ml) (normal: 0 400) 6,707 ± 1,477 7,455 ± 434 6,413 ± 1,972 p < 0.05 b Prothrombin fragment ,401 ± 0 1,980 ± 580 1,613 ± 633 p < 0.05 a,c Continuous variables were reported as means ± standard deviations, and compared using t test or Wilcoxon rank-sum test. Discrete variables were summarized using percentages and the differences were tested by X 2 or Fisher s exact test. All p-values are two-tailed, and p-values <0.05 were considered statistically significant R time to initial fibrin formation, K time to clot formation, a alpha angle, rate of clot formation, MA maximum amplitude, absolute clot strength, LY30 fibrinolysis at 30 min after MA a Group 1 versus Group 2, p < 0.05 b Group 2 versus Group 3, p < 0.05 c Group 1 versus Group 3, p < 0.05 odds ratio of DCI [95 %CI ( ); p < ]. In-hospital Mortality In total, 50 patients died, which represents 14.5 % of the entire cohort. The highest mortality rate was found among Group 1 patients who developed coagulopathy (66 %). In general, patients with severe TBI (Groups 1 and 2) had higher mortality rates when compared to Group 3 patients (21.6 vs %, p < 0.05). Although, Group 1 patients developed less commonly coagulopathy, the mortality among coagulopathic Group 1 patients was statistically higher than Group 1 patients with normal coagulation profile (66 vs %, p < 0.05). Also, when compared to Group 3 patients, the head-injured patients who developed

8 Table 4 Logistic regression models Logistic regression with coagulopathy as an outcome (n = 283; excluding 62 patients with missing data regarding tissue hypoperfusion) Variable Odds ratio (CI) p-value Age ( ) ISS 1.07 ( ) < Group overall Group 1 versus Group ( ) Group 1 versus Group ( ) Group 3 versus Group ( ) Tissue hypoperfusion 3.72 ( ) Logistic regression with coagulopathy as an outcome (n = 345; 62 patients with missing data regarding tissue hypoperfusion were assumed to be normal) Age ( ) ISS 1.07 ( ) < Group overall Group 1 versus Group ( ) Group 1 versus Group ( ) Group 3 versus Group ( ) Logistic regression with DIC as an outcome (n = 283; excluding 62 patients with missing data regarding tissue hypoperfusion) Age 0.99 ( ) ISS 1.07 ( ) Coagulopathy ( ) < Group overall any difference between any 2 groups Tissue hypoperfusion 3.63 ( ) Logistic regression with DIC as an outcome(n = 345; 62 patients with missing data regarding tissue hypoperfusion were assumed to be normal) Age 0.98 ( ) ISS 1.07 ( ) Coagulopathy ( ) < Group overall-any difference between any 2 groups Tissue hypoperfusion 3.14 ( ) Univariate logistic regression for in-hospital mortality Coagulopathy 8.49 ( ) < Group overall Group 1 versus Group ( ) Group 3 versus Group ( ) Group 1 versus Group ( ) Multivariate logistic regression for in-hospital mortality Coagulopathy 5.61 ( ) < Group overall < Group 1 versus Group ( ) Group 3 versus Group ( ) Group 1 versus Group ( ) < ISS ( ) <0.0001

9 coagulopathy combined (Groups 1 and 2), had extremely higher mortality rates (19 vs. 50 %, p < 0.05). In the univariate logistic regression model, the presence of isolated severe TBI had an OR of 7.6 for in-hospital mortality, when compared to patients with multisystem trauma without head injury. In the multivariate logistic regression model, the presence of coagulopathy, and isolated severe TBI were independent risk factors for inhospital mortality, when adjusted for ISS. Group 1 patients had ( CI, p < ) higher OR to die in hospital, when compared to Group 3 patients. Discussion This is the largest cohort of trauma patients to date to examine the role of severe TBI in the development of coagulopathy. We performed a comprehensive coagulation evaluation by means of classic tests associated with TEG, and advanced laboratory analysis, which included the measurement of coagulation factors and biomarkers of all phases of the hemostatic cascade (Fig. 1-initiation, amplification, propagation, and fibrinolysis). Our main finding suggests that patients with isolated blunt severe TBI do not differ from multisystem trauma patients with or without TBI from a coagulation stand point of view, even by the use of advanced laboratorial analysis. Our results support the concept that ACoTS is dependent on the severity of injury (ISS) [26 28] rather than the type of tissue damaged, and on the presence of tissue hypoperfusion [29]. Similarly to previous reports [20], in our large cohort patients with isolated blunt severe TBI developed coagulopathy only in a setting of tissue hypoperfusion, characterized by the laboratory findings of decreased basic deficits and arterial ph, and increased lactate levels (Table 1). Multiple mechanisms have been proposed as the pathophysiology of TBI-induced coagulopathy. In the early 1970 s Keimowitz and Annis [11] reported a case of DIC secondary to massive brain trauma. Likewise, Goodnight et al. [10] in a prospective study showed that 9 out 13 patients with brain tissue damage had signs of coagulopathy by means of low fibrinogen levels associated with increased levels of serum fibrinogen-related or fibrin-related antigen and low levels of factors V, VIII or platelets. Both pioneer studies suggested that the condition was caused by the release of TF into the circulation, activation of extrinsic pathway, and secondary consumption coagulopathy. Our results challenge the TF hypothesis, because TF levels were similar in all three groups, regardless the presence of coagulopathy. Hyperfibrinolysis is a second proposed mechanism. Two possible explanations emerge from the hyperfibrinolytic theory: the release of TF into the circulation is believed to over activate the extrinsic pathway (i.e., the increased endogenous fibrinolysis), represented by the elevation of tpa, fibrin degradation products, and decrease of depletion of a-2 plasmin inhibitor [30, 31]. Our results do not support the hyperfibrinolysis hypothesis, because patients with isolated blunt severe TBI (Group 1) did not differ from the other two groups in terms of tpa levels, fibrinogen degradation products (e.g., D-dimer, PF 1 + 2), or reduced plasminogen activator inhibitor-1 (PAI-1) levels. A third mechanism introduces the role of platelets into the pathophysiology of TBI-induced coagulopathy. Schnüriger et al. [17]. in a retrospective study of 310 patients with isolated severe TBI showed that platelet level below 100,000/mm 3 was associated with a ninefold increased risk of death (OR [95 % CI]: 9.5 [ ]; adjusted p = 0.029). Additionally, patients with platelet count below 175,000/mm 3 were at higher risk for hematoma expansion, need for craniotomy and death. Carrick et al., who found that patients with moderate and severe TBI were at risk of developing progressive thrombocytopenia, corroborated these findings. The authors showed that 46 % of TBI patients had low platelet count by day 3, and more strikingly 67 % of patients who died presented thrombocytopenia [16]. Likewise, platelets dysfunction assessed by modified TEG has been shown to be present after isolated TBI, which could contribute to hemorrhagic complications [18]. Thrombocytopenia was not a common finding in the Group 1 patients, presented only in six patients (12.5 %) with a mean platelet level of 99,000 ± 39.5/mm 3. Although, patients who developed coagulopathy had TEG abnormalities in clot formation time (K), alpha angle, maximal amplitude (MA) representing thrombocytopenia/ platelet dysfunction, these derangements were not statistically significant among the three groups. Interestingly, the coagulation derangements in Group 3 patients (multisystem trauma without TBI) were more profound when compared to Group 1 patients, including thrombocytopenia (Table 3). However, despite of the higher platelet, INR and aptt levels, the mortality among TBI patients (Groups 1 and 2) who developed coagulopathy was more than the double of patients without head injury (Table 1). The last mechanism believed to play a role in the development of coagulopathy after isolated TBI is the ACoTS and the activation of the Protein C pathway. The classic triad of death (coagulopathy, hypothermia, and acidosis) has been challenged in the recent years by some studies demonstrating that severe trauma can induce clinically significant early coagulopathy not related to the abovementioned triad [21]. In the new model, early coagulopathy can be present on hospital arrival regardless of fluid administration, clotting factor depletion or hypothermia. It is postulated that in the presence of tissue hypoperfusion, the endothelium expresses thrombomodulin, which activates

10 the protein C pathway. Activated protein C decreases plasminogen activator inhibitor (PAI-1) levels, increases tpa, leading with hyperfibrinolysis [29]. Although, protein C and soluble thrombomodulin levels were not measured in our cohort, and PAI-1 levels were in the normal range in the three groups, the development of coagulopathy was only present in the presence of tissue hypoperfusion (Table 1), which supports the concept of ACoTS [29]. Lastly, similar to smaller studies [22, 32], our large cohort showed that patients with TBI associated with multisystem trauma (Group 2) were more severely injured (i.e., higher ISS), which was translated into a higher incidence of coagulopathy, DIC, and higher mortality. However, isolated blunt severe TBI was associated with an odds ratio of ( CI, p < ) for in-hospital mortality. Additionally, our findings are supported by Genét et al. [32]., which showed in a prospective cohort of 80 trauma patients that isolated TBI and multisystem trauma patients do not differ in term of coagulation parameters. Despite of the fact that isolated severe blunt TBI was not an independent factor for the development of coagulopathy, 50 % of TBI patients who developed coagulopathy died (Group 1 + Group 2), which was more the two times the mortality rate of coagulopathic patients without head injury (Group 3). Conclusion We found that isolated severe TBI is not an independent risk factor for the development of coagulopathy, including DIC. No differences in the pathophysiologic mechanisms of trauma-induced coagulopathy among patients with or without TBI were found. However, severe TBI patients who develop coagulopathy in the course of the disease have extremely high mortality rates. Acknowledgments SB.R. received a salary award from the Canadian Institute of Health Research/NovoNordisk, honoraria and speaking fees from NovoNordisk. Conflict of interest disclose. References None of the authors have conflict of interest to 1. Boto GR, Gómez PA, De La Cruz J, Lobato RD. Severe head injury and the risk of early death. J Neurol Neurosurg Psychiatry. 2006;77: Shackford SR, Mackersie RC, Holbrook TL, et al. The epidemiology of traumatic death: a population-based analysis. Arch Surg. 1993;128: Lustenberger T, Talving P, Kobayashi L, et al. Early coagulopathy after isolated severe traumatic brain injury: relationship with hypoperfusion challenged. J Trauma. 2010;69: Harhangi BS, Kompanje EJO, Leebeek FWG, Maas AIR. Coagulation disorders after traumatic brain injury. Acta Neurochir. 2008;150: discussion Oertel M, Kelly DF, McArthur D, et al. Progressive hemorrhage after head trauma: predictors and consequences of the evolving injury. J Neurosurg. 2002;96: Allard CB, Scarpelini S, Rhind SG, et al. Abnormal coagulation tests are associated with progression of traumatic intracranial hemorrhage. J Trauma. 2009;67: Tian H-L, Chen H, Wu B-S, et al. D-dimer as a predictor of progressive hemorrhagic injury in patients with traumatic brain injury: analysis of 194 cases. Neurosurg Rev. 2010;33: discussion Talving P, Benfield R, Hadjizacharia P, Inaba K, Chan LS, Demetriades D. Coagulopathy in severe traumatic brain injury: a prospective study. J Trauma. 2009;66:55 61 discussion Wafaisade A, Lefering R, Tjardes T, et al. Acute coagulopathy in isolated blunt traumatic brain injury. Neurocrit Care. 2009; 12: Goodnight SH, Kenoyer G, Rapaport SI, Patch MJ, Lee JA, Kurze T. Defibrination after brain-tissue destruction: a serious complication of head injury. N Engl J Med. 1974;290(19): Keimowitz RM, Annis BL. Disseminated intravascular coagulation associated with massive brain injury. J Neurosurg. 1973;39: Scherer RU, Spangenberg P. Procoagulant activity in patients with isolated severe head trauma. Crit Care Med. 1998;26: Stein SC, Smith DH. Coagulopathy in traumatic brain injury. Neurocrit Care. 2004;1: Stein SC, Chen XH, Sinson GP, Smith DH. Intravascular coagulation: a major secondary insult in nonfatal traumatic brain injury. J Neurosurg. 2002;97: Hulka FF, Mullins RJR, Frank EHE. Blunt brain injury activates the coagulation process. Arch Surg. 1996;131:923 7 discussion Carrick MM, Tyroch AH, Youens CA, Handley T. Subsequent development of thrombocytopenia and coagulopathy in moderate and severe head injury: support for serial laboratory examination. J Trauma. 2005;58:725 9 discussion Schnüriger B, Inaba K, Abdelsayed GA, et al. The impact of platelets on the progression of traumatic intracranial hemorrhage. J Trauma. 2010;68: Nekludov M, Bellander B-M, Blombäck M, Wallen HN. Platelet dysfunction in patients with severe traumatic brain injury. J Neurotrauma. 2007;24: Engstrom M, Romner B, Schalen W, Reinstrup P. Thrombocytopenia predicts progressive hemorrhage after head trauma. J Neurotrauma. 2005;22: Cohen MJ, Brohi K, Ganter MT, Manley GT, Mackersie RC, Pittet J-F. Early coagulopathy after traumatic brain injury: the role of hypoperfusion and the protein c pathway. J Trauma. 2007;63: discussion Frith D, Brohi K. The acute coagulopathy of trauma shock: clinical relevance. Surgeon. 2010;8: Gando S, Nanzaki S, Kemmotsu O. Coagulofibrinolytic changes after isolated head injury are not different from those in trauma patients without head injury. J Trauma. 1999;46: discussion Rutherford EJ, Morris JA, Reed GW, Hall KS. Base deficit stratifies mortality and determines therapy. J Trauma. 1992; 33: Davis JW, Shackford SR, Holbrook TL. Base deficit as a sensitive indicator of compensated shock and tissue oxygen utilization. Surg Gynecol Obstet. 1991;173:473 6.

11 25. Davis JW, Parks SN, Kaups KL, Gladen HE, O Donnell-Nicol S. Admission base deficit predicts transfusion requirements and risk of complications. J Trauma. 1996;41: Frith D, Goslings JC, Gaarder C, et al. Definition and drivers of acute traumatic coagulopathy: clinical and experimental investigations. J Thromb Haemost. 2010;8: Brohi K, Singh J, Heron M, Coats T. Acute Traumatic Coagulopathy. J Trauma. 2003;54: Maegele M, Lefering R, Yucel N, et al. Early coagulopathy in multiple injury: an analysis from the German trauma registry on 8724 patients. Injury. 2007;38: Brohi K, Cohen MJ, Ganter MT, Matthay MA, Mackersie RC, Pittet J-FO. Acute traumatic coagulopathy: initiated by hypoperfusion. Ann Surg. 2007;245: Kushimoto S, Shibata Y, Yamamoto Y. Implications of fibrinogenolysis in patients with closed head injury. J Neurotrauma. 2003;20: Kushimoto S, Yamamoto Y, Shibata Y, Sato H, Koido Y. Implications of excessive fibrinolysis and alpha(2)-plasmin inhibitor deficiency in patients with severe head injury. Neurosurgery. 2001;49: Genét GF, Johansson PI, Meyer MAS, et al. Trauma-induced coagulopathy: standard coagulation tests, biomarkers of coagulopathy, and endothelial damage in patients with traumatic brain injury. J Neurotrauma. 2013;15(30):301 6.

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