The respective weights of head and extra-head injuries to the occurrence of coagulopathy following traumatic brain injury (TBI) remain unclear. We hypothesized that the severity of extra-head injuries would be the main contributor to coagulopathy following TBI. This was a retrospective study from a multicenter, prospective trauma registry. All adult patients directly admitted following TBI (Abbreviated Injury Score [AIS]) head ≥1) from 2012 to 2021 were included. Coagulopathy was defined as a prothrombin time ratio (PTr) >1.2, platelets <100 G.L-1, or fibrinogen level <1.5 g.L-1 on hospital admission. TBI severity was assessed by the Glasgow Coma Scale (GCS). Severe extracranial injuries were defined by at least one of the extra-head AIS scores ≥3 (AISextra-head ≥3). Incidences of coagulopathy were determined and compared according to TBI severity in patients with or without severe extracranial injuries. Risk factors for coagulopathy were identified using bivariate analysis and then multivariable analysis. In 9,610 TBI patients analyzed, the overall incidence of coagulopathy was 28.5% (n = 2,738). The incidence of coagulopathy increased gradually with TBI severity, from 8% for GCS 14-15% to 42% for GCS 3 in patients without severe extracranial injuries, and from 27% for GCS 14-15% to 70% for GCS 3 in patients with severe extracranial injuries. In multivariable analysis, AISextra-head ≥3 (odds ratio = 2 [1.8-2.3], p < 0.001) and GCS ≤8 (odds ratio = 1.3 [1.1-1.6], p = 0.001) were independent risk factors for coagulopathy. Coagulopathy was associated with both head and extra-head injury severities, yet to a greater extent with severe extracranial injuries.

Traumatic rhabdomyolysis (RM) is common and associated with the development of acute kidney injury and potentially with other organ dysfunctions. Thus, RM may increase the risk of death. The primary objective was to assess the effect of severe RM (Creatine Kinase [CK] > 5000 U/L) on 30-day mortality in trauma patients using a causal inference approach. In this multicenter cohort study conducted in France using a national major trauma registry (Traumabase) between January 1, 2012, and July 1, 2023, all patients admitted to a participating major trauma center hospitalized in intensive care unit (ICU) and with CK measurement were included. Confounding variables for both 30-day mortality and exposure were used to establish a propensity score. A doubly robust approach with inverse treatment weighting enabled the calculation of the average treatment effect on the treated (ATT). Analyses were performed in the overall cohort as well as in two subgroups: hemorrhagic shock subgroup (HS) and traumatic brain injury subgroup (TBI). Sensitivity analyses were conducted. Among the 8592 patients included, 1544 (18.0

INTRODUCTION:In recent years, hypocalcemia has been added to the "lethal triad" of the trauma patient, thus constituting the "lethal diamond". Nevertheless, its proper role remains debated. The aim of this study is to evaluate the association between severe hypocalcemia at admission and 24 h- transfusion requirements in severe trauma patients in a level 1 trauma center. STUDY DESIGN AND METHODS:In a monocentric retrospective observational study from January 2015 to May 2021, 137 traumatized adult patients transfused within 24 h after hospital admission was included in the study. The threshold for severe hypo ionized calcemia was ≤ 0.9 mmol/L. RESULTS:137 patients were included in the study, 23 presented with severe hypo-iCa at admission, 111 moderate hypo-iCa (0.9-1.2 mmol/L) and 3 normal iCa (≥ 1.2 mmol/L). Patients with severe hypo-iCa at admission had higher severity scores (SAPSII 58 IQR [51-70] vs. 45 IQR [32-56]; p = 0.001 and ISS 34 IQR [26-39] vs. 26 IQR [17-34]; p = 0.003). 24 h-transfusion requirements were greater for patients with severe hypo-iCa, regardless of the type of blood products transfused. There was a significant negative correlation between admission iCa and 24 h-transfusion (r = -0.45, p < 0.001). The difference in mortality was not significant between the two groups (24 h mortality: 17 % (4/23) for severe hypo-iCa vs. 8 % (9/114) for non-severe hypo-iCa; p = 0.3). DISCUSSION:This study highlights the high prevalence of severe hypocalcemia in trauma patients and its association with increased 24 h- transfusion requirements.

Abstract Background Following traumatic brain injury (TBI), coagulopathy on hospital admission is reported in 25–35% of patients and associated with increased morbimortality. The respective contributions of intracranial injury and concomitant extracranial lesions to coagulopathy have been poorly investigated. We hypothesized that the occurrence of post-TBI coagulopathy would not only be related to head injury severity, but also and to a greater extent to the presence and severity of the associated extra-cranial injuries.Methods Observational study from a multicenter prospective French trauma registry (Traumabase®). All adult patients directly admitted to one of the participating centers from January 2012 to December 2021 following TBI (AIS (Abbreviated Injury score) head ≥ 1) were included. Post-TBI coagulopathy was defined by at least 1 of the following criteria: prothrombin ratio (Quick %) < 70% or platelet count < 100 G.L− 1 or fibrinogenemia < 1.5 g.L− 1 on hospital admission. Severe associated extracranial lesions were defined by at least 1 of the extra-head AIS scores ≥ 3.Results Among 33875 patients admitted to 22 trauma centers, 9610 patients had TBI and were analyzed. The overall incidence of admission coagulopathy was 28.5%. Coagulopathic patients were significantly more severely injured and especially more severely head-injured, when compared to non-coagulopathic patients. The higher the AIShead, the higher the proportion of patients exhibiting coagulopathy (P < 0.001), whatever the presence of extracranial lesions. When compared to patients with AIShead = 1, the increased incidence of coagulopathy with TBI severity was observed at an earlier stage of TBI severity when severe extracranial lesions were present. In multivariable analysis, severe extracranial injury was independently associated with the risk of post-TBI coagulopathy (OR 2.0 (1.8–2.3), P < 0.001).Conclusions A continuously graded association between the severity of head injury and coagulopathy at hospital admission was observed, and this increased incidence of coagulopathy was observed at an earlier stage of TBI severity when severe extracranial lesions were present. The presence of severe extracranial injuries was one of the most important risk factors for coagulopathy following TBI. Intracranial and extra-cranial injury severity could be used to timely identify TBI patients most likely to present post-traumatic coagulopathy, that could benefit from early specific hemostatic resuscitation.

BACKGROUND: Traumatic rhabdomyolysis (RM) is common and contributes to the development of medical complications, of which acute renal failure is the best described. Some authors have described an association between elevated aminotransferases and RM, suggesting the possibility of associated liver damage. Our study aims to evaluate the relationship between liver function and RM in hemorrhagic trauma patients. METHODS: This is a retrospective observational study conducted in a level 1 trauma center analyzing 272 severely injured patients transfused within 24 hours and admitted to intensive care unit (ICU) from January 2015 to June 2021. Patients with significant direct liver injury (abdominal Abbreviated Injury Score [AIS] >3) were excluded. Clinical and laboratory data were reviewed, and groups were stratified according to the presence of intense RM (creatine kinase [CK] >5000 U/L). Liver failure was defined by a prothrombin time (PT)-ratio <50% and an alanine transferase (ALT) >500 U/L simultaneously. Correlation analysis was performed using Pearson’s or Spearman’s coefficient depending on the distribution after log transformation to evaluate the association between serum CK and biological markers of hepatic function. Risk factors for the development of liver failure were defined with a stepwise logistic regression analysis of all relevant explanatory factors significantly associated with the bivariate analysis. RESULTS: RM (CK >1000 U/L) was highly prevalent in the global cohort (58.1%), and 55 (23.2%) patients presented with intense RM. We found a significant positive correlation between RM biomarkers (CK and myoglobin) and liver biomarkers (aspartate transferase [AST], ALT, and bilirubin). Log-CK was positively correlated with log-AST (r = 0.625, P < .001) and log-ALT (r = 0.507, P < .001) and minimally with log-bilirubin (r = 0.262, P < .001). Intensive care unit stays were longer for intense RM patients (7 [4–18] days vs 4 [2–11] days, P < .001). These patients required increased renal replacement therapy use (4.1% vs 20.0%, P < .001) and transfusion requirements. Liver failure was more common (4.6% vs 18.2%, P < .001) for intense RM patients. It was associated with bivariate and multivariable analysis with intense RM (odds ratio [OR], 4.51 [1.11–19.2]; P = .034), need for renal replacement therapy, and Sepsis-Related Organ Failure Assessment Score (SOFA) score on day 1. CONCLUSIONS: Our study established the presence of an association between trauma-related RM and classical hepatic biomarkers. Liver failure was associated with the presence of intense RM in bivariate and multivariable analysis. Traumatic RM could have a role in the development of other system failures, specifically at the hepatic level, in addition to the already known and well-described renal failure.