Critical traumatic brain injury is associated with worse coagulopathy

Cucher, Daniel; Harmon, Laura; Myer, Brian S; Ngyuen, Andrew; Rankin, Timothy M.; Cook, Alan; Hu, Charles; Tesoriero, Ronald; Scalea, Thomas M.; Stein, Deborah M.

doi:10.1097/ta.0000000000003253

Cited by 15 publications

(9 citation statements)

References 21 publications

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“…2), suggesting that the platelet, an essential hemostatic ingredient, may contribute to thrombosis. It was recently demonstrated that critical TBI correlates with a signi cant worsening of traumatic coagulopathy in comparison with moderate/severe TBI [72]. Surprisingly, even our patients were severely injured, all the coagulation pro le was undistinguishable between the patients with and without DVT (Fig.…”

Section: Discussionmentioning

confidence: 59%

Prognostic Significance of Plasma Insulin Level for Deep Venous Thrombosis in Patients with Severe Traumatic Brain Injury in Critical Care

Zhang

Tang

et al. 2022

Neurocrit Care

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Background:Whether insulin resistance is underlying the deep venous thrombosis (DVT) development in patients with traumatic brain injury (TBI) is elusive. To associate kinetics of plasma insulin level in patients with TBI with developing DVT in ICU. Methods:A prospective observational study of 73 patients with TBI who had measurements of insulin, glucose, glucagon-like peptide 1 (GLP-1), in ammatory factors, and hematological pro le within 4 preset time periods during the 14 days after TBI. Ultrasonic surveillance of DVT was tracked weekly for time-to-event analyses. Two-way ANOVA analysis was applied to determine whether the above factors could discriminate between patients with and without DVT, or with and without insulin therapy. Partial correlations of insulin level with all the variables were carried out separately in patients with or without DVT. Factors associated with DVT were analyzed by multivariable logistic regression. Neurological outcome 6 months after TBI was assessed for Glasgow Outcome Scale (GOS).Results:Among patients with an average (SD) age of 53±16 years, DVT developed in 20 (27%) on mean (median) TBI day 10±8. The 14-day insulin levels were higher in patients with DVT (P=0.01). Platelet pro le discriminated signi cantly between patients with and without DVT. Surprisingly, none of other factors differed between the two groups. Patients with insulin therapy had signi cant higher insulin (P=0.006), glucose (P<0.001) and GLP-1 (P=0.01) levels, and were more likely to develop DVT (60% vs. 15%, P<0.001) with concomitant platelet depletion. Insulin levels correlated with glucose, GLP-1 levels, and platelet count exclusively in patients without DVT. Conversely, in patients with DVT, insulin correlated negatively with GLP-1 level (r=-0.297, P=0.016). Age (P=0.01) and elevated insulin level at day 4-7 (P=0.04) were independently associated with DVT. Patients with insulin therapy also showed worse GOS (P=0.001). Conclusions:Elevated insulin level in the rst 14 days after TBI may present insulin resistance in TBI, which was associated with consistent platelet activation, thus increasing risk of DVT. Our data suggest that insulin resistance index may be a predictive biomarker for DVT.

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Section: Discussionmentioning

confidence: 59%

Prognostic Significance of Plasma Insulin Level for Deep Venous Thrombosis in Patients with Severe Traumatic Brain Injury in Critical Care

Zhang

Tang

et al. 2022

Neurocrit Care

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“… 35 The cause of death in a majority of patients in our cohort was due to TBI. Although TBI is associated with an inherent coagulopathy, 36 the results from this investigation may not be applicable to all trauma patients. It is possible that low fibrinogen is simply a specific marker of injury severity in patients with severe TBI that is not captured by other traditional measures of coagulopathy, such as INR.…”

Section: Discussionmentioning

confidence: 95%

Raising the bar on fibrinogen: a retrospective assessment of critical hypofibrinogenemia in severely injured trauma patients

Richards

Fedeles

Chow

et al. 2023

Trauma Surg Acute Care Open

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ObjectivesFibrinogen depletion may occur at higher levels than historically referenced. We evaluated hypofibrinogenemia and associated mortality and multiple organ failure (MOF) after severe injury.MethodsRetrospective investigation including 417 adult patients with Injury Severity Score (ISS) >15. Demographics and injury characteristics were collected. Fibrinogen within 30 minutes of admission was described: <150 mg/dL, 150 mg/dL to 200 mg/dL and >200 mg/dL. Primary outcome: 28-day mortality. Secondary outcomes: 28-day MOF and blood product transfusion. Multivariable logistic regression model evaluated association of fibrinogen categories on risk of death, after controlling for confounding variables. Results presented as OR and 95% CIs.ResultsFibrinogen <150 mg/dL: 4.8%, 150 mg/dL to 200 mg/dL: 18.2%, >200 mg/dL: 77.0%. 28-day mortality: 15.6%. Patients with <150 mg/dL fibrinogen had over fourfold increased 28-day mortality risk (OR: 4.9, 95% CI 1.53 to 15.7) after adjusting for age, ISS and admission Glasgow Coma Scale. Patients with lower fibrinogen were more likely to develop MOF (p=0.04) and receive larger red blood cell transfusion volumes at 3 hours and 24 hours (p<0.01).ConclusionsFibrinogen <150 mg/dL is significantly associated with increased 28-day mortality. Patients with fibrinogen <150 mg/dL were more likely to develop MOF and required increased administration of blood products. The optimal threshold for critically low fibrinogen, the association with MOF and subsequent fibrinogen replacement requires further investigation.Level of evidenceLevel III

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“…As far as we know, this study is the largest cohort to date to examine the role of head and extra-head injuries and their association in the development of coagulopathy in trauma patients. All degrees of TBI severity, from mild (AIS head = 1) to currently untreatable (AIS head = 6) were included herein, whereas many previous studies restricted their analysis to moderate-to-severe TBI patients (excluding AIS head values of 0-1 and 6) (10,21,22). Moreover, all types of extracranial lesions associated to TBI, from none to extremely severe, were also included in the present study.…”

Section: Mainmentioning

confidence: 99%

Respective contributions of intracranial and extracranial injuries in early coagulopathy occurrence following traumatic brain injury.

Wildenberg

Rustin

Kallout

et al. 2023

Preprint

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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.

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Critical traumatic brain injury is associated with worse coagulopathy

Cited by 15 publications

References 21 publications

Prognostic Significance of Plasma Insulin Level for Deep Venous Thrombosis in Patients with Severe Traumatic Brain Injury in Critical Care

Prognostic Significance of Plasma Insulin Level for Deep Venous Thrombosis in Patients with Severe Traumatic Brain Injury in Critical Care

Raising the bar on fibrinogen: a retrospective assessment of critical hypofibrinogenemia in severely injured trauma patients

Respective contributions of intracranial and extracranial injuries in early coagulopathy occurrence following traumatic brain injury.

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