Comparative Analysis of Risk Factors for Venous Thromboembolism in Patients With Traumatic Brain Injury of Different Severity

Abstract

Background

Venous thromboembolism (VTE) is a major complication in patients with traumatic brain injury (TBI). However, most existing studies have focused on severe TBI, and it remains unclear whether VTE risk factors differ across injury severities.

Objective

To compare independent risk factors for VTE among patients with mild, moderate, and severe TBI.

Methods

This retrospective cohort study analyzed clinical data from 460 TBI patients admitted to a tertiary trauma center between January 2022 and December 2024. Patients were stratified by admission Glasgow Coma Scale (GCS) score into mild (GCS 13-15, n = 205), moderate (GCS 9-12, n = 50), and severe (GCS 3-8, n = 205) groups. VTE was screened by serial bedside Doppler ultrasonography of the upper and lower extremities. Univariate and multivariable logistic regression analyses were performed within each group to identify independent risk factors, which were then compared across groups.

Results

VTE incidence was 15.1%, 28.0%, and 49.3% in the mild, moderate, and severe TBI groups, respectively (χ² = 55.52, P < .001). Independent risk factors differed across groups: in mild TBI, length of hospital stay > 14 days (OR = 4.76) and mechanical ventilation (OR = 3.70); in moderate TBI, length of stay > 14 days (OR = 9.64), with tracheostomy showing a trend (OR = 5.68, P = .054); in severe TBI, admission fibrinogen ≥ 4 g/L (OR = 8.19), age ≥ 60 years (OR = 6.25), tracheostomy (OR = 3.56), length of stay > 14 days (OR = 3.43), surgery (OR = 2.76), and central venous catheterization (OR = 2.26). Length of stay > 14 days was the only common independent risk factor across all three groups.

Conclusion

VTE incidence increases substantially with TBI severity, and the spectrum of independent risk factors differs systematically across injury grades. Severity-stratified VTE prevention strategies should be considered in clinical practice.

Introduction

Venous thromboembolism (VTE) is an important complication in patients with traumatic brain injury (TBI) and significantly increases morbidity and mortality.^1-3 Owing to injury-related immobilization, prolonged bedrest, and the cumulative effects of multiple treatments, TBI patients are particularly prone to venous stasis, vascular endothelial injury, and hypercoagulability, with a 3- to 4-fold higher VTE risk compared with general trauma patients.^4,5 The reported VTE incidence in TBI patients without prophylaxis is as high as 40%, and remains around 20% even with prophylactic measures.^6,7

Previous studies on VTE risk factors in TBI have largely focused on severe TBI populations,^8-12 identifying age, Injury Severity Score (ISS), length of hospital stay, mechanical ventilation, surgery, transfusion, and admission coagulation abnormalities as recognized risk factors. Existing VTE risk assessment tools, such as the Caprini score, ¹³ the Risk Assessment Profile for Thromboembolism (RAPT), ¹⁴ and the Trauma Embolic Scoring System (TESS), ¹⁵ are widely used but were not specifically designed for TBI patients. Current clinical guidelines generally apply uniform VTE prevention strategies to TBI patients regardless of injury severity.^16-18

However, TBI patients exhibit substantial heterogeneity in injury severity, and it remains unclear whether the spectrum of VTE risk factors differs between mild, moderate, and severe TBI. If risk factor profiles differ systematically across severity grades, a stratified, severity-tailored approach to VTE prevention may be more rational than uniform prophylaxis. The present retrospective cohort study aimed to compare independent VTE risk factors among patients with different TBI severity grades, in order to provide evidence for stratified VTE prevention strategies.

Materials and Methods

Study Design and Patients

This was a single-center retrospective cohort study. We consecutively reviewed 460 TBI patients admitted to the Trauma Medical Center of a tertiary teaching hospital between January 2022 and December 2024. Inclusion criteria were: (1) TBI confirmed by head computed tomography (CT); (2) age ≥ 18 years; and (3) no anticoagulant or antiplatelet therapy before admission. Exclusion criteria were: (1) death or self-discharge within 3 days of admission; (2) prior history of VTE; (3) prior history of malignancy; (4) VTE present on admission; and (5) incomplete clinical data. The study flow is summarized in Figure 1.

Figure 1.

Participant flow diagram. Patients admitted to the Trauma Medical Center between January 2022 and December 2024 were screened for eligibility. After exclusion of patients who met any of the predefined exclusion criteria (death or self-discharge within 3 days of admission; prior history of venous thromboembolism [VTE]; prior history of malignancy; VTE present on admission; incomplete clinical data), 460 patients with traumatic brain injury (TBI) were included in the analysis and stratified by admission Glasgow Coma Scale (GCS) score into mild (n = 205), moderate (n = 50), and severe (n = 205) groups. Outcomes (VTE/non-VTE) within each stratum are shown at the bottom of the diagram

Patients were stratified by admission Glasgow Coma Scale (GCS) score into three groups: mild TBI (GCS 13-15), moderate TBI (GCS 9-12), and severe TBI (GCS 3-8). The study was approved by the institutional Medical Ethics Committee, which waived the requirement for individual informed consent given the retrospective design and the use of anonymized clinical data. No formal a priori sample size calculation was performed; all consecutive eligible TBI patients admitted during the study period were included to maximize statistical power.

VTE Screening

All patients underwent bedside color Doppler ultrasonography of the bilateral upper extremities (subclavian, axillary, brachial, cephalic, and basilic veins) and lower extremities (common femoral, superficial femoral, popliteal, posterior tibial, intramuscular calf, and greater saphenous veins) within 3-5 days of admission. Ultrasonography was repeated weekly until detection of venous thrombosis, at which point screening was discontinued. Patients with at least one positive ultrasonographic finding for venous thrombosis were classified into the VTE group, whereas patients with consistently negative findings were assigned to the non-VTE group. Pulmonary embolism was confirmed by CT pulmonary angiography in patients with clinical suspicion.

Data Collection

The following data were collected for each patient: sex, age, body mass index (BMI), ISS, GCS, injury severity grade, mechanism of injury, comorbidities (hypertension, diabetes, pulmonary infection, and others), treatment-related variables (intensive care unit [ICU] admission, mechanical ventilation, surgery, endotracheal intubation, duration of intubation, tracheostomy, central venous catheterization, transfusion, parenteral nutrition, mechanical prophylaxis, pharmacological prophylaxis), length of hospital stay, and laboratory parameters on admission and 3-5 days after admission (hemoglobin, platelet count, antithrombin III, prothrombin time [PT], thrombin time [TT], activated partial thromboplastin time [APTT], fibrinogen [FIB], D-dimer, and albumin).

Statistical Analysis

Statistical analyses were performed using SPSS version 26.0 (IBM Corp., Armonk, NY, USA). Normality of continuous variables was assessed using the Shapiro-Wilk test. Normally distributed continuous variables are presented as mean ± standard deviation, and were compared between groups using the Student t test or one-way analysis of variance. Non-normally distributed continuous variables are presented as median (Q1, Q3), and were compared using the Mann-Whitney U test or Kruskal-Wallis H test. Categorical variables are expressed as n (%), and were compared using the chi-square test or Fisher exact test as appropriate. Within each TBI severity group, univariate analyses were performed first; variables with P < .10 in univariate analysis were entered into a multivariable logistic regression model to identify independent risk factors. To minimize the risk of overfitting, the events-per-variable ratio was kept at approximately 10:1. All tests were two-sided, and P < .05 was considered statistically significant. Patients with missing data on key variables were excluded a priori, and no imputation was performed.

Results

Patient Characteristics and VTE Incidence

Of the patients consecutively assessed during the study period, 460 met all eligibility criteria and were included in the analysis (Figure 1). Complete data were available for all 460 included patients on every variable analyzed. The cohort comprised 349 males and 111 females, with a mean age of 54.7 ± 19.1 years. VTE occurred in 146 patients, yielding an overall incidence of 31.7%. VTE incidence increased progressively with injury severity, reaching 15.1% in mild TBI, 28.0% in moderate TBI, and 49.3% in severe TBI (χ² = 55.52, P < .001; Figure 2). The three groups also differed significantly in age, ISS, length of stay, ICU admission rate, mechanical ventilation rate, surgical rate, and several other treatment-related variables (Table 1).

Figure 2.

Incidence of venous thromboembolism (VTE) in patients with traumatic brain injury (TBI) of different severity grades. VTE incidence increased progressively from mild to severe TBI (χ² = 55.52, P < .001)

Table 1.

Clinical Characteristics of Patients With Traumatic Brain Injury (TBI) of Different Severity Grades

Variable	Mild TBI (n = 205)	Moderate TBI (n = 50)	Severe TBI (n = 205)	Statistic	P value
Age, years (mean ± SD)	58.3 ± 19.6	55.6 ± 19.9	50.8 ± 17.7	F = 8.23	< .001*
Male, n (%)	155 (75.6)	34 (68.0)	160 (78.0)	χ2 = 2.23	= .328
BMI, kg/m2 (mean ± SD)	22.7 ± 3.3	22.6 ± 3.5	23.0 ± 3.5	F = 0.53	= .589
ISS, median (Q1, Q3)	16 (13, 25)	25 (17, 33)	34 (25, 41)	H = 180.09	< .001*
Length of hospital stay, days, median (Q1, Q3)	8 (5, 13)	13.5 (7.2, 23.5)	18 (10, 32)	H = 68.53	< .001*
ICU admission, n (%)	44 (21.5)	12 (24.0)	126 (61.5)	χ2 = 74.27	< .001*
Mechanical ventilation, n (%)	61 (29.8)	24 (48.0)	175 (85.4)	χ2 = 130.64	< .001*
Surgery, n (%)	101 (49.3)	22 (44.0)	135 (65.9)	χ2 = 14.78	< .001*
Endotracheal intubation, n (%)	61 (29.8)	23 (46.0)	162 (79.0)	χ2 = 101.27	< .001*
Tracheostomy, n (%)	10 (4.9)	9 (18.0)	84 (41.0)	χ2 = 77.48	< .001*
Central venous catheterization, n (%)	12 (5.9)	12 (24.0)	102 (49.8)	χ2 = 99.66	< .001*
Transfusion, n (%)	45 (22.0)	16 (32.0)	138 (67.3)	χ2 = 88.84	< .001*
Parenteral nutrition, n (%)	53 (25.9)	26 (52.0)	126 (61.5)	χ2 = 53.87	< .001*
Mechanical prophylaxis, n (%)	21 (10.2)	7 (14.0)	42 (20.5)	χ2 = 8.40	= .015*
Hypertension, n (%)	61 (29.8)	11 (22.0)	29 (14.1)	χ2 = 14.58	< .001*
Pulmonary infection, n (%)	140 (68.3)	42 (84.0)	178 (86.8)	χ2 = 21.79	< .001*
Admission FIB, g/L, median (Q1, Q3)	2.7 (2.2, 3.5)	2.5 (2.0, 3.8)	2.5 (1.8, 4.4)	H = 0.73	= .694
Admission D-dimer, mg/L, median (Q1, Q3)	7.2 (1.2, 19.3)	8.8 (3.7, 21.7)	14.9 (4.9, 38.0)	H = 33.01	< .001*
VTE occurrence, n (%)	31 (15.1)	14 (28.0)	101 (49.3)	χ2 = 55.52	< .001*

Abbreviations: BMI, body mass index; F, F statistic (one-way ANOVA); FIB, fibrinogen; H, Kruskal-Wallis H statistic; ICU, intensive care unit; ISS, Injury Severity Score; Q1, first quartile; Q3, third quartile; SD, standard deviation; TBI, traumatic brain injury; VTE, venous thromboembolism; χ², chi-square statistic.

Note. Continuous variables were compared using one-way ANOVA (normally distributed) or the Kruskal-Wallis H test (non-normally distributed). Categorical variables were compared using the chi-square test. Two-sided P < .05 was considered statistically significant. An asterisk (*) denotes a statistically significant difference (P < .05).

Risk Factors for VTE in Mild TBI

In the mild TBI group, multivariable logistic regression identified length of hospital stay > 14 days and mechanical ventilation as independent risk factors for VTE, with transfusion showing a trend toward association (Table 2).

Table 2.

Multivariable Logistic Regression Analysis of Independent Risk Factors for Venous Thromboembolism (VTE) in Mild Traumatic Brain Injury (TBI) (n = 205)

Variable	β	SE	Wald	OR	95% CI	P value
Length of hospital stay > 14 days	1.561	0.476	10.74	4.76	1.87-12.12	= .001*
Mechanical ventilation	1.308	0.479	7.45	3.70	1.45-9.46	= .006*
Transfusion	0.868	0.500	3.02	2.38	0.90-6.35	= .082

Abbreviations: β, regression coefficient; CI, confidence interval; OR, odds ratio; SE, standard error; Wald, Wald statistic.

Note. Variables with P < .10 in univariate analysis were entered into the multivariable model. Two-sided P < .05 was considered statistically significant. An asterisk (*) denotes a statistically significant predictor (P < .05).

Risk Factors for VTE in Moderate TBI

In the moderate TBI group, length of hospital stay > 14 days was identified as an independent risk factor for VTE in multivariable logistic regression, and tracheostomy showed a trend toward association (Table 3).

Table 3.

Multivariable Logistic Regression Analysis of Independent Risk Factors for Venous Thromboembolism (VTE) in Moderate Traumatic Brain Injury (TBI) (n = 50)

Variable	β	SE	Wald	OR	95% CI	P value
Length of hospital stay > 14 days	2.266	0.870	6.77	9.64	1.75-53.08	= .009*
Tracheostomy	1.737	0.902	3.71	5.68	0.97-33.25	= .054

Abbreviations: β, regression coefficient; CI, confidence interval; OR, odds ratio; SE, standard error; Wald, Wald statistic.

Note. Variables with P < .10 in univariate analysis were entered into the multivariable model. Two-sided P < .05 was considered statistically significant. An asterisk (*) denotes a statistically significant predictor (P < .05). The small sample size of this subgroup may limit statistical power; results should be interpreted with caution.

Risk Factors for VTE in Severe TBI

In the severe TBI group, six independent risk factors for VTE were identified: admission FIB ≥ 4 g/L, age ≥ 60 years, tracheostomy, length of hospital stay > 14 days, surgery, and central venous catheterization (Table 4).

Table 4.

Multivariable Logistic Regression Analysis of Independent Risk Factors for Venous Thromboembolism (VTE) in Severe Traumatic Brain Injury (TBI) (n = 205)

Variable	β	SE	Wald	OR	95% CI	P value
Admission FIB ≥ 4 g/L	2.103	0.478	19.36	8.19	3.21-20.90	< .001*
Age ≥ 60 years	1.832	0.452	16.43	6.25	2.58-15.15	< .001*
Tracheostomy	1.269	0.425	8.90	3.56	1.55-8.19	= .003*
Length of hospital stay > 14 days	1.233	0.483	6.52	3.43	1.33-8.84	= .011*
Surgery	1.014	0.491	4.25	2.76	1.05-7.22	= .039*
Central venous catheterization	0.817	0.390	4.40	2.26	1.05-4.86	= .036*

Abbreviations: β, regression coefficient; CI, confidence interval; FIB, fibrinogen; OR, odds ratio; SE, standard error; Wald, Wald statistic.

Note. Variables with P < .10 in univariate analysis were entered into the multivariable model. Two-sided P < .05 was considered statistically significant. An asterisk (*) denotes a statistically significant predictor (P < .05).

Comparison of Risk Factor Profiles Across Severity Groups

Figure 3 presents a forest-plot comparison of independent VTE risk factors across TBI severity groups. Length of stay > 14 days was the only independent risk factor common to all three groups. Tracheostomy reached statistical significance as an independent risk factor only in severe TBI, while showing a trend toward association in moderate TBI (P = .054). Admission FIB ≥ 4 g/L, age ≥ 60 years, surgery, and central venous catheterization emerged as independent risk factors only in severe TBI, whereas mechanical ventilation was an independent risk factor only in mild TBI. The number of independent risk factors was substantially greater in severe TBI than in mild or moderate TBI.

Figure 3.

Forest plot comparing independent risk factors for VTE across TBI severity groups. Asterisks (*) indicate variables with P < .05 in multivariable logistic regression. For severe TBI, variables shown below the six significant predictors are from univariate analysis only

Discussion

Pathophysiological Basis of VTE in TBI

The pathophysiological mechanisms of VTE in TBI can be understood within the framework of the Virchow triad: venous stasis, vascular endothelial injury, and hypercoagulability. ¹⁹ Prolonged immobilization due to coma, sedation, and mechanical ventilation reduces lower-extremity muscle pump activity and promotes venous stasis. Direct trauma and surgery may damage the vascular endothelium, and central venous catheterization further contributes to focal endothelial injury. In addition, TBI is accompanied by complex coagulopathy, with an early hypocoagulable phase rapidly transitioning into a hypercoagulable state.^20,21 Release of tissue factor, pro-inflammatory cytokines (e.g., IL-6, TNF-α), and inflammation-driven elevation of FIB after TBI all contribute to this hypercoagulability.^22,23 These pathophysiological mechanisms provide a theoretical basis for the observed differences in VTE risk factor profiles across TBI severity grades.

VTE Incidence by Injury Severity

In this study, VTE incidence increased in a stepwise manner with TBI severity, reaching nearly 50% in severe TBI. This pattern is consistent with the linear relationship between VTE risk and head abbreviated injury scale (AIS) score reported by Van Gent et al. ²⁴ Skrifvars et al ¹² reported a 19.7% VTE incidence in 603 ICU-admitted moderate-to-severe TBI patients from the EPO-TBI study; the higher incidence observed in our severe TBI subgroup likely reflects greater diagnostic sensitivity due to weekly ultrasonographic surveillance and the high detection rate of asymptomatic thrombi. Notably, VTE incidence in our mild TBI group remained substantially higher than that reported for general trauma populations,^2,25 suggesting that even apparently mild TBI patients should not be excluded from VTE screening and prevention. Hoffman et al ⁹ demonstrated in a National Inpatient Sample analysis of more than 420,000 TBI patients that VTE substantially increases hospital length of stay, cost, and mortality, underscoring the importance of VTE prevention across all TBI severities.

Risk Factors in Mild and Moderate TBI

In mild TBI, the independent risk factors identified were all treatment-intensity-related variables. Mild TBI patients who require mechanical ventilation or prolonged hospitalization often have concomitant severe injuries, infections, or major comorbidities, and their overall clinical risk profile may approximate that of critically ill patients.^24,26 Therefore, VTE risk assessment based solely on the GCS may underestimate the true risk in such patients. Moderate TBI has received relatively limited attention in previous VTE studies and has often been combined with severe TBI under the label of “moderate-to-severe” injury.^3,12 The risk factor we identified in moderate TBI overlapped with that of the mild group (length of stay), while the trend toward an association with tracheostomy (P = .054) was directionally consistent with the severe group, suggesting that the pathogenesis of VTE in moderate TBI lies between these two extremes. Clinically, we suggest managing moderate TBI patients with VTE prevention strategies modeled after those for severe TBI in order to avoid underestimating their risk.

Risk Factors in Severe TBI

Severe TBI patients exhibited substantially more independent risk factors than mild or moderate TBI patients, indicating that VTE in this population results from complex, multifactorial interactions. Admission FIB elevation emerged as the strongest independent risk factor. FIB is a key procoagulant protein and a core component of thrombi, and elevated levels directly reflect a hypercoagulable state. ²² In severe TBI, massive release of tissue factor and inflammatory cytokines, compounded by surgery- or polytrauma-induced acute-phase responses, can markedly elevate FIB.^20,23 Wolberg ²² highlighted that elevated FIB not only increases VTE risk but also alters thrombus structure and stability, making clots more resistant to lysis. An elevated admission FIB therefore has strong predictive value and may serve as an early biomarker for VTE risk stratification in severe TBI.

Age ≥ 60 years was also a strong independent risk factor in severe TBI, consistent with previous reports.^11,27,28 Older patients exhibit reduced vascular endothelial function, imbalanced coagulation systems, more comorbidities, and slower recovery from immobilization, with these factors interacting to substantially increase VTE risk. Treatment-related factors such as tracheostomy, surgery, and central venous catheterization further contribute to VTE risk through prolonged sedation and immobilization, vascular endothelial injury, and local foreign-body-induced thrombus formation.^3,5,26 Although univariate analysis showed a significant association between transfusion and VTE in the severe TBI group, this association was not retained in multivariable analysis, in line with the findings of Goel et al ²⁹ suggesting that the transfusion-VTE association may be mediated by other clinical factors such as surgery or ISS.

Clinical Implications of Severity-Specific Risk Factor Profiles

The most clinically meaningful finding of this study is that the spectrum of VTE risk factors differs systematically across TBI severity grades: mild TBI is dominated by treatment-intensity-related factors; moderate TBI is characterized by prolonged airway management; and severe TBI exhibits a composite pattern of “physiological + treatment-related” factors. This pattern suggests that the underlying pathophysiology of VTE varies with TBI severity: as injury becomes more severe, primary coagulation activation (e.g., FIB elevation) and age-related coagulation imbalance contribute more substantially, whereas in milder injuries, VTE depends more on treatment-related iatrogenic factors and prolonged immobilization. Length of stay > 14 days was the only independent risk factor common to all three groups, emphasizing the universal value of early rehabilitation and shortened hospitalization for VTE prevention in TBI.^27,30 This systematic difference provides direct evidence supporting severity-tailored clinical prevention strategies.

Recommendations for Clinical Practice

Based on our findings, we suggest the following severity-tailored VTE prevention strategies for TBI patients: (1) All TBI patients, regardless of severity, should undergo VTE risk assessment and mechanical prophylaxis (e.g., intermittent pneumatic compression) on admission. ³⁰ (2) Mild TBI patients who require mechanical ventilation or have anticipated prolonged hospitalization should be considered high risk; once active intracranial hemorrhage progression is excluded, early initiation of pharmacological prophylaxis may be considered. (3) Moderate TBI patients undergoing tracheostomy or with anticipated prolonged stay should have intensified ultrasonographic surveillance, and pharmacological prophylaxis should be initiated according to the American Association for the Surgery of Trauma clinical consensus ¹⁷ and the Western Trauma Association critical decisions algorithm. ³¹ (4) Severe TBI patients with elevated admission FIB and older age should be the focus of particular attention; pharmacological prophylaxis should be initiated 24-72 hours after intracranial hemorrhage stabilization.^17,32 (5) Early initiation of pharmacological prophylaxis is encouraged. Systematic reviews and meta-analyses by Lu et al ³³ and Spano et al ³⁴ both demonstrated that early pharmacological prophylaxis significantly reduces VTE risk without increasing intracranial hemorrhage; large cohort studies by Byrne et al. (4,951 TBI patients undergoing neurosurgical intervention) ³² and Hecht et al (18,010 trauma patients) ³⁵ also showed that earlier prophylaxis is associated with lower VTE incidence. (6) Multidisciplinary collaboration is essential to reduce VTE risk through early weaning from mechanical ventilation, shortened intubation duration, and enhanced early rehabilitation.^16,17

Limitations

This study has several limitations. First, as a single-center retrospective study, selection bias is possible, and external validation is needed before generalizing the findings to other institutions. Second, the moderate TBI subgroup was relatively small, limiting the statistical power of multivariable regression analysis, and some potentially relevant risk factors may not have been retained in the final model due to limited event numbers. Sensitivity analyses such as Firth-penalized logistic regression were not pre-specified in the original protocol and could be considered in future validation studies to further verify the moderate-TBI findings. Third, VTE was diagnosed primarily on the basis of serial color Doppler ultrasonography. Although this approach enabled systematic, protocol-driven surveillance and high detection of asymptomatic thrombi, ultrasonography is operator-dependent and may miss asymptomatic pulmonary emboli or small deep thrombi; CT pulmonary angiography was performed only in patients with clinical suspicion of pulmonary embolism. The predominantly ultrasonography-based design should therefore be taken into account when interpreting the observed VTE incidence and risk-factor associations.

Fourth, although several common comorbidities (hypertension, diabetes, and pulmonary infection) were recorded and compared across groups (Table 1), the overall comorbidity burden was not systematically quantified using a composite index such as the Charlson Comorbidity Index, and certain conditions (e.g., chronic kidney disease, prior thrombophilia, and active inflammatory states) were not separately captured. Residual confounding by unmeasured comorbidities therefore cannot be excluded, and future studies incorporating a comprehensive, standardized assessment of comorbidity burden are warranted. Fifth, some potentially relevant variables (e.g., intracranial pressure monitoring, specific types of neurosurgical intervention, sedation regimens, and detailed regimens of low-molecular-weight heparin) were not included in our analysis.

Finally, although elevated admission FIB was the strongest independent predictor of VTE in severe TBI, our assessment of the coagulation system was limited to conventional plasma markers. FIB concentration reflects the quantity of circulating fibrinogen but does not capture the structure and function of the resulting fibrin clot, which are increasingly recognized as important determinants of thrombotic risk. As elevated FIB can alter clot architecture and resistance to fibrinolysis, ²² future studies that incorporate fibrin clot structure and function analyses (e.g., clot permeability, turbidity, viscoelastic testing, and lysis assays) may provide a more comprehensive and mechanistic assessment of VTE risk in TBI than fibrinogen concentration alone. The identified risk factors require further validation in prospective, multicenter studies.

Conclusion

VTE incidence increases substantially with TBI injury severity, and the spectrum of independent VTE risk factors differs systematically across severity grades. Mild TBI is dominated by treatment-related factors; moderate TBI is characterized by prolonged airway management; severe TBI exhibits a composite pattern of physiological and treatment-related factors. Length of hospital stay > 14 days is a common independent risk factor across all severity grades. Severity-tailored VTE prevention strategies should be considered in clinical practice to more precisely reduce VTE occurrence and improve patient outcomes.

ORCID iDs

Min Gong https://orcid.org/0009-0007-6385-9401

Jiayu Ye https://orcid.org/0009-0005-4058-4009

Ethical Considerations

This study was approved by the Medical Ethics Committee of West China Hospital, Sichuan University (Approval No.: 2021 Review (65)). The study was conducted in accordance with the Declaration of Helsinki. As this was a retrospective study based on existing medical records, the requirement for individual informed consent was waived; however, written informed consent was obtained from the families of all patients for the use of their de-identified clinical data.

Consent to Participate

Written informed consent was obtained from all patients' family members for the use of de-identified clinical data.

Consent for Publication

Not applicable. This manuscript does not contain any individual person’s identifying data in any form (including individual details, images, or videos).

Data Availability Statement

The de-identified data that support the findings of this study are available from the corresponding author upon reasonable request, subject to approval by the Medical Ethics Committee of West China Hospital, Sichuan University. Restrictions apply to the availability of these data due to patient privacy considerations.*