# Explainable machine learning reveals multifactorial drivers of early intracranial hematoma progression in traumatic brain injury: development of a SHAP-guided SVM nomogram

**Authors:** Xujie Wang, Rongfei Xie, Minmin Li, Ziyi Zhao, Zhaohui Liu, Biyun Wang, Xuhui Liu

PMC · DOI: 10.3389/fneur.2026.1718794 · Frontiers in Neurology · 2026-02-05

## TL;DR

A new machine learning model accurately predicts early brain bleeding progression in traumatic brain injury patients, helping guide timely treatment.

## Contribution

Development of an interpretable SVM model with SHAP-based explanations for predicting hematoma progression in TBI.

## Key findings

- An SVM model achieved high accuracy (AUC 0.937 in training, 0.925 in validation) in predicting hematoma progression.
- Seven key predictors were identified, including hematoma type, D-dimer, and monocyte-to-lymphocyte ratio.
- The model demonstrated strong clinical utility for risk stratification and individualized management.

## Abstract

Early intracranial hematoma progression is a common and life-threatening complication of traumatic brain injury (TBI), associated with rapid neurological deterioration and poor outcomes. Accurate early identification of patients at risk remains challenging due to the multifactorial and nonlinear nature of underlying mechanisms. This study aimed to develop and validate an interpretable machine learning (ML) model for predicting early hematoma progression in TBI patients.

We retrospectively analyzed clinical data from 356 patients with TBI admitted to Qinghai University Affiliated Hospital. Patients were randomly divided into training (70%) and internal validation (30%) cohorts. A total of 25 demographic, radiological, and laboratory variables were evaluated. Predictive features were selected using least absolute shrinkage and selection operator (LASSO) regression and further confirmed by multivariable logistic regression. Five ML algorithms were constructed and compared. The optimal model was interpreted using Shapley additive explanations (SHAP), followed by the development of a nomogram. Performance evaluation and risk-stratification analyses based on both model-derived probability estimates and nomoscore stratification were performed to assess the clinical utility of the model.

Early hematoma progression occurred in 49.7% (177/356) of patients. LASSO and logistic regression identified seven independent predictors: hematoma type, smoking history, age, D-dimer, monocyte-to-lymphocyte ratio (MLR), serum calcium, and multiple hematomas. Among the five algorithms, the support vector machine (SVM) achieved the best discrimination (training AUC = 0.937; validation AUC = 0.925), outperforming logistic regression, decision tree, XGBoost, and LightGBM. SHAP analysis confirmed the above variables as key contributors. The nomogram demonstrated strong predictive performance and interpretability. Rationality analyses showed that both model probability and nomoscore stratification exhibited stepwise increases in progression risk, validating the clinical robustness of the SVM-based model.

We developed and validated an interpretable SVM model that accurately predicts early hematoma progression in TBI patients. By integrating demographic, radiological, and laboratory features, this model provides a reliable tool for early risk stratification, guiding individualized management and timely intervention. Its strong performance across subgroups underscores its clinical applicability.

## Linked entities

- **Diseases:** traumatic brain injury (MONDO:0858950)

## Full-text entities

- **Genes:** ITIH1 (inter-alpha-trypsin inhibitor heavy chain 1) [NCBI Gene 3697] {aka H1P, IATIH, ITI-HC1, ITIH, SHAP}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, F2 (coagulation factor II, thrombin) [NCBI Gene 2147] {aka PT, RPRGL2, THPH1}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, FGB (fibrinogen beta chain) [NCBI Gene 2244] {aka HEL-S-78p}
- **Diseases:** endothelial injury (MESH:D057772), vascular dysfunction (MESH:D002561), ischemic stroke (MESH:D002544), atrial fibrillation (MESH:D001281), intracranial hematoma (MESH:D020198), coagulation (MESH:D001778), subarachnoid hemorrhage (MESH:D013345), intracerebral hemorrhage (MESH:D002543), death and disability (MESH:D003643), hypertension (MESH:D006973), brain injury (MESH:D001930), functional impairment of the brain (MESH:D001927), impaired consciousness (MESH:D003244), Hypocalcemia (MESH:D006996), thrombotic (MESH:D013927), term disability (MESH:D000088562), memory loss (MESH:D008569), sepsis (MESH:D018805), long (MESH:D000094024), cognitive disorders (MESH:D003072), Coma (MESH:D003128), DIC (MESH:D004211), neurological deterioration (MESH:D009422), epidural hematoma (MESH:D046748), systemic (MESH:D015619), intracranial lesion enlargement (MESH:D006332), contusion (MESH:D003288), intracranial lesions (MESH:D020765), TBI (MESH:D000070642), malignancy (MESH:D009369), diabetes (MESH:D003920), lymphopenia (MESH:D008231), psychiatric (MESH:D001523), head trauma (MESH:D006259), hemostatic dysregulation (MESH:D020141), Hematoma (MESH:D006406), cerebral hypoperfusion (MESH:D002547), inflammation (MESH:D007249), injury (MESH:D014947), damage (MESH:D020263), cerebral vascular fragility (MESH:D005600), neurological (MESH:D009461), fourth ventricle obstruction (MESH:D020432), bleeding (MESH:D006470), cerebral hypoxia (MESH:D002534), aggregation (MESH:D020914), subdural hematoma (MESH:D006408), intracranial hemorrhage (MESH:D020300)
- **Chemicals:** nicotine (MESH:D009538), potassium (MESH:D011188), D- (MESH:D003903), nomoscore (-), Ca (MESH:D002118), glucose (MESH:D005947), blood glucose (MESH:D001786), Glu (MESH:D018698)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

58 references — full list in the complete paper: https://tomesphere.com/paper/PMC12916409/full.md

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Source: https://tomesphere.com/paper/PMC12916409