Trajectories of systemic immune inflammation index and mortality risk in patients with moderate-to-severe traumatic brain injury: a retrospective cohort study.

Background: Some studies have shown a strong link between the central nervous system and peripheral immune system, but the prognostic implications of dynamic peripheral immune-inflammatory responses in patients with traumatic brain injury (TBI) remain unclear. This study aimed to determine the dynamic trajectory patterns of the Systemic Immune Inflammation Index (SII) in patients with TBI and assess its association with all-cause hospital mortality.

Methods: This retrospective cohort study utilized a large public database of patients with TBI sourced from the eICU Collaborative Research Database (eICU-CRD). Group-Based Trajectory Modeling (GBTM) was used to analyze daily SII trajectories during the initial 0-7 days of hospitalization. Logistic regression was employed to assess the relationship between different SII trajectory groups and hospital mortality. Receiver Operating Characteristic (ROC) curves were generated based on the logistic regression model.

Results: A total of 312 patients were included in this study, 52 of whom died during hospitalization. Using GBTM, three distinct SII trajectories were identified: Group 1 (low-level, rapid decline; 18.90%), Group 2 (moderate-level, slow decline; 60.20%), and Group 3 (sustained high-level; 20.80%). Compared to patients in Group 1, those in Groups 2 and 3 had a higher risk of all-cause hospital mortality (odds ratio [OR] 4.09; 95% confidence interval [CI] 1.21, 19.75) and (OR 5.84; 95% CI 1.52, 30.67), respectively. ROC analysis revealed an area under the curve (AUC) of 0.838, sensitivity: 75.0%, and specificity: 83.8% for mortality in this cohort.

Conclusion: This study identified three distinct SII trajectories, suggesting that post-TBI SII trajectories are heterogeneous patterns associated with mortality. The sustained high-level SII trajectory may serve as a marker of disease deterioration, highlighting the need for targeted interventions. Describing the evolution of SII through GBTM and its correlation with clinical outcomes can enhance our understanding of the link between neuroinflammation and the peripheral immune system.