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Background <p>Fat embolism syndrome (FES) is a serious complication of orthopedic trauma characterized by hypoxemia, hematologic abnormalities, and systemic inflammation. The dynamic interaction between triglycerides (TG), free fatty acid–mediated endothelial injury, and cytokine amplification has not been fully characterized in clinical cohorts. This study evaluated whether dexamethasone (DXM) modifies hematologic and inflammatory trajectories in FES and explored these findings within a proposed lipid pathological resonance (LPR) framework.</p> Methods <p>This retrospective cohort study included 134 adults diagnosed with FES between June 2020 and June 2024. Patients received either DXM (10&#xa0;mg/day for five days) or standard care. Daily TG, interleukin-6 (IL-6), red blood cell (RBC) counts, and platelet (PLT) counts were recorded for five days. Longitudinal trends were analyzed using generalized estimating equations (GEE), adjusting for transfusion volume and injury variables. Subgroup analyses compared survivors and non-survivors.</p> Results <p>Baseline characteristics were comparable. Beginning on day 3, the DXM group exhibited faster declines in TG and IL-6 and earlier improvements in RBC and PLT. Significant group × time interactions were observed for TG (P &lt; 0.01), IL-6 (P &lt; 0.001), RBC (P &lt; 0.05), and PLT (P &lt; 0.01). DXM-treated patients required fewer transfusions (P &lt; 0.001). Non-survivors showed persistent TG–IL-6 elevation and minimal hematologic recovery, consistent with failure to interrupt the lipid–cytokine amplification cycle proposed in the LPR model.</p> Conclusion <p>DXM was associated with improved inflammatory and hematologic trajectories in FES. These findings support the existence of a TG-driven cytokine amplification mechanism contributing to disease progression and suggest that DXM may attenuate this resonance loop. Prospective trials incorporating mechanistic biomarkers are warranted.</p>

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Impact of dexamethasone treatment on hematological indicators in patients with fat embolism syndrome

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月8日

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  • Yuwu Liu,
  • Qun Gao,
  • Fenfen Zhou,
  • Guangming Xiang,
  • Ming Chen,
  • Ping Shi

摘要

Background

Fat embolism syndrome (FES) is a serious complication of orthopedic trauma characterized by hypoxemia, hematologic abnormalities, and systemic inflammation. The dynamic interaction between triglycerides (TG), free fatty acid–mediated endothelial injury, and cytokine amplification has not been fully characterized in clinical cohorts. This study evaluated whether dexamethasone (DXM) modifies hematologic and inflammatory trajectories in FES and explored these findings within a proposed lipid pathological resonance (LPR) framework.

Methods

This retrospective cohort study included 134 adults diagnosed with FES between June 2020 and June 2024. Patients received either DXM (10 mg/day for five days) or standard care. Daily TG, interleukin-6 (IL-6), red blood cell (RBC) counts, and platelet (PLT) counts were recorded for five days. Longitudinal trends were analyzed using generalized estimating equations (GEE), adjusting for transfusion volume and injury variables. Subgroup analyses compared survivors and non-survivors.

Results

Baseline characteristics were comparable. Beginning on day 3, the DXM group exhibited faster declines in TG and IL-6 and earlier improvements in RBC and PLT. Significant group × time interactions were observed for TG (P < 0.01), IL-6 (P < 0.001), RBC (P < 0.05), and PLT (P < 0.01). DXM-treated patients required fewer transfusions (P < 0.001). Non-survivors showed persistent TG–IL-6 elevation and minimal hematologic recovery, consistent with failure to interrupt the lipid–cytokine amplification cycle proposed in the LPR model.

Conclusion

DXM was associated with improved inflammatory and hematologic trajectories in FES. These findings support the existence of a TG-driven cytokine amplification mechanism contributing to disease progression and suggest that DXM may attenuate this resonance loop. Prospective trials incorporating mechanistic biomarkers are warranted.