25dkou287 10.3205/25dkou287 urn:nbn:de:0183-25dkou2878 Meeting Abstract Klingebiel Klingebiel Felix Karl-Ludwig FKL

Universitätsspital Zürich, Zürich, Schweiz

author Kalbas Kalbas Yannik Y

Universitätsspital Zürich, Zürich, Schweiz

author Hübner Hübner Christian Thomas CT

Universitätsspital Zürich, Zürich, Schweiz

author Halvachizadeh Halvachizadeh Sascha S

Universitätsspital Zürich, Zürich, Schweiz

author Teuben Teuben Michel M

Universitätsspital Zürich, Zürich, Schweiz

author Ganse Ganse Bergita B

Saarland University, Homburg, Deutschland

author Cinelli Cinelli Paolo P

Universitätsspital Zürich, Zürich, Schweiz

author Pape Pape Hans-Christoph HC

Universitätsspital Zürich, Zürich, Schweiz

author Pfeifer Pfeifer Roman R

Universitätsspital Zürich, Zürich, Schweiz

author German Medical Science GMS Publishing House

Düsseldorf

610 20251031 engl This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). M0634 287 Deutsche Gesellschaft für Orthopädie und Unfallchirurgie Deutsche Gesellschaft für Orthopädie und Orthopädische Chirurgie Deutsche Gesellschaft für Unfallchirurgie Berufsverband für Orthopädie und Unfallchirurgie Deutscher Kongress für Orthopädie und Unfallchirurgie (DKOU 2025) Grundlagenforschung | Trauma & Inflammation 1 Berlin 20251028 20251031 AB42-4457 TextObjectives and questions: Severe injury is known to have systemic effects at multiple levels, with the inflammatory response being a major focus of research in recent years. However, little is known about the perturbation of metabolic pathways after polytrauma. Therefore, we performed a metabolomic analysis of patients from our in-hospital polytrauma biobank, which contains up to ten days of samples from each patient.Material and methods: Patients from the in-house polytrauma biobank with signed ethical consent were utilized. Sample time points were baseline (hospital admission), 8 h, 24 h, 48 h, 5 d and 10 days post trauma. Untargeted mass spectrometry was performed, while metabolites reliably identified using the KEGG/HMDB database were subset-analyzed in a semitargeted approach. Cluster analyses were performed and metabolite dynamics over time were assessed to investigate the metabolic response in between musculoskeletal trauma and hemorrhagic shock.Results: 97 severely injured patients (79.4% male/20.6% female) were included in the study. The median ISS of this cohort was 29 (IQR=19). 46 metabolites were reliably identified in the semitargeted analysis. The immediate response (0–8 h) shows increased activation of hemostasis and inflammation along with excessive corticosteroid production. In the 8–24 h period, there is an excessive catabolic state with energy mobilization from fatty and amino acids. At 24–48 hours, detoxification, immune regulation and metabolic adjustments are primarily active. In the 5–10 day period, energy requirements are still elevated but reduced compared to the previous time points. An elevation of acetylcarnitines in patients with hemorrhagic shock was observed over multiple timepoints starting from admission to the trauma bay.Discussion and conclusions: Severe trauma causes a major disruption in the metabolism. Immediately after trauma, the body activates life-saving pathways and begins to mobilize excessive energy resources by breaking down fats and amino acids for ATP production. Initial treatment and intensive care should take this excessive energy demand into account and assess the extent to which organ-protective treatment (e.g. liver) may be beneficial to the patient. Acetylcarnitines, which are indicative of mitochondrial dysfunction, have been identified as a promising marker for understanding the underlying mechanisms of traumatic ischemia. 0 0 0 0