ArticleEuropean journal of trauma and emergency surgery : official publication of the European Trauma Society2024
Limited impact of traumatic brain injury on the post-traumatic inflammatory cellular response.
Article in European journal of trauma and emergency surgery : official publication of the European Trauma Society, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Injury to the thorax is a dominant contributor to post-traumatic neutrophil mediated inflammatory response.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2026Article
- High interobserver reliability of neutrophil phenotyping based on visual determination of CD16/CD62L expression patterns.Langenbeck's archives of surgery · 2026Article
- MiR338-3p expression in extracellular vesicles after severe trauma with or without traumatic brain injury.Brain communications · 2025Article
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7 authors.
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Abstract
purposeTrauma triggers a systemic inflammatory cellular response due to tissue damage, potentially leading to a secondary immune deficiency. Trauma severity is quantified by the Injury Severity Score (ISS). Severe Traumatic Brain Injury (TBI) is associated with high ISSs due to high lethality, despite limited tissue damage. Therefore, ISS might overestimate the post-traumatic inflammatory cellular response. This study investigated the effect of TBI on the occurrence of different systemic neutrophil phenotypes as alternative read-out for systemic inflammation.
methodsA single-center retrospective cohort study was conducted at a level-1 trauma center. Patients aged ≥ 18 years, admitted between 01-03-2021-01-11-2022 and providing a diagnostic blood sample were included. Four groups were created: isolated TBI, isolated non-TBI, multitrauma TBI and multitrauma non-TBI. Primary outcome was occurrence of different neutrophil phenotypes determined by automated flow cytometry. Secondary outcome was infectious complications.
resultsIn total, 404 patients were included. TBI and non-TBI patients demonstrated similar occurrences of different neutrophil phenotypes. However, isolated TBI patients had higher ISSs than their isolated non-TBI controls who suffered similar post-traumatic inflammatory cellular responses. Regardless of the type of injury, patients exhibiting higher systemic inflammation had a high infection risk.
conclusionWhen TBI is involved, ISS tends to be higher compared to similar patients in the absence of TBI. However, TBI patients did not demonstrate an increased inflammatory cellular response compared to non-TBI patients. Therefore, TBI does not add much to the inflammatory cellular response in trauma patients. The degree of the inflammatory response was related to the incidence of infectious complications.
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