Inflammatory and Metabolic Mechanisms of Organ Dysfunction Following Severe Polytrauma: A Multidisciplinary Review

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Abstract
Olytrauma is a major cause of mortality, disability, and prolonged critical illness worldwide, particularly among young and economically active populations. Beyond the initial anatomical injury, severe trauma triggers a complex systemic response involving inflammatory activation, endothelial dysfunction, metabolic and endocrine alterations, coagulation abnormalities, immune dysregulation, and progressive organ failure. The objective of this review was to analyze current evidence regarding the inflammatory, metabolic, and organ dysfunction pathways associated with polytrauma from a multidisciplinary perspective integrating traumatology, orthopedics, internal medicine, endocrinology, and critical care medicine. A narrative and integrative literature review was conducted using scientific databases including PubMed/MEDLINE, Scopus, ScienceDirect, PMC, and Google Scholar. Peer-reviewed articles, clinical reviews, trauma guidelines, and observational studies related to systemic trauma physiology, trauma-induced coagulopathy, metabolic dysfunction, and multiple organ dysfunction syndrome were analyzed. The reviewed evidence demonstrated that inflammatory mediators such as interleukin-6, tumor necrosis factor-alpha, complement activation products, and oxidative stress pathways play fundamental roles in systemic deterioration after severe trauma. Simultaneously, hypercatabolism, stress hyperglycemia, insulin resistance, and prolonged endocrine activation contribute significantly to physiologic instability and delayed recovery. Trauma-induced coagulopathy emerged as a dynamic process strongly associated with endothelial injury, inflammatory signaling, hemorrhagic shock, and microvascular dysfunction. Pulmonary, cardiovascular, renal, hepatic, and neurological dysfunction represented the most frequent systemic complications identified during trauma progression.