PATHOPHYSIOLOGICAL MECHANISMS OF COMBAT INJURIES OF THE LOWER EXTREMITIES AND THEIR IMPACT ON THE CHOICE OF SURGICAL TACTICS
DOI:
https://doi.org/10.32345/USMYJ.3(164).2026.119-127Keywords:
blast injuries, compartment syndromes, necrosis, war-related injuries, wounds, gunshotAbstract
Introduction. Combat injuries of the lower extremities remain one of the leading causes of severe disability among military personnel. The high-energy nature of blast, gunshot, fragment, thermal, and barotraumatic injuries gives rise to complex local and systemic pathophysiological responses that largely determine the course of traumatic disease and the prospects for limb salvage.
Aim. To systematise current data on the pathophysiological mechanisms of tissue injury in the lower extremities across different types of combat trauma and to clarify their significance for the selection of surgical tactics.
Materials and methods. A narrative review of the literature indexed in PubMed/MEDLINE, Scopus, and Google Scholar for the period 2016–2026 was performed using the keywords “blast injury”, “gunshot wounds”, “fragment wounds”, “compartment syndrome”, “reperfusion injury”, “endothelial dysfunction”, and “combat trauma”. English-language full-text publications addressing the pathogenesis of combat trauma were included. After screening and removal of duplicates, 45 sources were assessed, of which 15 were included in the final analysis.
Results. Regardless of the physical mechanism of injury, combat trauma may be characterized by a three-zone pattern comprising a zone of primary necrosis, a zone of secondary injury (zone of molecular concussion), and an area of potentially reversible tissue changes. Blast injuries combine the effects of the blast wave, fragments, and thermal energy and may result in extensive muscle destruction and rhabdomyolysis; gunshot and fragment wounds are characterized by kinetic energy transfer, temporary cavitation, and substantial tissue contamination; thermal injury and barotrauma may produce zones of tissue stasis associated with increased capillary permeability and interstitial oedema. Progression of tissue injury within these zones is driven by a common cascade involving endothelial dysfunction and glycocalyx damage, the no-reflow phenomenon, intracellular calcium overload, mitochondrial dysfunction, reperfusion-associated oxidative stress, systemic inflammation, and compartment syndrome.
Conclusions. Despite differences in their physical mechanisms, various types of combat trauma share common pathogenetic mechanisms of secondary tissue injury and necrosis, providing a basis for unified approaches to monitoring tissue viability. Understanding these mechanisms supports the rational selection of surgical tactics, timely assessment of tissue viability, and improved limb salvage outcomes.
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