Aim: Severely injured patients experience substantial immunological stress upon traumatic insult. Next to the direct local tissue injury also other organs, which are not directly injured such as liver and lung, are frequently affected by a so-called remote organ damage (ROD) after trauma. Thus, we studied the inflammatory response of lung and liver either after isolated femur fracture as example for ROD, or after multiple trauma in a porcine polytrauma model.
Methods: Twenty-four male pigs (Sus scrofa) underwent either isolated standardized femoral fracture (monotrauma, MT, n = 12) or polytrauma (PT, n = 12). PT consisted of a femur fracture, lung contusion, liver laceration, hemorrhagic shock, subsequent resuscitation and surgical fracture fixation. Six animals served as controls (sham). After 72 h inflammatory changes were determined by analyses of the interleukin (IL)-6 gene expression and tissue infiltration of polymorphonuclear leukocyte (PMN, myeloperoxidase staining). ROD in MT, and lung as well as liver damage in PT were assessed histologically by hematoxylin-eosin staining. Expression of phosphorylated p65 NF-κB was evaluated by immunohistology.
Results: IL-6 increased in lungs and liver in both groups MT and PT, respectively, compared to sham. Similarly, PMN infiltration of the lungs and liver increased significantly after both MT and PT compared to sham. Histological evaluation demonstrated tissue damage notably in lungs after MT, while tissue damage after PT was found in both lung and liver after PT. p65 NF-κB tended to an increase upon MT, and was significantly enhanced after PT in both tissues.
Conclusion: Our data indicate that remote organ damage after MT notably in lungs was associated with an enhanced inflammatory response. Severe polytrauma substantially intensifies this response and organ damage in the underlying model.
Keywords: Fracture; Inflammation; Liver; Lung; Monotrauma; Polytrauma.