| Summary: | <p>Abstract</p> <p>Background</p> <p>Trauma such as found patients with femur fractures, induces a systemic inflammatory response, which ranges from mild SIRS to ARDS. Neutrophils (i.e. PMN) play an important role in the pathogenesis of this inflammatory condition. Additional activation of PMNs during intramedullary nailing (IMN) is thought to act as a second immunological hit. Damage control orthopedics has been developed to limit this putative exacerbation of the inflammatory response. The hypothesis is tested that IMN exacerbates systemic inflammation, thereby increasing the risk for ARDS.</p> <p>Methods</p> <p>Thirty-eight trauma patients who required IMN for femur fracture were included. The development of SIRS and ARDS was recorded. Blood samples were taken prior and 18 hours after IMN. Inflammatory response was analyzed by changes in plasma IL-6 levels, monocyte (HLA-DR) and PMN phenotype (MAC-1 and responsiveness for the innate immune stimulus fMLP in the context of active FcγRII).</p> <p>Results</p> <p>Plasma IL-6 was significantly enhanced in severely injured patients compared to patients with isolated femur fractures and matched controls (P = 0.005; P = 0.018). This enhanced inflammatory tone was associated with a lower percentage HLA-DR positive monocytes (P = 0.002). The systemic PMN compartment was activated, characterized by an increased MAC-1 expression and a significantly decreased sensitivity for the innate stimulus fMLP Interestingly the PMN compartment was not affected by IMN.</p> <p>Conclusions</p> <p>Multitrauma patients were characterized by a marked activation of the systemic inflammatory response, associated with a systemic activation of the monocyte and PMN compartments. IMN particularly affected the monocyte arm of the systemic innate immune system.</p>
|
|---|
