SIRS (systemic inflammatory response syndrome) is a complex immune response that is characterized by hyperdynamic cardiac function and low afterload. This syndrome is manifested by signs of inflammation including hyperthermia or hypothermia, tachycardia, tachypnea, and elevated or depressed white blood cell count. This state lies in a spectrum with septic shock with the notable exception that septic shock is associated with the presence of an infection. The multiple triggers of SIRS include trauma, surgery, medications, and transfusions. The proinflammatory reaction of SIRS correlates to the severity of tissue damage. Depending on the injury, the response can progress to a shock state including hypotension, oliguria, mental status changes, and coagulopathies.

One of the strongest surgical triggers of SIRS is spine surgery. During spine surgery, destruction of bone and soft tissue activates macrophages to release proinflammatory cytokines such as tumor necrosis factor α (TNF-α), and interleukin 1 (IL-1). These factors then induce the production of IL-6 and IL-8 from endothelial and epithelial cells, fibroblasts, and monocytes, propagating SIRS. The onset of these factors occurs immediately following the procedure and is manifested clinically as elevations of body temperature and erythrocyte sedimentation rate (ESR), leukocytosis, and an increase in C-reactive protein (CRP). In severe reactions, patients may experience hypotension, coagulopathies, and shifting of intravascular fluid to the interstitial space. Much of the proinflammatory phase peaks on postoperative day one but can continue to linger up to postoperative day four. ESR will continue to be elevated for weeks following surgery. The extent of SIRS is affected by the duration and extent of spinal surgery, the volume of blood loss, the level of postoperative pain, and the degree of instrumentation during the procedure. Instrumentation results in a dramatic increase in the inflammatory response possibly from increased tissue destruction with implant placement or a direct physiological reaction to the implant material.