A final component of the surgical stress response is activation of the immune system, a necessary factor in recovery and wound healing. In the early postoperative period, innate immune mechanisms (immunity that is naturally present and is not due to prior exposure) are activated leading to an influx of white blood cells into the wound and the production of inflammatory mediators (cytokines and chemokines). [4] If an infectious agent had been encountered by the patient prior to surgery itself, the acquired or adaptive immune system may also be activated. The inflammatory response associated with activation of the immune system is aimed at getting rid of the infectious agent, reducing tissue damage, removal of dead cells, and start of the healing process. A key part of that healing process is an increase in anti-inflammatory agents which reduce the severity and duration of the inflammatory response. Although the stress response is highly protective by design, under certain conditions, such as surgery, instead of the sympathetic, endocrine, and immune activation being self-limiting and restorative, the response can lead to further injury. Factors affecting the likelihood of an injurious response include the magnitude of surgery, the presence of co-existing diseases particularly those affecting the lungs, heart, and kidney (e.g. diabetes) , the occurrence of postoperative complications such as bleeding or infection, impaired exercise tolerance before surgery, and malnutrition.
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