Inflammatory response after abdominal surgery

Abstract

Surgical manipulation of the gut elicits an inflammatory cascade within the intestinal muscularis that contributes to postoperative bowel dysmotility. A range of cytokines is sequentially released into the peritoneal fluid following abdominal surgery, their concentrations reflecting the magnitude of surgical trauma. The overproduction of inflammatory mediators might have detrimental effects on organ function and contribute to the enhanced risk of anastomotic leakage in the presence of sepsis. Specific cellular immune functions such as the microbicidal activity of peritoneal phagocytes are depressed after elective surgery, imposing a risk of infectious complications. Laparoscopic surgery decreases the local and systemic production of cytokines and acute-phase reactants, and better preserves peritoneal immunity compared with open surgery. As concluded from animal studies, the gas used for the pneumoperitoneum may possess substantial immunomodulatory activity.