Epidemiology and pathophysiology of intraabdominal infections (IAI)

Intraabdominal infection continues to be one of the major challenges in general surgery. Whilst the term "peritonitis" means an inflammation of the peritoneum regardless of its etiology, intraabdominal infections encompass all forms of bacterial peritonitis, of intraabdominal abscesses and of infections of intraabdominal organs. Several classification systems have been suggested for peritonitis and intraabdominal infections, respectively. However, neither phenomenological classifications nor classification systems with respect to the origin of bacterial contamination have a proven relevance for the clinical course of this disease. Moreover, most of the studies dealing with secondary peritonitis or intraabdominal infections are ill-comparable because of wide variations of inclusion criteria. Thus the true incidence of secondary bacterial peritonitis is difficult to assess. With respect to its etiology perforation of hollow viscus is the leading cause followed by postoperative peritonitis, ischemic damage of bowel wall, infection of intraabdominal organs and translocation in nonbacterial peritonitis. The anatomic origin of bacterial contamination and microbiological findings are no major predictors of outcome. However, the preoperative physiological derangement, the surgical clearance of the infectious focus and the response to treatment are established prognostic factors. The pathogenesis of intraabdominal infections is determined by bacterial factors which influence the transition from contamination to infection. Intraabdominal adjuvants and the local host response are additionally important. Bacterial stimuli lead to an almost uniform activation response which is triggered by reaction of mesothelial cells and interspersed peritoneal macrophages and which also involves plasmatic systems, endothelial cells and extra- and intravascular leukocytes. The local consequences of this activation are the transmigration of granulocytes from peritoneal capillaries to the mesothelial surface and a dilatation of peritoneal blood vessels resulting in enhanced permeability, peritoneal edema and lastly the formation of protein-rich peritoneal exudate.