Operative management of intraabdominal infections still rests on the principles of elimination of focus, reduction of contamination of the peritoneal cavity, and treatment of residual infection. To control the source of contamination from a perforated viscus primary closure, exclusion or resection may be considered with respect to the severity of peritonitis and to the underlying disease. The principle of "peritoneal toilet" with complementary use of systemic and/or local antibiotics is generally accepted even if the value of aggressive debridement is still debated controversely. For the treatment of residual and the prevention of recurrent infection, closed and open lavage techniques, the left-open abdomen, and planned relaparotomy represent the major approaches in severe generalized peritonitis when the infectious focus might not be securely controlled. The values and disadvantages of different regimens are discussed, additional measures are briefly described, and an outlook on areas of further research is given.

According to these results, it may be expected that tumours with a VEGF/MIB-1 ratio of 1:6 or less prior to RCX will respond to this therapy.

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.

The study supports the view that these bacteria continue to play a minor role in secondary peritonitis. The point has to be emphasized, however, that the patients under study were in relatively good condition (APACHE II median 9 for cephalosporins and 10 for penicillins) and that postoperative cases of peritonitis were excluded.

Complexes of granulocyte elastase and alpha 1-antitrypsin are markers for granulocyte activation. In 75 patients with acute pancreatitis these complexes were immunologically determined daily in plasma during the first week of hospitalization. Patients were classified into three groups: mild pancreatitis (I, less than or equal to 1 complication, N = 34), severe pancreatitis (II, greater than or equal to 2 complications, N = 29), lethal outcome (III, N = 12). Initially, granulocyte elastase (mean +/- SEM) was lower in group I (348 +/- 39 micrograms/liter) as compared to groups II (897 +/- 183 micrograms/l) and III (799 +/- 244 micrograms/liter), P less than 0.001 for I vs II + III. Initial elastase concentrations greater than 400 micrograms/liter were consistent with a severe or fatal course of the disease but did not distinguish between severe and lethal pancreatitis. In patients with mild or severe disease, mean elastase concentrations decreased continuously during the following days (197 +/- 15 micrograms/liter in mild cases, 325 +/- 30 micrograms/liter in severe cases at day 7). In patients with lethal disease, however, mean elastase concentrations even increased at day 2 and remained higher than 700 micrograms/liter during the observation period. At days 1 and 2 the predictive value for severe or lethal disease of raised (greater than 400 micrograms/liter) elastase concentrations [positive predictive value (PPV) 82%, negative predictive value (NPV) 81%] was better than that of elevated (greater than 100 mg/liter) C-reactive protein (PPV 73%, NPV 73%), elevated (greater than 4.0 g/liter) alpha 1-antitrypsin (PPV 59%, NPV 50%), or decreased (less than 1.5 g/liter) alpha 2-macroglobulin (PPV 82%, NPV 67%).(ABSTRACT TRUNCATED AT 250 WORDS)