Peritonitis: update on pathophysiology, clinical manifestations, and management.

Peritonitis results from any local trigger of inflammation. titis, congestive heart failure, metastatic malignant disease, systemic lupus erythematosus, and lymphedema and, rarely, in Usually infection is the trigger, although infection may not necessarily be present at the earliest stage. For example, sterile adults with no underlying disease [3]. The presence of ascites appears to be the common link among these various conditions. peritonitis may occur in the localized peritoneal space surrounding an infected but resectable intraabdominal organ, such The route of infection in primary peritonitis is usually not as the appendix or gallbladder. In contrast, there may be conapparent but is thought to be hematogenous, lymphogenous, tamination of the peritoneum from a defect in the intestinal via transmural migration through an intact gut wall from the wall, before establishment of infection or onset of an inflamintestinal lumen, or, in women, from the vagina via the fallomatory response, e.g., immediately following penetrating abpian tubes. In cirrhotic patients the hematogenous route is most dominal trauma. Peritonitis has been categorized as primary, likely. Organisms removed from circulation by the liver may secondary, or (more recently) tertiary. Peritonitis complicating contaminate hepatic lymph and pass through the permeable peritoneal dialysis can be considered as an additional category. lymphatic walls into the ascitic fluid. In addition, portosystemic Each of these categories is reviewed herein, with an emphasis shunting greatly diminishes hepatic clearance of bacteremia, on recent developments in pathogenesis, evaluation, and manwhich would tend to perpetuate bacteremia and increase the agement. opportunity to cause metastatic infection at susceptible sites such as the ascitic collection. The infrequency of primary peritonitis in forms of ascites Primary Peritonitis other than that due to liver disease emphasizes the importance Pathogenesis. Primary peritonitis is an infection of the periof intrahepatic shunting in the pathogenesis of this disease. toneal cavity not directly related to other intraabdominal abnorThe hepatic reticuloendothelial system is known to be a major malities. The vast majority of cases are due to bacterial infecsite for removal of bacteria from blood, and animal studies tion; it is also commonly known as spontaneous bacterial have suggested that destruction of blood-borne bacteria by the peritonitis. Usually it occurs in the presence of ascites from reticuloendothelial system is impaired in experimental cirrhosis any of a variety of underlying conditions [1]. In the preantiand in alcoholic liver disease. The decrease in phagocytic activbiotic era, primary peritonitis accounted for Ç10% of all pediity seen in alcoholic cirrhosis is proportional to the severity of atric abdominal emergencies; it now accounts for õ1–2% [2]. the liver disease. The decline has been attributed to widespread use of antibiotics Enteric bacteria may also gain access to the peritoneal cavity for minor upper respiratory tract illness. by directly traversing the intact intestinal wall. In an animal Although primary peritonitis may occur in children without model, Escherichia coli passes from the bowel into the peritopredisposing disease, it is especially associated with postneal cavity after the introduction of hypertonic solutions into necrotic cirrhosis and nephrotic syndrome. In adults, primary the peritoneum. The infrequent occurrence of bacteremia and peritonitis develops in up to 25% of patients with alcoholic the multiplicity of species in peritoneal fluid when anaerobic cirrhosis but has also been reported to occur in adults with bacteria are involved suggest that transmural migration of bacpostnecrotic cirrhosis, chronic active hepatitis, acute viral hepateria is the probable route of infection of ascitic fluid in most of these patients. In prepubertal girls, the pathogenesis of primary peritonitis is likely related to an ascending infection of genital origin, as Received 21 January 1997; revised 10 February 1997. suggested by the simultaneous presence of pneumococci in Reprints or correspondence: Dr. Matthew E. Levison, Division of Infectious Diseases, Allegheny University–MCP, 3300 Henry Avenue, Philadelphia, vaginal secretions and peritoneal fluid. Alkaline vaginal secrePennsylvania 19129. tions that occur in this age group may be less inhibitory to Clinical Infectious Diseases 1997;24:1035–47 bacterial growth than the acidic secretions of postpubertal feq 1997 by The University of Chicago. All rights reserved. 1058–4838/97/2406–0001$02.00 males.