Peritonitis: Update on Pathophysiology, Clinical Manifestations, and Management

1035 STATE-OF-THE-ART CLINICAL ARTICLE Peritonitis: Update on Pathophysiology, Clinical Manifestations, and Management Caroline C. Johnson, James Baldessarre, and Matthew E. Levison Primary Peritonitis Pathogenesis. Primary peritonitis is an infection of the peritoneal cavity not directly related to other intraabdominal abnormalities. The vast majority of cases are due to bacterial infection; it is also commonly known as spontaneous bacterial peritonitis. Usually it occurs in the presence of ascites from any of a variety of underlying conditions [1]. In the preantibiotic era, primary peritonitis accounted for Ç10% of all pediatric abdominal emergencies; it now accounts for õ1 – 2% [2]. The decline has been attributed to widespread use of antibiotics for minor upper respiratory tract illness. Although primary peritonitis may occur in children without predisposing disease, it is especially associated with postnecrotic cirrhosis and nephrotic syndrome. In adults, primary peritonitis develops in up to 25% of patients with alcoholic cirrhosis but has also been reported to occur in adults with postnecrotic cirrhosis, chronic active hepatitis, acute viral hepa- Received 21 January 1997; revised 10 February 1997. Reprints or correspondence: Dr. Matthew E. Levison, Division of Infectious Diseases, Allegheny University – MCP, 3300 Henry Avenue, Philadelphia, Pennsylvania 19129. Clinical Infectious Diseases 1997;24:1035–47 q 1997 by The University of Chicago. All rights reserved. 1058–4838/97/2406–0001$02.00 / 9c2f$$ju45 05-07-97 17:21:37 titis, congestive heart failure, metastatic malignant disease, systemic lupus erythematosus, and lymphedema and, rarely, in adults with no underlying disease [3]. The presence of ascites appears to be the common link among these various conditions. The route of infection in primary peritonitis is usually not apparent but is thought to be hematogenous, lymphogenous, via transmural migration through an intact gut wall from the intestinal lumen, or, in women, from the vagina via the fallopian tubes. In cirrhotic patients the hematogenous route is most likely. Organisms removed from circulation by the liver may contaminate hepatic lymph and pass through the permeable lymphatic walls into the ascitic fluid. In addition, portosystemic shunting greatly diminishes hepatic clearance of bacteremia, which would tend to perpetuate bacteremia and increase the opportunity to cause metastatic infection at susceptible sites such as the ascitic collection. The infrequency of primary peritonitis in forms of ascites other than that due to liver disease emphasizes the importance of intrahepatic shunting in the pathogenesis of this disease. The hepatic reticuloendothelial system is known to be a major site for removal of bacteria from blood, and animal studies have suggested that destruction of blood-borne bacteria by the reticuloendothelial system is impaired in experimental cirrhosis and in alcoholic liver disease. The decrease in phagocytic activity seen in alcoholic cirrhosis is proportional to the severity of the liver disease. Enteric bacteria may also gain access to the peritoneal cavity by directly traversing the intact intestinal wall. In an animal model, Escherichia coli passes from the bowel into the peritoneal cavity after the introduction of hypertonic solutions into the peritoneum. The infrequent occurrence of bacteremia and the multiplicity of species in peritoneal fluid when anaerobic bacteria are involved suggest that transmural migration of bacteria 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 suggested by the simultaneous presence of pneumococci in vaginal secretions and peritoneal fluid. Alkaline vaginal secretions that occur in this age group may be less inhibitory to bacterial growth than the acidic secretions of postpubertal females. cida UC: CID Peritonitis results from any local trigger of inflammation. Usually infection is the trigger, although infection may not necessarily be present at the earliest stage. For example, sterile peritonitis may occur in the localized peritoneal space surrounding an infected but resectable intraabdominal organ, such as the appendix or gallbladder. In contrast, there may be contamination of the peritoneum from a defect in the intestinal wall, before establishment of infection or onset of an inflammatory response, e.g., immediately following penetrating abdominal trauma. Peritonitis has been categorized as primary, secondary, or (more recently) tertiary. Peritonitis complicating peritoneal dialysis can be considered as an additional category. Each of these categories is reviewed herein, with an emphasis on recent developments in pathogenesis, evaluation, and management. From the Division of Infectious Diseases, Allegheny University of the Health Sciences, and Veterans Affairs Medical Center, Philadelphia, Pennsylvania; and R. W. Johnson Pharmaceutical Research Institute, Raritan, New Jersey 1036 Johnson, Baldessarre, and Levison / 9c2f$$ju45 05-07-97 17:21:37 ings of peritoneal irritation. Fever (temperature of ú1007F) is the most common presenting sign, occurring in 50% – 80% of cases and even in the absence of abdominal signs or symptoms. Primary peritonitis should always be considered in the differential diagnosis of decompensation of previously stable chronic liver disease, especially hepatic encephalopathy. Primary tuberculous peritonitis usually is gradual in onset, causing fever, weight loss, malaise, night sweats, and abdominal distension. The abdomen may not be rigid and is often characterized as being ‘‘doughy’’ on palpation. The findings at surgery or laparoscopy consist of multiple nodules scattered over the peritoneal surface and omentum. Adhesions and a variable amount of peritoneal fluid are usually present. Similarly, C. immitis can cause a granulomatous peritonitis with variable clinical manifestations. Although the diagnosis of primary peritonitis can be established with certainty only after thorough laparotomy to exclude a primary intraabdominal site of infection, it can usually be surmised from examination of the peritoneal fluid. Fluid obtained at paracentesis should be analyzed for cell count, differential count, and protein concentration, and a gram stain and culture should be performed. Specimens for culture should be sent in an airless, capped syringe or injected directly into aerobic and anaerobic broth culture media; volumes of §10 mL will increase the yield of cultures [6]. A gram stain of the sediment is diagnostic when positive but is more commonly negative. Bacteremia occurs in up to 75% of patients with primary peritonitis due to aerobic bacteria, but it is rare in those with peritonitis due to anaerobes. Usually the same organisms isolated from the peritoneal fluid are recovered from the blood. The a (...truncated)