Peritonitis, bacterial

Spontaneous bacterial peritonitis Bacterial infection of the peritoneal fluid without an abdominal source. 

Immunological tests were performed for studying the reactive of peritoneal-exudative cells, especially peritonial macrophages, which are the main effector cells involved in natural resistance (host defence system) against bacterial infection. 

O Portal hypertension is the precipitating factor for the complications of cirrhotic liver disease—ascites, spontaneous bacterial peritonitis (SBP), variceal bleeding, and hepatic encephalopathy. Lowering portal pressure can reduce the complications of cirrhosis and decrease morbidity and mortality. 

Cirrhosis is the progressive replacement of normal hepatic cells by fibrous scar tissue. This scarring is accompanied by the loss of viable hepatocytes, which are the functional cells of the liver. Progressive cirrhosis is irreversible and leads to portal hypertension that is in turn responsible for many of the complications of advanced liver disease. These consequences include (but are not limited to) spontaneous bacterial peritonitis (SBP), hepatic encephalopathy, and variceal bleeding.1... 

Drug therapy for portal hypertension and cirrhosis can alleviate symptoms and prevent complications but it cannot reverse cirrhosis. Drug therapy is available to treat the complications of ascites, varices, spontaneous bacterial peritonitis, hepatic encephalopathy, and coagulation abnormalities. 

FIGURE 19-5. Approach to the patient with ascites and spontaneous bacterial peritonitis (SBP). 

Patients who have previously experienced spontaneous bacterial peritonitis and have low-protein ascites (ascitic fluid albumin less than 1 g/dL [less than 10 g/L]) are candidates for long-term prophylactic therapy. Recommended regimens include either a single trimethoprim-sulfamethoxazole doublestrength tablet 5 days per week (Monday through Friday) or ciprofloxacin 750 mg once weekly.19,46 Any patient who has experienced an episode of variceal bleeding should also receive prophylactic antibiotics. 

Rimola A, Garcia-Tsao G, Navasa M, et al. Diagnosis, treatment and prophylaxis of spontaneous bacterial peritonitis a consensus document. J Hepatol 2000 32 142-145. 

Peritonitis may be classified as primary, secondary, or tertiary. Primary peritonitis, also called spontaneous bacterial peritonitis, is an infection of the peritoneal cavity without an evident source of bacteria from the abdomen.1,2 In secondary peritonitis, a focal disease process is evident within the abdomen. Secondary peritonitis may involve perforation of the gastrointestinal (GI) tract (possibly because of ulceration, ischemia, or obstruction), postoperative peritonitis, or posttraumatic peritonitis (e.g., blunt or penetrating trauma). Tertiary peritonitis occurs in critically ill patients and is infection that persists or recurs at least 48 hours after apparently adequate management of primary or secondary peritonitis. 

An abscess occurs if peritoneal contamination is localized but bacterial elimination is incomplete. The location of the abscess often is related to the site of primary disease. For example, abscesses resulting from appendicitis tend to appear in the right lower quadrant or the pelvis those resulting from diverticulitis tend to appear in the left lower quadrant or pelvis. A mature abscess may have a fibrinous capsule that isolates bacteria and the liquid core from antimicrobials and immunologic defenses. 

Primary peritonitis is treated with antimicrobials and rarely requires drainage. Secondary peritonitis requires surgical removal of the inflamed or gangrenous tissue to prevent further bacterial contamination. If the surgical procedure is sub-optimal, attempts are made to provide drainage of the infected or gangrenous structures. 

Dougherty SH. Antimicrobial culture and susceptibility testing has little value for routine management of secondary bacterial peritonitis. Clin Infect Dis 1997 25(suppl 2) S258-261. 

A7. Aranow, J. S Zhuang, J., Wang, H Larkin, V., Smith, M., and Fink, M. P., A selective inhibition of inducible nitric oxide synthase prolongs survival in a rat model of bacterial peritonitis Comparison with two nonselective strategies. Shock 5, 16-121 (1996). 

Chang CS, Chen GH, Lien HC, Yeh HZ Small intestine dysmotility and bacterial overgrowth in cirrhotic patients with spontaneous bacterial peritonitis. Hepatology 1998 28 1187-1190. 

Rifaximin Rifamycin Antibiotic Gut bacteria Enteric infection Diarrhea, infectious Hepatic encephalopathy Small intestine bacterial overgrowth Inflammatory bowel disease Colonic diverticular disease Irritable bowel syndrome Constipation Clostridium difficile infection Helicobacter pylori infection Colorectal surgery Bowel decontamination, selective Pancreatitis, acute Bacterial peritonitis, spontaneous Nonsteroidal anti-inflammatory drug enteropathy... 

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