Spontaneous bacterial peritonitis: Prevention and therapy

Abstract

Spontaneous bacterial peritonitis (SBP) is a serious problem in patients with cirrhotic ascites, with an incidence of 10% to 25% on hospital admission (1) and accounting for 5% to 30% of all infections in cirrhotic patients (2, 3), 19% of documented bacteremic episodes (4) and 60% to 75% of all "serious" infections (5, 6). Recent studies (1,7,8) have focused attention on culture techniques, diagnosis, differentiation from secondary peritonitis, pathogenesis and predisposing factors. However, data on prevention and therapy have been scarce. Gin& et al. in this issue of HEPATOLOGY report the first prospective trial of prevention of SBP by use of longterm antibiotic prophylaxis (9). Is this rational with our present knowledge of the pathogenesis and therapy of SBP?Most organisms cultured from ascites in patients with SBP (1) are part of the normal aerobic flora of the gut (10-12). Low concentrations (one organism per milliliter) of a single organism are typical (13). SBP with multiple organisms or anaerobes is distinctly uncommon and probably represents secondary bacterial peritonitis. Sixty percent to 80% of the organisms in patients with SBP are aerobic gram-negative bacteria (1, 2, 5, 6, 11, 14-17). Escherichia coli is associated with 40% to 50% of cases of SBP (1, 2, 5, 6, 14), perhaps reflecting the abundance in stool (9-11). However, more frequent extraascitic dissemination with E. coli is compatible with greater virulence (9, 18, 19). The remaining organisms causing SBP are gram-positive cocci; half of which are found in the gut (1). Thus the gut appears to be the repository of most organisms causing SBP.Multiple mechanisms potentially predispose to SBP. Studies of the microbial flora in cirrhotic patients show no significant qualitative or quantitative difference from normal individuals (20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30). Thus an unusual spectrum or quantity of aerobic organisms or decreased colonization resistance by anaerobic bacteria does not appear to play a role. The decreased serum bactericidal and opsonic activity and abnormal polymorphonuclear cell function demonstrated in cirrhotic patients (31-34) have not been associated with SBP, and the degree of defect appears insufficient for such a role. Intrahepatic and extrahepatic shunting may predispose to SBP by increasing systemic bacteremia from the gut owing to Address reprint requests to:

Rapid emergence of quinolone resistance in cirrhotic patients treated with norfloxacin to prevent spontaneous bacterial peritonitis

“…As SBP is usually caused by commensal enteric organisms, selective digestive decontamination has been recommended (10). This antibiotic prophylaxis is aimed at eliminating members of the family Enterobacteriaceae while respecting the other components of the gut flora.…”

Diagnostic Usefulness of Carbohydrate Antigen-125 in Cancerous and Noncancerous Peritoneal Effusions

“…Several studies have tried to increase the sensitivity of the cytological examination by using the determination of lactate dehydrogenase (LDH) and its isoenzymes, C-reactive protein (CRP), neutrophil count, total protein content, tumor associated antigens or expression of different cellular antigens (Jacobs and Bast 1989;Hoefs 1990;Chi et al 1996). The evaluation of body fluids is more simple than the analysis of cellular parameters, especially tumor associated antigens, which are released by the tumour cells to the effused fluid, and could be of significance in the diagnostic differentiation of the cancerous from the noncancerous origin of effusions (Ricolleau et al 1984;Mezger et al 1998).…”

Randomized trial comparing ceftriaxone with cefonicid for treatment of spontaneous bacterial peritonitis in cirrhotic patients

“…A few studies have dealt specifically with the treatment of SBP in cirrhotics (14). Although some studies suggest that treatment with ceftriaxone results in higher concentrations than ceftriaxone in peritoneal fluid and has pharmacokinetic characteristics superior to those of cefotaxime, the concentrations of both agents in tissue and peritoneal fluid are greater than the minimum level necessary to inhibit the growth of peritoneal pathogens (5,12).…”