Aim: To evaluate effective alternative antibiotics in treatment of cefotaxime-resistant spontaneous bacterial peritonitis.

Methods: One hundred cirrhotic patients with spontaneous bacterial peritonitis [ascitic fluid polymorphonuclear cell count (PMNLs) ≥ 250 cells/mm(3) at admission] were empirically treated with cefotaxime sodium 2 g/12 h and volume expansion by intravenous human albumin. All patients were subjected to history taking, complete examination, laboratory tests (including a complete blood cell count, prothrombin time, biochemical tests of liver and kidney function, and fresh urine sediment), chest X-ray, a diagnostic abdominal paracentesis, and the sample subjected to total and differential cell count, chemical examination, aerobic and anaerobic cultures. Patients were divided after 2 d by a second ascitic PMNL count into group I; patients sensitive to cefotaxime (n = 81), group II (n = 19); cases resistant to cefotaxime (less than 25% decrease in ascitic PMNL count). Patients of group II were randomly assigned into meropenem (n = 11) or levofloxacin (n = 8) subgroups. All patients performed an end of treatment ascitic PMNL count. Patients were considered improved when: PMNLs decreased to < 250 cells/mm(3), no growth in previously positive culture cases, and improved clinical manifestations with at least 5 d of antibiotic therapy.

Results: Age, sex, and Child classes showed no significant difference between group I and group II. Fever and abdominal pain were the most frequent manifestations and were reported in 82.7% and 80.2% of patients in group I and in 94.7% and 84.2% of patients in group II, respectively. Patients in group II had a more severe ascitic inflammatory response than group I and this was demonstrated by more ascitic lactate dehydrogenase (LDH) [median: 540 IU/L (range: 150-1200 IU/L) vs median: 240 IU/L (range: 180-500 IU/L), P = 0.000] and PMNL [median: 15,000 cell/mm(3) (range: 957-23,822 cell/mm(3)) vs 3400 cell/mm(3) (range: 695-26,400 cell/mm(3)), P = 0.000] counts. Ascitic fluid culture was positive in 32% of cases. Cefotaxime failed in 19% of patients; of these patients, 11 (100%) responded to meropenem and 6 (75%) responded to levofloxacin. Two patients with failed levofloxacin therapy were treated according to the in vitro culture and sensitivity (one case was treated with vancomycin and one case was treated with ampicillin/sulbactam). In group II the meropenem subgroup had higher LDH (range: 108-860 IU/L vs 120-491 IU/L, P = 0.042) and PMNL counts (range: 957-23,822 cell/mm(3)vs 957-15,222 cell/mm(3), P = 0.000) at initiation of the alternative antibiotic therapy; there was no significant difference in the studied parameters between patients responsive to meropenem and patients responsive to levofloxacin at the end of therapy (mean ± SD: 316.01 ± 104.03 PMNLs/mm(3)vs 265.63 ± 69.61 PMNLs/mm(3), P = 0.307). The isolated organisms found in group II were; enterococci, acinetobacter, expanded-spectrum β-lactamase producing Escherichia coli, β-lactamase producing Enterobacter and Staphylococcus aureus.

Conclusion: Empirical treatment with cefotaxime is effective in 81% of cases; meropenem is effective in cefotaxime-resistant cases.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3587484PMC
http://dx.doi.org/10.3748/wjg.v19.i8.1271DOI Listing

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