Review Article

Spontaneous Bacterial Peritonitis – Bacteriology, Diagnosis, Treatment, Risk Factors and Prevention

J. B. Dever; M. Y. Sheikh


Aliment Pharmacol Ther. 2015;41(11):1116-1131. 

In This Article


Intravenous Antibiotics

If suspicion for SBP arises (i.e. fever, abdominal pain or tenderness, altered mental status, or otherwise unexplained decompensation in patients with cirrhosis and ascites), then antibiotics should be started immediately to reduce complications and improve survival. Third-generation, broad-spectrum cephalosporins are the agents of choice for SBP treatment because of their superiority in randomised controlled trials and rare side effect profile with minimal risk of nephrotoxicity compared to other antibiotics.[103–105] Cefotaxime covers most culprit pathogens, has excellent ascitic fluid penetration and achieves sterilisation in 94% of cases after initial antibiotic dosing.[106] Treatment efficacy and clinical resolution with cefotaxime 4 g/day has ranged from 77% to 98%. Higher dosing, i.e. 8 g/day has not provided a therapeutic advantage.[107] However, cefotaxime 2 g every 8 h (6 g/day) is considered the standard regimen and current guideline recommendation put forth by the American Association for the Study of Liver Diseases.[57] A 5-day course of cefotaxime 2 g every 8 h is as effective as 10 days of treatment. No differences were seen with infection cure, SBP recurrence and hospital mortality rates.[104]

Alternative intravenous antibiotic regimens for SBP include amoxicillin–clavulanic acid, which has comparable results to cefotaxime,[108] ampicillin and gentamicin,[103] and fluoroquinolones. Antibiotics other than third-generation cephalosporins have an increased risk for adverse events, and there is less evidence supporting their role in primary treatment. A second-line choice of third-generation cephalosporins is ceftriaxone, a strongly protein bound antibiotic, and because of poor protein synthesis in cirrhotic patients, is theoretically less effective for SBP treatment. Nevertheless, ceftriaxone has been well studied for primary treatment of SBP,[109,110] and although considered inferior to cefotaxime, ceftriaxone is effective therapy particularly at doses of 2 g/day for 5 days.[111,112] Aminoglycosides cause renal impairment in 5% of patients and should be avoided in patients with cirrhosis who have considerable risk for renal injury.[113] Fluoroquinolones have comparable ascitic fluid penetration to cephalosporins.[114] Levofloxacin has shown similar efficacy compared to (cefotaxime and cefepime) at providing E. coli coverage [71% vs. (82%)] and coagulase-negative Staphylococcus coverage [90% vs. (44%)] in patients with SBP not receiving fluoroquinolone prophylaxis.[26] In patients with penicillin allergy who are not receiving long-term fluoroquinolone therapy, levofloxacin is a reasonable and safe alternative treatment for SBP.[115]

Oral Antibiotics

Oral fluoroquinolones are generally acceptable for uncomplicated SBP (i.e. absence of sepsis and patients at risk for aspiration). Fluoroquinolones have excellent oral bioavailability ranging from 70% for ciprofloxacin to 95% for levofloxacin.[116] In a randomised controlled trial, oral ofloxacin and IV cefotaxime resolved SBP at the same rate (84% vs. 85%) respectively.[105]

Switch Therapy

In a randomised study in 2000, Terg et al. showed that patients with SBP can be adequately treated with oral ciprofloxacin after a short course of IV ciprofloxacin.[117] Switch therapy with oral ciprofloxacin was as effective as IV ciprofloxacin at infection resolution in a randomised study involving 116 patients with SBP and was more cost effective.[118]

Antibiotics for Multi-resistant Bacteria

Emergence of antibiotic resistance and changing profile to SBP-causing-bacteria have made standard treatment less reliable in some instances. In fact, 8–22% of Enterobacteriaceae have cephalosporin resistance.[33,119] A 5-year retrospective study of 67 patients with SBP revealed that long-term prophylactic norfloxacin treatment reduced the risk of Gram-negative infections but increased the risk of severe hospital-acquired staphylococcal infections, whereby 77% were methicillin-resistant.[120]


Albumin is a single chain peptide protein, made in the liver, with a half-life of approximately 21 days. It regulates plasma oncotic pressure, buffers plasma, scavenges free radicals, and transports hormones, fatty acids, unconjugated bilirubin, metals, ions, and drugs. The structure and function of albumin is abnormal in advanced liver disease thereby impairing many key physiological processes.[121] Hypoalbuminemia has myriad causes and is associated with increased morbidity and mortality regardless of aetiology.[122,123]

Albumin is cornerstone therapy for select patients with SBP in addition to antibiotics. A randomised, controlled trial involving patients with SBP treated with cefotaxime alone compared to cefotaxime and albumin (1.5 g/kg within 6 h of diagnosis, followed by 1 g/kg on day 3) demonstrated that by adding albumin patients avoided irreversible renal impairment (10 vs. 33%, P = 0.002) and had lower mortality both during hospitalisation (10 vs. 29%, P = 0.01) and at 3-month follow-up after discharge (22 vs. 41%, P = 0.03).[124] Renal impairment occurs in one-third of patients with SBP, and albumin is not indicated for all patients. Patients should be carefully screened to receive albumin infusion, because those at risk for renal impairment [i.e. serum creatinine > (1 mg/dL = 88.4 μmol/L), bilirubin > (4 mg/dL = 68.4 μmol/L), BUN > 30 mg/dL] have clearly shown benefit.[125] Patients with chronic kidney disease with or without dialysis dependency who develop SBP should receive albumin therapy.