Spontaneous bacterial peritonitisK65.-

Bacterial inflammation of the peritoneal cavity with no indication of any other intra-abdominal cause of infection (e.g. cholecystitis, diverticulitis, etc.), peritoneal metastases or tuberculosis SBP is a common complication of liver cirrhosis with an incidence of between 10 and 50 percent per year in the presence of ascites, but can also occur in other underlying diseases, for example malignant ascites. It is microbiologically defined as evidence of colonisation of the ascites with bacteria without increased PMN count in the ascites (i.e. <250 PMN/mm3).

Risk factors for the occurrence of spontaneous bacterial peritonitis are:

• an SBP that has already taken place
• a gastrointestinal haemorrhage
• a low total protein content in the ascites (<1.5 or <1.0g/dl).

Untreated SBP has a high mortality rate. If ascites persists, recurrence rates of 30 to 70% within one year are to be expected.

Spontaneous bacterial peritonitis is the most common spontaneous bacterial infection in liver cirrhosis and is reported in prospective case series with about 24% of all bacterial infections in hospitalized patients with liver cirrhosis. In the outpatient setting in asymptomatic patients with refractory ascites, the prevalence of SBP is max. 3.5%, in hospitalized patients 8-36%.

Signs of severe liver disease. The clinical symptoms of SBP are often mild and non-specific. Abdominal pain and fever are detectable in up to 80% of cases. The abdominal walls may be moderately tense during the examination, and peritonism with a board-like abdominal wall is rather untypical. In mild abdominal symptoms, the occurrence or worsening of hepatic encephalopathy, hypotension or renal failure may be the sole symptoms of SBP (Häussinger D et al. 2000).

The diagnosis is made by ascites puncture with detection of more than 250 neutrophil granulocytes per µl in the puncture and/or microbiological germ detection.

Antibiotic therapy should be started immediately after the diagnosis of an SBP. The choice of antibiotic is empirically based on the expected bacterial spectrum (predominantly gram-negative intestinal germs).

The intravenous administration of cefotaxime has been proven to be effective. Dosage 2x 2 g/day i.v. (Gines P et al. 1989). The main advantage is the low nephrotoxicity (clinical picture is often complicated by severe kidney dysfunction). Some authors recommend the additional administration of metronidazole (up to 10% anaerobic infections). Ampicillin combined with clavulanic acid, aztreonam, ampicillin with aminoglycosides or oral fluoroquinolones have also been shown to be effective in individual studies.

The success of antibiotic therapy of SBP should be assessed clinically as well as by diagnostic control puncture of the ascites approx. 48h after the start of therapy (Häussinger D et al. 2000; Song KH et al. 2009).

The hospital mortality of a first SBP episode is reported to be 10-50% depending on the concomitant risk factors. The 1-year mortality after the occurrence of a first SBP is between 31% and 93%.

The following factors can be identified as predictive risk factors for an unfavorable course in different collectives:

• Age of the patient (Thuluvath PJ et al. 2001)
• Child Pugh Score (Toledo C et al. 1993)
• Intensive stay
• nosocomial SBP (Toledo C et al. 1993)
• hepatic encephalopathy
• Serum creatinine and bilirubin
• cultural pathogen detection and occurrence of bacteremia (Cho JH et al. 2007)

In the presence of ascites with reduced total protein content (<1.5g/dl), primary prophylaxis with antibiotics can be carried out. In patients with additional presence of one of the two criteria:

• severe liver failure, i.e. Child-Pugh-Score>9 with bilirubin >3mg/dl
• Renal failure with serum creatinine >1.2mg/dl, urea >25mg/dl or sodium <130 mEq/l

antibiotic primary prophylaxis should be given. In case of gastrointestinal bleeding in liver cirrhosis (with or without ascites) antibiotic primary prophylaxis should always be taken.

In principle, the presence of SBP should be considered whenever the condition of a cirrhosis of the liver with ascites worsens, but also in cases of refractory ascites without pronounced signs of infection.

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