Overall Bottom Line
- SBP is observed predominantly in patients with advanced cirrhosis.
- Gram-negative aerobic bacteria are causative in approximately 80% of patients, anaerobic bacteria occur in no more than 5% of patients, but the prevalence of multidrug resistant organisms is increasing.
- Diagnostic paracentesis with ascitic fluid analysis (PMN count and culture) is the cornerstone of diagnosis.
- Primary and secondary prophylaxis improves survival.
- Treatment (third generation cephalosporins are first line antibiotics) leads to resolution of SBP in 70–90% of patients.
- Early diagnosis and treatment have reduced in-hospital mortality from approximately 80% to 15–20%.
Section 1: Background
Definition
- SBP is a life-threatening infection of ascites in the absence of an intra-abdominal source of infection and with no obvious source of bacteria.
Epidemiology
- SBP is observed predominantly in patients with advanced cirrhosis.
- The prevalence of SBP in outpatients is 1.5–3.5% and approximately 15–20% in hospitalized patients.
- SBP occurs in between 25% and 65% of cirrhotic patients with acute GI bleeding.
Etiology
- Gram-negative aerobic bacteria is most common (80% of cases; E. coli > Klebsiella species).
- Gram-positive cocci, mainly Streptococcus species (S. pneumoniae) occur in 20% of cases.
- Anaerobic bacteria occur in <5% of patients.
- Ninety percent of all SBP cases are monomicrobial.
- Epidemiology of bacterial infections differs between community-acquired (Gram-negative infections predominate) and nosocomial infections (Gram-positive infections predominate).
- Microbiology of SBP is changing with an increasing prevalence of MDR organisms. Suspect MDR organisms if:
- SBP is nosocomial.
- The patient was in hospital recently.
- The patient had intestinal decontamination.
- SBP is nosocomial.
Pathogenesis
- Multifactorial, not well understood.
- Dysfunction of the immune system in cirrhosis.
- Activity of the RES-system (chemotaxis, phagocytosis, intracellular killing) impaired.
- Deficient phospholipase C activity in blood neutrophils.
- Increased intestinal permeability.
- Bacterial overgrowth and translocation of intestinal micro-organisms.
- Endotoxemia.
- Reduced levels of antibacterial substances in ascites (e.g. opsonins, complement components).
Risk factors
- The risk of SBP is increased in cirrhotic patients with the following conditions:
- GI bleeding.
- Low total protein concentration (<1–1.5 g/dL) in ascites.
- Severe liver dysfunction.
- History of previous SBP.
- Use of proton pump inhibitors.
- GI bleeding.
Section 2: Prevention
- Primary prophylaxis is restricted to patients with high risk of SBP.
- Third generation cephalosporins are first line antibiotics in patients with acute GI bleeding.
- Fluoroquinolones may be used in patients with low total protein content in ascites.
- Primary prophylaxis improves survival.
- Whether prophylaxis should be given intermittently or continuously remains unsettled.
Screening
- A diagnostic paracentesis should be performed:
- In all cirrhotic patients with newly formed ascites.
- In any patient with cirrhosis and ascites on hospital admission.
- In patients with cirrhosis and ascites who develop compatible symptoms or signs of peritonitis (e.g. abdominal pain, fever).
- In any patient with cirrhosis and ascites with worsening renal, liver or mental function/hepatic encephalopathy without an obvious cause (see Chapter 19).
- In all cirrhotic patients with newly formed ascites.
Primary prevention
- Primary prophylaxis should be restricted to patients at high risk of SBP, i.e. those with:
- Low total protein content in ascites (1–1.5 g/dL), and/or
- Acute GI hemorrhage.
- Low total protein content in ascites (1–1.5 g/dL), and/or
- Patients with acute GI bleeding and severe liver disease:
- Ceftriaxone 1–2 g IV once a day for 3–4 days. May be switched to
- Norfloxacin 400 mg PO twice a day after bleeding has been controlled.
- Ceftriaxone 1–2 g IV once a day for 3–4 days. May be switched to
- Patients with acute GI bleeding and less severe liver disease:
- Norfloxacin 400 mg PO once to twice a day or
- Ciprofloxacin 500 mg PO twice a day or 750 mg PO once weekly.
- Norfloxacin 400 mg PO once to twice a day or
- Patients without GI bleeding with low total protein (<1–1.5 g/dL) in ascites:
- Norfloxacin 400 mg PO once a day for 12 months.
- Whether prophylaxis should be given intermittently or continuously currently is unsettled.
Secondary prevention
- Patients recovering from one episode of SBP should receive long-term secondary prophylaxis with:
- Norfloxacin 400 mg PO once a day (or another quinolone) or
- Co-trimoxazole (TMP/SMX) 1 double-strength tablet PO once a day, 5 days per week.
- Norfloxacin 400 mg PO once a day (or another quinolone) or
- Secondary prophylaxis should be continued until the disappearance of ascites or until liver transplantation.
- Long-term secondary prophylaxis will result in a:
- Change of bacterial spectrum towards Gram-positive cocci as well as
- Emergence of quinolone resistant Gram-negative organisms.
- Change of bacterial spectrum towards Gram-positive cocci as well as
- Patients who develop SBP on prophylactic quinolones respond as well to third generation cephalosporins as patients not on prophylaxis.
Section 3: Diagnosis
Clinical Pearls
- Clinical findings are unreliable and may be misleading.
- The diagnosis of SBP is based on the results of ascitic fluid analysis:
- Neutrophil cell count >250/mm3 (>0.25 × 109/L).
- Positive culture.
- Neutrophil cell count >250/mm3 (>0.25 × 109/L).
Differential diagnosis
Differential diagnosis | Features |
---|---|
Secondary bacterial peritonitis due to intestinal perforation | Suspect secondary bacterial peritonitis in patients with:
|
Peritoneal tuberculosis | Culture-negative peritonitis; sensitivity of ascites smear for mycobacteria is 0%, that of ascites culture is approximately 50% |
Peritoneal carcinomatosis | Culture-negative peritonitis; if three still warm ascites samples are examined without delay the sensitivity of cytological examination in diagnosing peritoneal carcinomatosis amounts to >90% |
Typical presentation
- The clinical signs and symptoms of SBP may be subtle and range from:
- Asymptomatic, to
- Fever, abdominal pain, abdominal tenderness, altered mental status (50–60% of patients),
- Diarrhea, paralytic ileus, hypotension, hypothermia (≤50% of patients).
- Asymptomatic, to
Clinical diagnosis
History
- Enquire about the presence of chronic liver disease/liver cirrhosis, history of previous SBP and the use of proton pump inhibitors.