Peritonitis, Acute



  • Definition: inflammation of the peritoneum
  • Classification:
    • Aseptic: chemical irritation or systemic inflammation of peritoneum
    • Bacterial: infection of peritoneal fluid
  • Bacterial peritonitis types:
    • Primary/spontaneous bacterial peritonitis (SBP): infection of ascitic fluid in the absence of an intra-abdominal source
    • Secondary bacterial peritonitis: infection of ascitic fluid from a detectable intra-abdominal source
      • Secondary bacterial peritonitis can be further classified as either perforation peritonitis or nonperforation peritonitis.
    • Tertiary bacterial peritonitis: >48 hours of infection despite source control
    • Peritoneal dialysis–associated (PD) peritonitis


Annual incidence of SBP is around one-third in hospitalized patients with cirrhosis (1).


  • In asymptomatic patients with cirrhosis and ascites, the prevalence of SBP is low in the outpatient setting.
  • In patients with cirrhosis and ascites, 5% of peritonitis is secondary.
  • Secondary peritonitis is the most common cause of sepsis in surgical ICU patients.

Etiology and Pathophysiology

  • Mechanism
    • SBP:
      • Bacterial translocation via lymphatic spread through mesenteric lymph nodes
      • Often develops in the setting of large-volume ascites in patients with advanced cirrhosis
      • Cirrhotic patients have:
        • Alterations to gut microbiota with higher prevalence of pathogenic organisms
        • Small intestinal bacterial overgrowth (SIBO) and increased intestinal mucosal permeability to bacteria
        • Decreased cellular and humoral immunity limiting peritoneal bacterial clearance
    • Secondary:
      • Translocation of bacteria from inflamed or perforated intraperitoneal (IP) organs or introduction of bacterial through instrumentation
    • Tertiary: evolves from secondary peritonitis
    • PD peritonitis:
      • Contamination with pathogenic skin flora during exchanges or exit-site infection
  • Microbiology
    • Most cases of SBP are monomicrobial.
      • Most common gram-negative pathogens are Escherichia coli and Klebsiella species.
      • Most common gram-positive pathogens are Streptococcus and Staphylococcus species.
    • Secondary: perforation of a viscus, small bowel strangulation, necrotizing pancreatitis. Organism depends on cause of peritonitis; gram-positive organisms more common with upper GI pathology whereas gram-negative organisms more common with lower GI pathology. Common species include E. coli, Klebsiella, Proteus, Streptococcus, Enterococcus, Bacteroides, and Clostridium (1).
    • PD peritonitis is most commonly due to Staphylococcus epidermidis and Staphylococcus aureus (2).

Risk Factors

  • SBP: advanced cirrhosis with ascites, malnutrition, variceal hemorrhage, acid-suppressive therapy, and prior SBP (1)
    • Acid suppression (most commonly with PPIs) promotes gut bacterial growth and translocation.
    • 70% of SBP cases are in patients with Child-Pugh class C cirrhosis.
    • Low ascites protein (<1 g/dL) increases risk.
  • Secondary:
    • Helicobacter pylori or NSAID-induced ulcers, vascular disease causing bowel ischemia, alcohol-related pancreatitis, trauma, or IBD causing bowel perforation
  • PD peritonitis:
    • Nonsterile technique
    • Recent instrumentation

General Prevention

  • SBP prophylaxis decreases mortality in patients at high risk (e.g., ascitic fluid protein concentration <1 g/dL, esophageal varices, or history of previous SBP).
    • Primary prophylaxis: antibiotics including norfloxacin, ciprofloxacin, trimethoprim-sulfamethoxazole
    • Patients with cirrhotic ascites who have low ascitic fluid protein (<1.5 g/dL), renal impairment (creatinine ≥1.2 mg/dL, BUN ≥25 mg/dL, serum sodium [Na] ≤130 mEq/L) or liver failure (Child-Pugh score ≥9 and serum bilirubin ≥3 mg/dL) should receive SBP prophylaxis (1).
  • Limit use of PPI therapy.
  • PD peritonitis:
    • Adherence to sterile technique
    • Antibiotic prophylaxis prior to selected procedures

Commonly Associated Conditions

SBP almost always occurs in the setting of decompensated cirrhosis (3).

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