DESCRIPTION

• 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 (PD)–associated peritonitis

EPIDEMIOLOGY

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).