• Inflammation of the peritoneal cavity in reaction to infection or chemical irritation by organic fluids (e.g., intestinal contents, bile, blood, or urine)
  • Infectious peritonitis can be classified as follows:
    • Primary or spontaneous bacterial peritonitis (SBP), which occurs without an obvious source or a break in continuity of the intestinal lumen
    • Secondary peritonitis occurs with visceral disruption from bowel perforation, abscess formation, ischemic necrosis, or penetrating abdominal injury; typically polymicrobial
    • Tertiary peritonitis is recurrent infection of the peritoneal cavity after presumed adequate treatment for primary or secondary peritonitis.


Rates of peritonitis vary based on the underlying abdominal processes but classically occurs in association with cirrhosis, nephrotic syndrome, and malignancy.


  • In children on peritoneal dialysis, SBP incidence increases with duration, but majority suffer episode in first 6 months.
  • Age may have inverse relationship on incidence rates: 0.79 peritoneal infections per year (in patients <1 year of age) versus 0.57 infections in children >12 years.


In children with chronic liver disease–related ascites, prevalence of SBP ranges from 19% to 56%.

Risk Factors

  • End-stage liver disease
  • Serum albumin <1.5 g/dL
  • Low serum levels of complement factors C3 and C4
  • Nephrotic syndrome (inability to clear organisms, most common is Streptococcus pneumoniae)
  • Splenectomy (encapsulated organisms: group A streptococci, Escherichia coli, S. pneumoniae, Bacteroides sp.)
  • Peritoneal dialysis
  • Presence of gastrointestinal hemorrhage
  • Prematurity
  • Proton pump inhibitor use

General Prevention

  • Children with chronic liver disease should receive all recommended childhood vaccinations.
  • Children with functional asplenia due to portal hypertension should receive the meningococcal and pneumococcal conjugate vaccines as early as possible.
  • Oral antibiotic prophylaxis reduces occurrence of SBP and improves short-term survival in adults with cirrhosis.


  • When bacteria or chemicals reach the peritoneal cavity, a local peritoneal and systemic host defense response is initiated:
    • Mechanical clearance of bacteria via lymphatics: Entrance of bacteria and bacterial products into the bloodstream contributes to the systemic response.
    • Phagocytosis and destruction of bacteria
    • Sequestration and walling off of bacteria with delayed clearance by phagocytic cells
    • Initial response is characterized by hyperemia, exudate of fluid into peritoneal cavity, and influx of macrophages followed by neutrophils.
    • Mesothelial cells secrete cytokines after stimulation (interleukins [IL-6, IL-8], tumor necrosis factor-α [TNF-α]). IL-6 stimulates T- and B-cell differentiation, and IL-8 is a selective chemoattractant for neutrophils.
    • Cytokines promote local resolution and compartmentalization through fibrin deposition.
  • In SBP, pathogenic bacteria are cultured from peritoneal fluid without any apparent intra-abdominal surgical treatable source of infection; recognized as a complication in patients with ascites as a result of cirrhosis of any etiology
    • Generalized bacteremia and translocation of organisms from the gut (E. coli, Klebsiella sp.) into the portal veins or lymphatics or, less likely, directly into the ascitic fluid may account for the source of the infection.
    • Clearance of bacteria from the bloodstream may be impaired in patients with cirrhosis and ascites.
      • Poor clearance is due to diminished phagocytic activity of the hepatic reticuloendothelial system secondary to cellular functional defects or shunting of blood away from the liver.
    • Complement, necessary for the opsonization of bacteria and ultimately clearance by phagocytes, is decreased in the ascitic fluid.
  • Infectious organisms include aerobic gram-negative organisms (E. coli and Klebsiella species) and aerobic gram-positive organisms (Streptococcus and Enterococcus species).
  • In secondary peritonitis, the underlying bacterial infection tends to be a complex polymicrobial infection. Most common isolates are a combination of E. coli and Bacteroides fragilis.
  • In tertiary peritonitis, the recurrence of infection is due to inadequate control of the infectious source or altered host immunity.


  • Primary peritonitis: liver cirrhosis or other conditions associated with ascites, such as the following:
    • Budd-Chiari syndrome
    • Congestive heart failure
    • Nephrotic syndrome
    • Systemic lupus erythematosus and other vasculitides
    • Rheumatoid arthritis
  • The etiology of secondary peritonitis varies with age.
    • Neonates and infants
      • Meconium peritonitis (begins prenatally)
      • Necrotizing enterocolitis
      • Idiopathic gastrointestinal perforation
      • Perforation due to Hirschsprung disease
      • Spontaneous biliary perforation
      • Omphalitis (common in developing countries due to poor umbilical cord care)
      • Perforation of a urachal cyst
    • Children and adolescents
      • Secondary to appendicitis
      • Perforation of Meckel diverticulum
      • Gastric ulcer perforation
      • Pancreatitis
      • Cholecystitis
      • Traumatic or spontaneous perforation of the intestine
      • Intussusception and other bowel obstruction leading to necrosis
      • Neutropenic enterocolitis (typhlitis)
      • Crohn disease with fistula and abscess formation
      • Toxic megacolon
      • Tuberculosis
      • Salpingitis and pelvic inflammatory disease
      • Toxins

Commonly Associated Conditions

  • Cirrhosis
  • Peritoneal dialysis
  • Perforated viscus (particularly if trauma/surgery)

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