5-Minute Pediatric Consult



  • Inflammation of the peritoneum in reaction to infection or chemical irritation by organic fluids (GI contents, bile, blood, or urine). Infectious peritonitis can be:
    • Primary or spontaneous bacterial peritonitis (SBP). Pathogens can reach the peritoneum by translocation from the intestinal lumen, from the bloodstream, from the lymphatics, by ascension from the vagina, foreign bodies inserted in the peritoneal cavity or from the pharyngeal or skin flora.
    • Secondary peritonitis occurs after bowel perforation, abscess formation, ischemic necrosis, or penetrating abdominal injury.
  • Infectious organisms include aerobic Gram-negative organisms: Escherichia coli (~50%), Klebsiella species (~13%), and aerobic Gram-positive organisms (Streptococcus [~19%] and Enterococcus [5%] species).
  • Anaerobes rarely cause SBP, and polymicrobial infections occur in relatively few patients (~8%).
  • Urine cultures have been found to be positive for the same organism in ~44% of patients.
  • Pneumonia and soft-tissue infections have also been suggested as sources.

Risk Factors

  • Liver cirrhosis (10–30% of adults hospitalized with cirrhosis have SBP), nephrotic syndrome (staphylococcal species, streptococci, enteric organisms, and fungi)
  • Splenectomy (encapsulated organisms: Group A streptococci, E. coli, Streptococcus pneumoniae, Bacteroides sp.)
  • Decreased serum complement levels
  • Decreased ascitic protein and complement levels
  • Presence of gastrointestinal hemorrhage


  • When bacteria or chemicals reach the peritoneal cavity, a local peritoneal and systemic response is initiated.
    • Hyperemia and exudation of fibrinogen, albumin, opsonins, and complement
    • Mesothelial cells secrete cytokines (interleukin [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 polymorphonuclear (PMN) leucocytes.
  • 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 because of diminished phagocytic activity of the hepatic reticulo-endothelial 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 of patients with ascites.
  • In secondary bacterial peritonitis, the underlying bacterial infection tends to be a complex polymicrobial infection with an average of 3 or 4 different isolates; the most common isolates are combinations of E. coli and Bacteroides fragilis, and the most common Gram-positive organisms are nonenterococcal streptococci and enterococci.


  • Primary peritonitis: Liver cirrhosis or other conditions associated with ascites, such as:
    • Budd-Chiari syndrome
    • CHF
    • Nephrotic syndrome
    • Systemic lupus erythematosus
    • Rheumatoid arthritis
  • The etiology of secondary peritonitis varies with age.
    • Neonate:
      • Necrotizing enterocolitis
      • Idiopathic gastrointestinal perforation
      • Perforation due to Hirschsprung disease
      • Spontaneous biliary perforation
      • Omphalitis
      • Perforation of an urachal cyst
    • Children and adolescents:
      • Secondary to appendicitis
      • Perforation of Meckel diverticulum
      • Gastric ulcer perforation
      • Pancreatitis
      • Traumatic perforation of the intestine
      • Intussusception
      • Neutropenic colitis (typhlitis)
      • Crohn disease with fistula and abscess formation
      • Toxic megacolon
      • Tuberculosis
      • Salpingitis

Signs and Symptoms

  • Dependent on stage, age, and etiology
  • Fever, chills, vomiting
  • Generalized abdominal pain with rebound tenderness
  • Decreased bowel sounds
  • In SBP, ~10% of cases are entirely asymptomatic.
  • Other less common findings include:
    • Hypothermia
    • Hypotension
    • Diarrhea
    • Increased ascites despite diuretics
    • Worsening encephalopathy
    • Unexplained decrease in renal function

Physical Exam
  • Swollen rigid and painful abdomen
  • Decreased bowel sounds
  • Evidence of chronic liver disease
  • Evidence of ascites


Diagnostic Procedures/Surgery

  • Leucocytosis, increased C-reactive protein (CRP), leucopenia, and thrombocytopenia are also possible.
  • Diagnosis may be confirmed with paracentesis. To improve culture yield, culture bottles should be inoculated immediately at the bedside in large-volume blood culture bottles.
  • Elevated PMN count in ascitic fluid is important in the early diagnosis of SBP and is considered the most important laboratory indicator of SBP:
    • Diagnostic criteria for SBP include PMN leukocyte counts of >250/mm3 in ascitic fluid culture usually positive for a single organism.
    • Diagnostic criteria for secondary bacterial peritonitis include ascitic fluid culture positive for polymicrobial infection, total protein >1 g/dL, glucose <50 mg/dL, and lactate dehydrogenase (LDH) level >225 mU/mL.
    • Ultrasound, abdominal radiography, and CT scan may reveal fluid, thickening of bowel wall, abscesses, and a pneumoperitoneum.

General Measures

  • Support the patient’s cardiovascular and respiratory systems.
  • Control the underlying infection with antibiotics or surgery (in secondary bacterial peritonitis).
  • Decompression with nasogastric tube
  • Patients at significant risk for SBP will benefit from selective intestinal decontamination as an effective preventive measure:
    • Antibiotics that have been studied for this use in adults include norfloxacin, ciprofloxacin, and trimethoprim-sulfamethoxazole.

Medication (Drugs)

  • Empiric antibiotic coverage should be directed primarily toward enteric Gram-negative aerobes and Gram-positive cocci:
    • After the organism is identified, the antibiotic coverage may be optimized.
    • No particular antibiotic regimen has been shown to be superior in controlled clinical trials. Both single agents and combination regimens have been used.
  • In SBP, cefotaxime has been shown to have higher resolution of infection and lower hospital mortality than the traditional ampicillin and an aminoglycoside as empiric coverage.


In secondary bacterial peritonitis, surgery is the primary management tool with control of the source of the intra-abdominal infection:

  • Control of the underlying source of the abdominal infection by repairing the affected bowel through laparotomy/laparoscopy should be considered.
  • The degree of contamination may be decreased through intraoperative peritoneal lavage, and débridement of loculations and abscesses.
  • Adding antibiotics to lavage fluid has lost favor after the discovery that this procedure appears to impair neutrophil chemotaxis, inhibit neutrophil bactericidal activity, and increase the formation of adhesions.
  • Catheters may be placed to drain a well-defined abscess cavity, form a controlled fistula, or provide access for continuous postoperative peritoneal lavage.


  • SBP is associated with a high mortality. In reports from the 1970s, the mortality exceeded 90%. Currently with intensive treatment the in-hospital mortality in adults is still between 10% and 30%.
    • The combination of underlying disease and the infection causes acute decompensation in a marginally compensated host.
  • Retrospective studies have indicated that SBP is a recurrent problem, with 60% of patients who survive the 1st episode going on to develop 1 or more recurrences.
  • Severe secondary peritonitis is associated with a mortality rate (30–55%) in adults.


  • Hypovolemia results from extravasation of fluid from the inflamed peritoneal membrane. Intravascular volume must be supported with crystalloids and blood products.
  • Respiration may be impaired via mechanical mechanisms through diaphragmatic spasm and reflex abdominal rigidity and through increased permeability of the pulmonary vasculature in response to systemic inflammation.
  • Long term complications include adhesions.


  • 567.9 Peritonitis


  • Q: Is peritonitis common in children with ascites?
    • A: Despite the frequency of ascites from many different causes, peritonitis occurs rarely. In the setting of children with chronic liver disease and ascites, SBP may occur.
  • Q: What are the most useful laboratory aids for this diagnosis?
    • A: Paracentesis and analysis of the fluid for pH, glucose content, and amount of inflammatory cells provides the most useful information regarding the diagnosis of peritonitis.


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  5. Nathans AB, Rotstein OD. Therapeutic options in peritonitis. Surg Clin North Am. 1994;74:6577–6592.
  6. Parsi MA, Atreja A, Zein NN. Spontaneous bacterial peritonitis: Recent data on incidence and treatment. Cleve Clin J Med. 2004;71(7):569–576.  [PMID:15320366]
  7. Robledo FA, Luque-De-Leon E, Suarez R Open versus closed management of the abdomen in the surgical treatment of severe secondary peritonitis: A randomized clinical trial. Surg Infect (Larchmt). 2007;8(1):63–72.  [PMID:17381398]
  8. Sabri M, Saps M, Peters JM. Pathophysiology and management of pediatric ascites. Curr Gastroenterol Rep. 2003;5:240–246.  [PMID:12734047]
  9. Schaefer F. Management of peritonitis in children receiving chronic peritoneal dialysis. Paediatr Drugs. 2003;5:315–325.  [PMID:12716218]


Vera De Matos, MDDror Wasserman, MD (4th Edition)

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