Basics
Description
- 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 the continuity of the intestinal lumen. Pathogens enter the peritoneum via translocation from the intestine; from the circulation; from vaginal, oropharyngeal, or skin flora; or from foreign bodies inserted into the peritoneal cavity.
- Secondary peritonitis occurs with visceral disruption from bowel perforation, abscess formation, ischemic necrosis, or penetrating abdominal injury.
- Tertiary peritonitis is recurrent peritonitis after presumed adequate treatment for secondary peritonitis.
- SBP almost always occurs in patients with cirrhosis and ascites.
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
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.
Pathophysiology
- 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 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.
- The most common gram-positive organisms are nonenterococcal streptococci and enterococci.
Etiology
- 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 colitis (typhlitis)
- Crohn disease with fistula and abscess formation
- Toxic megacolon
- Tuberculosis
- Salpingitis and pelvic inflammatory disease
- Toxins
Diagnosis
History
- Dependent on stage, age, and etiology
- Abdominal pain is the most common symptom.
- Young children may be unable to verbalize pain.
- Fever, chills, vomiting, diarrhea
- ¢ ¼10% of SBP cases are entirely asymptomatic; presentation may be subtle.
- Infants may present with poor feeding and lethargy.
- Other less common findings include the following:
- Hypothermia
- Hypotension
- Increasing ascites despite diuretics
- Worsening encephalopathy
- Unexplained decrease in renal function
Physical Exam
- Abdominal distension
- Rebound tenderness
- Decreased bowel sounds
- Evidence of chronic liver disease
- Evidence of ascites
Diagnostic Tests & Interpretation
Lab
- Blood
- Leukocytosis, elevated CRP
- There may be leukopenia and thrombocytopenia in sepsis.
- Urinalysis to exclude renal diseases which may mimic peritonitis
Imaging
- Abdominal x-ray may show evidence of ileus, obstruction, or perforation.
- Abdominal ultrasound or CT shows ascites, thickening of bowel wall, and abscesses.
Diagnostic Procedures/Other
- Paracentesis is diagnostic and should be performed in all cases of new-onset ascites and when SBP is suspected.
- To improve culture yield, inoculate blood culture bottles with 10 mL of fluid immediately at the bedside. A separate tube is sent for Gram stain.
- Elevated neutrophil count of ≥250/mm3 in ascitic fluid is the most important laboratory indicator of SBP.
- Fluid chemistries: albumin, total protein, glucose, LDH, amylase, bilirubin
- Serum-ascites albumin gradient = serum albumin minus fluid albumin. Difference >1.1 indicates portal hypertension.
- Diagnostic criteria for secondary peritonitis: positive ascitic fluid culture, neutrophil count of ≥250/mm3, and surgically treatable source of infection
Treatment
Medication
- Empiric antibiotic coverage should be initiated immediately and directed primarily toward enteric gram-negative aerobes and gram-positive cocci:
- After the organism is identified, the antibiotic coverage may be optimized.
- First line: Cefotaxime is drug of choice for SBP in pediatrics.
- Consider adding metronidazole for secondary SBP.
- Antibiotic resistance is increasing.
- Quinolones may be used in areas where resistance is low.
- Second line: carbapenems for severe nosocomially acquired cases
Additional Treatment
General Measures
- Fluid resuscitation with isotonic saline, 20 mL/kg boluses up to 60 mL/kg, or albumin if large amounts of fluid are required to restore intravascular volume
- Decompression with nasogastric tube
- Patients at significant risk for SBP will benefit from selective intestinal decontamination with fluoroquinolones, trimethoprim-sulfamethoxazole, or rifaximin as an effective preventive measure.
Surgery/Other Procedures
In secondary peritonitis, surgery is the primary management tool:
- Control of the underlying source of infection by closing, diverting, or resecting the affected bowel
- Intraoperative peritoneal lavage and debridement of loculations and abscesses decrease bacterial inoculum and help prevent recurrent sepsis.
- Older studies in adults show benefit of antibiotic peritoneal lavage; controversial, as it may impair the local response and promote adhesions
- Catheters may be placed to drain a well-defined abscess cavity, form a controlled fistula, or provide access for continuous postoperative peritoneal lavage.
Ongoing Care
Prognosis
- SBP in adults has in-hospital mortality of 10 " 50%.
- SBP markedly worsens the prognosis in patients with cirrhosis.
- Recurrence is common: 60% of patients who survive the 1st episode develop 1 or more recurrences.
- Severe secondary peritonitis in adults has a mortality rate of 30 " 55%.
Complications
- Hypovolemia from reduced fluid intake, vomiting, and third-space fluid extravasation
- Sepsis and multiorgan failure
- Intra-abdominal abscess
- Long-term: adhesions
Additional Reading
- European Association for the Study of the Liver. EASL clinical practice guidelines on the management of ascites, spontaneous bacterial peritonitis, and hepatorenal syndrome. J Hepatol. 2010;53(3):397 " 417. [View Abstract]
- Haecker FM, Berger D, Schumacher U, et al. Peritonitis in childhood: aspects of pathogenesis and therapy. Pediatr Surg Int. 2000;16(3):182 " 188. [View Abstract]
- Leonis MA, Balistreri WF. Evaluation and management of end-stage liver disease in children. Gastroenterology. 2008;134(6):1741 " 1751. [View Abstract]
- Saab S, Hernandez JC, Chi AC, et al. Oral antibiotic prophylaxis reduces spontaneous bacterial peritonitis occurrence and improves short-term survival in cirrhosis: a meta-analysis. Am J Gastroenterol. 2009;104(4):993 " 1001; quiz 1002. [View Abstract]
- Sabri M, Saps M, Peters JM. Pathophysiology and management of pediatric ascites. Curr Gastroenterol Rep. 2003;5(3):240 " 246. [View Abstract]
- Wiest R, Krag A, Gerbes A. Spontaneous bacterial peritonitis: recent guidelines and beyond. Gut. 2012;61(2):297 " 310. [View Abstract]
- Wong CL, Holroyd-Leduc J, Thorpe KE, et al. Does this patient have bacterial peritonitis or portal hypertension? How do I perform a paracentesis and analyze the results? JAMA. 2008;299(10):1166 " 1178. [View Abstract]
Codes
ICD09
- 567.9 Unspecified peritonitis
- 567.23 Spontaneous bacterial peritonitis
- 777.6 Perinatal intestinal perforation
- 567.81 Choleperitonitis
- 567.21 Peritonitis (acute) generalized
- 567.29 Other suppurative peritonitis
ICD10
- K65.9 Peritonitis, unspecified
- K65.2 Spontaneous bacterial peritonitis
- P78.1 Other neonatal peritonitis
- K65.3 Choleperitonitis
- K65.0 Generalized (acute) peritonitis
- P78.0 Perinatal intestinal perforation
SNOMED
- 48661000 Peritonitis (disorder)
- 197171003 Bacterial peritonitis (disorder)
- 276522000 Neonatal peritonitis (disorder)
- 36746002 Bile peritonitis
- 129129003 infectious peritonitis (disorder)
- 431873008 Peritonitis due to infected peritoneal dialysis catheter (disorder)
- 67602004 Acute peritonitis
- 87510000 Chronic peritonitis
- 57341009 Meconium peritonitis (disorder)
FAQ
- 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 neutrophil count provides the most useful information regarding the diagnosis of peritonitis. Fluid culture is not required for diagnosis but helps to guide therapy.