Peritonitis, Acute
Basics
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–associated (PD) peritonitis
Epidemiology
Incidence
Annual incidence of SBP is around one-third in hospitalized patients with cirrhosis (1).
Prevalence
- 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
- SBP:
- 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).
- Most cases of SBP are monomicrobial.
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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Citation
Domino, Frank J., et al., editors. "Peritonitis, Acute." 5-Minute Clinical Consult, 33rd ed., Wolters Kluwer, 2025. Medicine Central, im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/1688859/all/Peritonitis__Acute.
Peritonitis, Acute. In: Domino FJF, Baldor RAR, Golding JJ, et al, eds. 5-Minute Clinical Consult. Wolters Kluwer; 2025. https://im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/1688859/all/Peritonitis__Acute. Accessed October 13, 2024.
Peritonitis, Acute. (2025). In Domino, F. J., Baldor, R. A., Golding, J., & Stephens, M. B. (Eds.), 5-Minute Clinical Consult (33rd ed.). Wolters Kluwer. https://im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/1688859/all/Peritonitis__Acute
Peritonitis, Acute [Internet]. In: Domino FJF, Baldor RAR, Golding JJ, Stephens MBM, editors. 5-Minute Clinical Consult. Wolters Kluwer; 2025. [cited 2024 October 13]. Available from: https://im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/1688859/all/Peritonitis__Acute.
* Article titles in AMA citation format should be in sentence-case
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T1 - Peritonitis, Acute
ID - 1688859
ED - Domino,Frank J,
ED - Baldor,Robert A,
ED - Golding,Jeremy,
ED - Stephens,Mark B,
BT - 5-Minute Clinical Consult, Updating
UR - https://im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/1688859/all/Peritonitis__Acute
PB - Wolters Kluwer
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DB - Medicine Central
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