Medicine Central™ is a quick-consult mobile and web resource that includes diagnosis, treatment, medications, and follow-up information on over 700 diseases and disorders, providing fast answers—anytime, anywhere. Explore these free sample topics:
-- The first section of this topic is shown below --
- Definition: inflammation of the peritoneum
- 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; typically monomicrobial
- Secondary bacterial peritonitis: infection of ascitic fluid from a detectable intra-abdominal source (i.e., perforation, abscess); typically polymicrobial
- Tertiary bacterial peritonitis: persistent infection despite therapy
- In patients with ascites, the annual incidence of SBP is 10–25% (1).
- Secondary bacterial peritonitis correlates with underlying pathology (e.g., colitis, appendicitis, diverticulitis, PUD).
- 57% of patients with secondary bacterial peritonitis progress to tertiary peritonitis (2).
Etiology and Pathophysiology
- Bacterial translocation via lymphatic spread through mesenteric lymph nodes
- 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 bacterial peritonitis
- Spillage/translocation of bacteria from inflamed or perforated intraperitoneal organs or introduction of bacterial through instrumentation—including peritoneal dialysis, intraperitoneal chemotherapy
- Tertiary bacterial peritonitis
- Evolves from secondary peritonitis with inadequate source control and/or altered host immunity
- Escherichia coli (33%), Streptococcus spp. (15%), Staphylococcus (13%), Klebsiella (8%); reflects increasing rate of gram-positive and resistant organisms (e.g., extended-spectrum β-lactamase [ESBL]–producing E. coli, MRSA, Enterococcus) in the nosocomial setting (5)
- Secondary bacterial peritonitis:
- E. coli, Klebsiella, Proteus, Streptococcus, Enterococcus, Bacteroides, Clostridium
- SBP: advanced cirrhosis with ascites, malnutrition, upper GI bleed, PPI usage, prior SBP
- Factors associated with perforation or fluid translocation (e.g., peritoneal dialysis, Helicobacter pylori and NSAIDs causing ulcers, vascular disease causing bowel ischemia, alcohol abuse causing pancreatitis) increase risk for SBP.
- SBP prophylaxis in patients at high risk (e.g., ascitic fluid protein concentration <1.0 g/dL, esophageal varices, or history of previous SBP)
- Prior SBP: prophylactic norfloxacin or sulfamethoxazole and trimethoprim (Bactrim) PO daily (6)[A]
- Cirrhosis and GI bleed: 7-day course of ceftriaxone 1 g IV daily or norfloxacin BID; IV while bleeding, PO as tolerated. IV ceftriaxone is superior to oral norfloxacin (6)[A].
- Cirrhotic ascites: low ascitic fluid protein (<1.5 g/dL) with renal impairment (creatinine ≥1.2, BUN ≥25, or serum Na ≤130) or liver failure (child score ≥9, bilirubin ≥3): prophylactic norfloxacin or sulfamethoxazole and trimethoprim (Bactrim) PO daily (3,6)[A]
- Limit use of PPIs (6)[B].