Peritonitis, Acute

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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; 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

Epidemiology

Incidence
  • 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).

Prevalence
  • SBP: In asymptomatic patients with cirrhosis and ascites, the prevalence is <3% in outpatients. Nosocomial rates are 8–36% (3).
  • In patients with cirrhosis and ascites, 5% of peritonitis is secondary (4).

Etiology and Pathophysiology

  • Mechanism
    • SBP:
      • 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
  • Microbiology
    • SBP
      • 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

Risk Factors

  • SBP: advanced cirrhosis with ascites, malnutrition, upper GI bleed, PPI usage, prior SBP
    • Acid suppression (most commonly with PPIs) promotes SIBO increasing incidence of SBP. Hospitalized cirrhosis patients receiving PPIs are at increased risk for SBP (3,5).
    • 70% of SBP cases are in patients with Child-Pugh class C cirrhosis (1).
    • Low ascites protein (<1.0 g/dL) increases risk.
  • 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.

General Prevention

  • 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].

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