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%.
  • Secondary bacterial peritonitis correlates with underlying pathology (e.g., colitis, appendicitis, diverticulitis, peptic ulcer disease).
  • 57% of patients with secondary bacterial peritonitis progress to tertiary peritonitis.

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

Etiology and Pathophysiology

  • Mechanism
    • SBP:
      • Bacterial translocation via lymphatic spread through mesenteric lymph nodes
      • Usually 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 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
    • Peritoneal dialysis-related peritonitis (PD peritonitis)
      • Contamination with pathogenic skin flora during exchanges or exit-site infection
        • Intraluminal contamination: most common source of infection; associated with lack of appropriate sterile technique for connecting catheter and frequency of exchange
        • Periluminal contamination: extension of bacteria from exit-site or tunnel infection
        • Visceral contamination: due to gut flora
  • Microbiology
    • SBP. Most cases (>90%) of SBP are mono-microbial.
      • 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 (1)
    • Secondary bacterial peritonitis. Second most common cause of sepsis in ICU patients. Can be due to perforation of a viscus, small bowel strangulation, necrotizing pancreatitis. Organism depends on site of underlying pathology. Gram positive organisms more common with upper GI pathology. Gram negative organisms more common with lower GI pathology (and/or patients on chronic PPI therapy).
      • E. coli, Klebsiella, Proteus, Streptococcus, Enterococcus, Bacteroides, Clostridium
    • PD peritonitis
      • Most commonly due to Staphylococcus epidermidis and Staphylococcus aureus
      • Also by gram-negative organisms and fungi

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 (1).
    • 70% of SBP cases are in patients with Child-Pugh class C cirrhosis.
    • 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)
  • PD peritonitis
    • Recent instrumentation involving GI/GU tract (e.g., colonoscopy, cystoscopy, dental procedures)
    • Nasal Staphylococcus aureus carriage
    • Underlying GI pathology

General Prevention

  • SBP prophylaxis in patients at high risk (e.g., ascitic fluid protein concentration <1.0 g/dL, esophageal varices, history of previous SBP)
    • Prior SBP: prophylactic norfloxacin or sulfamethoxazole and trimethoprim (Bactrim) PO daily
    • 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.
    • 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
  • Limit use of PPIs.
  • PD peritonitis
    • Proper training in sterile techniques
    • Antibiotic prophylaxis prior to selected procedures
    • Drainage of peritoneal fluid prior to procedures

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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%.
  • Secondary bacterial peritonitis correlates with underlying pathology (e.g., colitis, appendicitis, diverticulitis, peptic ulcer disease).
  • 57% of patients with secondary bacterial peritonitis progress to tertiary peritonitis.

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

Etiology and Pathophysiology

  • Mechanism
    • SBP:
      • Bacterial translocation via lymphatic spread through mesenteric lymph nodes
      • Usually 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 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
    • Peritoneal dialysis-related peritonitis (PD peritonitis)
      • Contamination with pathogenic skin flora during exchanges or exit-site infection
        • Intraluminal contamination: most common source of infection; associated with lack of appropriate sterile technique for connecting catheter and frequency of exchange
        • Periluminal contamination: extension of bacteria from exit-site or tunnel infection
        • Visceral contamination: due to gut flora
  • Microbiology
    • SBP. Most cases (>90%) of SBP are mono-microbial.
      • 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 (1)
    • Secondary bacterial peritonitis. Second most common cause of sepsis in ICU patients. Can be due to perforation of a viscus, small bowel strangulation, necrotizing pancreatitis. Organism depends on site of underlying pathology. Gram positive organisms more common with upper GI pathology. Gram negative organisms more common with lower GI pathology (and/or patients on chronic PPI therapy).
      • E. coli, Klebsiella, Proteus, Streptococcus, Enterococcus, Bacteroides, Clostridium
    • PD peritonitis
      • Most commonly due to Staphylococcus epidermidis and Staphylococcus aureus
      • Also by gram-negative organisms and fungi

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 (1).
    • 70% of SBP cases are in patients with Child-Pugh class C cirrhosis.
    • 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)
  • PD peritonitis
    • Recent instrumentation involving GI/GU tract (e.g., colonoscopy, cystoscopy, dental procedures)
    • Nasal Staphylococcus aureus carriage
    • Underlying GI pathology

General Prevention

  • SBP prophylaxis in patients at high risk (e.g., ascitic fluid protein concentration <1.0 g/dL, esophageal varices, history of previous SBP)
    • Prior SBP: prophylactic norfloxacin or sulfamethoxazole and trimethoprim (Bactrim) PO daily
    • 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.
    • 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
  • Limit use of PPIs.
  • PD peritonitis
    • Proper training in sterile techniques
    • Antibiotic prophylaxis prior to selected procedures
    • Drainage of peritoneal fluid prior to procedures

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