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
    • 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 peritonitis

Epidemiology

Incidence
  • In cirrhotic patients with ascites, the annual incidence of SBP is 10–25%.
  • 25–75% of patients with secondary bacterial peritonitis progress to tertiary peritonitis.

Prevalence
  • SBP: In asymptomatic patients with cirrhosis and ascites, the prevalence of SBP is <4% in outpatients. Nosocomial rates are 10%.
  • In patients with cirrhosis and ascites, 5% of peritonitis is secondary.
  • Secondary peritonitis is the most common cause of sepsis in surgical ICU patients.
  • PD peritonitis is the primary reason for switching from PD to hemodialysis (HD).

Etiology and Pathophysiology

  • Mechanism
    • SBP:
      • Likely due to 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
    • 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
  • Microbiology
    • SBP. Most cases (>90%) of SBP are monomicrobial.
      • Most common gram-negative pathogens are Escherichia coli and Klebsiella spp.
      • Most common gram-positive pathogens are Streptococcus spp. and Staphylococcus aureus.
    • 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.
    • PD peritonitis is most commonly due to Staphylococcus epidermidis and S. aureus.

Risk Factors

  • SBP: advanced cirrhosis with ascites, malnutrition, upper GI bleed, PPI usage, and prior SBP
    • 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 (<1.0 g/dL) increases risk.
  • Secondary:
    • Helicobacter pylori or NSAIDs-induced ulcers, vascular disease causing bowel ischemia, alcohol abuse causing 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 <1.0 g/dL, esophageal varices, or history of previous SBP).
    • Antibiotics include norfloxacin, ciprofloxacin, or TMP/SMZ PO daily.
    • 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 also receive SBP prophylaxis.
  • Limit use of PPIs.
  • PD peritonitis:
    • Sterile techniques
    • Antibiotic prophylaxis prior to selected procedures

Commonly Associated Conditions

SBP almost always occurs in the setting of decompensated cirrhosis.

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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
    • 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 peritonitis

Epidemiology

Incidence
  • In cirrhotic patients with ascites, the annual incidence of SBP is 10–25%.
  • 25–75% of patients with secondary bacterial peritonitis progress to tertiary peritonitis.

Prevalence
  • SBP: In asymptomatic patients with cirrhosis and ascites, the prevalence of SBP is <4% in outpatients. Nosocomial rates are 10%.
  • In patients with cirrhosis and ascites, 5% of peritonitis is secondary.
  • Secondary peritonitis is the most common cause of sepsis in surgical ICU patients.
  • PD peritonitis is the primary reason for switching from PD to hemodialysis (HD).

Etiology and Pathophysiology

  • Mechanism
    • SBP:
      • Likely due to 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
    • 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
  • Microbiology
    • SBP. Most cases (>90%) of SBP are monomicrobial.
      • Most common gram-negative pathogens are Escherichia coli and Klebsiella spp.
      • Most common gram-positive pathogens are Streptococcus spp. and Staphylococcus aureus.
    • 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.
    • PD peritonitis is most commonly due to Staphylococcus epidermidis and S. aureus.

Risk Factors

  • SBP: advanced cirrhosis with ascites, malnutrition, upper GI bleed, PPI usage, and prior SBP
    • 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 (<1.0 g/dL) increases risk.
  • Secondary:
    • Helicobacter pylori or NSAIDs-induced ulcers, vascular disease causing bowel ischemia, alcohol abuse causing 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 <1.0 g/dL, esophageal varices, or history of previous SBP).
    • Antibiotics include norfloxacin, ciprofloxacin, or TMP/SMZ PO daily.
    • 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 also receive SBP prophylaxis.
  • Limit use of PPIs.
  • PD peritonitis:
    • Sterile techniques
    • Antibiotic prophylaxis prior to selected procedures

Commonly Associated Conditions

SBP almost always occurs in the setting of decompensated cirrhosis.

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