Primary (Spontaneous) Bacterial Peritonitis

• Epidemiology: Primary bacterial peritonitis (PBP) is most common among pts with cirrhosis (usually due to alcoholism) and preexisting ascites, but ≤10% of these pts develop PBP. PBP is also described in other settings (e.g., malignancy, hepatitis).
• Pathogenesis: PBP is due to hematogenous spread of organisms to ascitic fluid in pts in whom a diseased liver and altered portal circulation compromise the liver's filtration function.
• Microbiology: Enteric gram-negative bacilli such as Escherichia coli or gram-positive organisms such as streptococci, enterococci, and pneumococci are the most common etiologic agents.
  • A single organism is typically isolated.
  • If a polymicrobial infection including anaerobes is identified, the diagnosis of PBP should be reconsidered and a source of secondary peritonitis sought.
• Clinical manifestations: Although some pts experience acute-onset abdominal pain or signs of peritoneal irritation, other pts have only nonspecific and nonlocalizing manifestations (e.g., malaise, fatigue, encephalopathy). Fever is common (∼80% of pts).
• Diagnosis: PBP is diagnosed if peritoneal fluid is sampled and contains >250 PMNs/µL.
  • Culture yield is improved if a 10-mL volume of peritoneal fluid is placed directly into blood culture bottles.
  • Blood cultures should be performed because bacteremia is common.
• Prevention: Up to 70% of pts have a recurrence of PBP within 1 year. Prophylaxis with fluoroquinolones (e.g., ciprofloxacin, 500 mg weekly) or trimethoprim-sulfamethoxazole (TMP-SMX; one double-strength tablet daily) reduces this rate to 20% but increases the risk of serious staphylococcal infections over time.

Secondary Peritonitis

• Pathogenesis: Secondary peritonitis develops when bacteria contaminate the peritoneum as a result of spillage from an intraabdominal viscus.
• Microbiology: Infection almost always involves a mixed flora in which gram-negative bacilli and anaerobes predominate, especially when the contaminating source is colonic. The specific organisms depend on the flora present at the site of the initial process.
• Clinical manifestations: Initial symptoms may be localized or vague and depend on the primary organ involved. Once infection has spread to the peritoneal cavity, pain increases; pts lie motionless, often with knees drawn up to avoid stretching the nerve fibers of the peritoneal cavity. Coughing or sneezing causes severe, sharp pain. There is marked voluntary and involuntary guarding of anterior abdominal musculature, tenderness (often with rebound), and fever.
• Diagnosis: Although recovery of organisms from peritoneal fluid is easier in secondary than in primary peritonitis, radiographic studies to find the source of peritoneal contamination or immediate surgical intervention should usually be part of the initial diagnostic evaluation. Abdominal taps are done only to exclude hemoperitoneum in trauma cases.

Peritonitis In Pts Undergoing Capd

• Pathogenesis: In a phenomenon similar to that seen in intravascular device-related infections, organisms migrate along the catheter-a foreign body that serves as an entry point.
• Microbiology: CAPD-associated peritonitis usually involves skin organisms, with Staphylococcus spp. such as coagulase-negative staphylococci and Staphylococcus aureus accounting for ∼45% of cases; gram-negative bacilli and fungi (e.g., Candida) are occasionally identified. A polymicrobial infection should prompt evaluation for secondary peritonitis.
• Clinical manifestations: CAPD-associated peritonitis presents similarly to secondary peritonitis, in that diffuse pain and peritoneal signs are common.
• Diagnosis: Several hundred milliliters of removed dialysis fluid should be centrifuged and sent for culture.
  • Use of blood culture bottles improves the diagnostic yield.
  • The dialysate is usually cloudy and contains >100 WBCs/µL, with >50% neutrophils; the percentage of neutrophils is more important than the absolute WBC count.