primary peritonitis

DEFINITION: Peritoneal infection arising without a primary intra-abdominal source such as bowel perforation, appendicitis, or abscess. This distinguishes it from secondary peritonitis (due to a ruptured viscus or other intra-abdominal pathology) and tertiary peritonitis (persistent or recurrent infection after treatment of secondary peritonitis). Typically monomicrobial.

MAIN FORMS: 1) Spontaneous bacterial peritonitis (SBP): the classic form, in cirrhosis with ascites (also seen in nephrotic syndrome and, in children, with ascites from other causes). 2) Peritoneal dialysis–associated peritonitis: a related but separate entity from catheter contamination. Usually Staph epidermidis or Staph aureus. Cloudy dialysate is the classic sign. 3) Tuberculous peritonitis: lymphocytic ascites with high ADA. 4) Pediatric primary peritonitis: historically Strep pneumoniae or group A strep, mostly in girls (possible ascending genital tract spread), and with nephrotic syndrome.

PATHOPHYSIOLOGY OF SBP: - Cirrhosis with portal hypertension leads to intestinal bacterial overgrowth, increased gut permeability, and bacterial translocation to mesenteric lymph nodes and ascitic fluid. - Impaired host defenses add to this: reticuloendothelial (Kupffer cell) dysfunction, low ascitic fluid protein (<1.5 g/dL) with reduced opsonic activity, and complement deficiency. - Organisms are usually gram-negative enteric bacteria, most often E. coli and Klebsiella. Gram-positive cocci (Strep pneumoniae, viridans strep, Enterococcus) are also seen. Anaerobes are rare, and a polymicrobial culture suggests secondary peritonitis.

CLINICAL PRESENTATION: - Fever, abdominal pain or tenderness, and altered mental status (hepatic encephalopathy), often with worsening ascites. - It can be subtle or asymptomatic. Always tap ascites in any cirrhotic patient with ascites who is admitted to the hospital or has clinical deterioration, GI bleeding, AKI, or encephalopathy. - Complications include hepatorenal syndrome (type 1 HRS-AKI) and death.

DIAGNOSIS (diagnostic paracentesis): - Ascitic fluid PMN (absolute neutrophil count) ≥250 cells/mm³ is diagnostic. - Inoculate blood culture bottles at the bedside with ascitic fluid to increase yield. - SAAG ≥1.1 g/dL (portal hypertension) is usually present in cirrhotic ascites. - Variants: culture-negative neutrocytic ascites (PMN ≥250, negative culture) and monomicrobial non-neutrocytic bacterascites (positive culture, PMN <250). - Secondary peritonitis clues: multiple organisms, total protein >1 g/dL, glucose <50 mg/dL, LDH above the upper limit of normal for serum, very high PMN count, and failure to respond to antibiotics. Imaging is warranted if suspected.

TREATMENT: - Empiric IV third-generation cephalosporin (cefotaxime or ceftriaxone) for about 5 days. - IV albumin (1.5 g/kg on day 1 and 1 g/kg on day 3) reduces the risk of hepatorenal syndrome and mortality, especially if creatinine >1 mg/dL, BUN >30, or bilirubin >5. - Broaden coverage for nosocomial or healthcare-associated infection or if there is no response in 48 hours.

PROPHYLAXIS: - Secondary prophylaxis after an SBP episode: long-term norfloxacin, ciprofloxacin, or TMP-SMX. - Primary prophylaxis is considered for ascitic protein <1.5 g/dL with renal or liver dysfunction (Cr ≥1.2, BUN ≥25, Na ≤130, Child-Pugh ≥9 with bilirubin ≥3). - Prophylaxis with ceftriaxone (or a fluoroquinolone) for cirrhotics with acute GI (variceal) bleeding. - Avoid unnecessary PPIs, which are associated with increased SBP risk.

BOARD PEARLS: - Cirrhosis plus ascites plus fever or abdominal pain: do a paracentesis. - Think SBP when a cirrhotic has new encephalopathy or AKI. - Ascitic PMN ≥250 means treat. Correct the PMN count for a bloody tap by subtracting 1 PMN per 250 RBCs. - Primary peritonitis is usually monomicrobial. Polymicrobial infection points to secondary peritonitis requiring surgery.