Peritonitis: A High-Yield USMLE Review

Peritonitis is inflammation of the peritoneum, either from a chemical/bacterial insult after visceral perforation (secondary peritonitis) or from bacterial infection of pre-existing ascites (spontaneous bacterial peritonitis, SBP). It is a high-yield exam topic because the two flavors present very differently — a dramatic surgical abdomen versus a subtle infection in a cirrhotic — and because it is a defined trigger that converts a medical problem into an urgent surgical one.

Presentation

• Secondary peritonitis (e.g., perforated ulcer): sudden, severe epigastric pain that becomes diffuse, a 'board-like' rigid abdomen, and a patient who lies completely still because movement worsens the pain
• Signs of sepsis — tachycardia, fever, and hypotension
• Peritoneal signs and pain that localizes as inflammation spreads: early appendicitis causes vague periumbilical (visceral) pain that migrates to the right lower quadrant once the parietal peritoneum is involved
• SBP in a cirrhotic with ascites: may be subtle, presenting with increasing abdominal girth and evidence of decompensation rather than a dramatic acute abdomen
• Peritonitis can trigger an adynamic (paralytic) ileus, with distension, vomiting, obstipation, and absent bowel sounds

Diagnosis

• Diagnostic paracentesis of ascites: a PMN count ≥250 cells/mm³ establishes SBP; calculate the SAAG (serum albumin − ascites albumin), where ≥1.1 g/dL confirms portal hypertension as the source of the ascites
• Upright chest or abdominal X-ray in suspected perforation: free air under the diaphragm
• CT abdomen/pelvis when the diagnosis is unclear — used to look for extraluminal fluid, free air, or an abscess (e.g., to detect an anastomotic leak before classic peritonitis appears)

Management

• SBP: empiric antibiotics (ceftriaxone or cefotaxime), IV albumin (1.5 g/kg on day 1 and 1 g/kg on day 3) to reduce hepatorenal syndrome risk, repeat paracentesis in 48 hours to confirm improvement, and long-term prophylaxis after recovery (norfloxacin or TMP-SMX)
• Perforation-related peritonitis: NPO, NG decompression, IV antibiotics, and urgent surgical repair (e.g., Graham patch or primary closure)
• Prophylactic antibiotics (ceftriaxone, or oral norfloxacin) for 7 days after variceal bleeding to prevent SBP — this is standard of care and confers a proven survival benefit

High-yield

• Ascitic PMN ≥250 cells/mm³ = spontaneous bacterial peritonitis
• SAAG ≥1.1 g/dL indicates portal hypertension; SBP occurs with enteric organisms in cirrhotic ascites
• IV albumin in SBP reduces the risk of hepatorenal syndrome
• 'Board-like' rigid abdomen with the patient lying perfectly still = perforation with diffuse peritonitis; free air under the diaphragm confirms it
• Prophylactic antibiotics after variceal bleeding prevent SBP and improve survival
• Cirrhosis is a host factor that predicts SBP with enteric organisms
• Migrating periumbilical-to-RLQ pain reflects progression from visceral to parietal peritoneal inflammation (appendicitis)

Pitfalls

• Trusting the snapshot over the curve postoperatively: progressive tachycardia and a rising white count on POD 2–3 in a patient who appears 'fine' is an anastomotic leak until proven otherwise — tachycardia can precede radiologic evidence and classic peritonitis by 24–48 hours, so 'watch overnight' is the wrong move
• Missing SBP because it can be clinically subtle in a cirrhotic — always tap the ascites and check the PMN count rather than waiting for a florid acute abdomen
• Attempting non-operative management when peritonitis is present: an adhesive small bowel obstruction earns a trial of conservative therapy only if there is no ischemia or peritonitis — peritoneal signs are a trigger to operate