secondary peritonitis

**Definition:** Inflammation of the peritoneum caused by contamination from a defined intra-abdominal pathologic process, most often a breach in the GI tract wall (or, less commonly, the biliary/genitourinary tract).

**Common causes:** - Perforated peptic ulcer (free air under the diaphragm on upright CXR) - Acute appendicitis with rupture - Diverticulitis with perforation - Ischemic or necrotic bowel (mesenteric ischemia, strangulated hernia, volvulus) - Perforated cholecystitis, severe pancreatitis (chemical/sterile initially) - Malignancy, inflammatory bowel disease (toxic megacolon), trauma (penetrating/blunt) - Postoperative anastomotic leak - Iatrogenic: endoscopic or colonoscopic perforation

**Pathophysiology:** Spillage of gastric acid, bile, enzymes, enteric contents, and bacteria into the peritoneal cavity triggers an intense inflammatory response (chemical peritonitis, then bacterial). Inflammatory mediators (TNF-α, IL-1, IL-6) increase capillary permeability, causing third-spacing of fluid, hypovolemia, and ileus. Can progress to abscess formation, sepsis, and multi-organ failure. Upper GI perforations are initially chemical (low bacterial burden); lower GI (colonic) perforations are heavily bacterial.

**Microbiology:** Polymicrobial: Enterobacterales (E. coli, Klebsiella), Bacteroides fragilis and other anaerobes, enterococci, and streptococci. Distal source = higher bacterial load. Candida may be involved in upper GI perforations or in critically ill/health care-associated cases.

**Clinical features:** Acute severe abdominal pain worsened by movement/coughing; patient lies still. Fever, tachycardia, hypotension. Exam: rebound tenderness, guarding, rigidity ("board-like abdomen"), absent/decreased bowel sounds. Labs: leukocytosis, elevated lactate in sepsis.

**Diagnosis:** Largely clinical. Upright CXR or CT abdomen/pelvis with contrast shows free air, fluid, abscess, or the source. Peritoneal fluid analysis (if obtained) typically shows PMNs >250/µL, multiple organisms on Gram stain/culture, elevated protein and LDH, low glucose (<50 mg/dL), and elevated CEA/alkaline phosphatase (suggesting perforation).

**Management:** 1. Resuscitation (IV fluids, correct electrolytes) 2. Broad-spectrum antibiotics covering gram-negative enterics and anaerobes (e.g., piperacillin-tazobactam; or a third-generation cephalosporin/fluoroquinolone plus metronidazole; carbapenem if severe or resistant) 3. **Source control**: emergent surgery (exploratory laparotomy) or percutaneous drainage for localized abscesses

**Secondary vs. primary vs. tertiary:** - **Primary (spontaneous bacterial peritonitis, SBP):** no intra-abdominal source; monomicrobial (E. coli, Klebsiella, S. pneumoniae); seen in cirrhosis with ascites and in nephrotic syndrome (children, S. pneumoniae); ascitic fluid PMN ≥250/µL; treat with cefotaxime/ceftriaxone, albumin, and prophylaxis (e.g., ciprofloxacin or TMP-SMX) after an episode. No surgery. - **Secondary:** identifiable source, polymicrobial, requires source control. - **Tertiary:** persistent or recurrent peritonitis ≥48 hours after adequate treatment of secondary peritonitis, often with low-virulence or resistant organisms (Enterococcus, Candida, Staphylococcus epidermidis, Pseudomonas) in immunocompromised/critically ill patients.

**High-yield pearls:** - Free air under the diaphragm on upright CXR = perforated viscus until proven otherwise. - Ascitic fluid in secondary peritonitis: polymicrobial and often ≥2 of: glucose <50, protein >1 g/dL, LDH > serum upper limit (Runyon criteria). - Peritoneal dialysis–associated peritonitis (cloudy effluent) is typically from skin flora (S. epidermidis, S. aureus) and is classified separately. - Complications: intra-abdominal abscess, sepsis/septic shock, adhesions and small-bowel obstruction, fistula formation.