Definition & Classification

Acute Primary Peritonitis

Bacterial infection of peritoneal cavity without demonstrable intra-abdominal source.
Originates outside abdomen; seeds peritoneal cavity via hematogenous, lymphatic, or transmural spread.
Occurs predominantly in children with pre-existing ascites (cirrhosis, nephrotic syndrome).
Hypoalbuminemia increases infection risk.
Pathogens: Typically monomicrobial. Pneumococci (most common), group A streptococci, enterococci, staphylococci, Escherichia coli, Klebsiella pneumoniae.
Rare causes: Mycobacterium tuberculosis, Neisseria meningitidis.

Insidious or rapid onset.
Fever, abdominal pain, toxic appearance, vomiting, diarrhea.
Hypotension, tachycardia, shallow rapid respirations (due to breathing discomfort).
Rebound tenderness, abdominal rigidity, hypoactive or absent bowel sounds.
Signs may be subtle in cirrhotic patients; suspect in cases of unexplained leukocytosis, azotemia, or metabolic acidosis.

Results from enteric bacteria entering peritoneal cavity through necrotic defect in intestinal wall or viscus.
Causes: Perforated appendix (most common), incarcerated hernia, ruptured Meckel diverticulum, midgut volvulus, intussusception, peptic ulceration, inflammatory bowel disease, trauma.
Neonatal causes: Necrotizing enterocolitis, meconium ileus, spontaneous gastric/intestinal rupture.
Postpubertal females: Genital tract bacteria (Neisseria gonorrhoeae, Chlamydia trachomatis) gaining access via fallopian tubes.
Pathogens: Typically polymicrobial (gram-negative aerobes and anaerobes).
Pathogenesis: Direct toxic bacterial effects combined with local and systemic release of inflammatory mediators (lipopolysaccharide endotoxin).

Fever, diffuse abdominal pain, nausea, vomiting.
Rebound tenderness, abdominal wall rigidity, paucity of body motion (patient lies perfectly still).
Decreased or absent bowel sounds secondary to paralytic ileus.
Massive fluid exudation into peritoneal cavity and systemic vasodilative substances lead to rapid shock development.
Complications: Basilar atelectasis, intrapulmonary shunting, acute respiratory distress syndrome.

Feature	Acute Primary Peritonitis\|	Acute Secondary Peritonitis\|
Diagnostic Imaging	Dilated intestines, bowel wall thickening, increased loop separation.	Free air in peritoneal cavity, obliteration of psoas shadow, ileus.
Laboratory Findings	Peripheral leukocytosis with polymorphonuclear (PMN) predominance.	Peripheral WBC count >12,000 cells/mm³ with marked PMN predominance.
Ascitic Fluid Analysis	WBC count >250 cells/mm³, >50% PMNs.	Elevated total protein (>1 g/dL), low glucose (<50 mg/dL).
Microbiology	Monomicrobial.	Polymicrobial (mixed bacterial flora).
Medical Management	Broad-spectrum parenteral antibiotics (cefotaxime or ceftriaxone) for 5-10 days.	Aggressive fluid resuscitation, cardiovascular support, broad-spectrum antibiotics (ampicillin + gentamicin + clindamycin/metronidazole, or piperacillin/tazobactam).
Surgical Management	Not indicated. Diagnosed via paracentesis, CT, or laparoscopy.	Surgical emergency. Requires exploration, lavage, and repair of perforated viscus post-stabilization.

Localized collection of pus following visceral perforation (commonly appendiceal or pelvic abscess from perforated appendix).
Transmural inflammation with fistula formation (e.g., Crohn disease) leads to abscess.
Symptoms: Prolonged fever, anorexia, vomiting, lassitude.
Signs: Localized right lower quadrant tenderness and palpable mass (appendiceal), abdominal distention, rectal tenesmus, bladder irritability (pelvic).
Elevated peripheral WBC count and erythrocyte sedimentation rate.

Radiologic-guided (ultrasound or CT) or surgical drainage with indwelling catheter placement.
Broad-spectrum antibiotic therapy (ampicillin, gentamicin, and clindamycin; or ciprofloxacin and metronidazole) adjusted per culture sensitivities.
Appendiceal abscess may require 4-6 weeks of antibiotics followed by interval appendectomy.