Key Points

• Acute peritonitis is inflammation of the peritoneal lining, most often caused by microbial contamination from a perforated viscus or translocation of bacteria.
• Classify as primary (spontaneous bacterial), secondary (viscus perforation or intra-abdominal source), or tertiary (persistent/recurrent infection despite therapy).
• Presents with severe abdominal pain, guarding/rigidity, systemic inflammatory response, and signs of sepsis.
• Early management focuses on resuscitation, broad-spectrum antibiotics, and prompt source control (usually surgical or radiologic drainage).
• Delays in diagnosis or source control increase morbidity and mortality; multidisciplinary care and intensive monitoring improve outcomes.

Introduction

Acute peritonitis is a life-threatening condition caused by inflammation of the peritoneum. It ranges from localized peritonitis surrounding an inflamed organ (e.g., appendiceal phlegmon) to diffuse peritonitis with generalized contamination and sepsis. Rapid recognition and treatment are essential to limit progression to septic shock and multi-organ failure.

Classification and Causes

Primary (Spontaneous) Peritonitis

• Occurs without an obvious intra-abdominal source; bacteria access the peritoneal cavity via hematogenous spread, lymphatics, or transmural migration.
• Common in patients with ascites from cirrhosis, nephrotic syndrome, or immunosuppression.
• Typical pathogens: gram-negative enteric organisms (e.g., E. coli), Streptococcus spp., and occasionally Streptococcus pneumoniae in children.

Secondary Peritonitis

• Most common type; results from contamination of the peritoneal cavity by perforation or severe inflammation of an intra-abdominal organ.
• Common causes:
• Perforated appendicitis
• Perforated peptic ulcer
• Perforated diverticulitis
• Bowel ischemia with necrosis/perforation
• Traumatic bowel injury
• Postoperative anastomotic leak or intra-abdominal contamination
• Intra‑abdominal inflammatory disease (e.g., severe pancreatitis with infected necrosis, complicated cholecystitis)
• Gynecologic sources (e.g., tubo‑ovarian abscess, ruptured ectopic pregnancy)

Tertiary (Persistent/Recurrent) Peritonitis

• Ongoing or recurrent intra‑abdominal infection despite appropriate surgical source control and antibiotics.
• Often seen in critically ill or immunocompromised patients and associated with resistant organisms and fungal infections.

Pathophysiology

• Peritoneal contamination triggers an acute inflammatory response with neutrophil recruitment, cytokine release, and increased vascular permeability.
• Local inflammation leads to ileus, third‑spacing of fluids, and systemic inflammatory response syndrome (SIRS).
• Bacterial translocation and endotoxemia can precipitate sepsis and multi-organ dysfunction when host defenses are overwhelmed.

Clinical Presentation

• Abrupt or progressive abdominal pain; diffuse, severe pain suggests generalized peritonitis.
• Peritoneal signs: guarding, rigidity, rebound tenderness, and decreased bowel sounds.
• Systemic features: fever, tachycardia, hypotension, oliguria, altered mental status.
• In primary peritonitis, symptoms may be more insidious, especially in patients with ascites.
• History clues: recent abdominal surgery, peptic ulcer disease, diverticulitis, trauma, immunosuppression, or peritoneal dialysis.

Diagnostic Evaluation

Initial Assessment

• Rapid evaluation of airway, breathing, circulation; early aggressive resuscitation for unstable patients.
• Focused history and physical exam to localize source and assess severity.

Laboratory Studies

• CBC: leukocytosis with left shift (may be absent in immunocompromised patients).
• Basic metabolic panel: assess electrolytes, renal function, acid–base status.
• Liver function tests and coagulation profile where indicated.
• Serum lactate as a marker of tissue hypoperfusion and severity.
• Blood cultures prior to antibiotics when feasible.
• Ascitic fluid analysis (in patients with ascites): cell count (>250 PMNs/µL suggests infection), Gram stain, culture, serum-ascites albumin gradient (SAAG).

Imaging

• Upright chest and abdominal radiographs: free air under diaphragm suggests perforation.
• Contrast-enhanced CT abdomen/pelvis: preferred imaging to identify perforation, abscesses, inflammatory changes, bowel ischemia, and to guide percutaneous drainage.
• Ultrasound: useful in unstable patients, for evaluation of free fluid, gallbladder pathology, or guided drainage.

Management Principles

• Early resuscitation: aggressive IV fluids, oxygen, and hemodynamic support; follow sepsis protocols when appropriate.
• Broad‑spectrum empiric IV antibiotics covering gram‑negative, gram‑positive, and anaerobic organisms; tailor therapy to source and cultures.
• Prompt source control:
• Urgent laparotomy or laparoscopy for generalized peritonitis from perforation or uncontrolled contamination.
• Percutaneous drainage for localized abscesses or collections when feasible.
• Repair of perforation, resection of necrotic bowel, or diverting ostomy as indicated.
• Management of complications: ventilatory support, vasopressors, renal replacement therapy for organ failure.

Empiric Antibiotic Considerations

• Choose agents based on local resistance patterns, severity, and patient risk factors (healthcare exposure, immunosuppression).
• Examples (institution-specific selection required):
• Piperacillin–tazobactam or a carbapenem for high-risk or severe community-acquired secondary peritonitis.
• Ceftriaxone + metronidazole for stable patients without risk factors for resistant organisms.
• Add coverage for MRSA or antifungal therapy in select high‑risk patients (e.g., postoperative peritonitis, tertiary peritonitis).
• De-escalate based on culture results and clinical response; usual duration 4–7 days for adequately controlled sources, longer if source control is delayed or infection complicated.

Special Situations

Peritoneal Dialysis‑Related Peritonitis

• Often presents with cloudy effluent, abdominal pain; treat promptly with intraperitoneal antibiotics per dialysis unit protocols and consider catheter removal for refractory cases.

Cirrhotic Patients with Spontaneous Bacterial Peritonitis (SBP)

• Empiric therapy: third‑generation cephalosporin (e.g., cefotaxime) or broader agents in nosocomial cases; albumin infusion reduces renal failure risk in selected patients.

Nursing Considerations

• Frequent monitoring of vital signs, urine output, fluid balance, and abdominal exam for evolving peritoneal signs.
• Maintain large-bore IV access; assist with blood draws and timely administration of antibiotics and fluids.
• Provide wound and drain care postoperatively; ensure proper drain function and output recording.
• Monitor for signs of organ dysfunction: altered mental state, oliguria, rising lactate, or hypotension.
• Educate patient and family on the need for urgent intervention, potential need for surgery, and postoperative expectations.

Complications

• Intra‑abdominal abscess, persistent sepsis, septic shock, acute respiratory distress syndrome (ARDS), acute kidney injury, and multiple organ dysfunction syndrome (MODS).
• Adhesive small-bowel obstruction and incisional hernia as late postoperative complications.

Prognosis

• Dependent on etiology, timeliness of source control, patient comorbidities, and presence of sepsis or organ failure.
• Mortality rates higher in tertiary peritonitis and in patients with delayed diagnosis or inadequate source control.

Disposition and Follow-up

• Admit patients with suspected generalized peritonitis to a monitored setting (surgical ward or ICU depending on severity).
• Arrange timely surgical consultation; coordinate imaging and interventional radiology for drainage when indicated.
• Plan outpatient follow-up for recovery, wound checks, and investigation of underlying causes (e.g., malignancy, diverticular disease).

References

1. Sartelli M, Chichom-Mefire A, Labricciosa FM, et al. 2017 WSES guidelines for management of intra‑abdominal infections. World J Emerg Surg. 2017;12:1.
2. Solomkin JS, Mazuski JE, Bradley JS, et al. Diagnosis and management of complicated intra‑abdominal infection in adults and children: 2010 consensus guidelines by the Surgical Infection Society and the Infectious Diseases Society of America. Clin Infect Dis. 2010;50(2):133–164.
3. Runyon BA. Management of adult patients with ascites caused by cirrhosis: an update. Hepatology. 2009;49(6):2087–2107.