Definition and epidemiology
Peritonitis is inflammation of the peritoneal membrane that lines the abdominal cavity and covers the abdominal viscera. It is classified as primary (spontaneous), secondary, or tertiary based on etiology.
Primary (spontaneous) peritonitis occurs without an obvious intra-abdominal source, typically from hematogenous or lymphatic spread. It accounts for approximately 10% of cases and occurs predominantly in patients with ascites from cirrhosis or nephrotic syndrome.
Secondary peritonitis is the most common form, resulting from perforation or rupture of an intra-abdominal viscus. Common causes include perforated peptic ulcer, appendicitis, diverticulitis, and traumatic bowel injury. It accounts for approximately 80-85% of cases.
Tertiary peritonitis refers to persistent or recurrent intra-abdominal infection following treatment of secondary peritonitis, often with less virulent or resistant organisms.
Peritonitis carries significant morbidity and mortality, with case fatality rates of 10-40% depending on etiology, time to treatment, and patient comorbidities. Early recognition and intervention are critical to outcomes.
- Peritoneal signs (rigidity, rebound tenderness) indicate peritonitis and warrant urgent surgical evaluation.
- Spontaneous bacterial peritonitis is diagnosed by ascitic fluid neutrophil count ≥250 cells/mm³.
- Most common organisms in SBP: E. coli, Klebsiella, Streptococcus pneumoniae (monomicrobial).
- Treat SBP with third-generation cephalosporin plus IV albumin to prevent hepatorenal syndrome.
- Secondary peritonitis requires both broad-spectrum antibiotics and urgent surgical source control.
- Upright chest X-ray showing free air under the diaphragm indicates perforated viscus.
- CT abdomen with IV contrast is the imaging study of choice for secondary peritonitis.
- Runyon criteria help distinguish secondary from primary peritonitis: protein >1 g/dL, glucose <50 mg/dL, elevated LDH suggest secondary cause.
Etiology and risk factors
Primary (spontaneous) bacterial peritonitis
- Cirrhosis with ascites (80-90% of cases)
- Nephrotic syndrome
- Congestive heart failure with ascites
- Chronic kidney disease on peritoneal dialysis
Secondary peritonitis causes
- Perforation: Peptic ulcer, appendicitis, diverticulitis, toxic megacolon, bowel obstruction, malignancy
- Transmural inflammation: Acute pancreatitis, inflammatory bowel disease
- Trauma: Penetrating abdominal injury, blunt trauma with visceral rupture
- Iatrogenic: Post-operative anastomotic leak, endoscopic perforation
- Vascular: Mesenteric ischemia with bowel infarction
- Gynecologic: Pelvic inflammatory disease, ruptured ectopic pregnancy, ruptured ovarian cyst
Risk factors
- Advanced cirrhosis with low ascitic fluid protein (<1 g/dL)
- Prior episode of spontaneous bacterial peritonitis
- Gastrointestinal hemorrhage in cirrhotic patients
- Immunosuppression (corticosteroids, chemotherapy, HIV)
- Prolonged peritoneal dialysis catheter use
- Recent abdominal surgery
- Advanced age
- Multiple comorbidities (diabetes, chronic kidney disease)
Pathophysiology
In primary peritonitis, bacterial translocation from the gut is the presumed mechanism, facilitated by increased intestinal permeability, impaired immune function, and altered gut flora. In cirrhotic patients, portal hypertension and reduced reticuloendothelial system function allow bacteria to seed ascitic fluid hematogenously. The most common organisms are Escherichia coli (40-50%), Klebsiella pneumoniae (10-15%), and Streptococcus pneumoniae (10-15%). Monomicrobial infection is the rule.
Secondary peritonitis results from direct contamination of the peritoneal cavity with intestinal contents following perforation or transmural bacterial migration. The inoculum is typically polymicrobial, including gram-negative enteric organisms (E. coli, Klebsiella, Enterobacter), anaerobes (Bacteroides fragilis, Clostridium), and gram-positive cocci (Enterococcus, Streptococcus). When colonic perforation occurs, anaerobes predominate.
The peritoneum responds to bacterial or chemical insult with:
- Increased vascular permeability leading to fluid extravasation and third-spacing
- Fibrin deposition attempting to wall off infection
- Intense inflammatory cytokine release (IL-1, IL-6, TNF-α) causing systemic inflammatory response
- Paralytic ileus from inflammatory mediators affecting bowel motility
Without treatment, peritonitis progresses to septic shock, multiorgan dysfunction, and death. Bacterial translocation into the bloodstream causes bacteremia in 20-75% of cases. The inflamed peritoneum loses its normal absorptive and immune functions, allowing infection to persist or spread.
Clinical features
Symptoms
- Abdominal pain: Typically severe, diffuse, constant; may start localized then generalize
- Nausea and vomiting
- Anorexia
- Fever and chills
- Inability to pass stool or flatus (ileus)
- Abdominal distension
Signs
- Peritoneal signs (hallmark finding):
- Rigidity: Board-like abdominal wall stiffness from involuntary guarding
- Rebound tenderness (Blumberg sign): Pain worse on sudden release of palpation pressure
- Percussion tenderness: Pain with gentle tapping of abdomen
- Absent bowel sounds: From paralytic ileus
- Fever (may be absent in elderly or immunocompromised)
- Tachycardia
- Hypotension (if septic shock develops)
- Shallow, rapid breathing (pain limits diaphragmatic excursion)
- Patient lies still, knees flexed (movement worsens pain)
Special presentations
- Primary peritonitis in cirrhosis: May present subtly with fever, altered mental status, or worsening ascites without prominent abdominal signs
- Peritoneal dialysis-associated: Cloudy dialysate effluent is the cardinal feature; abdominal pain may be mild
- Perforated viscus: Sudden, severe pain, often with history of ulcer disease or recent abdominal symptoms
- Post-operative: Fever, tachycardia, and abdominal distension 5-7 days post-surgery suggest anastomotic leak
Clinical severity varies with etiology, extent of contamination, and time from onset. Elderly and immunosuppressed patients may have blunted inflammatory responses and atypical presentations.
Diagnosis
Diagnosis requires integration of clinical presentation, laboratory findings, and imaging.
Laboratory studies
- Complete blood count: Leukocytosis with left shift; leukopenia suggests overwhelming sepsis
- Basic metabolic panel: Assess for acute kidney injury, electrolyte abnormalities
- Lactate: Elevated in sepsis, indicates tissue hypoperfusion
- Blood cultures: Positive in 20-75% of secondary peritonitis; obtain before antibiotics
- Liver function tests and coagulation studies: Especially in suspected primary peritonitis
Ascitic fluid analysis (if ascites present)
Critical for diagnosing primary peritonitis:
- Cell count and differential: Absolute neutrophil count ≥250 cells/mm³ diagnostic of spontaneous bacterial peritonitis
- Gram stain and culture: Identify organism; inoculate blood culture bottles at bedside for optimal yield
- Albumin: Calculate serum-ascites albumin gradient (SAAG)
- Total protein: Low protein (<1 g/dL) increases SBP risk
Imaging
- Upright chest X-ray: Free air under diaphragm indicates perforation (present in only 50-70% of perforations)
- Abdominal X-ray: May show dilated bowel loops (ileus), free air, or calcifications
- CT abdomen/pelvis with IV contrast: Imaging study of choice for secondary peritonitis
- Identifies perforation, abscess, free fluid, bowel wall thickening, pneumoperitoneum, mesenteric fat stranding
- Sensitivity >95% for detecting most causes
- Ultrasound: Useful for detecting free fluid, guiding paracentesis, assessing for peritoneal dialysis catheter complications
Diagnostic paracentesis
Perform in all patients with ascites and suspected infection. Contraindications are few (severe coagulopathy, bowel obstruction with distension). Paracentesis distinguishes primary from secondary peritonitis:
| Feature | Primary (SBP) | Secondary |
|---|---|---|
| Neutrophil count | ≥250 cells/mm³ | Usually >10,000 cells/mm³ |
| Organisms | Monomicrobial | Polymicrobial |
| Glucose | Normal | Low (<50 mg/dL) |
| Protein | Low | High (>1 g/dL) |
| LDH | Normal/slightly elevated | Markedly elevated |
Runyon criteria for secondary peritonitis: 2 of the following suggest secondary rather than primary peritonitis: total protein >1 g/dL, glucose <50 mg/dL, LDH greater than upper limit of normal for serum.
Differential diagnosis
- Acute pancreatitis: Elevated lipase/amylase, epigastric pain radiating to back, no peritoneal signs unless complicated by pancreatic necrosis
- Bowel obstruction: Cramping pain, distension, hyperactive then absent bowel sounds, no rigidity unless ischemia/perforation
- Mesenteric ischemia: Pain out of proportion to exam, metabolic acidosis, often in elderly with atrial fibrillation
- Ruptured abdominal aortic aneurysm: Pulsatile mass, hypotension, back/flank pain, known AAA history
- Acute cholecystitis: Right upper quadrant tenderness, Murphy sign, fever, positive imaging
- Pelvic inflammatory disease: Lower abdominal/pelvic pain, cervical motion tenderness, vaginal discharge, younger sexually active women
- Ruptured ectopic pregnancy: Acute onset, positive pregnancy test, adnexal mass, hemodynamic instability
- Myocardial infarction: Inferior MI can present with epigastric pain; check ECG and troponin
- Diabetic ketoacidosis: Abdominal pain, nausea, altered mental status; hyperglycemia, ketones, anion gap acidosis
- Pneumonia: Lower lobe pneumonia may cause referred abdominal pain; chest imaging differentiates
The presence of peritoneal signs strongly suggests peritonitis and requires urgent surgical evaluation to exclude secondary causes.
Management
Management depends on whether peritonitis is primary or secondary.
Primary (spontaneous) bacterial peritonitis
Antibiotic therapy:
- Start empiric antibiotics immediately after diagnostic paracentesis, do not wait for culture results
- First-line: Third-generation cephalosporin (cefotaxime or ceftriaxone) for 5-7 days
- Alternative: Fluoroquinolone if no recent quinolone prophylaxis
- Adjust based on culture and susceptibility results
- Repeat paracentesis in 48 hours if clinical response is poor; neutrophil count should decrease by ≥25%
Albumin administration:
- Give IV albumin to prevent hepatorenal syndrome
- Administered at diagnosis and again on day 3
Secondary prophylaxis:
- After one episode, lifelong antibiotic prophylaxis or liver transplant evaluation
- Prophylactic regimen: Daily fluoroquinolone or trimethoprim-sulfamethoxazole
Secondary peritonitis
Immediate resuscitation:
- Aggressive IV fluid resuscitation with crystalloids
- Correct electrolyte abnormalities and coagulopathy
- Vasopressors if septic shock develops
- Supplemental oxygen or mechanical ventilation if needed
- Nasogastric decompression for ileus
- Foley catheter for urine output monitoring
Broad-spectrum antibiotics: Start empirically before source control:
- Community-acquired: Piperacillin-tazobactam, or ceftriaxone plus metronidazole, or a carbapenem
- Healthcare-associated or high-risk: Carbapenem or cefepime plus metronidazole; consider adding antifungal and gram-positive coverage
- Cover gram-negatives, anaerobes, and gram-positive cocci; adjust based on cultures
Urgent surgical source control: Essential for secondary peritonitis; medical management alone has high mortality.
- Exploratory laparotomy or laparoscopy: Identify and repair perforation, drain abscesses, remove necrotic tissue
- Procedures: Primary repair, resection with anastomosis or stoma, drainage of contaminated fluid
- Damage control surgery may be needed in unstable patients: abbreviated procedure, temporary abdominal closure, planned reoperation
Post-operative management:
- Continue antibiotics 4-7 days if adequate source control achieved; longer if persistent infection
- Nutritional support (enteral preferred)
- Monitor for tertiary peritonitis or intra-abdominal abscess
- Some cases require open abdomen management with serial washouts
Peritoneal dialysis-associated peritonitis
- Add antibiotics directly to dialysate
- Initial empiric: Vancomycin plus ceftazidime or aminoglycoside
- Most cases resolve with antibiotics; catheter removal if refractory or fungal infection
Supportive care
- Pain management (opioid analgesics after diagnosis established)
- VTE prophylaxis unless contraindicated
- Stress ulcer prophylaxis in ICU patients
- Early mobilization when feasible
Complications and prognosis
Complications
- Septic shock and multiorgan dysfunction: Most common cause of death; requires ICU care with vasopressor support
- Acute kidney injury: From sepsis, hypovolemia, or hepatorenal syndrome in cirrhotic patients
- Acute respiratory distress syndrome (ARDS): From systemic inflammation
- Intra-abdominal abscess: May require percutaneous or surgical drainage
- Tertiary peritonitis: Persistent infection after treatment of secondary peritonitis
- Adhesions and bowel obstruction: Late complication from fibrin deposition
- Wound complications: Dehiscence, infection, enterocutaneous fistula
- Hepatorenal syndrome: Specifically in primary peritonitis with cirrhosis
Prognosis
Primary peritonitis: With prompt treatment, resolution occurs in 90% of cases. In-hospital mortality is 10-30%, largely dependent on underlying liver disease severity. One-year survival after SBP is approximately 30-50%, reflecting advanced liver disease. Recurrence risk is 70% within one year without prophylaxis.
Secondary peritonitis: Overall mortality is 20-40%. Prognosis depends on:
- Time to source control (delay >24 hours significantly worsens outcomes)
- Adequacy of source control
- Organism virulence and presence of multidrug-resistant pathogens
- Patient age and comorbidities
- Severity of organ dysfunction at presentation
Favorable prognostic factors: Early diagnosis, prompt surgical intervention, appropriate antibiotic coverage, absence of immunosuppression, localized disease.
Poor prognostic factors: Delayed presentation, inadequate source control, fecal peritonitis, multiorgan failure, advanced age, malignancy, immunosuppression, nosocomial infection with resistant organisms, APACHE II score >15.
Tertiary peritonitis has mortality rates of 30-60% and often requires multiple operations.
Complete recovery is possible with early recognition and aggressive management, but peritonitis remains a life-threatening condition requiring urgent intervention.
Practice questions
1. A 58-year-old man with a history of alcohol-related cirrhosis presents to the emergency department with fever, confusion, and abdominal distension. He has known ascites. Vital signs: temperature 38.7°C, heart rate 105 bpm, blood pressure 95/60 mmHg. Abdominal examination shows mild diffuse tenderness without rigidity. Diagnostic paracentesis reveals cloudy fluid with 450 neutrophils/mm³, total protein 0.8 g/dL, glucose 65 mg/dL. Gram stain shows gram-negative rods. Which of the following is the most appropriate next step in management?
2. A 45-year-old woman presents with sudden-onset severe abdominal pain that began 6 hours ago. She has a history of peptic ulcer disease. On examination, her abdomen is rigid with diffuse rebound tenderness. Vital signs show temperature 38.2°C, heart rate 118 bpm, blood pressure 100/65 mmHg. Upright chest X-ray shows free air under the right hemidiaphragm. Laboratory studies show WBC 18,500/μL with 85% neutrophils. Which of the following is the most appropriate management?
3. A 62-year-old man with cirrhosis and ascites was hospitalized 2 days ago for spontaneous bacterial peritonitis and started on cefotaxime. Initial ascitic fluid showed 380 neutrophils/mm³ and grew E. coli sensitive to cefotaxime. Despite therapy, he remains febrile with worsening abdominal pain. Repeat paracentesis today shows 420 neutrophils/mm³, total protein 2.1 g/dL, glucose 35 mg/dL, LDH 300 U/L (serum upper limit 200 U/L). Gram stain shows multiple organism types. What is the most likely diagnosis?
Frequently asked questions
What causes peritonitis?
Peritonitis is caused by bacterial infection or chemical irritation of the peritoneum. Primary (spontaneous) peritonitis occurs mainly in cirrhotic patients with ascites from bacterial translocation. Secondary peritonitis, the most common form, results from perforation of an abdominal organ such as perforated peptic ulcer, appendicitis, diverticulitis, or bowel injury. Other causes include pancreatitis, pelvic inflammatory disease, peritoneal dialysis catheter infection, and post-surgical complications like anastomotic leaks.
What are the first symptoms of peritonitis?
The first symptoms of peritonitis are typically severe, diffuse abdominal pain that is constant and worsens with movement. Patients also experience nausea, vomiting, fever, and abdominal distension. On examination, the abdomen becomes rigid (board-like) with rebound tenderness when pressure is released. Patients prefer to lie still with knees bent because movement intensifies the pain. In cirrhotic patients with spontaneous bacterial peritonitis, symptoms may be more subtle, presenting with fever, confusion, or worsening ascites without prominent abdominal signs.
How is peritonitis diagnosed?
Peritonitis is diagnosed through clinical examination, laboratory tests, and imaging. Physical examination reveals peritoneal signs: abdominal rigidity, rebound tenderness, and absent bowel sounds. If ascites is present, diagnostic paracentesis is performed; an ascitic fluid neutrophil count ≥250 cells/mm³ confirms spontaneous bacterial peritonitis. CT scan of the abdomen with IV contrast is the imaging study of choice for secondary peritonitis, identifying perforations, abscesses, or free fluid. Upright chest X-ray may show free air under the diaphragm indicating perforation. Blood tests show elevated white blood cell count and lactate.
Is peritonitis curable?
Yes, peritonitis is curable with prompt, appropriate treatment. Primary (spontaneous) bacterial peritonitis resolves in about 90% of cases with antibiotics and albumin therapy. Secondary peritonitis requires both broad-spectrum antibiotics and urgent surgery to repair the source (such as closing a perforation or removing infected tissue). However, mortality remains 10-40% depending on cause, timing of treatment, and patient health. Without treatment, peritonitis progresses to septic shock and death. Early recognition and aggressive management are essential for cure and survival.
Peritonitis vs appendicitis — what is the difference?
Appendicitis is inflammation of the appendix, while peritonitis is inflammation of the peritoneal lining of the entire abdominal cavity. Appendicitis typically starts with periumbilical pain that migrates to the right lower quadrant (McBurney's point) with localized tenderness. Peritonitis causes diffuse abdominal pain with widespread rigidity and rebound tenderness throughout the abdomen. Appendicitis can cause peritonitis if the appendix ruptures and spills contents into the peritoneal cavity. Uncomplicated appendicitis is treated with appendectomy, while established peritonitis requires broader surgical exploration, washout, and source control.
Key drugs
Related conditions and differentials
Sources and further reading
StatPearls (NCBI Bookshelf)MedlinePlusWHO ICD-10: K65
Educational content for medical students, prepared by the WhiteCoat Pro editorial team with AI assistance; every page is reviewed by a second AI model for factual errors. It is not medical advice and does not replace the product label, local guidelines or a clinician.