Quick Recap
GI & Hepatology System, Protocol 11/13. Closely linked to Perforation (prior protocol) as the physiologic syndrome most perforations produce, but peritonitis has distinct primary/secondary/tertiary categories requiring different diagnostic and management approaches.
1. Classification
- Primary (spontaneous) peritonitis: infection of ascitic fluid WITHOUT an identifiable intra-abdominal source of contamination — the prototype is spontaneous bacterial peritonitis (SBP) in cirrhotic ascites (Section 3)
- Secondary peritonitis: infection secondary to a identifiable intra-abdominal process — perforation, anastomotic leak, ischemic bowel, abscess rupture (the most common ICU-relevant category, closely tied to the Perforation protocol)
- Tertiary peritonitis: persistent/recurrent intra-abdominal infection despite adequate initial source control and antibiotic therapy for secondary peritonitis, often with different (more resistant, opportunistic, or fungal) organisms — a distinct, more difficult-to-treat entity reflecting a dysregulated host response as much as ongoing infection
Critical distinction: SBP must be differentiated from secondary bacterial peritonitis due to bowel perforation or intra-abdominal abscess — the management pathways diverge completely (medical antibiotic therapy alone for SBP vs mandatory source control/surgery for secondary peritonitis), making this differentiation one of the most consequential diagnostic branch points in this protocol.
2. Secondary Peritonitis (Perforation/Leak-Associated) — Cross-Reference
See the Perforation protocol for full site-specific etiology, imaging approach, and source control management. The core principle: antibiotics alone cannot control secondary peritonitis from an ongoing GI leak — surgical or percutaneous source control is mandatory and time-sensitive, with antibiotics as an essential but insufficient-alone adjunct.
3. Spontaneous Bacterial Peritonitis (SBP) — Primary Peritonitis, Full Detail
The most common infectious complication of ascites. 10-27% of hospitalized cirrhotic ascites patients have SBP at time of admission. Infections including SBP carry a 4-FOLD increase in hospital mortality in cirrhosis — this is not a minor complication to treat casually.
Presentation is often SUBTLE/ATYPICAL: abdominal pain, fever, and leukocytosis are FREQUENTLY ABSENT — do not require classic peritonitis signs to suspect SBP; any unexplained clinical deterioration in a cirrhotic patient with ascites (worsening encephalopathy, renal function decline, hypotension) should prompt diagnostic paracentesis, mirroring the precipitant-search principle established in the Hepatic Encephalopathy protocol.
Diagnosis: ascitic fluid PMN (polymorphonuclear) cell count >=250 cells/mm3, OR positive ascitic fluid culture with a compatible clinical picture. Inoculate ascitic fluid directly into blood culture bottles at the bedside (as established in the Acute-on-Chronic Liver Failure protocol) — substantially improves culture yield over standard lab-based specimen handling.
Most common organisms: monomicrobial GRAM-NEGATIVE organisms (E. coli, Klebsiella most common) — a polymicrobial or mixed gram-positive/anaerobic picture on culture should raise suspicion for SECONDARY (not primary/spontaneous) peritonitis and prompt a search for a perforation/leak source.
Treatment:
- First-line: third-generation cephalosporin — ceftriaxone 1g q24h OR cefotaxime 2g q12h
- Multidrug-resistant (MDR) organism risk is RISING — risk factors: nosocomial infection, recent hospitalization, ICU patients. For first-line failure or suspected MDR organism: piperacillin-tazobactam, carbapenems, or vancomycin
- Renal protection with albumin: renal dysfunction occurs in up to 1/3 of SBP patients DESPITE adequate antimicrobial treatment — IV 25% albumin 1.5 g/kg on day 1 and 1 g/kg on day 3 reduces AKI risk. Strongly consider albumin in ALL SBP patients, particularly those with jaundice or pre-existing kidney disease
- Hold diuretics and beta-blockers at the time of SBP diagnosis — both can worsen the hemodynamic vulnerability associated with SBP (diuretics worsen effective volume depletion; beta-blockers blunt the compensatory tachycardic response to the septic/hemodynamic insult)
- Repeat paracentesis 2 days after treatment initiation to confirm response — failure to achieve at least a 25% reduction in PMN count from pretreatment levels should prompt a switch from first- to second-line antimicrobial therapy (and reconsideration of whether this is truly SBP vs an unrecognized secondary source)
Antibiotic prophylaxis (for high-risk cirrhotic patients, distinct from treatment of established SBP):
- Variceal hemorrhage: prophylactic antibiotics reduce SBP risk and rebleeding (see Upper GI Bleed protocol — ceftriaxone 1g/day x7 days)
- Primary SBP prevention in ascitic fluid protein <1.5 g/dL PLUS any of: BUN >25, serum Na <130, or bilirubin >3
- Secondary prevention in any patient with a prior SBP episode (recurrence risk is substantial without prophylaxis)
- Prophylactic antibiotics are LESS EFFECTIVE in patients colonized with MDR bacteria — the central tension is balancing prophylactic benefit against the inevitable selection pressure for antimicrobial resistance; this should inform a judicious, not blanket, approach to prophylaxis duration/breadth
4. Immediate Stabilization (ABCDE) — General Peritonitis Framework
Airway/Breathing: standard indications; abdominal distension can impair diaphragmatic excursion/ventilation in severe cases.
Circulation: treat as septic shock if hemodynamically unstable — apply full Septic Shock protocol principles (fluid resuscitation, blood cultures/ascitic fluid cultures before antibiotics where feasible without meaningful delay, empiric antibiotics within 1 hour, norepinephrine first-line for vasopressor-dependent shock).
Checklist:
5. Tertiary Peritonitis — Brief Note
Persistent/recurrent intra-abdominal infection after adequate source control and antibiotic therapy for an initial secondary peritonitis episode. Often reflects a combination of ongoing low-grade infection with more resistant/opportunistic organisms (including fungal pathogens) AND a dysregulated, immunosuppressed host inflammatory state rather than a single correctable anatomic problem. Management requires broadened microbiologic workup (including fungal cultures), reassessment for any missed or recurrent source requiring further intervention, and antimicrobial therapy informed by prior culture data and local resistance patterns — involve infectious disease early given the complexity.
6. Organ Support
Fluid resuscitation and vasopressor support per Septic Shock protocol if unstable; albumin for SBP-associated renal protection; source control (surgical/percutaneous) for secondary peritonitis; standard ICU supportive care; nutrition support once stabilizing.
7. Consultation Matrix
Consultation | Trigger | Timing |
Hepatology/Gastroenterology | SBP diagnosis/management, paracentesis | Immediate |
General Surgery | Any secondary peritonitis requiring source control | Immediate |
Infectious Disease | MDR organism, tertiary peritonitis, complex antibiotic management | As needed |
8. Monitoring Framework
Repeat paracentesis at 48h for SBP treatment response (25% PMN reduction target), serial abdominal exam and hemodynamics, renal function trend (esp. with albumin protection for SBP), culture data trending for antibiotic de-escalation, source control adequacy reassessment for secondary peritonitis.
9. Complications
SBP: renal failure/hepatorenal syndrome (despite treatment, in up to 1/3), recurrence without adequate secondary prophylaxis, progression to septic shock. Secondary peritonitis: abscess formation, fistula, multi-organ failure, progression to tertiary peritonitis. Prevention: prompt diagnostic paracentesis for at-risk patients, appropriate SBP prophylaxis in high-risk cirrhotic patients (balanced against MDR selection pressure), timely source control for secondary peritonitis. Rescue: second-line antibiotics for SBP treatment failure, repeat surgical/percutaneous source control for secondary/tertiary peritonitis.
10. Escalation & De-escalation
Escalate: SBP with <25% PMN reduction at 48h -> switch to second-line antibiotics, reconsider secondary peritonitis; secondary peritonitis with ongoing instability -> repeat source control intervention.
De-escalate: SBP responding (>=25% PMN reduction), clinical improvement -> continue definitive antibiotic course, resume diuretics/beta-blockers once stable, arrange secondary SBP prophylaxis at discharge; secondary peritonitis source-controlled and improving -> narrow antibiotics per culture, advance nutrition.
11. ICU Discharge Criteria
SBP: hemodynamically stable, PMN response confirmed, renal function stable/improving, antibiotic course completed or on track, secondary prophylaxis plan established. Secondary peritonitis: source controlled, hemodynamically stable off vasopressors, antibiotics narrowed to definitive course, nutrition established.
12. Documentation & Medicolegal Checklist
13. Key Guidelines
Biggins SW, Angeli P, Garcia-Tsao G, et al. Diagnosis, evaluation, and management of ascites, spontaneous bacterial peritonitis and hepatorenal syndrome: 2021 AASLD practice guidance. Hepatology. 2021;74(2):1014-1048. Mazuski JE, Tessier JM, May AK, et al. The Surgical Infection Society revised guidelines on the management of intra-abdominal infection. Surg Infect. 2017;18(1):1-76.
14. Controversies
The balance between SBP prophylaxis benefit and antimicrobial resistance selection pressure remains a genuinely unresolved tension — practice varies in how aggressively primary prophylaxis is pursued given this tradeoff. Tertiary peritonitis management (empiric antifungal threshold, optimal antibiotic duration/combination) lacks strong RCT-level guidance given the heterogeneity and complexity of this patient population.
15. References
- Al-Obaid L, Korenblat KM. End-Stage Liver Disease (SBP section). Washington Manual of Critical Care, 4th ed, 2025 (Ch. 51).
- Biggins SW, Angeli P, Garcia-Tsao G, et al. Diagnosis, evaluation, and management of ascites, SBP, and HRS: 2021 AASLD practice guidance. Hepatology. 2021;74(2):1014-1048.
- Mazuski JE, Tessier JM, May AK, et al. The Surgical Infection Society revised guidelines on the management of intra-abdominal infection. Surg Infect. 2017;18(1):1-76.
- Sort P, Navasa M, Arroyo V, et al. Effect of intravenous albumin on renal impairment and mortality in patients with cirrhosis and SBP. N Engl J Med. 1999;341(6):403-409 (foundational albumin dosing trial).
See also: Perforation (secondary peritonitis source), Acute-on-Chronic Liver Failure (cirrhotic ascites context), Upper GI Bleed (variceal bleeding SBP prophylaxis) — GI & Hepatology System.