Peritonitis & Abdominal Sepsis

1. Classification of Peritonitis

By Pathogenesis (Hamburg Classification — most widely used surgically)

By Extent

• Local (localized) — contained by omentum/adjacent organs → abscess formation
• Diffuse (generalized) — free contamination of the entire peritoneal cavity

By Exudate Character

• Serous → Fibrinous → Fibrinopurulent → Purulent → Fecal (fecal peritonitis = worst prognosis)

By Etiology

• Bacterial (most common): E. coli, Bacteroides fragilis, streptococci, enterococci, C. perfringens
• Chemical (sterile): bile peritonitis, pancreatic enzyme leakage, gastric acid (perforated PU within first hours)
• Granulomatous: tuberculous, foreign body, ruptured dermoid cyst, talc

2. Sources and Infection Spread in Acute Surgical Diseases

1. Direct extension along peritoneal surfaces (gravity-dependent pooling: pelvis, paracolic gutters, subphrenic spaces)
2. Lymphatic dissemination → bacteremia/septicemia
3. Hematogenous seeding (especially in primary peritonitis)

3. Clinical Presentation

Symptoms

• Abdominal pain: sudden onset (perforation) or gradual; classically constant, worsened by movement
• Nausea, vomiting, anorexia
• Fever (38–39°C; high fever or hypothermia in sepsis/elderly)
• Cessation of flatus/stool (paralytic ileus)

Signs

• Board-like (muscular) rigidity — involuntary guarding (most reliable sign of diffuse peritonitis)
• Rebound tenderness (Blumberg sign)
• Absent bowel sounds (paralytic ileus)
• Tachycardia, hypotension (septic shock in severe cases)
• Facies Hippocratica (late): sunken eyes, dry lips, ashen face — sign of advanced/terminal peritonitis
• Positive percussion tenderness; obliteration of hepatic dullness (free air in pneumoperitoneum)

Special Presentations

• Elderly / immunosuppressed: signs may be minimal/absent despite severe disease
• Post-operative peritonitis: masked by analgesia, tachycardia may be the only clue
• Children: generalized voluntary guarding, diffuse tenderness

4. Diagnosis

Laboratory

• CBC: leukocytosis (>12,000) with left shift; leukopenia is ominous
• CRP, PCT (procalcitonin) — elevated; PCT >2 ng/mL suggests bacterial infection/sepsis
• Lactate: elevated in sepsis; >4 mmol/L → septic shock
• Blood cultures (before antibiotics)
• BMP: electrolytes, renal function (AKI in sepsis); LFTs, amylase (source identification)
• Urinalysis (to exclude renal/urological source)

Imaging

• Upright CXR: free air under diaphragm (pneumoperitoneum) — confirms perforation
• Plain AXR: dilated bowel loops, absent psoas shadow, ground-glass opacity
• CT abdomen/pelvis (with IV contrast): gold standard — localizes source, identifies free air, fluid collections, abscesses, bowel wall thickening; guides drainage planning
• Ultrasound: useful for free fluid, biliary pathology, pelvic assessment; limited by ileus/gas

Diagnostic Peritoneal Lavage / Laparoscopy

• Used when imaging inconclusive and clinical deterioration continues
• Laparoscopy: diagnostic + therapeutic (appendectomy, washout, ulcer repair)

Scoring Systems

• MPI (Mannheim Peritonitis Index): 8 variables (age, sex, organ failure, malignancy, duration >24h, non-colonic source, diffuse spread, exudate type); score >26 → high mortality (>50%)
• APACHE II, SOFA — for severity of abdominal sepsis / ICU triage
• Peritonitis Severity Score (PSS)

5. Modern Principles of Comprehensive Treatment

The Three Pillars

1. SOURCE CONTROL  +  2. ANTIMICROBIAL THERAPY  +  3. ORGAN SUPPORT

A. Source Control (Priority #1)

• Eliminate the source of contamination (perforation closure, bowel resection, appendectomy, cholecystectomy)
• Peritoneal lavage (mechanical reduction of bacterial load)
• Drainage of residual infected collections
• Timing: within 6–12 hours of diagnosis (delay increases mortality); for septic shock: within 6 hours

B. Antimicrobial Therapy

• Start empirically within 1 hour of diagnosis; obtain cultures first when feasible
• Duration: typically 4–7 days after adequate source control; de-escalate based on culture results

• Monotherapy: ertapenem, piperacillin-tazobactam, or moxifloxacin
• Combination: cephalosporin (1st–3rd gen) OR fluoroquinolone + metronidazole
• Note: ampicillin-sulbactam avoided (high E. coli resistance); cefoxitin falling out of favor

• Broaden to cover P. aeruginosa, ESBL producers, Enterococcus, anaerobes
• Piperacillin-tazobactam, or imipenem/meropenem/doripenem, or cefepime + metronidazole
• Add vancomycin if MRSA suspected; antifungals (fluconazole/micafungin) if upper GI source or immunocompromised

C. Organ Support (ICU/Sepsis Bundles — Surviving Sepsis Campaign)

• Fluid resuscitation: 30 mL/kg crystalloid IV within 3 hours
• Vasopressors (norepinephrine first-line) if MAP <65 mmHg despite fluids
• Hydrocortisone if vasopressor-refractory shock
• Mechanical ventilation (lung-protective) if ARDS
• Renal replacement therapy if AKI with metabolic dysfunction

D. Nutritional Support

• Early enteral nutrition (within 24–48h of ICU admission) preferred over parenteral
• Prevents gut mucosal atrophy and translocation

6. Indications for Laparotomy (Emergency / Urgent)

Absolute Indications

• Free air (pneumoperitoneum) on imaging → hollow viscus perforation
• Fecal / diffuse purulent peritonitis with clinical deterioration
• Strangulated bowel / mesenteric ischemia with necrosis
• Ruptured abdominal aortic aneurysm with peritoneal signs
• Uncontrolled abdominal hemorrhage
• Failure of conservative / percutaneous management (worsening sepsis)
• Anastomotic leak with peritonitis / sepsis

Relative / Elective Indications (if no improvement in 12–24h)

• Localized abscess not amenable to percutaneous drainage
• Peritonitis from cholecystitis not responding to conservative management
• Appendiceal mass (plastron) with signs of complication

Approach Options

• Open laparotomy: standard for diffuse peritonitis, fecal contamination, bowel resection
• Laparoscopy: selected cases — perforated peptic ulcer repair, appendectomy, diagnostic lavage

7. Types of Abdominal Cavity Drainage

Drain Placement Principles

• Drain to dependent areas: pelvis (Morrison's pouch, Douglas pouch), paracolic gutters, subphrenic spaces
• Do not drain over anastomoses (increases leak rate)
• Prophylactic drains after elective surgery have not been shown to reduce complications in clean cases

8. Abdominal Sepsis

Definition

Patho-Mechanism

1. Intra-abdominal contamination → local inflammatory response (IL-1, IL-6, TNF-α)
2. Bacterial translocation + endotoxin release → systemic inflammatory response syndrome (SIRS)
3. Activated complement, coagulation cascades → microvascular thrombosis
4. End-organ hypoperfusion → MODS (lung → ARDS; kidney → AKI; liver → jaundice; gut → further translocation)

Classification (Sepsis-3, 2016)

• Sepsis: infection + organ dysfunction (SOFA ≥2 points)
• Septic shock: sepsis + vasopressor requirement to maintain MAP ≥65 mmHg + lactate >2 mmol/L despite adequate fluid resuscitation

Abdominal Sepsis vs. Other IAI

Management of Abdominal Sepsis (Hour-1 Bundle — Surviving Sepsis Campaign)

1. Measure lactate (remeasure if >2 mmol/L)
2. Blood cultures ×2 before antibiotics
3. Broad-spectrum antibiotics within 1 hour
4. IV crystalloid 30 mL/kg for hypotension or lactate ≥4 mmol/L
5. Vasopressors for MAP <65 mmHg despite resuscitation
6. Source control within 6–12 hours (emergent surgery / percutaneous drainage)

Prognostic Markers

• Lactate: best early predictor of mortality; clearance >10% within 2h = favorable
• PCT: guides antibiotic de-escalation
• SOFA score: predicts ICU mortality
• Mannheim Peritonitis Index >26: mortality >50%

Key References

• Robbins, Cotran & Kumar Pathologic Basis of Disease — Peritonitis morphology and etiology
• Current Surgical Therapy 14e — Intra-abdominal infection, source control, antibiotic regimens
• Tintinalli's Emergency Medicine — PD-related peritonitis diagnosis and management
• Goldman-Cecil Medicine — Intra-abdominal inflammation and sepsis
• Surviving Sepsis Campaign 2021 Guidelines
• IDSA Guidelines on Complicated Intra-abdominal Infections