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Intraabdominal Infections and Abscesses

Chapter 137 | Part 5: Infectious Diseases · Part 5 – Infectious Diseases: Bacterial · Chapter 137

Key Clinical Points

  1. Primary Bacterial Peritonitis (PBP) diagnosis requires ascitic fluid PMN count >250/μL; absence of this finding excludes PBP.
  2. Secondary peritonitis is characterized by mixed flora (aerobes + anaerobes) and requires surgical source control.
  3. Bacteroides fragilis is the most common anaerobe in intraabdominal abscesses, uniquely virulent due to its capsular polysaccharide complex.
  4. Liver abscesses: Elevated alkaline phosphatase is the single most reliable lab finding (70%); fever of unknown origin should prompt abdominal imaging.
  5. CAPD peritonitis diagnosis: Dialysate must be cloudy with >100 WBC/μL (>50% PMNs); clear fluid requires a second exchange with dwell time ≥2 h.
  6. Empirical therapy for secondary peritonitis must cover gram-negative bacilli and anaerobes; drainage is the mainstay of therapy for abscesses.
  7. PBP mortality: 17.6% in-hospital, 23% at 30 days, and 37% at 90 days in tertiary centers.
  8. PBP prevention: Chronic antibiotic prophylaxis (fluoroquinolones or rifaximin) for high-risk cirrhotics (ascitic protein <1.5 g/dL, renal impairment, liver failure).
  9. Liver abscesses: 26% of all intraabdominal abscesses; 48% of all visceral abscesses; biliary tract disease is the most common source.
  10. Diabetic foot infection: MRSA prevalence 5–43%; ESBL-producing gram-negative bacilli are common in Asia; vancomycin indicated for high MRSA risk.

1. DEFINITION & OVERVIEW

Intraabdominal infections arise from disruption of normal anatomic barriers (e.g., appendicitis, diverticulitis, ulcer rupture). Pathogenesis involves two stages: peritonitis followed by abscess formation if untreated. Microbial flora differs between primary and secondary peritonitis.

1.1 Classification of Peritonitis

• Primary (Spontaneous): Occurs in cirrhosis with ascites; single organism typically isolated (gram--negative bacilli, streptococci). • Secondary: Results from viscus rupture/spillage; mixed flora (aerobes + anaerobes) predominate. Requires surgical intervention. • CAPD-Associated: Caused by skin organisms (staphylococci); catheter removal often required.

1.2 Anatomy of the Peritoneal Cavity

• Compartmentalization: Divided into upper and lower compartments by transverse mesocolon. • Anatomical Landmarks: Greater omentum lines lower peritoneal cavity; anterior retroperitoneal space contains pancreas, duodenum, and colon; posterior retroperitoneal space includes kidneys, ureters, adrenals. • Fluid Dynamics: Peritoneal cavity lined with serous membrane; normal fluid has <30 g/L protein and <300 WBCs/μL.

2. EPIDEMIOLOGY

Primary Bacterial Peritonitis (PBP) occurs in 10% of cirrhotic patients with ascites. Risk factors include alcoholism, postnecrotic cirrhosis, and chronic active hepatitis. Secondary peritonitis is more common in trauma or perforation cases. Diabetic foot infections show rising MRSA rates (5–43%) and ESBL-producing gram-negative bacilli prevalence in Asia.

2.1 Diabetic Foot Infection Epidemiology

• Risk Factors: Poor glycemic control, prolonged infection duration, large ulcer size. • Regional Trends: MRSA prevalence 5–43% globally; gram-negative pathogens more common than gram-positive in Asia.

3. ETIOLOGY & PATHOPHYSIOLOGY

PBP pathogenesis involves hematogenous spread of organisms in cirrhosis with altered portal circulation. Secondary peritonitis results from bacterial spillage (e.g., appendicitis, diverticulitis). Bacteroides fragilis virulence linked to capsular polysaccharide complex that induces abscess formation via T lymphocyte activation.

3.1 Liver Abscess Pathogenesis

• Transmission Routes: Hematogenous spread (e.g., from biliary tract, pelvis) or local extension. • Biliary Tract: Most common source; mixed flora, B. fragilis predominant. • Pylephlebitis: Portal vein thrombosis with infection also contributes to abscess formation. • Amebic Infection: >95% serology positive; PCR used for confirmation.

4. CLINICAL FEATURES

PBP presents with fever (80% of cases), ascites, and nonlocalizing symptoms (malaise, encephalopathy). Absent PMN >250/μL excludes diagnosis. Secondary peritonitis has acute abdominal pain, guarding, and rebound tenderness. CAPD peritonitis shows cloudy dialysate with >100 WBCs/μL (>50% PMNs). Liver abscesses may present with fever of unknown origin, right upper quadrant tenderness, or no symptoms in 50% of cases.

4.1 CAPD Peritonitis Presentation

• Clinical Signs: Diffuse abdominal pain and peritoneal signs. • Diagnostic Criteria: Dialysate cloudy with >100 WBC/μL (>50% PMNs). • Short Dwell Times: PMN percentage >50% is diagnostic even if WBC <100/μL. • Management of Sample: If no fluid available, infuse 1 L dialysate for 1–2 h before analysis.

4.2 Liver Abscess Presentation

• Primary Symptoms: Fever most common; 50% have hepatomegaly/right upper quadrant tenderness. • Non-specific Symptoms: Chills, anorexia, weight loss. • Elderly Patients: Fever of unknown origin may be sole manifestation.

5. DIFFERENTIAL DIAGNOSIS

PBP diagnosis requires exclusion of secondary sources (e.g., appendicitis). Contrast-enhanced CT identifies intraabdominal infection sources. Dialysate culture with >1 organism suggests secondary peritonitis. Liver abscess may be suggested by right hemidiaphragm elevation on chest X-ray or fever of unknown origin.

5.1 PBP vs Secondary Peritonitis

• PBP: Fever, ascites predating infection; PMN >250/μL diagnostic. • Secondary peritonitis: Acute onset, peritoneal irritation, mixed flora in cultures.

5.2 CAPD Peritonitis vs Tunnel Infection

• Dialysate culture with >1 organism → suggests secondary peritonitis. • Exit-site infection may coexist but is not diagnostic. • Single organism typically isolates in CAPD-associated peritonitis.

6. INVESTIGATIONS & DIAGNOSIS

Ascitic fluid PMN >250/μL is diagnostic for PBP. Contrast-enhanced CT identifies intraabdominal infection sources. Liver abscess: elevated alkaline phosphatase (70% of cases), leukocytosis (77%), and hypoalbuminemia (33%).

6.1 Diagnostic Criteria for PBP

• Ascitic Fluid Analysis: 1. PMN count → >250/μL (Diagnostic threshold). 2. Protein → <30 g/L (Normal peritoneum). 3. WBC → <300/μL (Normal peritoneum). • Imaging: 1. Chest X-ray → Free air indicates perforation. 2. Contrast-enhanced CT → Identifies intraabdominal infection sources.

6.2 Liver Abscess Diagnostic Labs

• Alkaline Phosphatase: Elevated in 70% of cases (most reliable). • Bilirubin & AST: Elevated in 50% and 48% respectively. • Leukocytosis: Present in 77%. • Anemia: Present in 50%. • Hypoalbuminemia: Present in 33%.

7. MANAGEMENT & TREATMENT

  1. Primary Bacterial Peritonitis (PBP):
  2. Empirical: Cefotaxime 2 g IV q6h OR Ceftriaxone 2 g IV daily.
  3. Anaerobic coverage: Add Metronidazole 500 mg IV q8h.
  4. Duration: 2–4 weeks; adjust based on response and culture results.
  5. Secondary Peritonitis:
  6. Empirical: Piperacillin-tazobactam 4.5 g IV q6h OR Meropenem 1 g IV q8h.
  7. Anaerobic coverage: Add Metronidazole.
  8. Definitive: Surgical source control (e.g., appendectomy, cholecystectomy).
  9. CAPD Peritonitis:
  10. Initial: Vancomycin 15 mg/L dialysate + Ceftazidim 2 g/L.
  11. Escalation: Catheter removal if tunnel infection suspected; discontinue CAPD if peritonitis persists despite treatment.
  12. Intraabdominal Abscesses:
  13. Initial: Percutaneous drainage (ultrasound/CT-guided).
  14. Antibiotics: Piperacillin-tazobactam or meropenem + metronidazole.
  15. Duration: 2–6 weeks depending on abscess size and response.

7.4 Intraabdominal Abscess Management Pathway

  1. Percutaneous Drainage
  2. Assessment of Response (at 24–48 h):
  3. Defervescence achieved?
  4. YES → Successful drainage and defervescence → Drain out when criteria for catheter removal satisfied.
  5. NO → Perform repeat CT scan with dilute Hippaque injection into cavity and attempt further drainage.
  6. Evaluation of Repeat Attempt:
  7. Success (Successful drainage and defervescence)?
  8. YES → Drain out when criteria for catheter removal satisfied.
  9. NO (No drainage or no improvement) → Surgery.

8. PROGNOSIS & COMPLICATIONS

• PBP Mortality: - In-hospital: 17.6% (2018 study). - 30-day mortality: 23%. - 90-day mortality: 37% in tertiary centers. • Complications: Sepsis, multiorgan failure, and recurrence (up to 70% within 1 year). • Liver Abscess Progression: May progress to septicemia or rupture if untreated.

9. SPECIAL CONSIDERATIONS

• PBP Prevention in Cirrhotics: - Criteria: Ascitic protein <1.5 g/dL, renal impairment, or liver failure. - Prophylaxis: Fluoroquinolones or rifaximin. • Diabetic Foot Infections: Require culture-guided antibiotics and offloading.

10. KEY PEARLS & CLINICAL TRAPS

• Diagnostic Thresholds: - PMN >250/μL is the definitive threshold for PBP; absence of this finding excludes PBP. - Dialysate must be cloudy with >100 WBC/μL (>50% PMNs) to diagnose; clear dialysate → 2nd exchange with dwell time ≥ 2 h. • Clinical Indicators: - Elevated alkaline phosphatase (70%) is the most reliable lab finding for liver abscess. - Fever of unknown origin should prompt immediate abdominal imaging. • Exclusion Criteria: - Absence of PMN >250/μL excludes PBP. - Single organism in dialysate culture suggests CAPD-associated peritonitis.