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Intraabdominal Infections and Abscesses

Chapter 137 | Part 5: Infectious Diseases

KEY CLINICAL POINTS

  • Intraabdominal infections progress through two stages: peritonitis (inflammatory) and abscess formation (localized collection).
  • Primary bacterial peritonitis (PBP) is associated with cirrhosis and gram-negative pathogens, while secondary peritonitis involves mixed flora including anaerobes.
  • Imaging (CT, ultrasound) is critical for diagnosing abscesses, with percutaneous drainage being a mainstay for treatment.
  • Antibiotic regimens vary by infection type: third-gen cephalosporins for PBP, broad-spectrum coverage for secondary peritonitis, and specific agents for CAPD or fungal infections.
  • Multidrug-resistant organisms are increasingly common, requiring tailored antibiotic selection based on local resistance patterns.

1. DEFINITION & OVERVIEW

Intraabdominal infections arise from disruption of anatomical barriers, leading to peritonitis or abscess formation. Peritonitis occurs in two stages: initial inflammatory response (bacterial sepsis) and subsequent abscess formation if untreated. Abscesses are localized collections of pus, often secondary to peritonitis or direct spillage of intestinal contents.

Peritoneal Fluid Analysis

Parameter Normal Value Infection Indicators
Protein (g/L) <30 ‡30
WBCs/mL <300 ‡250 (PMNs)
PMNs (%) 0–5% ‡50% (bacterial)

1.1 Peritoneal Anatomy

The peritoneal cavity is divided into compartments (e.g., subphrenic, pelvis, Morrison’s pouch). The retroperitoneal space contains organs like the pancreas, kidneys, and adrenal glands. Peritoneal fluid is a serous membrane lining, with normal fluid containing <30 g/L protein and <300 WBCs/ µ L.

1.2 Types of Infections

Primary bacterial peritonitis (PBP) occurs in cirrhosis due to hematogenous spread, while secondary peritonitis results from spillage of intestinal contents. Abscesses may form in the peritoneal cavity or visceral organs (e.g., liver, spleen).

2. EPIDEMIOLOGY

PBP occurs in 10% of cirrhotic patients, with 17.6% in-hospital mortality in the U.S. Multidrug-resistant organisms (MDROs) are prevalent in diabetic foot infections (5–43% MRSA prevalence). Risk factors include poor glycemic control, prolonged infection, and prior antibiotic use.

2.1 PBP Incidence

PBP occurs in ≤ 10% of cirrhotic patients, with 23% mortality at 30 days in tertiary centers. Mortality is highest in patients with serum creatinine ≥ 1 mg/dL or total bilirubin ≥ 5 mg/dL.

2.2 Abscess Prevalence

74% of intraabdominal abscesses are intraperitoneal or retroperitoneal. Liver abscesses account for 13% of all intraabdominal abscesses, with 26% of cases linked to biliary tract disease.

3. ETIOLOGY & PATHOPHYSIOLOGY

PBP is caused by hematogenous spread of gram-negative bacilli (e.g., E. coli) or gram-positive cocci (e.g., streptococci). Secondary peritonitis involves mixed flora (aerobes/anaerobes) from spillage of intestinal contents. Bacteroides fragilis is the most common anaerobic pathogen in abscesses, with virulence factors including capsular polysaccharides and zwitterionic properties.

3.1 Pathogenesis

Abscess formation involves containment of microbes by fibrous capsules, preventing systemic spread. B. fragilis adheres to mesothelial cells, stimulating cytokine release and abscess localization.

3.2 Microbial Factors

Gram-negative bacilli (e.g., E. coli, Klebsiella) dominate in secondary peritonitis. Anaerobes (e.g., B. fragilis) are common in abscesses. Fungal abscesses (e.g., Candida) occur in immunocompromised patients.

4. CLINICAL FEATURES

PBP presents with fever, ascites, and nonlocalizing symptoms (e.g., malaise). Secondary peritonitis has localized pain, guarding, and marked leukocytosis. Abscesses cause localized pain, fever, and systemic symptoms. CAPD peritonitis mimics secondary peritonitis with cloudy dialysate and >100 WBCs/ µ L.

4.1 PBP vs. Secondary Peritonitis

PBP: Fever, ascites, nonlocalizing symptoms. Secondary: Localized pain, guarding, marked leukocytosis. PBP is more common in cirrhosis, while secondary peritonitis follows bowel perforation.

4.2 Abscess Presentation

Localized pain, fever, and systemic symptoms. Liver abscesses may present with right upper quadrant pain, while renal abscesses cause flank pain. Psoas abscesses may mimic musculoskeletal pain.

5. DIFFERENTIAL DIAGNOSIS

Appendicitis, diverticulitis, pancreatitis, and pelvic inflammatory disease must be considered. Differentiate PBP from secondary peritonitis using clinical context and imaging. Fungal abscesses (e.g., Candida) require culture confirmation.

5.1 Mimicking Conditions

Pancreatic pseudocysts, diverticular abscesses, and tuberculous peritonitis may mimic intraabdominal infections. Fungal abscesses (e.g., Candida) require specific diagnostic tests.

5.2 Imaging Role

CT is most sensitive for abscess detection. Ultrasound is useful for renal/perinephric abscesses. Gallium scans may detect abscesses in neutropenic patients.

6. INVESTIGATIONS & DIAGNOSIS

Imaging (CT, ultrasound, MRI) is essential. Peritoneal fluid analysis (WBCs, PMNs, Gram stain) confirms peritonitis. Dialysate analysis (WBCs >100/ µ L) detects CAPD peritonitis. Gallium scans and indium-labeled WBCs help localize abscesses.

6.1 Diagnostic Imaging

CT is the gold standard for abscess detection. Ultrasound is preferred for renal/perinephric abscesses. MRI may be used for soft tissue delineation.

6.2 Laboratory Tests

Elevated ALP, bilirubin, and AST suggest liver abscesses. Blood cultures and peritoneal fluid cultures identify pathogens. PCR and serology aid in diagnosing amebic or tuberculous peritonitis.

7. MANAGEMENT & TREATMENT

Antibiotics (broad-spectrum for secondary peritonitis, targeted for PBP) and drainage (percutaneous or surgical) are mainstays. CAPD peritonitis requires antibiotic therapy and catheter management. Fungal abscesses require antifungal agents (e.g., amphotericin B).

Antibiotic Regimens for Intraabdominal Infections

Infection Type Recommended Regimen
Primary Bacterial Peritonitis Ceftriaxone (2 g q24h) or cefotaxime (2 g q8h)
Secondary Peritonitis Piperacillin/tazobactam (3.375 g q6h) + metronidazole (500 mg q8h)
CAPD Peritonitis Vancomycin (1 g q12h) + metronidazole (500 mg q8h)

7.1 Antibiotic Regimens

PBP: Third-gen cephalosporins (e.g., ceftriaxone). Secondary peritonitis: Broad-spectrum coverage (e.g., piperacillin/tazobactam + metronidazole). CAPD: Target S. aureus, gram-negative bacilli, and anaerobes.

7.2 Drainage Procedures

Percutaneous drainage is preferred for single abscesses (<3 cm). Surgical intervention is needed for complex abscesses or when drainage fails. CAPD catheter removal may be required for recurrent infections.

8. PROGNOSIS & COMPLICATIONS

PBP has 17.6% in-hospital mortality in the U.S. Abscesses may lead to sepsis, multi-organ failure, or recurrence. Complications include abscess rupture, septic emboli, and chronic infection in immunocompromised patients.

8.1 Mortality

PBP mortality: 17.6% in-hospital, 23% at 30 days. Liver abscesses have 15% mortality despite treatment. Renal abscesses may have higher mortality in immunocompromised patients.

8.2 Long-Term Outcomes

Chronic infection may lead to fibrosis or organ dysfunction. Recurrence rates for PBP are up to 70% within 1 year. Abscesses may require long-term antibiotic therapy.

9. SPECIAL CONSIDERATIONS

Pregnancy: Avoid certain antibiotics (e.g., fluoroquinolones). Pediatrics: Monitor for sepsis and adjust dosages. Elderly: Higher risk of complications and drug interactions. Diabetic patients: Risk of multidrug-resistant infections and poor wound healing.

9.1 Renal Failure

Adjust antibiotic dosages for renal impairment (e.g., vancomycin, piperacillin/tazobactam). Avoid nephrotoxic agents in patients with preexisting renal disease.

9.2 Dialysis Patients

CAPD patients require specific antibiotic regimens. Fungal abscesses (e.g., Candida) require antifungal therapy (e.g., amphotericin B).

10. KEY POINTS & CLINICAL PEARLS

  1. Intraabdominal infections progress through peritonitis and abscess formation. 2. PBP is associated with cirrhosis and requires targeted antibiotics. 3. Secondary peritonitis needs broad-spectrum coverage and drainage. 4. Imaging is critical for abscess diagnosis. 5. Multidrug-resistant organisms require tailored antibiotic selection.