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Lung Abscess

Chapter 132 | Part 5: Infectious Diseases · Part 5 – Infectious Diseases: Bacterial · Chapter 132

Key Clinical Points

  1. Lung abscess is defined as necrosis and cavitation of the lung following microbial infection, typically a single dominant cavity >2 cm in diameter.
  2. Primary lung abscesses (~80% of cases) arise from aspiration of oral flora (anaerobes) in susceptible hosts without underlying pulmonary/systemic conditions.
  3. Secondary lung abscesses arise in the setting of underlying conditions (e.g., bronchial obstruction, immunocompresssion) or septic emboli.
  4. Putrid sputum is virtually diagnostic of anaerobic infection.
  5. Right lung is affected more commonly than the left due to the less angulated right mainstem bronchus.
  6. Diagnosis relies on chest imaging: CXR shows thick-walled cavity with air-fluid level; CT provides better definition and identifies underlying causes (e.g., malignancy).
  7. Treatment of primary abscesses involves clindamycin or a beta-lactam/beta-lactamase combination followed by oral amoxicillin-clavulanate.
  8. Treatment duration ranges from 3–4 weeks to 14 weeks, with at least 6 weeks suggested for better outcomes.
  9. Complications include empyema (requiring drainage), bronchoscopy spillage, and pneumothorax/bronchopleural fistula from CT-guided aspiration.
  10. Non-infectious causes of cavitary lesions include malignancy, infarction, and sarcoidosis.

1. DEFINITION & CLASSIFICATION

• Definition: Lung abscess is defined as necrosis and cavitation of the lung following microbial infection; typically a single dominant cavity >2 cm in diameter. • Classification by Origin: ◦ Primary Lung Abscesses: Arise from aspiration (anaerobes) in susceptible hosts without underlying pulmonary/systemic conditions (~80% of cases). ◦ Secondary Lung Abscesses: Occur in the setting of bronchial obstruction, immunocompresssion, or septic emboli. • Classification by Chronicity: ◦ Acute: <4–6 weeks. ◦ Chronic: ~40% of cases.

2. EPIDEMIOLOGY

• Demographics: Primary lung abscesses are more common in middle-aged men. • Anatomical Predilection: Right lung is affected more commonly than the left due to the less angulated right mainstem bronchus. • Risk Factors for Aspiration: ◦ Modifiable: Alcoholism, drug overdose, poor dentition, gastroesophageal reflux, recumbent position. ◦ Non-modifiable: Neuromuscular disease, prior cerebrovascular/cardiovascular events, esophageal lesions. ◦ Specific Subgroups: Altered mental status, seizures, bulbar dysfunction, and esophageal dysmotility.

3. ETIOLOGY & PATHOPHYSIOLOGY

• Pathogenesis: ◦ Aspiration of oral flora into lung parenchyma. ◦ Pneumonitis develops initially (potentially from gastric acid damage). ◦ Parenchymal necrosis and cavitation occur over 7–14 days. ◦ Anaerobes cause more extensive tissue necrosis in polymicrobial infections. • Pathogen Profiles: ◦ Primary: Anaerobes (Peptostreptococcus spp., Prevotella spp., Bacteroides spp., milleri group streptococci) and microaerophilic streptococci. ◦ Secondary: S. aureus, Pseudomonas aeruginosa, opportunistic fungi. ◦ Embolic: S. aureus (endocarditis), Fusobacterium necrophorum (Lemierre’s syndrome). ◦ Endemic: Mycobacterium tuberculosis, Coccidioides spp., Histoplasma capsulatum. ◦ Miscellaneous: S. aureus post-viral infection, Actinomyces spp.

Table 132-1: Examples of Microbial Pathogens That Can Cause Lung Abscesses

• Primary lung abscess (often with risk factors for aspiration): Anaerobes (e.g., Peptostreptococcus spp., Prevotella spp., Bacteroides spp., milleri group streptococci), microaerophilic streptococci • Embolic lesions: Staphylococcus aureus (often from endocarditis), Fusobacterium necrophorum (Lemierre’s syndrome) • Miscellaneous conditions: Bacterial pathogen (often S. aureus) after influenza or another viral infection, Actinomyces spp.

4. CLINICAL FEATURES

• General Presentation: Initial manifestations resemble pneumonia (fevers, cough, sputum production). • Anaerobic Specifics: Chronic symptoms including night sweats, fatigue, and anemia; putrid sputum is virtually diagnostic of anaerobic infection. • S. aureus Specifics: May present as fulminant illness with high fevers. • Physical Examination Findings: ◦ Fevers, poor dentition, gingival disease. ◦ Amphoric/cavernous breath sounds. ◦ Digital clubbing. ◦ Absent gag reflex.

5. DIFFERENTIAL DIAGNOSIS

• Non-infectious Cavitary Lesions: ◦ Lung infarction. ◦ Malignancy. ◦ Sequestration. ◦ Cryptogenic organizing pneumonia. ◦ Sarcoidosis. ◦ Vasculitides (e.g., granulomatosis with polyangiitis). ◦ Lung cysts/bullae with fluid. • Infectious/Other: ◦ Septic emboli (tricuspid endocarditis). ◦ Extrapulmonary diseases (e.g., inflammatory bowel disease).

6. INVESTIGATIONS & DIAGNOSIS

  1. Imaging: ◦ Chest Radiograph: Identifies thick-walled cavity with air-fluid level. ◦ CT Scan: Provides better definition, identifies underlying causes (e.g., malignancy), and distinguishes peripheral abscess from pleural infection.
  2. Microbiology: ◦ Sputum Gram stain/culture: Noninvasive; may identify pathogens but results may not reflect anaerobes. ◦ Putrid sputum: Virtually diagnostic of anaerobic infection. ◦ Blood cultures: Advised in secondary abscess or treatment failure. ◦ Serologic studies: For opportunistic pathogens in immunocompromised hosts.
  3. Invasive Procedures (if indicated): ◦ Bronchoscopy/BAL: Risk of spillage of abscess contents. ◦ CT-guided aspiration: Risk of pneumothorax or bronchopleural fistula.

7. MANAGEMENT & TREATMENT

  1. Pharmacologic Therapy: ◦ Clindamycin: 600 mg IV three times daily → 300 mg PO four times daily (post-improvement). ◦ Beta-lactam/beta-lactamase combination: IV administration → transition to oral amoxicillin-clavulanate once condition is stable.
  2. Duration of Therapy: ◦ Range: 3–4 weeks to 14 weeks. ◦ Goal: Continue until imaging shows abscess resolution (at least 6 weeks recommended for better outcomes).
  3. Surgical Considerations: ◦ Historically common, now less frequent due to antibiotics. ◦ Indicated for complications such as empyema or when empirical therapy fails.

• Clindamycin: 600 mg IV (3x daily) → 300 mg PO (4x daily) • Amoxicillin-clavulanate: Oral (once condition is stable) • Beta-lactam/Beta-lactamase: IV (until stable) → Amoxicillin-clavulanate

8. COMPLICATIONS & PROGNOSIS

• Pleural Space Infection: Empyema requiring urgent drainage. • Procedure-related Risks: ◦ Spillage of abscess contents during bronchoscopy. ◦ Pneumothorax or bronchopleural fistula from CT-guided aspiration.

9. SPECIAL CONSIDERATIONS

• Immunocompromised Hosts: ◦ Higher risk for infection with opportunistic organisms (Table 132-1). ◦ Less likely to respond to empirical therapy. ◦ Culture material essential for targeted therapy.

10. KEY PEARLS & CLINICAL TRAPS

• Putrid-smelling sputum: Virtually diagnostic of anaerobic infection. • Anatomical Rule: Right lung more commonly affected due to less angulated bronchus. • Primary Abscess Composition: Polymicrobial (anaerobes + microaerophilic streptococci). • Secondary Abscess Pathogens: S. aureus, Pseudomonas aeruginosa, or opportunistic fungi. • Imaging Utility: CT is superior for identifying underlying causes and distinguishing abscess from pleural infection. • Clinical Clues: Thick-walled cavity with air-fluid level on CXR; amphoric/cavernous breath sounds; digital clubbing.

Reference Tables

TABLE 132-1 Examples of Microbial Pathogens That Can Cause Lung Abscesses

Harrison's 22e, p.1034

CLINICAL CONDITION PATHOGENS
Primary lung abscess
(often with risk factors
for aspiration)		 Anaerobes (e.g., Peptostreptococcus spp., Prevotella
spp., Bacteroides spp., milleri group streptococci),
microaerophilic streptococci
Embolic lesions Staphylococcus aureus (often from endocarditis),
Fusobacterium necrophorum (Lemierre’s syndrome; see
text for details)
132 Lung Abscess
Rebecca M. Baron, Beverly W. Baron,
Miriam Baron Barshak
Miscellaneous
conditions		 Bacterial pathogen (often S. aureus) after influenza or
another viral infection, Actinomyces spp.