Primary Causes & Pathophysiology
A lung abscess typically develops following aspiration of oropharyngeal contents, leading to a polymicrobial infection dominated by anaerobic bacteria. The infection triggers a severe inflammatory response, causing suppurative necrosis of the lung parenchyma. As the necrotic tissue liquefies, it is expelled through the tracheobronchial tree, creating a cavity that communicates with an airway. This communication allows air to enter the cavity, resulting in the classic air-fluid level seen on upright chest radiographs. Secondary abscesses may arise from bronchial obstruction (e.g., malignancy), septic emboli (e.g., right-sided endocarditis), or contiguous spread from an empyema.
Inhalation of anaerobic and aerobic bacteria from the gingival crevices into dependent lung segments (e.g., superior segments of lower lobes, posterior segments of upper lobes), leading to necrotising infection.
Severe infection by virulent pathogens such as Staphylococcus aureus, Klebsiella pneumoniae, or Pseudomonas aeruginosa causing extensive parenchymal destruction and cavity formation.
Tumours, foreign bodies, or enlarged lymph nodes obstruct airway clearance, leading to post-obstructive pneumonia and subsequent abscess formation (secondary abscess).
Infected thrombi, typically from right-sided infective endocarditis or infected central venous catheters, lodge in the pulmonary vasculature, causing multifocal infarction and abscess formation.