Aspiration Syndromes & Lung Abscess

Who aspirates, and where it goes

Risk factors. Aspiration happens when glottic closure and cough fail to protect the airway. Impaired consciousness is the leading setup: alcohol intoxication, seizures, sedatives or overdose, and general anesthesia. Dysphagia from stroke, neuromuscular disease or esophageal disorders, repeated vomiting, and nasogastric or feeding tubes add risk. Poor dentition and periodontal disease raise the bacterial load of what is aspirated; an edentulous patient with a lung abscess has few oral anaerobes, so an obstructing carcinoma should be suspected. Prevention includes raising the head of the bed to 30–45°, formal swallow evaluation after stroke, and fasting before elective anesthesia.

Bronchial anatomy. The right main bronchus is wider and shorter than the left and leaves the trachea at a steeper, more vertical angle, so aspirated material and inhaled foreign bodies usually enter the right lung. A toddler who chokes on a peanut typically has unilateral wheeze and decreased breath sounds; the object can act as a ball valve, and an expiratory film then shows unilateral hyperinflation with the mediastinum shifting away. Removal is by bronchoscopy.

Gravity and position. Aspirate runs to whatever segment is dependent at the time.

• Supine (unconscious, intoxicated, anesthetized): posterior segment of the right upper lobe and superior segment of the right lower lobe.
• Upright (sitting or standing, as in dysphagia while eating): basal segments of the right lower lobe, the most common aspiration site overall.

Aspiration pneumonitis versus aspiration pneumonia

Mendelson syndrome. Aspiration of acidic gastric contents, first described during obstetric anesthesia, chemically burns alveolar epithelium and capillary endothelium. Injury is greater when the aspirate is very acidic (pH below about 2.5). Within hours, neutrophilic inflammation and leaky capillaries cause abrupt dyspnea, hypoxemia, bronchospasm, low-grade fever and dependent infiltrates that can progress to ARDS. The process is initially sterile, so care is supportive; antibiotics are not routinely given early and glucocorticoids do not help.

Aspiration pneumonia. Silent aspiration of colonized oropharyngeal secretions seeds a polymicrobial infection dominated by oral anaerobes (Peptostreptococcus, Fusobacterium, Prevotella and Bacteroides) mixed with oral streptococci; in hospitalized patients, gram-negative rods and S. aureus also contribute. It develops over days to weeks with fever, cough and foul-smelling sputum in a dependent segment, and it can progress to necrotizing pneumonia, lung abscess or empyema.

Why anaerobes behave as they do. Obligate anaerobes lack catalase and superoxide dismutase, so oxygen radicals kill them. They thrive in necrotic, poorly oxygenated tissue, ferment to foul-smelling short-chain fatty acids and gas, and form abscesses. Aminoglycosides do not work against them because drug uptake requires oxygen-dependent transport.

Lung abscess

Formation. In a necrotizing pneumonia, neutrophil enzymes digest dead lung (liquefactive necrosis) into a cavity larger than about 2 cm. When the cavity erodes into a bronchus, pus drains and air enters, producing the air-fluid level seen on imaging and the putrid sputum. Symptoms smolder for weeks: fever, night sweats, weight loss and cough; chronic abscesses cause clubbing. Complications include empyema with bronchopleural fistula and hemoptysis.

• Aspirated oral anaerobes: the most common cause; usually a single cavity in a dependent segment.
• S. aureus (often after influenza, including MRSA) and Klebsiella pneumoniae (alcohol use, diabetes; thick currant-jelly sputum, upper lobes) cause cavitating necrotizing pneumonia; Pseudomonas, Nocardia and fungi do so in immunocompromised hosts.
• Post-obstructive: an abscess behind a bronchus blocked by bronchogenic carcinoma or a foreign body.
• Septic emboli: multiple peripheral cavitating nodules, classically from S. aureus tricuspid endocarditis in people who inject drugs, or from Lemierre syndrome (Fusobacterium necrophorum pharyngitis → septic internal jugular thrombophlebitis).

Treatment and differential diagnosis

Antibiotics. Many oral anaerobes, especially Prevotella and Bacteroides, produce β-lactamase. Clindamycin or a β-lactam/β-lactamase inhibitor (ampicillin-sulbactam IV, amoxicillin-clavulanate orally) is given for weeks, until imaging shows the cavity resolving. Most abscesses drain through the airway and heal without surgery; percutaneous drainage or resection is reserved for failures. Clindamycin carries a high risk of C. difficile colitis.

Metronidazole alone fails in lung abscess because it misses the aerobic and microaerophilic streptococci of mixed oral flora.