INTRODUCTION AND EPIDEMIOLOGY
Lung abscess is defined as a localized necrosis of the lung parenchyma, typically caused by suppurative microbial infection. This initial infection is usually caused by aspiration of oral contents. Lung abscess may also develop as a result of hematogenous spread of infectious material to the lung parenchyma or lung infarct. Other less common causes of pulmonary abscess include infection as a result of penetrating chest trauma, fungal and parasitic infections, primary and metastatic neoplasms, and inflammatory conditions such as Wegener's granulomatosis and sarcoidosis.
Primary lung abscess occurs in individuals in good health or in those prone to aspiration. Approximately 80% of lung abscesses are primary.1 The in-hospital mortality rate is 10% to 15%. Secondary lung abscess is associated with malignancy, immunosuppression, extrapulmonary infection or sepsis, or complication of surgery; the mortality is higher than seen in primary lung abscess, often over 50%. Lung abscesses present for less than 1 month are acute, with the rest being considered chronic.1
The incidence of lung abscess and short-term mortality have both declined over the last four decades, presumably secondary to improved treatment regimens for pneumonia. The mortality rate for community-acquired (anaerobic) lung abscess is considerably lower than that of hospital-acquired (aerobic) lung abscess.
Lung abscess typically is caused by a breakdown or overwhelming of the usual pulmonary defense mechanisms. This allows a parenchymal infection to evolve into an abscess. It takes approximately 7 to 14 days for aspiration pneumonia to develop into an abscess. Anaerobic bacteria are the most common isolates from lung abscess in immunocompetent patients.8 Generally, both aerobic and anaerobic bacteria cause lung abscess, but anaerobes are more common.1,9 Aerobic bacteria are found more commonly in lung abscesses in immunocompromised patients and include S. aureus, Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, Streptococcus pyogenes, Burkholderia pseudomallei, Haemophilus influenzae, Legionella pneumophila, Nocardia asteroides, Actinomyces species, and rarely pneumococci. Aerobic infections are often hospital-acquired and have a higher mortality rate; anaerobic infections usually are community-acquired and associated with aspiration. Typical anaerobic lung abscess pathogens are pigmented Prevotella, Porphyromonas, Bacteroides, Fusobacterium, and Peptostreptococcus species.
Aspiration predisposes patients to developing pneumonia and lung abscesses. Conditions increasing the frequency of aspiration are chronic alcoholism, chronic debility with extension neck contractures, chronically depressed mental status, poor dentition and gingival disease, therapeutic or recreational drug overdose, and gastric and jejunostomy tubes. These risk factors are covered in more detail in the chapter on aspiration pneumonia.
Lung abscesses caused by hematogenous spread tend to be multilobar; risk factors include IV drug use, endocarditis, and tricuspid valve endocarditis. Jugular vein suppurative thrombophlebitis (Lemierre's syndrome) is a complication of tonsillitis that can spread to the lungs with Fusobacterium necrophorum bacterial seeding.10,11
Lung abscesses typically occur in the basal segments of the lower lobes or the posterior segment of the upper lobes. When abscesses occur in the anterior lung, a neoplasm often underpins the infection. Cancer is associated with 8% to 18% of all lung abscesses; this rate increases to 30% in those older than 45 years.
Patients with lung abscess classically present with an indolent course of cough, fever, pleuritic chest pain, weight loss, and night sweats, often for 2 or more weeks. There may be cough productive of putrid sputum that layers out when allowed to stand. Hemoptysis occurs in up to 25% of cases. Because the infection is more indolent, tachycardia, tachypnea, and fever are often absent. Laboratory findings usually are nonspecific but commonly include an elevated WBC count and erythrocyte sedimentation rate.
The diagnosis is usually made by a chest radiograph showing an area of dense consolidation with an air-fluid level inside of a cavitary lesion, indicating that the abscess cavity communicated with a bronchiole. Bronchiole communication occurs in about three fourths of patients with lung abscesses (Figure 66-1). In the remaining quarter of patients, chest CT detects the cavitary lesion (Figure 66-2). Multiple abscesses are unusual but can be seen in septic emboli or Lemierre's syndrome (streptococcal sepsis from peritonsillar abscess).10
Posteroanterior and lateral chest x-ray. A. Chest radiograph demonstrating air-fluid level of abscess cavity at arrow. B. Lateral chest radiograph showing air-fluid level of abscess cavity at arrow.
CT of the chest, demonstrating air-fluid level of abscess cavity at arrow.
The differential diagnosis of cavitary lesions includes infected bullae, pleural fluid collection with bronchopleural fistula, and loop of bowel extending through a diaphragmatic hernia. Infected bullae have thin walls. Pleural fluid collection with bronchopleural fistula will demonstrate an air-fluid level that extends to the chest wall and tapers at the apex. A loop of bowel extending through a diaphragmatic hernia may result in nausea, vomiting, and abdominal pain due to incarceration or audible bowel sounds in the chest on the side on the hernia (Figure 66-3). Table 66-2 lists different causes of cavitary lung lesions.
TABLE 66-2Cavitary Lung Lesions ||Download (.pdf) TABLE 66-2 Cavitary Lung Lesions
Anaerobic abscess (immunocompetent)
Aerobic abscess (immunocompromised)
| Fungal || |
| Parasitic || |
|Neoplastic || |
Bronchogenic carcinoma (squamous cell or adenocarcinoma)
Metastatic cancer (colorectal or renal)
Lymphoma or Hodgkin's disease
|Inflammatory || |
Hiatal hernia mimicking the appearance of cavity lesion.
Medical management will resolve most lung abscesses. Initial treatment consists of clindamycin, 600 milligrams IV every 8 hours, or ampicillin-sulbactam, 1.5 to 3.0 grams IV every 6 hours, for those who cannot take clindamycin.1,11 Alternative treatments include piperacillin-tazobactam, 3.375 grams IV every 6 hours, or meropenem or doripenem. Methicillin-resistant S. aureus infections are treated with linezolid, 600 milligrams IV every 12 hours, or vancomycin, 15 milligrams/kg IV every 12 hours (target trough level 15 to 20 μg/mL).12
Drainage usually occurs spontaneously from communication of the abscess cavity with the tracheobronchial tree. This is signaled by the development of an air-fluid level on the chest radiograph. Reasons for poor outcomes include aerobic infection, large abscess cavity, advanced age, debilitation, immunosuppression, malignancy, malnutrition, and sepsis. Reasons for failure of medical treatment include bronchial obstruction, nonbacterial cause of abscess, large cavity size, and concomitant empyema.
Surgical treatments for a nondraining lung abscess include image-guided percutaneous drainage or thoracotomy with pulmonary resection.
Admit patients with new lung abscess; hospitalization usually lasts several weeks. After resolution of symptoms, patients can be discharged on oral antibiotics for 4 to 8 weeks. Chest radiographic findings will lag behind clinical progress and will take more than 2 months to resolve.
Complications of lung abscess include empyema, massive hemoptysis, contamination of the uninvolved lung, and failure of the abscess cavity to resolve. Approximately 10% of bacterial lung abscesses require surgical intervention.13