LUNG ABSCESS
A lung abscess is a localized (usually >2 cm in diameter), suppurative, and necrotizing infectious process within the pulmonary parenchyma caused by either a respiratory or systemic illness. Most abscesses are primary and result from necrosis in an existing pulmonary process (usually an infectious pneumonia), although necrotization and secondary infection may result from a lung neoplasm. Between 8% and 18% of lung abscesses are associated with neoplasms in all age groups, but in patients older than age 45 years, as many as 30% have an associated cancer. Primary squamous carcinoma of the lung is the most common malignancy associated with abscess formation. An abscess can also result from a systemic process such as a septic vascular embolus (e.g., from right-sided endocarditis) or can be a secondary complication of a pulmonary process such as bronchial emboli (e.g., aspirated foreign bodies) or rupture of an extrapulmonary abscess into the lung (e.g., empyema).
Although any necrotizing pathogen can cause an abscess
(such as Staphylococcus aureus, Pseudomonas aeruginosa,
parasites, or mycobacteria), the classic lung abscess is caused by anaerobic
bacteria. In the past 40 years, the incidence has declined 10-fold, although
the mortality rate has decreased to 5% to 10%, presumably because of improved
availability of antibiotics to treat pneumonia.
PATHOGENESIS
Most lung abscesses are caused by a mixed bacterial
flora, including anaerobes, up to 90% of the time. Aerobic organisms may be
present in up to 50% of patients, but in most cases, they coexist with
anaerobes. Typically, an abscess occurs when infected orogingival material is
present in a host who has a predisposition to aspirate this material into a
lung and who cannot adequately clear the challenge either because of impaired
consciousness or because of exposure to a large inoculum (as in massive
aspiration). Impaired consciousness can predispose to aspiration, as well as
causing impaired clearance, but aspiration can also occur in those with
oropharyngeal or esophageal dysfunction. At-risk patients are those with a
history of alcoholism, seizure disorders, drug overdose, general anesthesia,
protracted vomiting, neurologic disorders (e.g., stroke, myasthenia gravis,
amyotrophic lateral sclerosis), esophageal diverticulum, and gastropulmonary
fistulas. Aspiration of orogingival material, especially from a patient with
poor dental hygiene, is pathogenic, although aspiration of gastric contents may
not always lead to infection, especially if the aspirate is only acid, in which
case chemical pneumonitis may result.
Based on animal and some human data, the development
of a lung abscess occurs 7 to 14 days after aspirating infectious orogingival
material into the terminal bronchioles. The location of the abscess is
determined by gravity and body position at the time of aspiration, making the
most common sites the basal segments of the lower lobes, the superior segment
of the lower lobe, and the posterior segments of the upper lobes. In general,
the right lung is involved more than the left because of the straight direction
of its take off from the
trachea. (see Plate 4-79). Based on these principles, if an abscess occurs in
an edentulous patient (without oral anaerobes) or in a location other than the ones dictated by
gravity, there should be suspicion of an endobronchial obstruction, a
gastropulmonary fistula, or infection with a non-anaerobic organism (e.g.,
tuberculosis [TB]).
The most common anaerobic organisms causing lung
abscess are Peptostreptococcus spp. (an anaerobic grampositive coccus), Fusobacterium
nucleatum, Fusobacterium necrophorum, Porphyromonas spp.
(formerly classified in the genus Bacteroides), and Prevotella melaninogenicus (also
formerly classified in the genus Bacteroides). Although most necrotizing
lung processes are caused by anaerobic organisms, other necrotizing pathogens
include Staphylococcus aureus, Escherichia coli, Klebsiella
pneumoniae, Pseudomonas aeruginosa Streptococcus pyogenes, Pseudomonas
pseudomallei (melioidosis), Haemophilus influenzae (especially type
b), Legionella pneumophila, Nocardia asteroides, Actinomyces, and
rarely pneumococcus, parasites (Paragonimus westermani, Entamoeba
histolytica), fungi, and mycobacteria.
CLINICAL FEATURES
An acute lung abscess presents with symptoms of less
than 2 weeks’ duration and is commonly caused by a virulent aerobic bacterial
pathogen, although patients with a chronic lung abscess (symptoms lasting >4-6
weeks) are more likely to have an underlying cancer or an infection with a less
virulent anaerobic agent. Most patients with lung abscess have an insidious
presentation, with symptoms lasting at least 2 weeks before evaluation.
Findings include cough, foul-smelling sputum that forms layers on standing,
hemoptysis (in 25% of patients), fever, chills, night sweats, anorexia,
pleuritic chest pain (in 60% of patients), weight loss, and clubbing. The
presence of foul-smelling or putrid sputum is highly suggestive of anaerobic
infection. A history of weight loss is also common, occurring in 60% of
patients, with an average loss of between 15 and 20 lb, and this finding further
raises the suspicion of malignancy.
DIAGNOSTIC TESTING
Sputum culture may have some value if it shows a
specific nonanaerobic pathogen, but because the sample is expectorated through
the oropharynx, the finding of anaerobes (which must be specifically sought) is
of limited usefulness. Bronchoscopy may be valuable for ruling out
endobronchial obstruction and for promoting abscess drainage. If the abscess is
associated with an empyema, as is the case 30% of the time, then culture of the
pleural fluid may be valuable. Radiography is needed to define the presence of a
cavitary lung lesion and typically shows a solitary cavitary lesion measuring 2
to 4 cm in diameter with an air-fluid level. When there is extensive inflammation
surrounding the abscess, infection is likely; neoplasms tend to have less
surrounding radiographic infiltrate. Lung cavities caused by TB appear different
and tend to be thin-walled and without air-fluid levels. Sometimes it is
necessary to use a computed tomography (CT) scan to distinguish a lung abscess
from an empyema, the latter usually being confined to the pleural space. On the
CT scan, whereas a lung abscess usually appears as a thick, irregular-walled
cavity with no associated lung compression, an empyema has a thin, smooth wall
with compression of the uninvolved lung. When a lung abscess is complicated by
a bronchopleural fistula, it may be difficult to distinguish from an empyema. If
the radiograph reveals multiple cavitary lesions, it usually suggests a
necrotizing pneumonitis caused by a virulent nonanaerobic organism and the
possibility of septic pulmonary emboli.
THERAPY
Before the availability of antibiotics, treatment included
supportive care, postural drainage with or without bronchoscopy, and surgery.
Currently, the mainstay of therapy is antibiotics directed at orogingival
anaerobes. The initial antibiotic is usually intravenous penicillin or
clindamycin. Although penicillin has historically been the first choice of therapy, recent trials have
compared clindamycin with penicillin and found clindamycin to be associated
with fewer treatment failures and a shorter time to symptom resolution.
Metronidazole is not recommended and has had failure rates above 40%. Therapy
is usually for a long duration, and until the pulmonary infiltrates have
resolved or until the residual lesion is small and stable and the cavity
closed. Many patients require a total of 6 to 8 weeks of antimicrobial therapy.
Complications of lung abscess include empyema formation resulting from a bronchopleural fistula, massive
hemoptysis, spontaneous rupture into uninvolved lung segments, and
nonresolution of the abscess cavity. Although uncommon, these complications
often require prolonged medical therapy as well as surgical intervention,
either with tube thoracostomy in the case of empyema or lung resection in the
case of massive hemoptysis. Surgery for lung abscess is also used in the
setting of fulminant infection and in patients who fail medical therapy.
