The term lung abscess refers to a microbial infection of the lung that results in necrosis of the pulmonary parenchyma. Necrotizing pneumonia or lung gangrene refers to multiple small pulmonary abscesses in contiguous areas of the lung, usually resulting from a more virulent infection.
Lung abscesses are classified by clinical and pathologic features including the tempo of progression, the presence or absence of an associated underlying lesion, and the microbial pathogen responsible. Duration defines the infection as acute versus chronic, with the dividing line usually at 4–6 weeks. Abscesses occurring in the presence of underlying pulmonary lesions, including tumors or systemic conditions (e.g., HIV infection), are referred to as secondary; those that occur in the absence of underlying pulmonary lesions are considered primary. The term nonspecific lung abscess refers to cases in which no likely pathogen is recovered from expectorated sputum; most such cases are presumed to be due to anaerobic bacteria. Putrid lung abscess is a term applied to anaerobic bacterial lung abscesses, which are characterized by distinctive foul-smelling breath, sputum, or empyema fluid.
The likely etiologic agent, appropriate diagnostic testing, and appropriate treatment are frequently indicated by the characteristics of the host and the disease process. A variety of microbial pathogens cause lung abscess (Table 258-2). Most nonspecific lung abscesses are presumed to be due to anaerobic bacteria. Mycobacteria, especially M. tuberculosis, are a very important cause of pulmonary infections and abscess formation. Fungi and some parasites also cause lung abscess. An acute lung abscess developing in a young, previously healthy patient, especially in conjunction with influenza, is likely to involve Staphylococcus aureus; this pathogen generally is seen easily on sputum Gram's stain and culture, and presumptive treatment for methicillin-resistant S. aureus is urgent. In an immunocompromised host, suspected pathogens include enteric gram-negative bacilli—especially Klebsiella pneumoniae but also agents that are found almost exclusively in patients with defective cell-mediated immunity, such as Nocardia asteroides and Rhodococcus equi. Lung abscess acquired in other countries may involve Burkholderia pseudomallei or Paragonimus westermani.
Table 258-2 Microbial Pathogens Causing Cavitary Lung Infection |Favorite Table|Download (.pdf)
Table 258-2 Microbial Pathogens Causing Cavitary Lung Infection
|Anaerobic bacteria plus microaerophilic and/or anaerobic streptococci, Gemella spp.|
|Embolic (endovascular) lesions: usually Staphylococcus aureus, Pseudomonas aeruginosa, Fusobacterium necrophoruma|
|Endemic fungi: Histoplasma, Blastomyces, Coccidioides spp.|
|Mycobacteria: M. tuberculosis, M. kansasii, M. avium|
|M. tuberculosis, Nocardia asteroides, Rhodococcus equi, Legionella spp., P. aeruginosa, Enterobacteriaceae (especially Klebsiella pneumoniae), Aspergillus spp., Cryptococcus spp.|
|Previously Healthy Host|
|Bacteria: S. aureus,b S. milleri, K. pneumoniae, group A Streptococcus; Gemella, Legionella, and Actinomyces spp.|
|Parasites: Entamoeba histolytica, Paragonimus westermani, Strongyloides stercoralis|
Multiple pulmonary lesions that are not caused by microbes may resemble lung abscess. These include the lesions of pulmonary infarction, bronchiectasis, necrotizing carcinoma, pulmonary sequestration, vasculitides [e.g., periarteritis nodosa, granulomatosis with polyangiitis (Wegener's), Goodpasture syndrome], and cysts or bullae with fluid collections. In some cases, multiple lung abscesses result from septic emboli, most commonly in association with tricuspid valve endocarditis.
The classic presentation of nonspecific lung abscess is an indolent infection that evolves over several days or weeks, usually in a host who has a predisposition to aspiration. A common feature is periodontal infection with pyorrhea or gingivitis. Anaerobes and aerobic or microaerophilic streptococci that colonize the upper airways are implicated in these lesions. The usual symptoms are fatigue, cough, sputum production, and fever. Chills are uncommon. Many patients have evidence of chronic disease, such as weight loss and anemia. Some patients have putrid-smelling sputum indicative of the presence of anaerobes; the foul odor is presumably due to the organisms' production of short-chain fatty acids, such as butyric or succinic acid. Some patients have pleurisy due to pleural involvement by contiguous spread or by a bronchopleural fistula. The pleurisy may be severe and may be the symptom that prompts medical evaluation. Sequential x-rays or CT scans show the evolution of this lesion from pneumonitis to cavitation, a process that generally requires 7–14 days in experimental animals (Fig. 258-2).
Representative chest CT demonstrating development of lung abscesses. This patient was immunocompromised due to underlying lymphoma and developed severe Pseudomonas aeruginosa pneumonia, as represented by a left lung infiltrate with concern for central regions of necrosis (panel A, black arrow). Two weeks later, areas of cavitation with air fluid levels were visible in this region and were consistent with the development of lung abscesses (panel B, white arrow). (Images provided by Dr. Ritu Gill, Division of Chest Radiology, Brigham and Women's Hospital, Boston.)
Lung abscess can usually be detected with standard imaging, including chest x-ray and CT (Fig. 258-2). The latter is clearly preferred for precise definition of the lesion and its location and possibly for detection of underlying lesions. Lymphadenopathy is not associated with bacterial lung abscess; thus this finding suggests an alternative diagnosis.
Microbiologic studies include stains and cultures of expectorated sputum to detect aerobic bacterial pathogens. However, clinical correlations are very important because sputum cultures (especially those that do not satisfy standard cytologic criteria) are unreliable. In appropriate settings, it is important to consider cultures for fungi and mycobacteria. Anaerobic bacteria, the most common causes of primary lung abscess, are not detected in expectorated sputum cultures, and in any case the specimen is subject to anaerobic contamination as it traverses the upper airways. Alternative specimens that may be useful include pleural fluid obtained by thoracentesis in patients who have empyema and quantitative bronchoalveolar lavage (BAL) specimens if they are processed promptly and appropriately for anaerobic bacteria. Many reports describe the use of transtracheal aspiration to bypass the upper airways and obtain a specimen for meaningful anaerobic culture. This procedure, which was used extensively in the 1970s, has largely been abandoned out of concern about adverse consequences and because of a general decline in the pursuit of an etiologic agent in pulmonary infections. Another invasive method for bypassing contamination by the flora of the upper airways is transthoracic needle aspiration under CT guidance; the popularity of this procedure has increased in recent years. In most cases, the etiology of anaerobic lung abscess is clear: the host is prone to aspiration and has an abscess in a dependent pulmonary segment, with no other likely cause. As stated above, putrid breath, sputum, or empyema fluid indicates anaerobic infection.
Treatment depends on the presumed or established etiology. Infections caused by anaerobic bacteria should usually be treated with clindamycin; the initial IV dosage of 600 mg four times daily can be changed to an oral dosage of 300 mg four times daily once the patient becomes afebrile and improves clinically. The duration of therapy is arbitrary, but many experts recommend continuation of oral treatment until imaging shows that chest lesions have cleared or have left a small, stable scar. A shorter course may be effective. An alternative to clindamycin is any β-lactam/β-lactamase inhibitor combination; parenteral treatment may be followed by orally administered amoxicillin/clavulanate. Carbapenems are also effective against anaerobic bacteria as well as streptococci, but the published data with these drugs in the treatment of anaerobic pulmonary infections are sparse. Penicillin was previously regarded as a preferred drug for these infections, but many oral anaerobes produce β-lactamases, and clindamycin proved superior to penicillin G in a randomized clinical trial. Metronidazole is highly active against virtually all anaerobes but not against aerobic microaerophilic streptococci, which play an important role in mixed infections. In therapeutic trials, metronidazole has done poorly unless combined with a β-lactam or another agent active against aerobic and microaerophilic streptococci.
Persistence of fever beyond 5–7 days or progression of the infiltrate suggests failure of therapy and a need to exclude factors such as obstruction, complicating empyema, and involvement of antibiotic-resistant bacteria. Many patients with uncomplicated lung abscesses and all those with atypical presentations or unresponsive abscesses should undergo bronchoscopy and/or CT to detect a possible associated anatomic lesion, such as a tumor, or a foreign body. Quantitative bacteriologic studies using a protected brush catheter or BAL are much less reliable when done after antibiotic therapy. Postural drainage was previously popular for patients with lung abscess, but aggressive attempts to implement this strategy may result in spillage to other pulmonary segments, leading to airway obstruction and clinical deterioration.
Lung abscess due to S. aureus is usually treated with vancomycin at a dosage that targets a trough serum level of 15–20 μg/mL. The main alternative is linezolid. Daptomycin should not be used for pulmonary infections. Lung abscesses caused by aerobic gram-negative bacteria need to be treated according to the results of antibiotic sensitivity tests. Most common among the pathogens involved are K. pneumoniae (especially the K1 strain in Taiwan) and P. aeruginosa in patients with severe chronic lung disease or compromised immune defenses. Pseudomonal lung abscesses usually require prolonged courses of parenteral antibiotics. Carbapenems or β-lactams are frequently combined with aminoglycosides; oral fluoroquinolones are often effective initially, but resistance is common with prolonged use. Aerosolized colistin and aminoglycosides are sometimes used to augment other therapy, but the efficacy of this approach is variable.
Surgery for lung abscesses was developed at the time penicillin became available in the late 1940s. The relative roles of penicillin and resectional surgery were hotly debated at that time, but by the late 1950s penicillin was favored. Initially the standard choice for most lung abscesses, penicillin was subsequently supplanted by the options summarized above. Recent large-scale reviews indicate that, in general, surgery is now reserved for ~10–12% of patients. The major indications for surgery are failure to respond to medical management, suspected neoplasm, and hemorrhage. Failure to respond to antibiotics is usually due to an obstructed bronchus and an extremely large abscess (>6 cm in diameter) or to infection involving relatively resistant bacteria, such as P. aeruginosa. The usual procedure is lobectomy. An alternative intervention that is becoming popular is percutaneous drainage under CT guidance. Aspirate samples for assay of possible pathogens should be carefully collected.
Patients with lung abscess usually show clinical improvement, with decreased fever, within 3–5 days of initiation of antibiotic treatment. Defervescence can be expected within 5–10 days. Patients with fevers persisting for 7–14 days should undergo bronchoscopy or other diagnostic tests to better define anatomic changes and microbiologic findings. Cultures of expectorated sputum are not likely to be helpful at this juncture except for detecting pathogens such as mycobacteria and fungi. The response to therapy apparent on serial chest radiographs is delayed in comparison with the clinical course. In fact, infiltrates usually progress during the first 3 days of treatment in approximately one-half of patients. Pleural involvement is relatively common and may develop in dramatic fashion. The most common causes of failures of medical management include a failure to drain pleural collections, an inappropriate choice of antimicrobial therapy, an obstructed bronchus that prevents drainage, a "giant" abscess, a resistant pathogen, or refractory lesions due to immunocompromise.