Hospital Medicine

Lung abscess

Lung Abscess

I. What every physician needs to know.

Primary lung abscess is a collection of pus-containing material due to a polymicrobial infection, most commonly occurring after aspiration of bacteria-containing material into the lung parenchyma, resulting in a necrotic lesion with air-fluid levels. Lung abscesses can be classified in three different ways:

  1. Chronicity: Acute (< 6 weeks) vs chronic (> 6 weeks);

  2. Etiology: primary vs secondary;

  3. Spread of the infection: bronchogenic vs hematologic.

Primary lung abscesses can be associated with aerobic bacteria, mycobacteria, pyogenic bacteria, anaerobic bacteria, fungi, or parasites in immunocompetent or immunosuppressed hosts. Secondary lung abscesses can be associated with certain rheumatologic conditions such as rheumatoid arthritis or granulomatosis with polyangiitis, neoplasms, foreign body aspiration, bronchiectasis, and pulmonary infarctions.

Clinically, lung abscesses have symptoms of community-acquired pneumonia but have usually a more prolonged course characterized by night sweats, foul-smelling sputum, possible hemoptysis, and weight loss.

Radiologic studies are needed to diagnose a lung abscess. Typical features on a radiograph include a cavity with a thick wall and air-fluid levels. Compared to chest x-rays, chest computed tomography (CT) scanning detects smaller abscesses, distinguishes empyema associated pleural air-fluid levels from abscesses, and may demonstrate an underlying neoplasm. A bronchoscopy may be required to distinguish an abscess from other diagnoses.

The optimal duration of therapy for primary lung abscess is not clear. In general, it is recommended to treat lung abscesses with a 4-6 week course of antibiotics, guided by microbiological data when available. Microbiological data can be obtained from expectorated sputum, blood or cultures from the abscess itself by invasive biopsies.

II. Diagnostic Confirmation: Are you sure your patient has Lung Abscess?

To diagnose a lung abscess, certain features should be present which include:

  1. Clinical signs and symptoms suggestive of a lung abscess;

  2. Radiographic features suggestive of a lung abscess;

  3. Exclusion of secondary causes that can mimic a lung abscess.

Bronchoscopy is now an important element of the diagnostic work-up to rule out the above-mentioned causes that can mimic a lung abscess.

A. History Part I: Pattern Recognition

Primary lung abscess presents classically with fever, night sweats, putrid sputum, pleuritic chest pain, and weight loss occurring over 2-3 weeks. The presence of these symptoms along with known risk factors increases the suspicion for an abscess. Physical examination shows poor dentition, clubbing, and localized cavernous breath sounds. About 80% of lung abscesses arise due to aspiration of oropharyngeal contents.

Clinical, epidemiologic, and historic features help distinguish primary from secondary lung abscesses and guide diagnosis and treatment.

Features that should raise concern for the presence of an underlying neoplasm include an edentulous patient, extensive smoking history, age >50 years, and unusual abscess location.

The epidemiologic history may suggest tuberculosis or less common bacterial, fungal or parasitic pathogens.

In some cases of anaerobic pulmonary infection, a fulminant necrotizing clinical course with rapid evolution (<1 week), early empyema formation and marked leukocytosis (WBC > 20,000 cells/milliliter [mL]) may be observed and is termed pulmonary gangrene.

B. History Part II: Prevalence

Primary lung abscesses generally occur following aspiration of oropharyngeal contents. Radioactive tracer studies have shown that 45% of healthy individuals and 70% of patients with altered consciousness aspirate during sleep. Aspiration evolves to lung necrosis and abscess formation within 1 to 2 weeks.

Sputum contains 109 bacteria/ml. The low incidence of lung abscess attests to the effectiveness of normal lung defense mechanisms such as mucociliary clearance mechanisms, surface immunoglobulin A, and macrophage activity.

When host defenses are impaired or overwhelmed by larger volume aspirates, pneumonia and subsequent lung abscess formation can develop. These situations include:

  • Altered consciousness - due to alcoholism, stroke, anaesthesia, drug overdose, or seizure.

  • Neurologic disease - stroke, neurodegenerative disease.

  • Esophageal disease – gastroesophageal reflux disease (GERD), achalasia.

  • Mechanical barriers - nasogastric or endotracheal tubes.

As noted, alterations in the host’s barrier, humoral, and cellular defenses render affected patients susceptible to opportunistic pathogens.

C. History Part III: Differential diagnosis.

The differential diagnosis of a lung abscess includes the following:

1. Bronchogenic carcinoma;

2. Tuberculosis;

3. Empyema;

4. Infected bullae or cyst;

5. Cavitary pneumoconiosis;

7. Pulmonary infarct;

8. Granulomatosis with polyangiitis;

9. Pulmonary sequestration.

Diagnosis of lung abscess in a patient with a cavitary pulmonary lesion requires exclusion of non-infectious causes of cavitary lung disease.

Non-infectious causes

Table I lists non-infectious causes of cavitary lung lesions and distinguishing features.

Table I.

Noninfectious causes of cavitary lung lesions
Neoplasm Primary lung - ~80% of cases SCCA. Small cell lung CA does not cavitate.Lymphoma - multiple lesions, upper lobe predominance.Metastatic CA - esp. head and neck SCCA.
Vasculitis Wegener's - single or multiple lesions, cANCA present in >90%.Rheumatoid arthritis -multiple, lower lobes, systemic disease evident, may coexist with malignancy.
Pulmonary infarct ~15% of PEs infarct; cavitation occurs in ~5% of infarcts. Bacterial superinfection rare.
Structural lung abnormalities with air-fluid levels-blebs, cystic bronchiectasis, pulmonary sequestration, bullae usually distinguished by CT
Sarcoid multiple in ~90%, median diameter 2 cm

Endovascular infections

Hematogenous spread of staphylococcal infections from conditions like septic phlebitis or tricuspid valve endocarditis in injection drug users can result in septic embolization to multiple sites, with predilection for the lungs.

Oropharyngeal infection causing septic internal jugular vein thrombophlebitis and Fusobacterium necrophorum bacteremia produces multifocal septic pulmonary infarcts (Lemierre's syndrome). Progression to frank cavitation is less commonly seen now than in the pre-antibiotic era.

Health care associated infection

The recognition that chronically-ill patients with extensive health care system exposure develop oral colonization with aerobic gram-negative rods and Staphylococcus aureus is well-documented and reflected in the treatment guidelines for health-care associated pneumonia. Virulent pathogens such as Pseudomonas aeruginosa, Klebsiella pneumoniae and Staphylococcus aureus may cause cavitary pneumonia, and, in severe cases, pulmonary gangrene.

Infections in altered hosts

Patients with cell-mediated immune defects are susceptible to infection with fungi and intracellular bacterial pathogens. Granulocytopenic patients are more prone to infection with aerobic gram-negative rods and Staphylococcus aureus.

The likelihood of opportunistic infection increases with the intensity of endogenous or exogenous immunosuppression. Many opportunistic pathogens also cause infection in immunocompetent adults; conversely, conventional pathogens may cause more severe or unusual disease manifestations in patients with altered immunity.

Nocardia asteroides is an aerobic gram-positive actinomycete with a predilection for lung, CNS, and cutaneous involvement. A third of cases of nocardiosis occurs in immunocompromised patients. Approximately 40% of cases of nocardiosis are confined to the lung.

Rhodococcus equi is a gram-positive acid fast coccobacillus that has been associated with the human immunodeficiency virus (HIV) epidemic. It produces isolated pulmonary involvement in ~80% of cases. Cavitary disease is more frequently seen with Rhodococcus than with mycobacterial or nocardia infections in HIV-infected patients.

Invasive pulmonary aspergillosis has been most frequently described in heavily immunosuppressed populations, such as hematopoietic or solid organ transplant recipients. Invasive disease is well-described, however, in chronic obstructive pulmonary disease (COPD) patients on high doses or protracted courses of corticosteroids.

Mycobacteria

Reactivation tuberculosis leading to cavitation occurs in elderly patients as a consequence of waning immunologic surveillance. Immunosuppressed states such as HIV infection, post-transplantation, tumor necrosis factor (TNF)-alpha therapy, silicosis, dialysis, and head and neck cancer are associated with the highest risk for reactivation disease in patients with latent tuberculous infection (LTBI).

The nontuberculous mycobacteria Mycobacterium avium-intracellulare (MAC) and M. kansasii also cause cavitary lung disease. Illness classically presents with slowly-progressive cavitary disease in older men with underlying COPD. Cavitary disease is less commonly seen in HIV infected patients.

Endemic mycoses

Histoplasma capsulatum is endemic to the St. Lawrence, Ohio, and Mississippi River Valleys. Underlying COPD predisposes to chronic pulmonary histoplasmosis, in which the host inflammatory response mediates a chronic fibrosing process. Resulting upper lobe cavitary disease closely mimics tuberculosis; dual infection or coexisting lung cancer are well-described.

Coccidioides immitis is endemic to the southwest United States. Cavity formation is a late sequelae of primary infection. Patients may develop thin-walled cavities, typically peripheral and solitary, and often asymptomatic. Alternatively, chronic fibrocavitary disease, more frequent in diabetic patients, produces progressive systemic symptoms, infiltrates with thick walled cavitation, and often hilar adenopathy.

Less common fungal pathogens associated with cavitary lung disease include blastomycosis, cryptococcosis, and sporotrichosis. Cavitary disease caused by Pneumocystis jiroveci is well-described in HIV infected patients and typically features thin-walled lesions.

Other reported pathogens

Microaerophilic streptococci (Streptococcus anginosus group, formerly S. milleri) are a subgroup of viridans streptococci with a unique propensity for causing abscess formation. Monomicrobial lung abscesses have been described. Metastatic infection should be considered in bacteremic cases.

Type 3 Streptococcus pneumoniae has been reported as a sole abscess pathogen, but its role is unclear as coexisting anaerobic infection may have been contributory.

Actinomyces israelii is an anaerobic actinomycete most commonly associated with cervicofacial and abdominal infection. Isolated thoracic actinomycosis is uncommon but notoriously mimics lung cancer.

Other bacteria reported as pathogens in lung abscesses include Pasturella multocida, Haemophilus influenzae, Legionella, and Burkholderia cepacia.

Less common infections acquired abroad

Burkholderia pseudomallei, a gram negative intracellular bacterial pathogen, is the cause of melioidosis. This environmental saprophyte, endemic in Southeast Asia and the northern region of Australia, is transmitted by inoculation and presents with diverse clinical manifestations including lung abscess. The incubation period varies widely from days to years.

Klebsiella pneumoniae infection has been reported as a lung and liver abscess pathogen in Taiwan. Published experience is limited and the true prevalence of Klebsiella and its role as a sole pathogen in lung abscess is incompletely defined.

Entamoeba histolytica lung abscesses most commonly result from extension of a liver abscess into the lung and are therefore generally seen in the right lower or middle lobe.

Paragonimus westerman is a lung fluke endemic to Asia. Infection is acquired through ingestion of undercooked fresh water shellfish. Late infection may be associated with peripheral lung cavities, rarely with air-fluid levels, consequent to inflammatory lung changes around adult flukes. Lesions are typically small, peripheral, and found in the lower lung fields.

Echinococcus granulosa, the dog tapeworm, the etiologic agent of cystic echinococcal disease, is widely distributed throughout the world and classically produces a thin-walled cyst on CT that may demonstrate a crescent sign. Coexisting liver involvement is seen in ~20% of patients.

D. Physical Examination Findings.

Physical examination may support a diagnosis of anaerobic lung abscess. Associated findings include fever, poor dentition with gingival disease, digital clubbing, and putrid sputum in ~50% of patients. Pulmonary exam abnormalities may include amphoric breath sounds, and signs of consolidation or effusion.

1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

Laboratory testing is directed at establishing a microbiologic diagnosis, particularly in cases not clearly consistent with primary lung abscess.

Blood cultures are routinely sterile in anaerobic lung infection. Routine sputum cultures are of limited utility in primary lung abscess as they are routinely contaminated with aerobic upper airway flora. A putrid odor to sputum is characteristic of anaerobic infection. Sputum cultures should be obtained when health-care associated pathogens are suspected or in post-influenza settings when Staphylococcus aureus superinfection is a concern.

Blood cultures may be positive in Lemierre's syndrome for Fusobacterium necrophorum and in endovascular infections for Staphylococcus aureus.

Tuberculosis should always be excluded in any atypical case of lung abscess. All patients should be placed in respiratory isolation and sputum for acid fast smear and culture obtained.

Blood testing for galactomannan, a component of the Aspergillus cell wall, should be obtained if invasive aspergillosis is a concern. Testing for beta-glucan (Fungitell), a fungal cell wall component with utility in diagnosing aspergillosis and Pneumocystis, may also be obtained if available. Antibody and antigen testing for histoplasmosis and coccidioidomycosis is available and should be sent in suspect cases; antigen testing for cryptococcus is also available. Laboratory lag times prevent these tests from informing initial decision-making in atypical cases but results may be useful in the event of a desultory clinical response.

Antinuclear cytoplasmic antibodies should be sent if vasculitis is a consideration. As noted, cavitary rheumatoid disease generally occurs in the setting of clinically-apparent disease. Cavitation of a pulmonary infarct is an unusual initial presentation for thromboembolic disease; D-dimer elevations would be expected in systemic inflammatory disease and would not be useful.

2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

Lung abscess is generally a radiographic diagnosis. The typical location for a lung abscess is in a lung segment where gravity drainage carries aspirated material, i.e., the apical segment of the right lower lobe or posterior segment of the right upper lobe. Most aspirations occur in supine or recumbent patients. The right lung is favored because of the larger size and less acute angulation of the right mainstem bronchus. Primary lung abscesses are most often unilateral. Unusual (i.e. anterior) abscess location raises concern for an underlying neoplasm.

If an abscess is detected on chest radiograph, chest computed tomography (CT) provides enhanced assessment for an underlying endobronchial lesion, hilar adenopathy which is not usual in primary lung abscess, and additional underlying parenchymal lung disease or small abscesses. Chest CT also helps differentiate peripheral lung abscess from empyema with an air-fluid level indicative of bronchopleural fistula. In addition, CT chest may detect unsuspected lung abscess when performed in patients with non-resolving pneumonias.

III. Management.

Initial management necessitates determining whether a cavitary lung lesion is likely to represent a primary lung abscess. If the clinical presentation supports this diagnosis, therapy active against oral anaerobes is initiated. Commonly isolated pathogens include peptostreptococci, Prevotella spp, non-fragilis Bacteroides, and Fusobacteria spp. Parenteral clindamycin has supplanted penicillin as the standard of care, as several oral anaerobes (Fusobacterium, Prevotella sp, non-fragilis Bacteroides sp) now produce penicillinase.

Limited clinical data exists for other regimens, but based on in-vitro susceptibility of the usual pathogens, a number of other regimens may be used. These include combination beta-lactamase inhibitors (e.g., ampicillin-sulbactam, amoxicillin-clavulanate, piperacillin-tazobactam), carbapenems, second-generation cephalosporins (e.g., cefoxitin, cefotetan), and quinolones with good anaerobic activity (e.g. moxifloxacin). Concern has been raised that the anti-tuberculous activity of newer quinolones may lead to partial responses and diagnostic delays. As this question is unresolved, it may be preferable to select another drug regimen if tuberculosis is a serious consideration.

Metronidazole as monotherapy is not recommended for primary lung abscess since it is associated with a 50% failure rate due to poor activity against peptostreptococci; however it has been used effectively in combination with penicillin. Tetracyclines have variable anaerobic activity and poor penetrance through the abscess membranes, and are not recommended.

If health care-associated pathogens are likely, coverage for gram-negatives and Staphylococcus aureus should be initiated.

Patients should be treated for 4-6 weeks, ensuring sustained abatement of fever, resolution of putrid sputum, and improvement of radiographic findings.

A. Immediate management.

Initial management should include:

  • Ensuring hemodynamic stability and adequate oxygenation;

  • Initiation of antibiotics;

  • If tuberculosis is a consideration, initiate respiratory isolation and sputum collection;

  • If the patient is an alcoholic, thiamine repletion and withdrawal protocol.

Early bronchoscopy should be considered in patients with secondary lung abscess if CT suggests a neoplasm. Bronchoscopy may also be performed to obtain specimen for microbiologic studies if sputum cultures are non-diagnostic, particularly if unusual bacterial, mycobacterial, fungal or other opportunistic pathogens are suspected.

Medical management failure occurs in 10-15% of cases. Early engagement of appropriate consulting services in such cases is prudent. Clinical factors associated with treatment failure include:

  • Abscesses >6 centimeters (cm);

  • Severe hemoptysis (rare);

  • Resistant flora, e. g., Pseudomonas;

  • Presence of obstructing neoplasm.

Management of malignant post-obstructive abscesses often requires a multidisciplinary approach including medical oncology, radiation oncology and thoracic surgery consultations. Bronchoscopic lavage and drainage of abscesses is not recommended because of the potential for large volume pus spillage into other lung segments causing acute respiratory distress syndrome (ARDS) or mechanical asphyxiation.

There has been limited published experience with CT-guided percutaneous drainage of large or poorly responding pyogenic abscesses. Endoscopic placement of pigtail catheter for drainage under bronchoscopic visualization has also been reported. Expertise in these potential treatment modalities is institution specific. For patients failing medical therapy in whom less invasive modalities are not available, surgical options should be considered. These includes chest tube drainage, surgical resection via lobectomy (central or large abscesses) or video-assisted thoracoscopy.

If chest tube drainage is performed, it is usually continued for 10-14 days. Potential complications include empyema, bronchopleural fistula, and bleeding.

Indications for surgical resection include hemoptysis, prolonged sepsis, bronchopleural fistula, abscess rupture with empyema formation, failure of medical therapy (i.e., 4-6 weeks of antibiotics), cavity larger than 6 cm, and suspicion for malignancy.

B. Physical Examination Tips to Guide Management.

Patient monitoring should include daily assessment of fever trend, oxygenation, and any lung exam abnormalities. Watch for signs of alcohol withdrawal and adverse reactions to antibiotics (e.g., rash, diarrhea, drug fever.)

C. Laboratory Tests to Monitor Response to, and Adjustments in, Management.

Laboratory monitoring should include periodic complete blood count (CBC), to assess for resolution of infection-related leucocytosis and anemia. The frequency of monitoring is determined by the clinical evolution of the patient. Initially daily monitoring may be necessary. Once the patient is improving every 2-3 days testing is adequate.

Baseline renal and hepatic function should be assessed in anticipation of protracted antibiotic therapy in the event that symptoms or signs of drug toxicity subsequently appear. Baseline renal function will also inform the need for dosage adjustment of agents excreted by the kidneys.

D. Long-term management.

Initial improvement in patient symptoms and fever should appear in the first 2-3 days of therapy, with defervescence in 7-10 days. If there is no clear improvement by 10-14 days further evaluation is necessary. In addition to the previously outlined unfavorable prognostic features, diagnostic considerations include:

  • Drug fever-particularly if the clinical appearance and fever curve are discordant;

  • Inaccurate microbiologic diagnosis;

  • Non-infectious etiology of cavitary lung disease or superinfection of non-infectious condition.

In such cases, results of serologic testing for unusual pathogens (e.g., endemic mycoses in patients with travel history) should be reviewed and further epidemiologic history should be explored for clues suggesting an unusual infectious exposure. Diagnostic bronchoscopy for biopsy, culture (fungal, mycobacterial, bacterial), and exclusion of radiographically-occult cancer or occluding foreign body should be performed on poor responders.

The optimal frequency of serial chest imaging in patients progressing favorably has not been established. Initial worsening of chest imaging during the first week of therapy is described. Repeat imaging while in-hospital will be generally reserved for patients in whom the clinical response is uncertain or poor.

V. Transitions of Care.

Weekly CBC should be monitored to assess therapy response and monitor for drug toxicity. Weekly renal function testing is prudent in patients with underlying renal insufficiency. Chest x-rays should be obtained weekly to biweekly while the patient is under treatment. As noted there are no strict guidelines regarding the total duration of therapy. Many experts treat to radiographic resolution or stable small residual scarring. Abscess cavities and surrounding infiltrates often require weeks to months to resolve, typically lagging behind clinical improvement.

VI. Placement Considerations.

Patients receiving parenteral therapy for the duration of treatment will require peripherally inserted central catheter (PICC) placement. Skilled nursing facility placement may be necessary if there are logistic issues related to the complexity of the treatment regimen or if the patient requires physical and occupational therapy for debility.

Patients with primary lung abscesses responding well to initial therapy may be transitioned to oral therapy with clindamycin, amoxicillin-clavulanic acid, or moxifloxacin to complete therapy. Therapy regimens for hospital associated and opportunistic pathogens require individualization.

VII. Prognosis and Patient Counseling.

Primary lung abscesses have a favorable prognosis; approximately 90% of treated patients are cured. Underlying altered immunity, neoplastic bronchial obstruction, and hospital associated infection confer a much worse prognosis with fatal outcomes in 2/3 or more of patients reported.

VIII. What's the Evidence?

Kuhajda, I, Zarogoulidis, K, Tsirgogianni, K, Tsavlis, D, Kioumis, C, Tsakiridis, K, Mpakas, A, Zarogoulidis, P, Zissimopoulos, A, Baloukas, D, Kuhajda, D. "Lung abscess-etiology, diagnostic and treatment options". Ann Transl Med. vol. 3. 2015. pp. 183.

Wali, SO. "An update on the drainage of pyogenic lung abscesses". Ann Thorac Med. vol. 7. 2012. pp. 3-7.

Mandell, LA, Wunderink, RG, Anzueto, A. "Infectious Diseases Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults". Clin Infect Dis. vol. 44. 2007. pp. S27-72.

You must be a registered member of Clinical Pain Advisor to post a comment.

Sign Up for Free e-Newsletters