Lung Abscess: Diagnosis and Treatment
Authors: Hugh A. Cassiere, MD, Alan M. Fein, MD, SUNY at Stony Brook, Winthrop University Hospital

thumbnail Click here to see a CXR (chest radiograph) demonstrating
a cavitary lesion. 		Click here to see a CT scan of a lung abscess. thumbnail

Back Abstract: Lung abscess is defined as a localized suppurative necrotizing collection occurring within the pulmonary parenchyma. Infections and neoplasms are the most common causes. Anaerobic bacteria are causative in 90% of lung abscesses and aspiration of orogingival material is the most frequent etiology. Signs and symptoms usually begin at least 2 weeks before presentation and include cough, hemoptysis, fever, chills, night sweats, anorexia, pleuritic chest pain, and weight loss.ABSC. Foul smelling sputum, found in 50% to 60% of patients, is pathognomonic for anaerobic infection. Physical examination may reveal fever, altered sensorium, poor dental hygiene, and clubbing. The typical chest radiograph reveals a solitary cavitary lesion measuring 4.0 cm in diameter with an air fluid level. In contrast to an infectious abscess, neoplasm tends to have less surrounding radiographic infiltrate. The mainstay of therapy are antimicrobials which target orogingival anaerobes, usually intravenous penicillin or clindamycin. Many patients require 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 non-resolution of abscess cavity. [Medscape Respiratory Care 1(7), 1997. © 1997 Medscape, Inc.]

Key words: infection, abscess, infiltrate, aspiration pneumonia

Contents


Back Introduction

A lung abscess is defined as a localized (usually >2.0 cm in diameter), suppurative necrotizing collection occurring within the pulmonary parenchyma. Several processes, either respiratory or systemic, can lead to abscess formation. Most abscesses are primary, meaning they result from necrosis in an existing parenchymal process (usually an infectious pneumonia). Among the causes of necrotizing pneumonitis (which, if progressive, can become a lung abscess), infections and neoplasms are the most frequently identified.[2] When an abscess complicates septic vascular emboli (e.g. right sided endocarditis), bronchial emboli (e.g. aspirated foreign bodies) or rupture of an extrapulmonary abscess into the lung (e.g. empyema) it is termed secondary.

Numerous different infectious agents can be responsible for abscess formation including aerobic bacilli, fungi, parasites, and mycobacteria. However, anaerobes have been identified as the most common infectious agents leading to lung abscess. [1,2,3,4] Among neoplastic causes, primary squamous carcinoma is the most common malignancy associated with lung abscess. [8]

In the post-antibiotic era, the incidence of lung abscesses has declined, presumably as a result of improved treatment regimens for pneumonia. In fact, over the past 40 years , the incidence has declined 10-fold, while the mortality rate has fallen to 5% to10%. [3] Diagnosis and treatment have changed little over the years and are largely dictated by past clinical practices since lung abscesses are uncommon and it is difficult to obtain enough patients to perform controlled clinical trials. Nonetheless, the mainstay of therapy is antibiotics, and surgery is rarely needed. The role of newer antimicrobials is still controversial, but they may represent an advance over traditional therapeutic agents (penicillin), especially as drug-resistant bacteria become more prevalent.

Back Pathogenesis

Most lung abscesses are caused by infectious agents, including bacteria, fungi, parasites, and mycobacteria. However, the majority of cases involve a mixed bacterial flora that includes anaerobes in up to 90% of the time. Aerobic bacilli may be present in up to 50% of patients, but in most cases they coexist with anaerobes. The proposed pathogenesis is a combination of infective orogingival material in a host who has a predisposition to aspirate this material into a lung that cannot adequately clear the infectious challenge. [2]

Aspiration, is more likely in patient populations who have altered consciousness or oropharyngeal and esophageal dysfunction. This includes patients with alcoholism, seizure disorders, drug overdosage, general anesthesia, protracted vomiting, or neurological disorders such as cerebrovascular accidents, myasthenia gravis, Amyotropic Lateral Sclerosis (ALS), and other bulbar processes. (Table I.)

The aspirated material must contain a large concentration of potentially pathogenic bacteria. Aspiration of gastric contents may not always lead to infection, especially if the aspirate is only acid, in which case a chemical pneumonitis will result. On the other hand, orogingival material often contains a large bacterial inoculum and can lead to lung abscess, especially if the inoculum size is enhanced by poor dentition or gingival disease. Bartlett and Finegold found that approximately 73% of patients with lung abscess had at least one predisposing factor for aspiration and many had gingival disease found after careful dental evaluation.[1] Obviously not all patients with risk factors develop abscesses, and other factors, particularly underlying comorbidities and impaired host defenses also play a key role in the development of lung abscess.

According to some experimental evidence, lung abscesses form 7-14 days after aspirating infectious orogingival material into the terminal bronchioles. [2] When aspirated in large amounts, a single species of anaerobic bacteria, or a combination of multiple organisms, can cause a necrotizing pneumonitis. Progressive pneumonitis can lead to lung abscess localized according to gravity and body position at the time of aspiration. Since most patients aspirate while upright or supine, a lung abscess is typically located in the basal segments of the lower lobes, the superior segment of the lower lobe, or the posterior segments of the upper lobes (see Fig. 1). With these pathogenetic principles in mind, it is clear that an abscess arising in an otherwise healthy patient or in a location other than the ones mentioned, should raise suspicion of another pathogenic process (like non-anaerobic infection or an endobronchial obstructing lesion).

Back Microbiology and Classification

Approximately 90% of lung abscesses are associated with anaerobic bacteria either as the primary pathogens or in combination with aerobic bacterial agents. [5] This observation may be explained by the fact that anaerobic bacteria commonly cause necrosing infection, but other bacteria that can cause lung abscess include: S. aureus, E. coli, K. pneumoniae, P. aeruginosa and other gram negative bacilli; S. pyogenes, H. influenzae (especially type b), L. pneumophila, N. asteroides, Actinomyces species, and rarely pneumococcus. Parasites, including P. westermani, E. histolytica, fungi and mycobacteria may also cause lung abscess (Table II).

In those infections caused only by anaerobes, the average number of organisms isolated is three. Thus most lung abscesses are polymicrobial infections, involving either strictly anaerobes or a combination of aerobic-anaerobic bacteria.[4] Only 10% of lung abscesses are caused by aerobes alone, without anaerobic involvement. Although the bacteriology of this process has not changed much in recent years the taxonomy of the bacteria has changed, and the current names of the most clinically relevant organisms include the following: Peptostreptococcus species (anaerobic gram negative cocci), F. nucleatum, F. necrophorum, Porphyromonas species (formally classified in the genus Bacteriodes) and P. melaninogenicus (formerly classified into the genus Bacteriodes). [5]

In the past, lung abscesses have been categorized using several methods, but the separation into an acute versus a chronic process has the most clinical utility. This distinction is not absolute, but can aid the clinician by helping plan treatment regimens and by identifying patients who may need further diagnostic evaluation, such as bronchoscopy. An acute lung abscess is defined as occurring in a patient who presents with symptoms of less than 2 weeks duration. This type of patient is less likely to have an underlying neoplastic process and is more likely to have infection caused by a virulent aerobic bacterial agent such as S. aureus or K. pneumoniae. A patient with a chronic lung abscess, defined by symptoms lasting greater than 4-6 weeks, either has an underlying cancer or an infection with a less virulent, anaerobic agent.

Back Clinical Features

Signs and symptoms. Most patients with lung abscess have an insidious presentation, with symptoms lasting at least two weeks prior to evaluation. Signs and symptoms include cough, foul smelling sputum which layers on standing, hemoptysis (in 25% of patients), fever, chills, night sweats, anorexia, pleuritic chest pain ( in 60% of patients), weight loss, and clubbing. Although most of these signs and symptoms are sensitive, their specificity is extremely low. This is not the case for foul smelling or putrid sputum. This is a highly specific sign which is pathognomonic for anaerobic infection, although it is only found in 50% to 60% of patients. [1,2,4] A history of weight loss is also common, occurring in 60% of patients, with an average loss of between 15-20 lbs. As described earlier, historical data may also include risk factors for aspiration such as alcoholism, drug overdose, seizures, head injury, or stroke, and the absence of such risk factors should prompt a search for a diagnosis other than primary lung abscess.

Physical examination. Physical examination may reveal fever, altered sensorium, poor dental hygiene, and clubbing. Fever is found in approximately 60% to 90% of patients with lung abscess with an average maximal temperature of 39.10 C. Clubbing is present in approximately 20% of patients, but like other findings it lacks sensitivity and specificity.

Laboratory data. Laboratory data are generally non-specific. Culture information is generally not helpful unless the abscess is caused by non-anaerobic agents such as mycobacteria, fungi, or aerobic bacteria. Sputum examination is useful only in helping diagnose non-anaerobic pulmonary infections because sputum can pick up anaerobes as it is expectorated through the oral cavity and thus the finding of these organisms is not specific. More invasive methods like transtracheal aspiration and bronchoscopy are rarely employed since the majority of patients are treated empirically. If the patient presents in an atypical way or is not responding to therapy, then invasive techniques are justified to look for an endobronchial obstructing lesion. If the abscess is associated with an empyema, as is the case in 30% of the time, then culture of the empyema fluid may yield reliable bacteriologic data.

Radiologic data. Although certain historical information may suggest the presence of a lung abscess, a radiograph is needed to define the presence of a cavitary lung lesion (Table III). The typical chest radiograph reveals a solitary cavitary lesion measuring 4.0 cm in diameter with an air fluid level (Fig. 1). The amount of inflammation, seen radiographically surrounding the abscess, can help to identify those patients who are more likely to have an underlying non-malignant abscess.[8] In contrast to an infectious abscess, neoplasms tend to have less surrounding radiographic infiltrate.

thumbnail Figure 1. (click here to see the autorad) Chest radiograph reveals a solitary cavitary lesion with an air fluid level.

If a lung abscess fails to communicate with a bronchus, the characteristic cavity with an air fluid level will not be seen radiographically. This often leads to initial misdiagnosis since no clear abscess can be visualized. When the radiograph reveals multiple cavitary lesions it usually indicates that a necrotizing pneumonitis is present. This type of presentation is usually acute and fulminant and secondary to virulent aerobic bacteria such as S. aureus or K. pneumoniae. The presence of multiple bilateral cavities should raise suspicion of a hematogenously disseminated process, such as a right-sided endocarditis. Multiple cavities are rarely secondary to an anaerobic process unless the individual is severely immunocompromised, is recurrently aspirating, or the anaerobe(s) is virulent causing a necrotizing pneumonitis, instead of the typical lung abscess.

Radiographically, empyema and lung abscess are sometimes difficult to distinguish from one another. An empyema is a purulent infection which, in most cases, is confined to the pleural space, although it can develop as a complication of, or serve as a cause of a lung abscess. Both entities can have air-fluid levels, but one is intraparenchymal (lung abscess) while the other is extraparenchymal (empyema). If an empyema contains an air-fluid level, then a bronchopleural fistula is usually present. When the chest radiograph cannot distinguish these entities, a CT scan should be performed. On the CT scan, a lung abscess usually appears as a thick, irregular walled cavity with no associated lung compression (Fig. 2), as compared to an empyema, which has a thin smooth wall with compression of uninvolved lung.

thumbnail Figure 2. (click here to zoom image) On the CT scan, a lung abscess usually appears as a thick, irregular walled cavity with no associated lung compression.

Back Treatment

In the pre-antibiotic era the only treatment modalities available for lung abscess were supportive care, postural drainage with and without bronchoscopy, and surgery. All three have the same mortality rate (30% to 35%). Since the 1950's, when antibiotics became available for the treatment of lung abscess, mortality has fallen to 5% to 10%

Choosing an anitmicrobial. Currently, the mainstay of therapy for lung abscess is antimicrobial therapy which targets orogingival anaerobes, the organisms present in 90 % of lung abscesses. The choice of initial antibiotics is usually between intravenous penicillin and clindamycin, although past practices have also employed oral antibiotics, usually 3.0 gm of penicillin V daily. With the growing concern over penicillin-resistant anaerobes, two trials compared clindamycin to penicillin in a prospective study design. Both studies found that clindamycin therapy was associated with fewer treatment failures and a shorter time to symptom resolution.[7]

When metronidazole was evaluated as a single treatment modality it was found to have a 43% rate of treatment failure and hence, is not recommended for single agent therapy. Metronidazole, in combination with penicillin, is considered an appropriate treatment regimen for lung abscess because the penicillin will be active against the aerobic and microaerophilic streptococci that are often resistant to metronidazole.[3]

Many other antibiotics have in vitro activity against orogingival anaerobes but have not been evaluated in clinical trials to gain FDA approval for use in these infections. These antibiotics include chloramphenicol, imipenem, erythromycin, azithromycin, c larithromycin, and beta-lactams with a beta-lactamase inhibitor, e.g. ampicillin with sublactam.

Duration of Therapy. After selecting the appropriate antimicrobial agent, the next issue is determining the length of therapy. Although there is considerable controversy in the literature, the approach taken by Bartlett seems the most conservative and appropriate. He recommends treating most patients until the pulmonary infiltrates have resolved or until the residual lesion is small and stable.[3] The initial stages of treatment are with intravenous antibiotics until the patient is afebrile and shows clinical improvement (4-8 days). This is followed by oral medications usually for a prolonged time, although the length of time needed is variable from patient to patient. Many patients require a total of 6-8 weeks of antimicrobial therapy.

Bronchoscopy to treat? In the past, bronchoscopy was part of the standard care of lung abscess patients. Its uses included helping to promote drainage and ruling out underlying malignancy. Currently, bronchoscopy is reserved for patients with atypical presentations who are suspected of having an underlying malignancy, or an aspirated or obstructing foreign body. Bronchoscopy is no longer routinely used for abscess drainage because the majority spontaneously communicate with the airways and drain. And because drainage rupturing an abscess during bronchoscopy can cause contamination of previously uninvolved lung segments.

Surgery. Surgical treatment for lung abscess is usually reserved for complications such as massive hemoptysis, bronchopleural fistula, and empyema. It is also used in the setting of fulminant infection and in those patients who fail medical therapy. Approximately 10% of lung abscesses require surgical intervention. Prognostic factors which are associated with medical treatment failures include recurrent aspiration, large cavity size (>6.0 cm), prolonged symptom complex prior to presentation, abscess associated with an obstructing lesion, abscesses with thick walled cavities, and serious comorbidities such as advanced age, neoplasm, and other chronic medical conditions. An alternative to surgical drainage is percutaneous catheter placement.[7] At this time, percutaneous drainage should be reserved for patients who are unresponsive to medical therapy and have lung abscesses located peripherally. These patients should also continue on intravenous antibiotics during and after percutaneous drainage of lung abscess.

Complications. Complications of lung abscess include empyema formation resulting from a bronchopleural fistula, massive hemoptysis, spontaneous rupture into uninvolved lung segments, and non-resolution of 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.

Back Conclusion

The incidence of and mortality from lung abscess have decreased since the introduction of antibiotics. The mainstay of therapy since then has been antibiotics, and surgery is rarely needed. The role of newer antimicrobials is still controversial, but they may represent an advance over penicillin, the traditional therapeutic agent, especially as drug-resistant bacteria become more prevalent.

Back About the Authors

Dr. Cassiere is Assistant Clinical Instructor in Medicine at SUNY at Stony Brook and Cardiac Surgical Intensivist at Winthrop University Hospital at Mineola, NY. Dr. Fein is Professor of Medicine at SUNY at Stony Brook and Chief, Pulmonary & Critical Care Division at Winthrop University Hospital in Mineola, NY.

Back Related Web sites:

Back References

  1. Bartlett JG and Finegold SM: Anaerobic infections of the lung and pleural space. American Review of Respiratory Disease 110: 56-77, 1974.
  2. Bartlett JG and Gorbach SL: The triple threat of aspiration pneumonia. Chest 68: 560-566, 1975.
  3. Bartlett JG: Antibiotics in lung abscess. Seminars in respiratory infections 6(2): 103-111, 1991.
  4. Bartlett JG: Anaerobic bacterial infections of the lung and pleural space. Clinical Infectious Diseases 16S: S248-255, 1993.
  5. Geppert EF: Lung abscess and other subacute pulmonary infections. In: Niederman MS, et al., ed. Respiratory Infections: W.B. Saunders:291-305, 1994.
  6. Ha HK, Kang MW, Park JM, Yang WJ, Shinn KS, Bahk YW. Lung abscess: Percutaneous catheter therapy. Acta Radiologica 34: 362-365, 1993.
  7. Levison ME, Mangura CT, Lorber B, Abrutyn E, Pesanti EL, Levy RS, MacGregor RR, Schwartz AR.Clindamycin compared with pencillin for the treatment of anaerobic lung abscess. Annals of Internal Medicine 98: 466-471, 1983.
  8. Sosenko A and Glassroth J. Fiberoptic bronchoscopy in the evaluation of lung abscesses. Chest 87: 489-494, 1985.

Back Tables

Back Table I - Risk Factors For Aspiration

Back Table II - Micobiology of Lung Abscess

Back Table III - Differential Diagnosis of Cavitary Lesion on Chest Radiograph

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Last updated 2-03-03; Mary T. Johnson, Ph.D.