THE MERCK MANUAL: The Merck Manual of Diagnosis and Therapy
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Lung Abscess

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Lung abscess is a necrotizing lung infection characterized by a pus-filled cavitary lesion. It is almost always caused by aspiration of oral secretions by patients who have impaired consciousness. Symptoms are persistent cough, fever, sweats, and weight loss. Diagnosis is based primarily on chest x-ray. Treatment usually is with clindamycin or combination β-lactam/β-lactamase inhibitors.

Most lung abscesses develop after aspiration of oral secretions by patients with gingivitis or poor oral hygiene. Typically, patients have altered consciousness as a result of alcohol intoxication, illicit drugs, anesthesia, sedatives, or opioids. Older patients and those unable to handle their oral secretions, often because of neurologic disease, are also at risk.

A less common cause of lung abscess is necrotizing pneumonia that may develop from hematogenous seeding of the lungs due to suppurative thromboembolism (eg, septic embolism due to IV drug use) or right-sided endocarditis. In contrast to aspiration, these conditions typically cause multiple rather than isolated lung abscesses.

The most common pathogens of lung abscesses due to aspiration are anaerobic bacteria, but about half of all cases involve both anaerobic and aerobic organisms (see Table 1: Lung Abscess: Infectious Causes of Cavitary Lung LesionsTables). The most common aerobic pathogens are streptococci and staphylococci—sometimes methicillin-resistant Staphylococcus aureus (MRSA). An unusual but very important acute and often lethal form of lung necrosis is caused by S. aureus with genes for Panton-Valentine leukocidin. Very serious and fulminant cases may be caused by MRSA (USA 300 strain), which has become a rare but very important cause of necrotizing pneumonia in young previously healthy adults and children. Occasionally, cases are due to gram-negative bacteria, especially Klebsiella. Immunocompromised patients with lung abscess may have infection with Nocardia, Mycobacteria sp, or fungi. Some people, especially those from developing countries, are at risk of abscess due to Mycobacterium tuberculosis, and rare cases are due to amebic infection (eg, with Entamoeba histolytica), paragonimiasis, or Burkholderia pseudomallei.

Table 1

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Introduction of these pathogens into the lungs first causes inflammation, which leads to tissue necrosis and then abscess formation. The abscess usually ruptures into a bronchus, and its contents are expectorated, leaving an air- and fluid-filled cavity. In about one third of cases, direct or indirect extension (via bronchopleural fistula) into the pleural cavity results in empyema.

Cavitary pulmonary lesions are not always caused by infection. Noninfectious causes include the following:

  • Bullae with air-fluid level
  • Bronchiectasis
  • Lung cancer
  • Lung infarction
  • Nodular silicosis nodule with central necrosis
  • Pulmonary embolism
  • Pulmonary sequestration
  • Sarcoidosis
  • Wegener's granulomatosis

Symptoms of abscess due to anaerobic bacteria or mixed anaerobic and aerobic bacteria are usually chronic (eg, over weeks or months) and include productive cough, fever, sweats, and weight loss. Severe prostration may occur. Sputum may be purulent or blood-streaked and classically smells or tastes foul. Symptoms of abscess due to aerobic bacteria develop more acutely and resemble bacterial pneumonia. Abscesses due to organisms other than anaerobes (eg, Mycobacteria , Nocardia) lack putrid respiratory secretions and may be more likely to occur in nondependent lung regions.

Signs of lung abscess, when present, are nonspecific and resemble those of pneumonia: decreased breath sounds indicating consolidation or effusion, temperature 38° C, crackles over the affected area, egophony, and dullness to percussion in the presence of effusion. Patients typically have signs of periodontal disease and a history of a predisposing cause of aspiration, such as dysphagia or a condition causing impaired consciousness.

  • Chest x-ray
  • CT as needed
  • Sputum cultures (unless anaerobic infection is very likely), including for fungi and mycobacteria
  • Bronchoscopy as needed to exclude cancer

Lung abscess is suspected based on history in a patient who is aspiration-prone due to altered consciousness or dysphagia and is confirmed by chest x-ray. In an anaerobic infection due to aspiration, chest x-ray classically shows consolidation with a single cavity containing an air-fluid level in portions of the lung that would be dependent when the patient is recumbent (eg, the posterior segments of the upper lobes or the superior or lateral basal segments of the lower lobes). This pattern helps distinguish anaerobic abscess from other causes of cavitary pulmonary disease, because diffuse or embolic pulmonary disease often causes multiple cavitations, and TB typically involves the apices.

CT is not routinely needed but may be useful when the x-ray suggests a cavitating lesion or when an underlying pulmonary mass obstructing the drainage of a lung segment is suspected.

Bronchial carcinoma can lead to obstruction that causes pneumonia and abscess formation. This should be suspected in smokers, recent smokers, and patients with unexplained cavitary lesions and no fever. Bronchoscopy is sometimes done to exclude cancer or the presence of a foreign body or to detect unusual pathogens, such as fungi.

Cultures

Anaerobic bacteria are rarely identifiable on culture because uncontaminated specimens are difficult to obtain and because most laboratories do not culture anaerobes well or often. If sputum is putrid, then anaerobic infection is assumed to be the cause. However, if empyema is present, pleural fluid provides a good source for anaerobic culture.

When clinical findings make anaerobic infection less likely, aerobic, fungal, or mycobacterial infection should be suspected, and attempts should be made to identify a pathogen. Cultures of sputum, bronchoscopic aspirates, or both are helpful. MRSA is generally found in both the sputum and blood cultures.

  • IV antibiotics or, for less seriously affected patients, oral antibiotics
  • Percutaneous drainage or surgery if empyema present or no response to antibiotics

Treatment is with antibiotics. Clindamycin 600 mg IV q 6 to 8 h is usually the drug of choice because it has excellent activity against streptococci and anaerobic organisms. The primary alternative is a combination β-lactam/β-lactamase inhibitor (eg, ampicillin/sulbactam 1 to 2 g IV q 6 h, ticarcillin/clavulanate 3 to 6 g IV q 6 h, piperacillin/tazobactam 3 g IV q 6 h). Metronidazole 500 mg q 8 h may be used but must be combined with penicillin 2 million units q 6 h IV. Less seriously ill patients may be given oral antibiotics such as clindamycin 300 mg po q 6 h or amoxicillin/clavulanate 875/125 mg po q 12 h. IV regimens can be converted to oral ones when the patient defervesces. For very serious infections involving MSRA, the best treatment is vancomycin or linezolid.

Optimal duration of treatment is unknown, but common practice is to treat until the chest x-ray shows complete resolution, which generally takes 3 to 6 wk or longer. In general, the larger the abscess, the longer it will take for x-rays to show resolution.

Most authorities do not recommend chest physical therapy and postural drainage because they may cause spillage of infection into other bronchi with extension of the infection or acute obstruction. If the patient is weak or paralyzed or has respiratory failure, tracheostomy and suctioning may be necessary. Rarely, bronchoscopic aspiration helps facilitate drainage. An accompanying empyema must be drained. Percutaneous or surgical drainage of lung abscesses is necessary in the roughly 10% of patients in whom lesions do not respond to antibiotics. Resistance to antibiotic treatment is most common with large cavities and with infections that complicate obstructions.

When surgery is necessary, lobectomy is the most common procedure; segmental resection may suffice for small lesions (< 6 cm diameter cavity). Pneumonectomy may be necessary for multiple abscesses or for pulmonary gangrene unresponsive to drug therapy.

Last full review/revision February 2008 by John G. Bartlett, MD

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