eMedicine Specialties > Pulmonology > Infectious Lung Diseases

Lung Abscess

Nader Kamangar, MD, FACP, FCCP, FAASM,, Associate Professor of Clinical Medicine, Director of Hospitalist/Intensivist Program, Division of Pulmonary, Critical Care and Sleep Medicine, David Geffen School of Medicine at University of California Los Angeles; Associate Director, Combined Pulmonary and Critical Care Fellowship Program, Cedars-Sinai/Olive View-UCLA/West Los Angeles Veterans Affairs Medical Center
Curtis C Sather, MD, Fellow, Divison of Pulmonary/Critical Care Medicine, Cedars-Sinai Medical Center; Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital

Updated: Aug 19, 2009

Introduction

Background

Lung abscess is defined as necrosis of the pulmonary tissue and formation of cavities containing necrotic debris or fluid caused by microbial infection. The formation of multiple small (<2 cm) abscesses is occasionally referred to as necrotizing pneumonia or lung gangrene. Both lung abscess and necrotizing pneumonia are manifestations of a similar pathologic process. Failure to recognize and treat lung abscess is associated with poor clinical outcome.
 
In the 1920s, approximately one third of patients with lung abscess died; Dr David Smith postulated that aspiration of oral bacteria was the mechanism of infection. He observed that the bacteria found in the walls of the lung abscesses at autopsy resembled the bacteria noted in the gingival crevice. A typical lung abscess could be reproduced in animal models via an intratracheal inoculum containing, not 1, but 4 microbes, thought to be Fusobacterium nucleatum, Peptostreptococcus species, a fastidious gram-negative anaerobe, and, possibly, Prevotella melaninogenicus.
 
Lung abscess was a devastating disease in the preantibiotic era, when one third of the patients died, another one third recovered, and the remainder developed debilitating illnesses such as recurrent abscesses, chronic empyema, bronchiectasis, or other consequences of chronic pyogenic infections. In the early postantibiotic period, sulfonamides did not improve the outcome of patients with lung abscess until the penicillins and tetracyclines were available. Although resectional surgery was often considered a treatment option in the past, the role of surgery has greatly diminished over time because most patients with uncomplicated lung abscess eventually respond to prolonged antibiotic therapy.
 
Lung abscesses can be classified based on the duration and the likely etiology. Acute abscesses are less than 4-6 weeks old, whereas chronic abscesses are of longer duration. Primary abscess is infectious in origin, caused by aspiration or pneumonia in the healthy host; secondary abscess is caused by a preexisting condition (eg, obstruction), spread from an extrapulmonary site, bronchiectasis, and/or an immunocompromised state. Lung abscesses can be further characterized by the responsible pathogen, such as Staphylococcus lung abscess and anaerobic or Aspergillus lung abscess.

A thick-walled lung abscess.

Pathophysiology

Most frequently, the lung abscess arises as a complication of aspiration pneumonia caused by mouth anaerobes. The patients who develop lung abscess are predisposed to aspiration and commonly have periodontal disease. A bacterial inoculum from the gingival crevice reaches the lower airways, and infection is initiated because the bacteria are not cleared by the patient's host defense mechanism. This results in aspiration pneumonitis and progression to tissue necrosis 7-14 days later, resulting in formation of lung abscess.
 
Other mechanisms for lung abscess formation include bacteremia or tricuspid valve endocarditis, causing septic emboli (usually multiple) to the lung. Lemierre syndrome, an acute oropharyngeal infection followed by septic thrombophlebitis of the internal jugular vein, is a rare cause of lung abscesses. The oral anaerobe F necrophorum is the most common pathogen.
 
Microbiology
 
Because of the difficulty obtaining material uncontaminated by nonpathogenic bacteria colonizing the upper airway, lung abscesses rarely have a microbiologic diagnosis.
 
Published reports since the beginning of the antibiotic area have established that anaerobic bacteria are the most significant pathogens in lung abscess. In a study by Bartlett et al in 1974, 46% of patients with lung abscesses had only anaerobes isolated from sputum cultures, while 43% of patients had a mixture of anaerobes and aerobes.¹ The most common anaerobes are Peptostreptococcus species, Bacteroides species, Fusobacterium species, and microaerophilic streptococci.
 
Aerobic bacteria that may infrequently cause lung abscess include Staphylococcus aureus, Streptococcus pyogenes, Streptococcus pneumoniae (rarely), Klebsiella pneumoniae, Haemophilus influenzae, Actinomyces species, Nocardia species, and gram-negative bacilli.
 
Challenging current expert opinion, a study by Wang et al suggested that the bacteriologic characteristics of lung abscess have changed.² In a series of 90 patients with community-acquired lung abscess in Taiwan, anaerobes were recovered from just 28 patients (31%); the predominant bacterium was K pneumoniae, in 30 patients (33%). Another significant finding was that the rate of resistance of anaerobes and Streptococcus milleri to clindamycin and penicillin increased compared with previous reports.
 
Nonbacterial and atypical bacterial pathogens may also cause lung abscesses, usually in the immunocompromised host. These microorganisms include parasites (eg, Paragonimus and Entamoeba species), fungi (eg, Aspergillus, Cryptococcus, Histoplasma, Blastomyces, and Coccidioides species), and Mycobacterium species.

Frequency

United States

The frequency of lung abscess in the general population is not known.

Mortality/Morbidity

Most patients with primary lung abscess improve with antibiotics, with cure rates documented at 90-95%.
 
Host factors associated with a poor prognosis include advanced age, debilitation, malnutrition, human immunodeficiency virus infection or other forms of immunosuppression, malignancy, and duration of symptoms greater than 8 weeks.³ The mortality rate for patients with underlying immunocompromised status or bronchial obstruction who develop lung abscess may be as high as 75%.⁴
 
Aerobic organisms, frequently hospital acquired, are associated with poor outcomes. A retrospective study reported the overall mortality rate of lung abscesses caused by mixed gram-positive and gram-negative bacteria at approximately 20%.⁵

Sex

A male predominance for lung abscess is reported in published case series.

Age

Lung abscesses likely occur more commonly in elderly patients because of the increased incidence of periodontal disease and the increased prevalence of dysphagia and aspiration. However, a case series from an urban center with high prevalence of alcoholism reported a mean age of 41 years.⁶

Clinical

History

Symptoms depend on whether the abscess is caused by anaerobic or other bacterial infection.

• Anaerobic infection in lung abscess
  • Patients often present with indolent symptoms that evolve over a period of weeks to months.
  • The usual symptoms are fever, cough with sputum production, night sweats, anorexia, and weight loss.
  • The expectorated sputum characteristically is foul smelling and bad tasting.
  • Patients may develop hemoptysis or pleurisy
• Other pathogens in lung abscess
  • These patients generally present with conditions that are more emergent in nature and are usually treated while they have bacterial pneumonia.
  • Cavitation occurs subsequently as parenchymal necrosis ensues.
  • Abscesses from fungi, Nocardia species, and Mycobacteria species tend to have an indolent course and gradually progressive symptoms.

Physical

The findings on physical examination of a patient with lung abscess are variable. Physical findings may be secondary to associated conditions such as underlying pneumonia or pleural effusion. The physical examination findings may also vary depending on the organisms involved, the severity and extent of the disease, and the patient's health status and comorbidities.

• Patients with lung abscesses may have low-grade fever in anaerobic infections and temperatures higher than 38.5°C in other infections.
• Generally, patients with in lung abscess have evidence of gingival disease.
• Clinical findings of concomitant consolidation may be present (eg, decreased breath sounds, dullness to percussion, bronchial breath sounds, course inspiratory crackles).
• The amphoric or cavernous breath sounds are only rarely elicited in modern practice.
• Evidence of pleural friction rub and signs of associated pleural effusion, empyema, and pyopneumothorax may be present. Signs include dullness to percussion, contralateral shift of the mediastinum, and absent breath sounds over the effusion.
• Digital clubbing may develop rapidly.

Causes

The bacterial infection may reach the lungs in several ways. The most common is aspiration of oropharyngeal contents.

• Patients at the highest risk for developing lung abscess have the following risk factors:
  • Periodontal disease
  • Seizure disorder
  • Alcohol abuse
  • Dysphagia
• Other patients at high risk for developing lung abscess include individuals with an inability to protect their airways from massive aspiration because of a diminished gag or cough reflex, caused by a state of impaired consciousness (eg, from alcohol or other CNS depressants, general anesthesia, or encephalopathy).
• Infrequently, the following infectious etiologies of pneumonia may progress to parenchymal necrosis and lung abscess formation:
  • Pseudomonas aeruginosa
  • K pneumoniae
  • S aureus (may result in multiple abscesses)
  • Streptococcus pneumoniae
  • Nocardia species
  • Fungal species
• An abscess may develop as an infectious complication of a preexisting bulla or lung cyst.
• An abscess may develop secondary to carcinoma of the bronchus; the bronchial obstruction causes postobstructive pneumonia, which may lead to abscess formation.

Differential Diagnoses

Other Problems to Be Considered

Cavitating lung cancer
Localized empyema
Infected bulla containing a fluid level
Infected congenital pulmonary lesion, such as bronchogenic cyst or sequestration
Pulmonary hematoma
Cavitating pneumoconiosis
Hiatus hernia
Lung parasites (eg, hydatid cyst, Paragonimus infection)
Actinomycosis
Wegener granulomatosis and other vasculitides
Cavitating lung infarcts
Cavitating sarcoidosis

Workup

Laboratory Studies

• A complete white blood cell count with differential may reveal leukocytosis and a left shift.
• Obtain sputum for Gram stain, culture, and sensitivity.
• If tuberculosis is suspected, acid-fast bacilli stain and mycobacterial culture is requested.
• Blood culture may be helpful in establishing the etiology.
• Obtain sputum for ova and parasite whenever a parasitic cause for lung abscess is suspected.

Imaging Studies

• Chest radiography⁷
  • A typical chest radiographic appearance of a lung abscess is an irregularly shaped cavity with an air-fluid level inside. Lung abscesses as a result of aspiration most frequently occur in the posterior segments of the upper lobes or the superior segments of the lower lobes.
  • The wall thickness of a lung abscess progresses from thick to thin and from ill-defined to well-circumscribed as the surrounding lung infection resolves. The cavity wall can be smooth or ragged but is less commonly nodular, which raises the possibility of cavitating carcinoma.
  • The extent of the air-fluid level within a lung abscess is often the same in posteroanterior or lateral views. The abscess may extend to the pleural surface, in which case it forms acute angles with the pleural surface.
  • Anaerobic infection may be suggested by cavitation within a dense segmental consolidation in the dependent lung zones.
  • Lung infection with a virulent organism results in more widespread tissue necrosis, which facilitates progression of underlying infection to pulmonary gangrene.
  • Up to one third of lung abscesses may be accompanied by an empyema.

Pneumococcal pneumonia complicated by lung necrosis and abscess formation.

A lateral chest radiograph shows air-fluid level characteristic of lung abscess.

A 54-year-old patient developed cough with foul-smelling sputum production. A chest radiograph shows lung abscess in the left lower lobe, superior segment.

A 42-year-old man developed fever and production of foul-smelling sputum. He had a history of heavy alcohol use, and poor dentition was obvious on physical examination. Chest radiograph shows lung abscess in the posterior segment of the right upper lobe.

Chest radiograph of a patient who had foul-smelling and bad-tasting sputum, an almost diagnostic feature of anaerobic lung abscess.

• Computed tomography^7,8
  • CT scanning of the lungs may help visualize the anatomy better than chest radiography. CT scanning is very useful in the identification of concomitant empyema or lung infarction.
  • On CT scans, an abscess often is a rounded radiolucent lesion with a thick wall and ill-defined irregular margins.
  • The vessels and bronchi are not displaced by the lesion, as they are by an empyema.
  • The lung abscess is located within the parenchyma compared with loculated empyema, which may be difficult to distinguish on chest radiographs.
  • The lesion forms acute angles with the pleural surface chest wall.

A 42-year-old man developed fever and production of foul-smelling sputum. He had a history of heavy alcohol use, and poor dentition was obvious on physical examination. Lung abscess in the posterior segment of the right upper lobe was demonstrated on chest radiograph (see Image 6). CT scan shows a thin-walled cavity with surrounding consolidation.

•  Ultrasonography
  • Peripheral lung abscesses with pleural contact or included inside a lung consolidation are detectable using lung ultrasonography at the bedside.
  • Lung abscess appears as a rounded hypoechoic lesion with an outer margin.
  • If a cavity is present, additional nondependent hyperechoic signs are generated by the gas-tissue interface.⁹

Procedures

Diagnostic material uncontaminated by bacteria colonizing the upper airway may be obtained for anaerobic culture from the following:

• Blood culture
• Pleural fluid (if empyema present)
• Transtracheal aspirate
• Transthoracic pulmonary aspirate
• Surgical specimens
• Fiberoptic bronchoscopy with protected brush  
• Bronchoalveolar lavage with quantitative cultures

Histologic Findings

Lung abscesses begin as small zones of necrosis developing within the consolidated segments in pneumonia. These areas may coalesce to form single or multiple areas of suppuration, which are referred to as lung abscesses. If antibiotics interrupt the natural history at an early stage, the healing results in no residual changes. When the progressive inflammation erodes into the adjacent bronchi, the contents of the abscess are expectorated as malodorous sputum. Subsequently, fibrosis occurs, which causes a dense scar and separates the abscess. The abscess may still occur, and spillage of pus into the bronchial tree may disseminate the infection.

Histology of a lung abscess shows dense inflammatory reaction (low power).

Histology of a lung abscess shows dense inflammatory reaction (high power).

Treatment

Medical Care

Treatment of lung abscess is guided by the available microbiology and knowledge of the underlying or associated conditions. No treatment recommendations have been issued by major societies specifically for lung abscess; however, a guideline summary from the Infectious Diseases Society of America, Practice guidelines for outpatient parenteral antimicrobial therapy, is available.¹² Some clinical trials referred to below have included patients with aspiration pneumonia with or without lung abscess.

Antibiotic therapy

• Standard treatment of an anaerobic lung infection is clindamycin (600 mg IV q8h followed by 150-300 mg PO qid). This regimen has been shown to be superior over parenteral penicillin in published trials. Several anaerobes may produce beta-lactamase (eg, various species of Bacteroides and Fusobacterium) and therefore develop resistance to penicillin.¹³
• Although metronidazole is an effective drug against anaerobic bacteria, the experience with metronidazole in treating lung abscess has been rather disappointing because these infections are generally polymicrobial. A failure rate of 50% has been reported.^14,15
• In hospitalized patients who have aspirated and developed a lung abscess, antibiotic therapy should include coverage against S aureus and Enterobacter and Pseudomonas species.
• Ampicillin plus sulbactam is well tolerated and as effective as clindamycin with or without a cephalosporin in the treatment of aspiration pneumonia and lung abscess.¹⁶
• Moxifloxacin is clinically effective and as safe as ampicillin plus sulbactam in the treatment of aspiration pneumonia and lung abscess.¹⁷  

• Although the duration of therapy is not well established, most clinicians generally prescribe antibiotic therapy for 4-6 weeks.
• Expert opinion suggests that antibiotic treatment should be continued until the chest radiograph has shown either the resolution of lung abscess or the presence of a small stable lesion.
• The rationale for extended treatment maintains that risk of relapse exists with a shorter antibiotic regimen.

Response to therapy

• Patients with lung abscesses usually show clinical improvement, with improvement of fever, within 3-4 days after initiating the antibiotic therapy. Defervescence is expected in 7-10 days. Persistent fever beyond this time indicates therapeutic failure, and these patients should undergo further diagnostic studies to determine the cause of failure.
• Considerations in patients with poor response to antibiotic therapy include bronchial obstruction with a foreign body or neoplasm or infection with a resistant bacteria, mycobacteria, or fungi.
• Large cavity size (ie, > 6 cm in diameter) usually requires prolonged therapy. Because empyema with an air-fluid level could be mistaken for parenchymal abscess, a CT scan may be used to differentiate this process from lung abscess.
• A nonbacterial cause of cavitary lung disease may be present, such as lung infarction, cavitating neoplasm, and vasculitis. The infection of a preexisting sequestration, cyst, or bulla may be the cause of delayed response to antibiotics.

Surgical Care

Surgery is very rarely required for patients with uncomplicated lung abscesses. The usual indications for surgery are failure to respond to medical management, suspected neoplasm, or congenital lung malformation. The surgical procedure performed is either lobectomy or pneumonectomy.

When conventional therapy fails, either percutaneous catheter drainage or surgical resection is usually considered. Endoscopic lung abscess drainage is considered if an airway connection to the cavity can be demonstrated. Success of this treatment represents an additional option other than percutaneous catheter drainage or surgical resection.¹⁸

Consultations

Consulting a pulmonary medicine or infectious diseases specialist is often helpful in workup and follow-up of patients with lung abscess.

Medication

Most abscesses develop secondary to aspiration and are caused by anaerobes. A history suggestive of community acquired pneumonia or a history of development of abscess in a hospitalized patient is important in deciding the appropriate antibiotic coverage.

Antibiotics

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens suspected in this clinical setting.

Clindamycin (Cleocin)

Lincosamides are used for treatment of serious skin and soft tissue staphylococcal infections. Also effective against aerobic and anaerobic streptococci, except enterococci. Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

Dosing

Adult

600 mg IV q8h, followed by 150-300 mg PO qid

Pediatric

25-40 mg/kg/d IV divided tid/qid

Interactions

Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium; erythromycin may antagonize effects of clindamycin; antidiarrheals may delay absorption

Contraindications

Documented hypersensitivity; regional enteritis; ulcerative colitis; hepatic impairment; antibiotic-associated colitis

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in severe hepatic dysfunction; no adjustment necessary in renal insufficiency; associated with severe and possibly fatal colitis

Cefoxitin (Mefoxin)

Second-generation cephalosporin indicated for gram-positive cocci and gram-negative rod infections. Infections caused by cephalosporin- or penicillin-resistant gram-negative bacteria may respond to cefoxitin.

Dosing

Adult

2 g IV q6-8h

Pediatric

80-160 mg/kg/d IV divided q4-6h

Interactions

Probenecid may increase effects of cefoxitin; coadministration with aminoglycosides or furosemide may increase nephrotoxicity (closely monitor renal function)

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Bacterial or fungal overgrowth of nonsusceptible organisms may occur with prolonged use or repeated treatment; caution in patients with previously diagnosed colitis

Penicillin G (Pfizerpen)

Interferes with synthesis of cell wall mucopeptide during active multiplication, resulting in bactericidal activity against susceptible microorganisms.

Dosing

Adult

2 million U IV q4h

Pediatric

150,000 U/kg/d IV divided q4h

Interactions

Probenecid can increase effects of penicillin; coadministration of tetracyclines can decrease effects of penicillin

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in impaired renal function; traditional agent to treat lung abscess, but spectrum of activity is narrow

Metronidazole (Flagyl)

Imidazole ring-based antibiotic active against various anaerobic bacteria and protozoa. Used in combination with other antimicrobial agents (except for Clostridium difficile enterocolitis). Not standard practice to use metronidazole alone because some anaerobic cocci and most microaerophilic streptococci are resistant.

Dosing

Adult

Loading dose: 15 mg/kg IV (or 1 g for 70-kg adult) over 1 h
Maintenance dose: 6 h following loading dose, infuse 7.5 mg/kg IV (or 500 mg for 70-kg adult) over 1 h q6-8h; not to exceed 4 g/d

Pediatric

Administer as in adults using body weight

Interactions

May increase toxicity of anticoagulants, lithium, and phenytoin; cimetidine may increase toxicity of metronidazole; disulfiram reaction may occur with orally ingested ethanol

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in hepatic disease; monitor for seizures and development of peripheral neuropathy

Follow-up

Further Inpatient Care

• For the following reasons, inpatient care is advisable in patients with lung abscess:
  • Evaluation and management of patient's respiratory status
  • Administration of intravenous antibiotics
  • Drainage of the abscess or empyema as needed

Further Outpatient Care

• In patients who have small lung abscess, who are not clinically ill, and who are reliable, outpatient care may be considered after obtaining appropriate diagnostic studies such as sputum culture, blood culture, and blood work.
• Following initial intravenous antibiotic therapy, the patient may be treated on an outpatient basis for completion of prolonged therapy, which is often required for cure.

Deterrence/Prevention

• Prevention of aspiration is important to minimize the risk of lung abscess. Early intubation in patients who have diminished ability to protect the airway from massive aspiration (cough, gag reflexes), should be considered.
• Positioning the supine patient at a 30° reclined angle minimizes the risk of aspiration. Vomiting patients should be placed on their sides.
• Improving oral hygiene and dental care in elderly and debilitated patients may decrease the risk of anaerobic lung abscess.

Complications

• Complications of pulmonary abscess
  • Rupture into pleural space causing empyema
  • Pleural fibrosis
  • Trapped lung
  • Respiratory failure
  • Bronchopleural fistula
  • Pleural cutaneous fistula
• In a patient with coexisting empyema and lung abscess, draining the empyema while continuing prolonged antibiotic therapy is often necessary.

Prognosis

• The prognosis for lung abscess following antibiotic treatment is generally favorable. Over 90% of lung abscesses are cured with medical management alone, unless caused by bronchial obstruction secondary to carcinoma.

Patient Education

• For excellent patient education resources, visit eMedicine's Infections Center, Lung and Airway Center, Pneumonia Center, and Procedures Center. Also, see eMedicine's patient education articles Bacterial Pneumonia, Antibiotics, and Bronchoscopy.

Miscellaneous

Medicolegal Pitfalls

• A lung abscess may be asymptomatic in a small proportion of patients in the early stages; a chest radiograph may be helpful.
• In any patient who is producing foul-smelling or bad-tasting sputum, suspect a lung abscess.
• A shorter course of antibiotics may increase risk of a relapse. Therefore, antibiotic therapy for anaerobic lung abscess is prolonged, often extending up to 6-8 weeks.
• A lack of response to antibiotic therapy should lead to consideration of a cavitating lung neoplasm, lung infarction, or Wegener granulomatosis.

Multimedia

Media file 1: Histology of a lung abscess shows dense inflammatory reaction (low power).

Media file 2: A thick-walled lung abscess.

Media file 3: Pneumococcal pneumonia complicated by lung necrosis and abscess formation.

Media file 4: A lateral chest radiograph shows air-fluid level characteristic of lung abscess.

Media file 5: A 54-year-old patient developed cough with foul-smelling sputum production. A chest radiograph shows lung abscess in the left lower lobe, superior segment.

Media file 6: A 42-year-old man developed fever and production of foul-smelling sputum. He had a history of heavy alcohol use, and poor dentition was obvious on physical examination. Chest radiograph shows lung abscess in the posterior segment of the right upper lobe.

Media file 7: A 42-year-old man developed fever and production of foul-smelling sputum. He had a history of heavy alcohol use, and poor dentition was obvious on physical examination. Lung abscess in the posterior segment of the right upper lobe was demonstrated on chest radiograph (see Image 6). CT scan shows a thin-walled cavity with surrounding consolidation.

Media file 8: Chest radiograph of a patient who had foul-smelling and bad-tasting sputum, an almost diagnostic feature of anaerobic lung abscess.

Media file 9: Histology of a lung abscess shows dense inflammatory reaction (high power).

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Keywords

lung abscess, lung abscesses, necrotizing pneumonia, lung gangrene, necrosis of pulmonary tissue, lung cavities, aspiration pneumonia, periodontal disease, bacteremia, tricuspid valve endocarditis

Contributor Information and Disclosures

Author

Nader Kamangar, MD, FACP, FCCP, FAASM,, Associate Professor of Clinical Medicine, Director of Hospitalist/Intensivist Program, Division of Pulmonary, Critical Care and Sleep Medicine, David Geffen School of Medicine at University of California Los Angeles; Associate Director, Combined Pulmonary and Critical Care Fellowship Program, Cedars-Sinai/Olive View-UCLA/West Los Angeles Veterans Affairs Medical Center
Nader Kamangar, MD, FACP, FCCP, FAASM, is a member of the following medical societies: American Academy of Sleep Medicine, American Association of Bronchology, American College of Chest Physicians, American College of Physicians, American Lung Association, American Medical Association, American Thoracic Society, California Thoracic Society, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Curtis C Sather, MD, Fellow, Divison of Pulmonary/Critical Care Medicine, Cedars-Sinai Medical Center
Curtis C Sather, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Medical Association, and American Thoracic Society
Disclosure: Nothing to disclose.

Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital
Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Stephen P Peters, MD, PhD, Professor, Department of Medicine, Wake Forest University
Stephen P Peters, MD, PhD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American Association of Immunologists, American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Thoracic Society, and Sigma Xi
Disclosure: See below for list of all activities None None

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

,, Kathy Roarty Placeholder
Disclosure: Nothing to disclose.

CME Editor

Timothy D Rice, MD, Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, Saint Louis University School of Medicine
Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians
Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD, Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild Pulmonary Disease Institute, Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center; Professor of Medicine, David Geffen School of Medicine at UCLA
Zab Mosenifar, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, and American Thoracic Society
Disclosure: Nothing to disclose.

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