Lung abscess in adults

INTRODUCTION — A lung abscess is circumscribed, purulent infection contained within the lung parenchyma. Most lung abscesses arise as a complication of aspiration. As such, they are typically polymicrobial and indolent in onset. Less commonly, lung abscesses complicate acute monomicrobial infections with pyogenic bacteria (eg, Staphylococcus aureus, Klebsiella pneumoniae, and Pseudomonas aeruginosa). Lung abscesses can also result from secondary infection of pre-existing lung cavities, bronchial obstruction, septic embolization, or direct extension from local infections such as empyema.

The clinical features, pathogenesis, evaluation, and treatment of lung abscesses will be reviewed here. Aspiration pneumonia, which may precede the development of a lung abscess, is discussed separately. (See "Aspiration pneumonia in adults".)

DEFINITIONS — Lung abscess is defined as a circumscribed area of pus or necrosis in the pulmonary parenchyma caused by microbial infection. Lung abscesses can be classified as primary or secondary [1].

●Primary lung abscesses result from direct infection of the pulmonary parenchyma in an otherwise healthy person. Most result from aspiration of oral or gastric contents. Primary lung abscesses can also arise within an area of pneumonia caused by necrotizing organisms (eg, S. aureus).

●Secondary lung abscesses occur when there is a predisposing condition such as bronchial obstruction (eg, foreign body, neoplasm), hematogenous spread (eg, right-sided endocarditis), thoracic surgery, or impaired host defenses.

The terms "necrotizing pneumonia" or "lung gangrene" are used to describe pneumonia that is complicated by necrosis and numerous small abscesses [2].

PATHOGENESIS — Most lung abscesses arise as a complication of aspiration that leads to one or more localized areas of pneumonia, followed by necrosis and cavitation. Other mechanisms include embolization (blood–borne), direct extension, endobronchial obstruction, or infection of lung cysts.

●Aspiration – Lung abscess is classically caused by aspiration of oropharyngeal secretions especially in patients with recurrent aspiration who have dental, gingival, or periodontal infection or paranasal sinusitis. Anaerobes from the gingival crevice or sinuses reach the lower airways [3]. Impaired swallowing and enteral feeding while supine are risk factors. Infection is initiated either because the secretions are not cleared due to suppressed consciousness, because the inoculum size is large, or due to impaired host defenses. Pneumonitis arises first and then progresses to tissue necrosis after 7 to 14 days. Risk factors for aspiration are discussed separately. (See "Aspiration pneumonia in adults", section on 'Predisposing conditions'.)

●Hematogenous spread – Lung abscesses can occur as a consequence of septic embolization during bacteremia (eg, tricuspid valve endocarditis, intravascular catheters, intravenous (IV) drug use, or Lemierre syndrome [ie, jugular vein suppurative thrombophlebitis]). (See "Right-sided native valve infective endocarditis" and "Catheter-related septic thrombophlebitis" and "Lemierre syndrome: Septic thrombophlebitis of the internal jugular vein", section on 'Complications'.)

●Direct extension – A lung abscess may develop by direct extension of an empyema, subphrenic, or mediastinal abscess or a tracheo- or broncho-esophageal fistula. (See "Bronchopleural fistula in adults" and "Tracheo- and broncho-esophageal fistulas in adults".)

●Bronchial obstruction – Endobronchial obstruction from a bronchogenic or mediastinal mass (eg, aneurysm, lymphadenopathy, tumor), bronchial stenosis, or from an inhaled foreign body may result in postobstructive pneumonia that progresses to abscess formation presumably due to impaired drainage of local pulmonary secretions [4-6]. (See "Clinical presentation, diagnostic evaluation, and management of malignant central airway obstruction in adults".)

●Superinfection or spread of airway infection – Lung abscess may develop as a superinfection of pulmonary infarcts, congenital malformations, or lung contusion. Flares of bronchiectasis can lead to parenchymal infection that evolves into a lung abscess in a minority of patients [7,8]. The mechanism is likely multifactorial and includes poor drainage and impaired clearance of microbiologic flora from the lower airways.

MICROBIOLOGY — The microbiology of lung abscesses varies with the route of infection.

●Aspiration — Lung abscesses that result from aspiration are typically polymicrobial, reflecting oral and gingival flora. The most commonly isolated pathogens are microaerophilic Streptococci and anaerobes. The most common anaerobes include Peptostreptococcus, Prevotella, Bacteroides (usually not B. fragilis), and Fusobacterium [9-18]. Common streptococci include Streptococcus anginosus and other members of the Streptococcus milleri group and oral streptococci such as Streptococcus mitis. Gram-negative organisms may be present in up to one-third of cases [16,19,20]. These organisms may be a part of a polymicrobial infection or may be the sole pathogens. (See "Infections due to the Streptococcus anginosus (Streptococcus milleri) group".)

●Pneumonia caused by pyogenic bacteria — Aerobic bacteria that can cause monomicrobial lung abscess include Staphylococcus aureus (eg, in a patient with influenza) [21,22], Klebsiella pneumoniae (eg, in a patient with structural lung disease) [16,17,23,24], other Gram-negative bacilli (eg, Pseudomonas aeruginosa) [25], Streptococcus pyogenes [26], Burkholderia pseudomallei [27,28], Haemophilus influenzae type b, Legionella [29,30], Nocardia, and Actinomyces. There have been occasional case reports of lung abscess caused by Streptococcus pneumoniae, although superinfection by anaerobic bacteria may be the cause in such cases [31]. (See "Clinical manifestations of Staphylococcus aureus infection in adults", section on 'Pulmonary infection' and "Virulence determinants of community-acquired methicillin-resistant Staphylococcus aureus" and "Clinical features, diagnosis, and treatment of Klebsiella pneumoniae infection", section on 'Lung abscess' and "Nocardia infections: Epidemiology, clinical manifestations, and diagnosis", section on 'Lungs' and "Clinical manifestations and diagnosis of Legionella infection", section on 'Clinical features'.)

The bacteriology of lung abscess may be subject to geographic variability. For example, in a retrospective evaluation of 90 Taiwanese adults with lung abscess, Gram-negative bacilli (especially K. pneumoniae) accounted for 36 percent of isolates (see "Clinical features, diagnosis, and treatment of Klebsiella pneumoniae infection") [16]. Other organisms included anaerobes (34 percent), Gram-positive cocci (26 percent), and Gram-positive bacilli (4 percent).

●Nonbacterial pathogens — Selected nonbacterial pathogens can generate or colonize cavitary lesions and radiographically resemble lung abscess. Culprit pathogens include many fungi (eg, Aspergillus spp, Cryptococcus spp, Histoplasma capsulatum, Blastomyces dermatitidis, Coccidioides spp, the agents of mucormycosis), Mycobacterium tuberculosis, nontuberculous mycobacteria (eg, M. avium, M. kansasii, M. abscessus), and parasites (eg, Entamoeba histolytica, Paragonimus westermani, Echinococcus [hydatid cyst]). Pyogenic bacteria can also superinfect cavities caused by mycobacterial, fungal, and parasitic infections, leading to accumulation of liquid in an otherwise empty cavity. (See "Epidemiology and clinical manifestations of invasive aspergillosis", section on 'Pulmonary aspergillosis' and "Cryptococcus neoformans infection outside the central nervous system" and "Pathogenesis and clinical features of pulmonary histoplasmosis" and "Clinical manifestations and diagnosis of blastomycosis", section on 'Pulmonary involvement' and "Primary pulmonary coccidioidal infection", section on 'Clinical manifestations' and "Mucormycosis (zygomycosis)", section on 'Pulmonary mucormycosis' and "Pulmonary tuberculosis: Clinical manifestations and complications" and "Overview of nontuberculous mycobacterial infections" and "Nocardia infections: Epidemiology, clinical manifestations, and diagnosis", section on 'Lungs' and "Extraintestinal Entamoeba histolytica amebiasis", section on 'Pleuropulmonary infection' and "Paragonimiasis", section on 'Pulmonary paragonimiasis'.)

●Opportunistic infections — In the immunocompromised host, the most common causes of lung abscess are Pseudomonas aeruginosa and other aerobic Gram-negative bacilli, Nocardia spp, and fungi (Aspergillus and Cryptococcus spp). A number of other organisms can occasionally cause lung abscess in immunocompromised hosts, such as the agents of mucormycosis, Rhodococcus equi, Mycobacterium tuberculosis, and nontuberculous mycobacteria (table 1). (See "Pseudomonas aeruginosa pneumonia" and "Nocardia infections: Epidemiology, clinical manifestations, and diagnosis" and "Epidemiology and clinical manifestations of invasive aspergillosis" and "Cryptococcus neoformans infection outside the central nervous system" and "Mucormycosis (zygomycosis)" and "Clinical features, diagnosis, therapy, and prevention of Rhodococcus equi infections" and "Pulmonary tuberculosis: Clinical manifestations and complications" and "Overview of nontuberculous mycobacterial infections".)

An overview of pulmonary infections in immunocompromised patients is presented separately. (See "Epidemiology of pulmonary infections in immunocompromised patients".)

CLINICAL FEATURES — The clinical features of a lung abscess are typically nonspecific and mimic those of pneumonia, albeit with a more subacute presentation. It is typically the identification of one or more cavities filled with fluid or with an air-fluid interface on chest imaging that raises the suspicion for lung abscess.

Symptoms and signs — The presenting signs and symptoms include fever and chills (80 percent), productive cough (often putrid, sour-tasting; 55 to 90 percent), dyspnea (10 percent), chest pain when the pleural space is involved (20 to 35 percent), and hemoptysis (10 percent) [17,24,32-34]. Since abscesses of the lung are usually chronic, unlike pneumonia, most patients have symptoms that evolve over weeks to months. Systemic symptoms such as night sweats, weight loss, anorexia, and fatigue may also be present [12,13,35].

More rapid presentations with fulminant disease (eg, shock) may also occur with acute abscesses (eg, Staphylococcus aureus, Klebsiella pneumoniae), particularly in those who are immunocompromised, and those with septic emboli.

Typical findings on physical examination are fever, gingival crevice disease (eg, gingivitis, dental caries), associated conditions that reduce consciousness or cause dysphagia (eg, facial or tongue weakness, bulbar speech, neurologic disease with deconditioning, alcohol intoxication). Chest auscultation may be normal or may demonstrate egophony or increased vocal fremitus, reflecting consolidation, particularly if the abscess is large and subpleural.

Chest radiograph — Lung abscesses are often visible on the chest radiograph, manifest as a fluid-filled space, typically with an air-fluid interface, within an area of consolidation, mass, or nodule (image 1 and image 2), although more subtle forms of cavitation may only be appreciated on computed tomography of the chest (see 'Chest computed tomography' below). Most often, lung abscesses are unilateral [32]. Because most cases are due to aspiration, abscesses are frequently located in a segment of the lung that is dependent in the recumbent position (eg, the superior segment of a lower lobe or a posterior segment of the upper lobes), or in the right middle lobe if aspiration occurred in the upright or prone position [32].

Lung abscesses caused by hematological dissemination may be distributed randomly or predominately in the lower lobes.

DIAGNOSTIC EVALUATION — A lung abscess should be suspected in a patient with clinical features of an indolent pulmonary infection (eg, fever, sweats, dyspnea, putrid or bloody sputum, weight loss, leukocytosis) and a cavitating or fluid-filled lung mass on imaging (see 'Clinical features' above). The focus of investigation is the identification of the probable pathogen and reasonable exclusion of other serious pathologies, particularly malignancy. After obtaining initial samples of blood and sputum, empiric antibiotic therapy should be initiated; antibiotic choices can be revised based on culture results. (See 'Initial empiric antibiotics' below.)

Clinical assessment

●The medical history should include questions about risk factors, such as dental pain or procedures, episodes of altered consciousness, neurologic disease, esophageal disease, alcohol or injection drug use, symptoms of extrapulmonary infection, history of immune deficiency or bronchiectasis, and prior similar episodes. Patients should also be asked about the timing of symptom onset, the presence of associated symptoms (eg, pharyngeal or neck pain, difficulty swallowing or coughing after swallowing, weight loss, night sweats), and smoking history since these may provide clues to the underlying etiology or organisms.

●Physical examination should include a thorough examination of the oral cavity for halitosis, gingivitis, tonsillar enlargement, caries, loose, or tender teeth, and neck masses or tenderness. The patient should be asked to swallow a few sips of water to screen for dysphagia. (See "Complications of stroke: An overview", section on 'Dysphagia'.)

●Routine laboratory tests such as complete and differential blood count, chemistries, and liver and kidney function tests should be obtained. Laboratory findings are generally non-specific and include leukocytosis and anemia of chronic disease.

●For patients who are immunocompromised, the potential causes of infection are broader and additional testing is often needed. (See "Epidemiology of pulmonary infections in immunocompromised patients" and "Approach to the immunocompromised patient with fever and pulmonary infiltrates".)

●Patients with concomitant skin, nasal, kidney, or neurologic disease that suggests granulomatosis with polyangiitis should be tested for antineutrophil cytoplasmic antibodies (ANCA). (See 'Differential diagnosis' below and "Granulomatosis with polyangiitis and microscopic polyangiitis: Respiratory tract involvement".)

Microbiologic testing — All patients should have two sets of blood cultures for both aerobic and anaerobic culture. Additional cultures from any suspected source are also appropriate (eg, intravascular catheter or wound). Sputum should be obtained for Gram stain and culture, ideally before antibiotics are started; however, antimicrobial therapy should not be withheld for those with signs of sepsis or septic shock. For patients who do not expectorate sputum, bronchoscopic sampling and/or percutaneous needle aspiration or (rarely) biopsy may be indicated. (See 'Additional testing' below.)

A micro-organism present on Gram stain and abundant in culture is often a pathogen. However, care must be exercised in interpreting the results, particularly when antimicrobials have already been started, since sputum samples can yield contaminants from upper airway flora that do not need to be treated (eg, Corynebacterium spp) and may not reveal the presence of anaerobes that do need to be treated [36]. Regardless of culture results, a putrid odor of expectorated sputum suggests an anaerobic infection and should be treated with an agent that includes activity against anaerobes. (See "Sputum cultures for the evaluation of bacterial pneumonia".)

Despite obtaining respiratory cultures, up to 50 percent of patients do not have a positive culture and so antimicrobial therapy is empiric [17,18].

As bacterial infection can complicate mycobacterial cavities leading to an air-fluid interface, acid fast stains and mycobacterial cultures of sputum are prudent, especially if the cavity walls are thin or the patient has risk factors for M. tuberculosis. (See "Diagnosis of pulmonary tuberculosis in adults".)

Chest computed tomography — When a lung abscess is suspected, chest computed tomography (CT) should be performed. CT provides more precise anatomic definition than chest radiography (image 1 and image 2) and can identify other abscesses and thoracic lesions (eg, associated malignancy, lymphadenopathy, bullae) not clearly delineated on the chest radiograph [1,35,37,38]. (See 'Chest radiograph' above.)

CT findings of acute lung abscess include an area of cavitation surrounded by consolidation. The necrotic region tends to be irregular in shape. The wall of an acute abscess is often thick but can vary widely; the cavity wall typically becomes thin and uniform as the abscess heals. Air fluid levels within the abscess are common.  

A CT can also distinguish between a parenchymal lesion and a pleural collection (eg, parapneumonic effusion or empyema), which are managed very differently (image 3) and determine whether the abscess is due to an infected cyst or bulla, underlying congenital lesion (eg, infected sequestration), airway obstruction (eg, tumor, inhaled foreign body), or sub-diaphragmatic or pleural infection. Last, if surgery is indicated, CT facilitates decision-making regarding resection. (See 'Differential diagnosis' below and "Imaging of pleural effusions in adults", section on 'Empyema' and 'Surgical intervention' below.)

Differentiating between peripheral lung abscesses and empyemas can occasionally be difficult [39]. Abscesses tend to be more irregular in shape, spherical, and cavitated whereas empyemas tend to be better defined, elliptical, homogeneous, and have a smooth and uniform wall. Empyema may displace the blood vessels leading from the hilum to the periphery whereas abscesses typically do not.

Additional testing — Additional testing may be warranted for patients who are unable to produce sputum, have an atypical presentation (eg, suspected cancer, noninfectious granulomatous disease), are immunocompromised, or do not respond to empiric antibiotics. As an example, bronchoscopy may be pursued more quickly in patients who are unable to raise sputum or have sputum that is not putrid and those who are at increased risk for opportunistic organisms due to immune deficiency or underlying lung disease (table 1), as early diagnosis and specific therapy of opportunistic infections are the cornerstone of successful management in such patients.

Bronchoscopy — Flexible bronchoscopy is not routinely needed but is reserved for patients without a microbiologic diagnosis after noninvasive testing (sputum and blood cultures) and those with atypical presentations, uncertain diagnosis, or immunocompromised state. (See 'Additional testing' above.)

When performing bronchoscopy, the clinician should evaluate the airways in the areas of lung abscesses for endobronchial stenosis, foreign bodies, and lesions suspicious for malignancy that may be responsible for or mimic lung abscess. Samples of secretions observed in the affected region of the lung can be aspirated directly or by gentle washing of the area. However, caution is required as aggressive suctioning and sampling, including brushing, bronchoalveolar lavage, and transbronchial biopsy of the cavity, can cause sudden spillage of the abscess contents and acute respiratory distress syndrome [40].

Samples should be sent for cytology, routine Gram stain, aerobic culture and anaerobic culture, and special stains for Nocardia, Actinomyces, fungi, Pneumocystis, mycobacteria, and antigen testing for galactomannan. Visible airway lesions should be biopsied or brushed per usual practice. Further details on bronchoscopy are provided separately. (See "Flexible bronchoscopy in adults: Overview" and "Flexible bronchoscopy in adults: Indications and contraindications" and "Flexible bronchoscopy in adults: Preparation, procedural technique, and complications".)

Obtaining samples using a protected specimen brush and subjecting them to quantitative cultures may reduce the chances of oral contamination and provide a better idea of the degree of growth; however, this approach is inconsistently available, costly, and may still be of low yield for anaerobic pathogens.

Other

●Transthoracic needle aspiration or biopsy – Transthoracic needle aspiration of the abscess or needle biopsy of the abscess wall under ultrasound, fluoroscopic, or CT guidance may be indicated for microbiologic sampling in rare patients who fail to improve with empiric antibiotic therapy and in whom sputum cultures and bronchoscopy are not revealing [41,42]. Careful review of the CT scan is needed to ensure that the suspected abscess is not an infected bulla, since the risk of pneumothorax with needle aspiration may be high. Pneumothorax and pleural seeding appear less likely to occur if the abscess abuts the pleura and the needle or catheter can be passed through an area of pleural thickening into the cavity. Transthoracic drainage of lung abscess is described below. (See 'Needle or catheter drainage' below.)

●Echocardiography – For patients with multiple lung abscesses, transthoracic echocardiography is advised to assess for right-sided valve infective endocarditis [43-46]. If transthoracic echocardiography is negative when the suspicion for endocarditis is high, a transesophageal echocardiogram should be performed. (See "Right-sided native valve infective endocarditis", section on 'Cardiac imaging'.)

●Thoracentesis – If pleural fluid is present on the chest radiograph, a thoracentesis is performed to obtain a sample for microbiologic testing and to exclude empyema (fluid appearance, cell count and differential, chemistries including LDH and glucose, pH). (See "Epidemiology, clinical presentation, and diagnostic evaluation of parapneumonic effusion and empyema in adults", section on 'Thoracentesis and pleural fluid analysis'.)

●Transtracheal aspiration - While popular in the past, transtracheal aspiration is no longer performed due to safety concerns. [36,47-49]. (See "Diagnostic evaluation of the incidental pulmonary nodule", section on 'Transthoracic needle biopsy'.)

DIAGNOSIS — The diagnosis of lung abscess is a clinical one, based on the radiographic appearance (most often one or more cavities with an air-fluid interface), supportive clinical features and microbiologic tests, and response to antimicrobial therapy. Clinicians should understand that in many cases, (approximately half), the offending pathogen is not isolated [17,18].

For patients with lung abscess without a clear predisposing factor, post-diagnostic testing may be appropriate to assess for dysphagia, episodes of altered consciousness, underlying bronchiectasis, or immune deficits.

DIFFERENTIAL DIAGNOSIS — The key processes to consider in the differential diagnosis of lung abscess are other causes of a fluid or air-fluid filled mass in the lung parenchyma (eg, lung cancer, granulomatosis with polyangiitis [GPA], infected lung cyst or bulla, hydatid cyst, or superinfected fungal or mycobacterial cavity) (table 2). Additionally, an empyema with an air-fluid interface can mimic a lung abscess on conventional chest radiographs. While less common in adults, intralobar pulmonary sequestrations can develop abscesses.

●Malignancy – Primary lung cancer and metastatic cancer can present with cavitary lesions that mimic lung abscess or become superinfected. Additionally, endobronchial cancer can cause a postobstructive lung abscess. A solitary thick-walled cavity (wall >15 mm diameter) without surrounding consolidation is concerning for lung cancer. Diagnostic cytology and/or biopsy are warranted if the patient does not have systemic features suggestive of infection (fever, productive cough, leukocytosis) or if the lesion fails to improve despite antibiotics. Note, however, that endobronchial tumor can lead to postobstructive pneumonia and lung abscess, so it is possible for both malignancy and infection to be present. (See "Overview of the initial evaluation, diagnosis, and staging of patients with suspected lung cancer".)

●Noninfectious granulomatous disease – Several noninfectious granulomatous and inflammatory diseases form cavitating lung nodules, such as GPA [50], rheumatoid arthritis, sarcoidosis, nodular silicosis, and pulmonary Langerhans cell histiocytosis. (See "Clinical manifestations and diagnosis of sarcoidosis" and "Granulomatosis with polyangiitis and microscopic polyangiitis: Respiratory tract involvement", section on 'Computed tomography' and "Overview of pleuropulmonary diseases associated with rheumatoid arthritis", section on 'Rheumatoid lung nodules' and "Silicosis" and "Pulmonary Langerhans cell histiocytosis".)

●Tuberculosis with or without bacterial superinfection – Postprimary Mycobacterium tuberculosis in the lung is associated with thin-walled cavities or cavities on a background of patchy airspace opacity. An air-fluid interface may be present in the cavity in as many as 20 percent of cases, due to bleeding or bacterial superinfection [51,52]. (See "Pulmonary tuberculosis: Clinical manifestations and complications", section on 'Radiologic findings'.)

●Chronic pulmonary aspergillosis – Chronic cavitary aspergillosis can present with several months of weight loss, productive cough, hemoptysis of variable severity, shortness of breath, and sometimes fever. Cavities may contain fungus balls, debris, or fluid, and the walls are usually thin. Aspergillus antibody (precipitins) is elevated in over 90 percent of patients. (See "Chronic pulmonary aspergillosis: Epidemiology, clinical manifestations and diagnosis", section on 'Clinical manifestations'.)

●Hydatid cyst – For patients with travel or residence in an area endemic for Echinococcus, computed tomography (CT) imaging can identify single or multilocular cysts that may have an air crescent sign, germinative membranes floating in cyst fluid (water lily sign), or are empty. Liver cysts are also present in about 20 percent of patients with lung cysts and provide an etiologic clue. Peripheral blood eosinophilia is uncommon and serologic tests are variably helpful. (See "Echinococcosis: Clinical manifestations and diagnosis".)

●Empyema with air-fluid interface – It can sometimes be difficult to determine from a chest radiograph whether an air-fluid interface is in the pleural space or lung parenchyma. Empyema can be associated with chest pain, but a lung abscess abutting the pleura can also cause chest pain. Chest CT is the procedure of choice for making this differentiation and guiding therapy. Abscesses tend to be more irregular in shape, spherical, and cavitated whereas empyemas tend to be better defined, elliptical, homogeneous, and have a smooth and uniform wall. Empyema may displace the blood vessels leading from the hilum to the periphery whereas abscesses typically do not. Empyemas will need to be drained via chest tube. (See "Epidemiology, clinical presentation, and diagnostic evaluation of parapneumonic effusion and empyema in adults" and "Management and prognosis of parapneumonic pleural effusion and empyema in adults".)

●Infected sequestration – Infection is a well-described complication of pulmonary intralobar sequestration and may undergo abscess formation [53-55]. Diagnosis of sequestration is important because sequestration infections tend to be recurrent and generally require surgical resection. (See "Bronchopulmonary sequestration".)

TREATMENT — Treatment of lung abscess is based on prompt initiation of an empiric antibiotic regimen, adjustment of the regimen based on culture results, and a prolonged course of therapy (algorithm 1). This approach is successful in most patients, while a few require a drainage procedure or surgical resection (about 10 percent).

The role of postural drainage and chest percussion (chest physiotherapy) is less clear; it has been used with the rationale that it would facilitate intrabronchial drainage [32]. However, efficacy has not been demonstrated and fatal cases of intrabronchial abscess rupture have been reported. We reserve cautious chest physiotherapy for patients with cystic fibrosis and noncystic fibrosis bronchiectasis who are on a routine program of bronchial hygiene.

Initial empiric antibiotics — Empiric antimicrobial therapy should be started promptly in patients with lung abscess to reduce the risk of abscess rupture into the airways or pleural space or invasion of local structures (eg, blood vessels). The initial regimen can be adjusted, if needed, based on culture results and response to therapy, remembering that anaerobic organisms are difficult to grow in culture and susceptibility testing is rarely performed.

For patients with suspected lung abscess from aspiration, empiric intravenous (IV) regimens should penetrate the lung parenchyma and target both strict anaerobes and microaerophilic streptococci.

●For most patients, acceptable regimens include any combination of a beta-lactam–beta-lactamase inhibitor (eg, ampicillin-sulbactam 3 g intravenously [IV] every six hours) or a carbapenem (eg, imipenem, meropenem). This choice is based upon in vitro data, our experience, and the increasing rates of penicillin-resistance among anaerobes including Bacteroides ruminicola, black-pigmenting strains of Prevotella (formally Bacteroides melaninogenicus group), Bacteroides gracilis, Bacteroides ureolyticus, Fusobacteria, and others [14,56-59]. (See "Combination beta-lactamase inhibitors, carbapenems, and monobactams".)

●For patients who are allergic to penicillin, we generally use moxifloxacin 400 mg orally daily [19,60], or combination therapy with levofloxacin (750 mg orally daily) plus metronidazole (500 mg orally three times daily). For hospitalized patients, ceftriaxone (or other third-generation cephalosporin) plus metronidazole is a reasonable option. For outpatients who are allergic to penicillin, we favor a fluoroquinolone-based regimen when starting treatment because these regimens have better bioavailability.

Clindamycin monotherapy (600 mg IV every eight hours followed by 300 mg orally four times daily) is also a potential alternative [61,62]. However, clindamycin has the potential to fail, as abscesses are caused by gram negatives or resistant gram positives in 20 to 30 percent of patients [16,19,20].

Adjusting antimicrobial regimen — Once culture results are available, empiric antimicrobial therapy can be tailored to cover identified pathogens, although the empiric regimens described above remain appropriate for most patients with aspiration-related mixed anaerobic and streptococcal lung abscess (see 'Initial empiric antibiotics' above). When a single pathogen that is not a typical part of the oral flora is detected (eg, K. pneumoniae, S. aureus), it is often appropriate to tailor the regimen to target that pathogen based upon the results of in vitro susceptibility testing. However, as culture of anaerobes from the lung is difficult, continuing empiric anaerobic coverage in addition may be prudent, particularly in patients with suspected aspiration who have putrid sputum.

●For suspected methicillin-susceptible S. aureus (MSSA), the agents of choice are cefazolin (2 g IV every eight hours), nafcillin (2 g IV every four hours), or oxacillin (2 g IV every four hours).

●For methicillin-resistant S. aureus (MRSA), linezolid (600 mg IV every 12 hours) or vancomycin are acceptable (table 3) [63]. Other options are ceftaroline, trimethoprim-sulfamethoxazole, and telavancin. Ceftaroline is active in vitro against virtually all strains of MRSA [64], but it has not been approved by the US Food and Drug Administration (FDA) for MRSA pneumonia because of limited data on using it for this indication [65,66]. Daptomycin should not be used for pulmonary infections due to inadequate activity in the lung [67]. (See "Treatment of hospital-acquired and ventilator-associated pneumonia in adults", section on 'Methicillin-resistant S. aureus'.)

Duration of antibiotics — In general, we switch from IV to oral agents once the patient has defervesced and become clinically stable; for some patients this takes a few days while in others it may be one to three weeks. Appropriate oral regimens depend upon the identified or suspected infecting pathogens. For patients with a mixed anaerobic and streptococcal infection, amoxicillin-clavulanate is an appropriate regimen [68], but the choice of regimen should be guided by the causative pathogen(s) and susceptibility results when available.

The optimal total duration of therapy (IV plus oral) is unknown; reported ranges include 21 to 48 days [1,17]. Some experts treat for three weeks as a standard and others treat based upon the response. Our practice is to continue antibiotic treatment until chest imaging (preferably computed tomography [CT]) shows a small, stable residual lesion or is clear. This generally requires several weeks of treatment, most of which can be accomplished with an oral regimen on an outpatient basis.

Response to therapy — Most patients are followed clinically, but repeat imaging is prudent for new onset or recurrent fevers, chest pain, hemoptysis, dyspnea, or failure to improve.

Patients with aspiration-related lung abscesses usually show clinical improvement with decreased fever and leukocytosis within three to four days after beginning antibiotic treatment. Defervescence is expected in 7 to 10 days [9,10,69-71]. The disappearance of putrid sputum may take longer.

Persistent fevers beyond one to two weeks may indicate delayed response, and such patients should undergo further diagnostic tests to better define the underlying anatomy and microbiology of the infection; typically, another chest CT is performed to look for progression of the abscess, development of complications (eg, empyema or new abscesses), or an underlying precipitant that may not have been picked up on the initial CT scan (algorithm 1). In addition, further respiratory sampling via flexible bronchoscopy is usually indicated. (See 'Additional testing' above.)

Major considerations in patients with a delayed response include:

●An associated condition that precludes response, such as obstruction with a foreign body or neoplasm, or a pulmonary sequestration.

●Erroneous microbiologic diagnosis with infection due to bacteria, mycobacteria, or fungi that are not being treated.

●Failure of medical therapy despite appropriate antibiotics. Drainage may be required to facilitate recovery. This is more typical in patients with large cavities but there is no clear size cut-off that mandates intervention, and drainage has been reported to be helpful even for some smaller abscesses that fail to improve with antibiotics [38,72-75].

●An alternative, nonbacterial cause of cavitary lung disease, such as cavitating neoplasm, vasculitis. (See 'Differential diagnosis' above.)

●Conditions that mimic an abscess such as an infected cyst or empyema. (See 'Differential diagnosis' above.)

●Other causes of persistent fever, such as drug fever or Clostridioides difficile–associated colitis. (See "Drug fever" and "Clostridioides difficile infection in adults: Clinical manifestations and diagnosis".)

Patients who fail to improve by 7 to 10 days despite appropriate antimicrobial therapy may need a drainage procedure or surgery. (See 'Failure of antimicrobial therapy' below.)

Failure of antimicrobial therapy — Most lung abscesses respond to a prolonged course of antimicrobials. However, a small proportion fail antimicrobials and require a drainage procedure or surgical therapy (approximately 10 percent) [76,77].

Needle or catheter drainage — For patients who fail to improve after 7 to 10 days of antibiotic therapy that has been adjusted based on microbiologic results, drainage of the abscess via transthoracic or transbronchial catheters can often lead to clinical improvement [38,72,73,78-85]. Among these options, percutaneous drainage is preferred since experience with this option is more extensive than with bronchoscopic drainage. Patients continue with their systemic antimicrobial until the abscess cavity closes or is small and stable. The typical duration of drainage catheter placement is approximately three days to three weeks and patients generally continue with their systemic antimicrobial.

●Transthoracic (percutaneous) catheter drainage – Transthoracic (percutaneous) catheter drainage can be performed under imaging guidance; depending on the available facilities, computed tomography, ultrasound, or fluoroscopy may be utilized [74,85]. The transthoracic route is generally preferred when the abscess abuts or is close to the chest wall.

Transthoracic drainage procedures carry a small risk of infecting the pleural space. In addition, they are also associated with a small risk of hemorrhage or pneumothorax.

●Transbronchoscopic catheter drainage – The bronchoscopic approach may be preferred for more centrally located lesions and for those that do not abut the pleura; ultrasound-guided bronchoscopy may be used for localization [38,72,73]. Bronchoscopic drainage is performed by placing a pigtail catheter into the abscess cavity via the nose under bronchoscopic visualization, leaving the catheter in place until the cavity has drained [72]. In some cases, the cavity is rinsed daily with sterile saline and directed antibiotics (eg, gentamicin or antifungal).

One of the risks associated with bronchoscopic drainage is spillage of infected material to other parts of the lung. Intracavitary fibrinolytic therapy is not recommended due to the potential development of a bronchopleural fistula. This procedure is not universally available and is restricted to centers with pulmonary interventional expertise. Bronchoscopy for drainage, in the absence of catheter placement, is of little use and can result in spillage of abscess contents into other airways [40].

Treating endobronchial obstruction — For postobstructive lung abscess due to bronchial stenosis or tumor, efforts should be directed at relieving the obstruction or possibly curative surgical resection of the tumor (typically lobectomy) (algorithm 1). Foreign body removal is often achieved with flexible or rigid bronchoscopy. For bronchial stenosis or tumor, endobronchial balloon dilation with stent placement may be an option pending definitive therapy. Obstruction from mediastinal lesions (eg, aneurysms or lymphadenopathy) require individualized assessment and treatment. The management of airway obstruction is discussed separately. (See "Clinical presentation, diagnostic evaluation, and management of malignant central airway obstruction in adults" and "Flexible bronchoscopy balloon dilation for nonmalignant airway strictures (bronchoplasty)" and "Airway stents".)

Surgical intervention — For patients who fail to improve clinically or radiographically with antibiotic therapy with or without catheter drainage or who develop complications during therapy (eg, significant hemorrhage, bronchopleural fistula), surgery may very rarely be indicated.

Factors that may contribute to a slow response or no response are obstruction of the bronchus, an extremely large size abscess, and abscesses involving antibiotic-resistant organisms, such as P. aeruginosa.

The usual procedure in such cases is a lobectomy or pneumonectomy but small peripheral abscesses may be amenable to segmentectomy or wedge resection [86]. Video-assisted thoracic surgery (VATS) is the procedure of choice and attention should be paid to removing all infected material in order to avoid stump infection and resultant bronchopleural fistula [87].

Mortality with surgery is as high as 15 to 20 percent although the high mortality rate likely reflects the severity of lung abscess in patients referred for lung surgery as well as their underlying conditions, in addition to the risk of surgery itself [88,89].

OUTCOMES — Patients with primary lung abscess (about 60 percent overall) with typical aspiration-related lung abscesses, including those with alcohol or injection drug use, generally do well with antibiotic treatment with cure rates of 90 to 95 percent [1,10,17,24,32,74,90]. Patients who require surgery, are immunocompromised, or have malignancy or irreversible bronchial obstruction have higher mortality rates [91]. Associated disease in the host is an important factor in determining the outcome of a lung abscess.

In one illustrative series of 252 patients with aspiration lung abscess, antibiotic therapy (mainly penicillin and clindamycin) was successful in 200 [32]. Drainage of the abscess was performed in 6 patients, drainage of empyema in 24, and pulmonary resection in 22. There were 10 deaths.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Hemoptysis".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topic (see "Patient education: Aspiration pneumonia (The Basics)")

SUMMARY AND RECOMMENDATIONS

●Definition – Lung abscess is defined as a circumscribed area of pus or necrosis in the pulmonary parenchyma caused by microbial infection. While most lung abscesses are single, the term "necrotizing pneumonia" or "lung gangrene" may be used to describe necrosis with multiple small abscesses within an area of pneumonia. (See 'Introduction' above and 'Definitions' above.)

●Pathogenesis – Aspiration is the most common cause of lung abscesses, accounting for approximately 80 percent of cases. Less commonly, lung abscesses arise as complications of pneumonia caused by pyogenic bacteria (eg, Klebsiella pneumoniae, S. aureus). Other mechanisms include septic emboli from tricuspid valve endocarditis, other forms of hematogenous spread (eg, Lemierre syndrome), direct extension (eg, traumatic inoculation), and endobronchial obstruction. (See 'Pathogenesis' above.)

●Microbiology – Lung abscesses that result from aspiration are typically polymicrobial, composed of the oral flora that inhabits the gingival crevices. This flora typically includes microaerophilic streptococci and anaerobes (Peptostreptococcus, Prevotella, Bacteroides [usually not B. fragilis]), and Fusobacterium spp (table 4), but Gram-negative organisms are also seen, particularly in immunocompromised patients and patients with multiple comorbidities. (See 'Microbiologic testing' above.)

●Clinical features – Classically, the onset of illness associated with lung abscesses is indolent, with symptoms arising over weeks to months. Typical symptoms include cough (often with putrid-smelling sputum), dyspnea, and/or chest pain. Systemic symptoms can include fever, chills, night sweats and weight loss. (See 'Clinical features' above.)

●Diagnostic evaluation

•Imaging – For most patients, the diagnosis can be made based on radiographic findings in a patient with compatible clinical features (eg, history of aspiration). Chest radiograph typically shows a thick-walled cavity with an air-fluid level, with or without a surrounding opacity (image 1 and image 2). We typically obtain a chest CT to better characterize the extent and possible cause of lung abscesses (image 1 and image 2). (See 'Diagnosis' above.)

•Diagnostic testing – In all patients, we obtain sputum Gram stain, sputum culture, and blood cultures to help direct therapy. More invasive testing (eg, bronchoscopy or percutaneous needle aspiration of the abscess) is usually reserved for cases in which there is diagnostic uncertainty, clinical instability, suspicion for unusual pathogen, and/or when patients are not responding to empiric therapy. (See 'Diagnostic evaluation' above.)

●Differential diagnosis – The differential diagnosis includes other forms of infectious cavitary lung disease (eg, necrotizing pneumonia, nocardiosis, tuberculosis, septic emboli) and noninfectious cavitary lung disease (eg, malignancy, pulmonary vasculitides) (table 2). (See 'Differential diagnosis' above.)

●Typical empiric therapy – For patients with suspected lung abscess from aspiration, empiric antibiotics that penetrate the lung parenchyma and target both strict anaerobes and facultatively anaerobic streptococci should be chosen (algorithm 1). (See 'Initial empiric antibiotics' above.)

•We suggest a beta-lactam with a beta-lactamase inhibitor for most patients (eg, ampicillin-sulbactam 3 g intravenously [IV] every six hours) or a carbapenem (eg, imipenem, meropenem) because of rising penicillin resistance rates among anaerobes (Grade 2C).

•For patients who cannot use beta-lactams, we typically use moxifloxacin alone, or combination therapy with levofloxacin plus metronidazole.

•Most patients with a lung abscess caused by aspiration will recover with antibiotic treatment alone. The duration of treatment varies based on clinical and radiographic response. Generally, we assess response (symptoms, fevers, leukocytosis) after 7 to 10 days of antibiotic treatment. In those who respond, we continue antibiotic treatment until chest imaging shows a small, stable residual lesion or is clear. This generally requires several weeks of outpatient therapy. (See 'Duration of antibiotics' above and 'Response to therapy' above.)

●Special populations – Modifications to this regimen (eg, broader empiric therapy) may be needed for patients with clinical instability, immunocompromised patients, and/or when specific pathogens are suspected based on clinical or radiographic features (eg, coverage for S. aureus or Pseudomonas in a patient with necrotizing pneumonia). (See 'Initial empiric antibiotics' above.)

●Management of endobronchial obstruction – If there is concurrent endobronchial obstruction (eg, due to tumor, stenosis, foreign body), that obstruction should be relieved when possible (eg, tumor resection/cytoreduction, stenting for bronchial stenosis, or foreign body removal). (See 'Treating endobronchial obstruction' above.)

●Failure of antimicrobial therapy – For patients who do not improve despite antibiotic treatment, abscess drainage is indicated. When the abscess is accessible percutaneously, we prefer transthoracic drainage over transbronchial catheter drainage because it is technically easier and the risk of endobronchial spread of infection is less. Surgical resection is rarely necessary and reserved for those with abscesses that cannot be drained or do not respond to drainage with less invasive approaches. (See 'Failure of antimicrobial therapy' above.)

ACKNOWLEDGMENT — UpToDate gratefully acknowledges John G Bartlett, MD (deceased), who contributed as author on earlier versions of this topic and was a founding Editor-in-Chief for UpToDate in Infectious Diseases.