Lung Abscess in Adults

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Lung abscess in adults

Author: Michael Klompas, MD, MPH
Section Editor: Stephen B Calderwood, MD
Deputy Editors: Helen Hollingsworth, MD, Sheila Bond, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jan 2021. | This topic last updated: Jan 26, 2021.
INTRODUCTION
A lung abscess is circumscribed, purulent infection contained with 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 and, less commonly, from
infection with pyogenic bacteria (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), or immunocompromise.
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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 those with risk factors for aspiration who have dental, gingival,
or periodontal infection or para nasal sinusitis). Anaerobes from the gingival crevice or
sinuses reach the lower airways [3], which usually occurs while the patient is in the
recumbent position. Infection is initiated either because the bacteria 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 from poor local drainage [4-6]. (See "Clinical presentation,
diagnostic evaluation, and management of 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 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 anginosis and other members of the
Streptococcus milleri group and oral streptococci such as Streptococcus mitis. These
organisms may be a part of a polymicrobial infection or may be the sole pathogens.
● Pneumonia caused by pyogenic bacteria — Aerobic bacteria that can cause

monomicrobial lung abscess include Staphylococcus aureus (eg, in a patient with
influenza) [19,20], Klebsiella pneumoniae (eg, in a patient with structural lung disease)
[16,17,21,22], other Gram-negative bacilli (eg, Pseudomonas aeruginosa) [23],
Streptococcus pyogenes [24], Burkholderia pseudomallei [25,26], Haemophilus influenzae
type b, Legionella [27,28], Nocardia, and Actinomyces. There have been occasional case
reports of lung abscess caused by Streptococcus pneumoniae, although superinfection by
anaerobic bacteria may be causative microbes in such cases [29]. (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 "Clinical manifestations and
diagnosis of nocardiosis", section on 'Pulmonary' 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 (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 "Clinical manifestations and complications of pulmonary
tuberculosis" and "Overview of nontuberculous mycobacterial infections" and "Clinical
manifestations and diagnosis of nocardiosis", section on 'Pulmonary' 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 "Clinical manifestations and diagnosis of nocardiosis" 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
"Clinical manifestations and complications of pulmonary tuberculosis" 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 non-specific and mimic those of
pneumonia, albeit with 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) [17,22,30-32]. 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
[12,13,33].
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). 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 chest computed tomography (see 'Chest computed tomography' below).
Most often, lung abscesses are unilateral [30]. 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 occurs in the upright or prone position
[30].
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, leukocytosis, dyspnea, putrid or bloody sputum) and a
cavitating or fluid-filled lung mass on imaging (see 'Clinical features' above). The focus of
investigations 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 promptly; 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 thorough examination of the oral cavity for
halitosis, gingivitis, tonsillar enlargement, carious, 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 is 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 acute presentations such as 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 on Gram stain that is heavy in culture is often a pathogen. However, care
must be exercised in interpreting the results, particularly when antimicrobials have already
been started, since most sputum samples yield deceptive 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 [34]. Regardless of culture results, a putrid

odor of expectorated sputum is indicative of anaerobic infection and, in most cases of

aspiration-associated lung abscess, should be treated empirically. (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 anti-microbial 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 [1,33,35,36]. (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 [37]. 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
immunocompromise. (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 [38].
Samples should be sent for cytology, routine Gram stain and 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 bronchoscopy is not revealing
[39,40]. 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 used to assess for right-sided valve infective endocarditis [41-44]. 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 counts, chemistries, 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. [34,45-47]. (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 [48], rheumatoid
arthritis, sarcoidosis, nodular silicosis, and pulmonary Langerhans cell histiocytosis. (See
"Clinical manifestations and diagnosis of pulmonary sarcoidosis" and "Granulomatosis
with polyangiitis and microscopic polyangiitis: Respiratory tract involvement", section on
'Computed tomography' and "Overview of lung disease 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
[49,50]. (See "Clinical manifestations and complications of pulmonary tuberculosis",
section on 'Radiographic 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 "Clinical manifestations and diagnosis of chronic pulmonary
aspergillosis", section on 'Chronic cavitary pulmonary aspergillosis'.)
● 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 "Clinical manifestations and diagnosis of echinococcosis".)

● 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 is likely to be associated with chest pain, but a lung abscess
abutting the pleura can also cause chest pain. Chest computed tomography is the
procedure of choice for making this differentiation and guiding therapy. Abscesses tend
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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 [51-53]. 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. 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 [30]. 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 [14,54-57]. (See "Combination beta-lactamase inhibitors, carbapenems, and
monobactams".)
● For patients who are allergic to penicillin, clindamycin (600 mg IV every eight hours,
followed by 150 to 300 mg orally four times daily), moxifloxacin 400 mg orally daily
[58,59], or combination therapy with levofloxacin (750 mg orally daily) plus
metronidazole (500 mg orally three times daily) are alternatives [60,61]. If a patient fails
to respond to clindamycin alone then Gram-negative coverage should be added with a
quinolone or cephalosporin.
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) [62]. Other options are ceftaroline, trimethoprim-
sulfamethoxazole, and telavancin. Ceftaroline is active in vitro against virtually all strains
of MRSA [63], but it has not been approved by the US Food and Drug Administration
(FDA) for MRSA pneumonia because the experience is too limited [64,65]. Daptomycin
should not be used for pulmonary infections due to inadequate activity in the lung [66].
(See "Treatment of hospital-acquired and ventilator-associated pneumonia in adults",
section on 'Methicillin-resistant Staphylococcus aureus'.)
Duration of antibiotics — In general, we switch from IV to oral agents once the patient has
defervesced and becomes clinically stable; for some patients this takes a few days while in
others it may be one to three weeks. Appropriate oral regimens will depend upon the
identified or suspected infecting pathogens. For patients with a mixed anaerobic and
streptococcal infection, amoxicillin-clavulanate is an appropriate regimen [67], 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, or dyspnea and for 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 [9,10,68-70]. 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 reason that may not have been picked up on the initial CT scan. 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 [36,71-74].
● 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 C. difficile–associated colitis. (See
"Drug fever" and "Clostridioides (formerly Clostridium) 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) [75,76].
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
[36,71,72,77-83]. 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
[73]. The transthoracic route is generally preferred when the abscess abuts or is close to
the chest wall. Drainage catheters typically remain in place for approximately three days
to three weeks, although they may need to be replaced if dislocated or blocked. Patients
generally continue with their systemic antimicrobial.
Transthoracic drainage procedures carry a small risk of infecting the pleural space. In
addition, they are also associated with a small risk of hemorrhage and pneumothorax.
● Transbronchoscopic catheter drainage – The bronchoscopic approach may be

preferred for more centrally located lesions or those that do not abut the pleura;
ultrasound-guided bronchoscopy may be used for localization [36,71,72]. 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 [71]. In some cases, the cavity is rinsed daily with sterile saline and appropriate
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 [38]
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). 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
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 [84]. 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
[85].
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 [86,87].
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 [1,10,17,22,30,73,88]. Patients who
require surgery, are immunocompromised, or have malignancy or irreversible bronchial

obstruction have higher mortality rates [89]. 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 [30]. 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 5th to 6th
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 10th to 12th
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
● 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 multiple
small abscesses that develop within an area of pneumonia. (See 'Introduction' above
and 'Definitions' above.)
● 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, tricuspid valve endocarditis, Lemierre syndrome), direct
extension (eg, traumatic inoculation), and endobronchial obstruction. (See
'Pathogenesis' above.)
● 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.)
● 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.)
● For most patients, the diagnosis can be made based on radiographic findings in a
patient with compatible clinical features (eg, 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 computed tomography (CT) to
better characterize the extent and possible cause of lung abscesses ( image 1 and
image 2). (See 'Diagnosis' above.)
● 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.)
● 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.)
● For patients with suspected lung abscess from aspiration, empiric antibiotics should
penetrate the lung parenchyma and target both strict anaerobes and facultatively
anaerobic streptococci. (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, monotherapy with clindamycin,

moxifloxacin, or combination therapy with levofloxacin plus metronidazole are
reasonable alternatives.
● 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.)
● 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.)
● 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 after 7 to 10 days of antibiotic treatment.
Those who are improving generally require two to three weeks of treatment. (See
'Duration of antibiotics' above and 'Response to therapy' above.)
● 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
We are saddened by the death of John Bartlett, MD, who passed away in January 2021.
UpToDate wishes to acknowledge Dr. Bartlett's past work as an author for this topic.
Use of UpToDate is subject to the Subscription and License Agreement.
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Topic 7030 Version 22.0

GRAPHICS
Lung abscess microbiology in patients with cell-mediated immune defects
Common Uncommon
Bacteria Bacteria
Pseudomonas aeruginosa Rhodococcus equi
Enterobacteriaceae Legionella spp
Nocardia spp Mycobacteria
Anaerobic bacteria and microaerophilic streptococci (eg, M. avium complex
Streptococcus milleri)
Other nontuberculous
Staphylococcus aureus mycobacteria
Mycobacteria Fungi
M. tuberculosis Agents of mucormycosis
M. kansasii Blastomyces dermatitidis
Fungi Pneumocystis jirovecii
Cryptococcus spp (formerly P. carinii)
Aspergillus spp
Histoplasma capsulatum
Graphic 57589 Version 4.0

Necrotizing right lower lobe pneumonia due to anaerobes
Postanterior (A) and lateral (B) chest radiographs show areas of

consolidation and several air-fluid levels within the right lower lobe. Less
extensive consolidation is evident in the right middle lobe. Computed
tomography (CT) image (C) confirms the radiographic findings and also
demonstrates a few centrilobular nodules in the right middle lobe
(arrow). The patient was a 50-year-old man with pneumonia due to
anaerobic organisms.
Reproduced with permission from: Müller NL, Franquet T, Lee KS, Silva CIS.
Bacterial pneumonia. In: Imaging of pulmonary infections, Lippincott
Williams & Wilkins, Philadelphia 2007. Copyright © 2007 Lippincott Williams &
Wilkins. www.lww.com.

Lung abscess
Postanterior (A) and lateral (B) chest radiographs show dense right
upper airspace consolidation. Contrast-enhanced computed
tomography (CT) scan (C) demonstrates large focal area of decreased
attentuation with rim enhancement (arrow) characteristic of lung
abscess. Postanterior (D) and lateral (E) chest radiographs three weeks
later show decreased size of lung abscess and development of
cavitation with fluid level (arrows). The patient was a 43-year-old
woman with lung abscess secondary to Haemophilus aphrophilus.
Williams & Wilkins, Philadelphia 2007. Copyright © 2007 Lippincott
Williams & Wilkins. www.lww.com.

Empyema due to Staphylococcus aureus
Posterior (A) and lateral (B) chest radiographs show large loculated right
pleural effusion (arrows). Cross-sectional (C) contrast-enhanced
multidetector computed tomography (CT) image and sagittal reformation
(D) demonstrate the extent of the loculated effusion, pleural thickening,
and enhancement (arrows). The patient was a 44-year-old man and an
intravenous drug user. He had no radiologic evidence of the septic
embolism.
Williams & Wilkins, Philadelphia 2007. Copyright © 2007 Lippincott Williams
& Wilkins. www.lww.com.

Differential diagnosis of cavitary lung lesions
Infections
Necrotizing infections
Anaerobic bacteria, often mixed with aerobic and microaerophilic streptococci
Other bacteria
Staphylococcus aureus, Klebsiella pneumoniae, Enterobacteriaceae, Pseudomonas
aeruginosa, Legionella spp, Haemophilus influenzae type B, Nocardia spp, Actinomyces spp,
Burkholderia pseudomallei
Mycobacteria
Mycobacterium tuberculosis, M. avium, M. kansasii, other nontuberculous mycobacteria
Fungi
Aspergillus spp, Coccidioides spp, Histoplasma spp, Blastomyces dermatitidis, Cryptococcus
spp, agents of mucormycosis, Pneumocystis jirovecii
Parasites
Echinococcus, Entamoeba histolytica, Paragonimus westermani
Empyema with air-fluid level (hydropneumothorax)
Septic pulmonary emboli (eg, tricuspid valve endocarditis, intravascular catheters,
intravenous drug use, Lemierre syndrome)
Non-infectious diseases
Pulmonary embolism with infarction
Vasculitis (eg, granulomatosis with polyangiitis)
Neoplasm (eg, bronchogenic cancer, lymphoma, and metastatic head and neck,
bladder, colon, pancreatic, and uterine cancer).
Pulmonary sequestration
Bullae or cysts with air fluid level
Bronchiectasis
Cryptogenic organizing pneumonia
Sarcoidosis
Rheumatoid nodules
Pulmonary Langerhans histiocytosis
Foreign body aspiration

Approach to vancomycin dosing for adults with normal kidney function*
Loading dose (for patients with known or Load 20 to 35 mg/kg (based on actual body
suspected severe Staphylococcus aureus weight, rounded to the nearest 250 mg
infection) ¶ increment; not to exceed 3000 mg). Within this
range, we use a higher dose for critically ill
patients; we use a lower dose for patients who
are obese and/or are receiving vancomycin via
continuous infusion.
Initial maintenance dose and interval Typically 15 to 20 mg/kg every 8 to 12 hours
for most patients (based on actual body
weight, rounded to the nearest 250 mg
increment).
In general, the approach to establishing the
vancomycin dose/interval is guided by a
nomogram. Δ
Subsequent dose and interval adjustments Based on AUC-guided (preferred for severe
infection) [1] or trough-guided serum
concentration monitoring. ◊
AUC: area under the 24-hour time-concentration curve.
* Refer to the UpToDate topic on vancomycin dosing for management of patients with abnormal
kidney function.
¶ For patients with known or suspected severe S. aureus infection, we suggest administration of a
loading dose to reduce the likelihood of suboptimal initial vancomycin exposure. Severe S. aureus
infections include (but are not limited to) bacteremia, endocarditis, osteomyelitis, prosthetic joint
infection, pneumonia warranting hospitalization, infection involving the central nervous system, or
infection causing critical illness.
Δ If possible, the nomogram should be developed and validated at the institution where it is used, to
best reflect the regional patient population. Refer to UpToDate topic on vancomycin dosing for
sample nomogram.
◊ Refer to the UpToDate topic on vancomycin dosing for discussion of AUC-guided and trough-guided
vancomycin dosing. For patients with nonsevere infection who receive vancomycin for <3 days (in the
setting of stable kidney function and absence of other risk factors for altered vancomycin kinetics),
vancomycin concentration monitoring is often omitted; the value of such monitoring prior to
achieving steady state (usually around treatment day 2 to 3) is uncertain.
Reference:
1. Rybak MJ, Le J, Lodise TP, et al. Therapeutic Monitoring of Vancomycin for Serious Methicillin-Resistant
Staphylococcus Aureus Infections: A Revised Consensus Guideline and Review by the American Society
of Health-System Pharmacists, the Infectious Diseases Society of America, the Pediatric Infectious
Diseases Society, and the Society of Infectious Diseases Pharmacists. Am J Health Syst Pharm 2020;
77:835.

Bacteriology of lung abscess
Organisms Number of cases (percent)

Total cases
Aerobic bacteria only 10 (11)
Anaerobes only 43 (46)
Mixed aerobes and anaerobes 40 (43)
Predominant isolates
Aerobes
Staphylococcus aureus 13 (4)
Escherichia coli 9 (0)
Klebsiella pneumoniae 7 (3)
Pseudomonas aeruginosa 7 (1)
Streptococcus pneumoniae 6 (1)
Anaerobes
Peptostreptococcus 40 (12)
Fusobacterium nucleatum 34 (5)
Prevotella (black-pigmented) 32 (1)
Adapted from: Bartlett JG. Chest 1987; 91:901.

Contributor Disclosures
Michael Klompas, MD, MPH Nothing to disclose Stephen B Calderwood, MD Equity Ownership:
Pulmatrix [Infectious diseases]. Consultant/Advisory Boards: Day Zero Diagnostics [Whole genome
sequencing for microbial identification and determination of antimicrobial susceptibility]. Helen
Hollingsworth, MD Nothing to disclose Sheila Bond, MD Nothing to disclose
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these
are addressed by vetting through a multi-level review process, and through requirements for
references to be provided to support the content. Appropriately referenced content is required of all
authors and must conform to UpToDate standards of evidence.
Conflict of interest policy

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18/2/2021 Lung abscess in adults - UpToDate

Official reprint from UpToDate®

Lung abscess is defined as a circumscribed area of pus or necrosis in the pulmonary

● Secondary lung abscesses occur when there is a predisposing condition such as

● Aspiration – Lung abscess is classically caused by aspiration of oropharyngeal

● Hematogenous spread – Lung abscesses can occur as a consequence of septic

● Direct extension – A lung abscess may develop by direct extension of an empyema,

● Bronchial obstruction – Endobronchial obstruction from a bronchogenic or mediastinal

● Superinfection or spread of airway infection – Lung abscess may develop as a

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abscess in a minority of patients [7,8]. The mechanism is likely multifactorial and

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

● Pneumonia caused by pyogenic bacteria — Aerobic bacteria that can cause

● Nonbacterial pathogens — Selected nonbacterial pathogens can generate or colonize

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nontuberculous mycobacteria (eg, M. avium, M. kansasii, M. abscessus), and parasites (eg,

● Opportunistic infections — In the immunocompromised host, the most common

An overview of pulmonary infections in immunocompromised patients is presented

Lung abscesses caused by hematological dissemination may be distributed randomly or

A lung abscess should be suspected in a patient with clinical features of an indolent

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odor of expectorated sputum is indicative of anaerobic infection and, in most cases of

Despite obtaining respiratory cultures, up to 50 percent of patients do not have a positive

As bacterial infection can complicate mycobacterial cavities leading to an air-fluid interface,

Chest computed tomography — When a lung abscess is suspected, chest computed

CT findings of acute lung abscess include an area of cavitation surrounded by consolidation.

Differentiating between peripheral lung abscesses and empyemas can occasionally be

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Bronchoscopy — Flexible bronchoscopy is not routinely needed, but is reserved for

● Transthoracic needle aspiration or biopsy – Transthoracic needle aspiration of the

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● Echocardiography – For patients with multiple lung abscesses, transthoracic

● Thoracentesis – If pleural fluid is present on the chest radiograph, a thoracentesis is

● Transtracheal aspiration - While popular in the past, transtracheal aspiration is no

features suggestive of infection (fever, productive cough, leukocytosis) or if the lesion

● Noninfectious granulomatous disease – Several noninfectious granulomatous and

● Tuberculosis with or without bacterial superinfection – Postprimary Mycobacterium

● Chronic pulmonary aspergillosis – Chronic cavitary aspergillosis can present with

● Empyema with air-fluid interface – It can sometimes be difficult to determine from a

to be more irregular in shape, spherical, and cavitated whereas empyemas tend to be

● Infected sequestration – Infection is a well-described complication of pulmonary

Treatment of lung abscess is based on prompt initiation of an empiric antibiotic regimen,

Initial empiric antibiotics — Empiric antimicrobial therapy should be started promptly in

● For most patients, acceptable regimens include any combination of a beta-lactam–beta-

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melaninogenicus group), Bacteroides gracilis, Bacteroides ureolyticus, Fusobacteria, and

Adjusting antimicrobial regimen — Once culture results are available, empiric

● For methicillin-resistant S. aureus (MRSA), linezolid (600 mg IV every 12 hours) or

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Major considerations in patients with a delayed response include:

● An associated condition that precludes response, such as obstruction with a foreign

● Erroneous microbiologic diagnosis with infection due to bacteria, mycobacteria, or fungi

● Failure of medical therapy despite appropriate antibiotics. Drainage may be required to

● An alternative, nonbacterial cause of cavitary lung disease, such as cavitating neoplasm,

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Failure of antimicrobial therapy — Most lung abscesses respond to a prolonged course of

Needle or catheter drainage — For patients who fail to improve after 7 to 10 days of

● Transthoracic (percutaneous) catheter drainage – Transthoracic (percutaneous)

● Transbronchoscopic catheter drainage – The bronchoscopic approach may be

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available and is restricted to centers with pulmonary interventional expertise.

Treating endobronchial obstruction — For postobstructive lung abscess due to