LUNG ABSCESS

dr Budi Enoch SpPD

THE TERM LUNG ABSCESS REFERS TO A MICROBIAL INFECTION OF THE LUNG
THAT RESULTS IN NECROSIS OF THE PULMONARY PARENCHYMA. NECROTIZING
PNEUMONIA OR LUNG GANGRENE REFERS TO MULTIPLE SMALL PULMONARY
ABSCESSES IN CONTIGUOUS AREAS OF THE LUNG, USUALLY RESULTING FROM A
MORE VIRULENT INFECTION
 CLASSIFICATION
 Lung abscesses are classified by clinical and pathologic features
including the tempo of progression, the presence or absence of an
associated underlying lesion, and the microbial pathogen
responsible.
 Duration defines the infection as acute versus chronic, with the
dividing line usually at 4–6 weeks.
 Abscesses occurring in the presence of underlying pulmonary
lesions, including tumors or systemic conditions (e.g., HIV
infection), are referred to as secondary; those that occur in the
absence of underlying pulmonary lesions are considered primary.
 The term nonspecific lung abscess refers to cases in which no
likely pathogen is recovered from expectorated sputum; most such
cases are presumed to be due to anaerobic bacteria.
 Putrid lung abscess is a term applied to anaerobic bacterial lung
abscesses, which are characterized by distinctive foul-smelling
breath, sputum, or empyema fluid
 ETIOLOGY
 The likely etiologic agent, appropriate diagnostic testing, and
appropriate treatment are frequently indicated by the characteristics of
the host and the disease process.
 A variety of microbial pathogens cause lung abscess.
 Most nonspecific lung abscesses are presumed to be due to anaerobic
bacteria.
 Mycobacteria, especially M. tuberculosis, are a very important cause of
pulmonary infections and abscess formation.
 Fungi and some parasites also cause lung abscess.
 An acute lung abscess developing in a young, previously healthy patient,
especially in conjunction with influenza, is likely to involve
Staphylococcus aureus; this pathogen generally is seen easily on sputum
Gram's stain and culture, and presumptive treatment for methicillin-
resistant S. aureus is urgent.
 In an immunocompromised host, suspected pathogens include enteric
gram-negative bacilli—especially Klebsiella pneumoniae but also agents
that are found almost exclusively in patients with defective cell-
mediated immunity, such as Nocardia asteroides and Rhodococcus equi.
Lung abscess acquired in other countries may involve Burkholderia
pseudomallei or Paragonimus westermani.
 CLINICAL FEATURES
 The classic presentation of nonspecific lung abscess is an indolent
infection that evolves over several days or weeks, usually in a host
who has a predisposition to aspiration.
 A common feature is periodontal infection with pyorrhea or gingivitis.
Anaerobes and aerobic or microaerophilic streptococci that colonize
the upper airways are implicated in these lesions.
 The usual symptoms are fatigue, cough, sputum production, and fever.
Chills are uncommon.
 Many patients have evidence of chronic disease, such as weight loss
and anemia.
 Some patients have putrid-smelling sputum indicative of the presence
of anaerobes; the foul odor is presumably due to the organisms'
production of short-chain fatty acids, such as butyric or succinic acid.
 Some patients have pleurisy due to pleural involvement by contiguous
spread or by a bronchopleural fistula. The pleurisy may be severe and
may be the symptom that prompts medical evaluation. Sequential x-
rays or CT scans show the evolution of this lesion from pneumonitis to
cavitation, a process that generally requires 7–14 days in experimental
animals
DIAGNOSIS
 Lung abscess can usually be detected with
standard imaging, including chest x-ray and
CT .
 The latter is clearly preferred for precise
definition of the lesion and its location and
possibly for detection of underlying lesions.
 Lymphadenopathy is not associated with
bacterial lung abscess; thus this finding
suggests an alternative diagnosis
 Microbiologic studies include stains and cultures of expectorated sputum
to detect aerobic bacterial pathogens. However, clinical correlations are
very important because sputum cultures (especially those that do not
satisfy standard cytologic criteria) are unreliable.
 In appropriate settings, it is important to consider cultures for fungi and
mycobacteria.
 Anaerobic bacteria, the most common causes of primary lung abscess, are
not detected in expectorated sputum cultures, and in any case the
specimen is subject to anaerobic contamination as it traverses the upper
airways.
 Alternative specimens that may be useful include pleural fluid obtained
by thoracentesis in patients who have empyema and quantitative
bronchoalveolar lavage (BAL) specimens if they are processed promptly
and appropriately for anaerobic bacteria.
 Another invasive method for bypassing contamination by the flora of the
upper airways is transthoracic needle aspiration under CT guidance; the
popularity of this procedure has increased in recent years. In most cases,
the etiology of anaerobic lung abscess is clear: the host is prone to
aspiration and has an abscess in a dependent pulmonary segment, with
no other likely cause.
 As stated above, putrid breath, sputum, or empyema fluid indicates
anaerobic infection.
TREATMENT
 ANTIBIOTIC SELECTION
 Treatment depends on the presumed or established etiology.
 Infections caused by anaerobic bacteria should usually be treated with
clindamycin; the initial IV dosage of 600 mg four times daily can be changed to an
oral dosage of 300 mg four times daily once the patient becomes afebrile and
improves clinically. The duration of therapy is arbitrary, but many experts
recommend continuation of oral treatment until imaging shows that chest lesions
have cleared or have left a small, stable scar. A shorter course may be effective.
 An alternative to clindamycin is any -lactam/-lactamase inhibitor combination;
parenteral treatment may be followed by orally administered
amoxicillin/clavulanate.
 Carbapenems are also effective against anaerobic bacteria as well as streptococci,
but the published data with these drugs in the treatment of anaerobic pulmonary
infections are sparse.
 Penicillin was previously regarded as a preferred drug for these infections, but
many oral anaerobes produce -lactamases, and clindamycin proved superior to
penicillin G in a randomized clinical trial.
 Metronidazole is highly active against virtually all anaerobes but not against
aerobic microaerophilic streptococci, which play an important role in mixed
infections. In therapeutic trials, metronidazole has done poorly unless combined
with a -lactam or another agent active against aerobic and microaerophilic
streptococci
 Persistence of fever beyond 5–7 days or progression of the infiltrate suggests
failure of therapy and a need to exclude factors such as obstruction,
complicating empyema, and involvement of antibiotic-resistant bacteria. Many
patients with uncomplicated lung abscesses and all those with atypical
presentations or unresponsive abscesses should undergo bronchoscopy and/or
CT to detect a possible associated anatomic lesion, such as a tumor, or a
foreign body. Quantitative bacteriologic studies using a protected brush
catheter or BAL are much less reliable when done after antibiotic therapy.
Postural drainage was previously popular for patients with lung abscess, but
aggressive attempts to implement this strategy may result in spillage to other
pulmonary segments, leading to airway obstruction and clinical deterioration.
 Lung abscess due to S. aureus is usually treated with vancomycin at a dosage
that targets a trough serum level of 15–20 g/mL. The main alternative is
linezolid. Daptomycin should not be used for pulmonary infections. Lung
abscesses caused by aerobic gram-negative bacteria need to be treated
according to the results of antibiotic sensitivity tests. Most common among the
pathogens involved are K. pneumoniae (especially the K1 strain in Taiwan) and
P. aeruginosa in patients with severe chronic lung disease or compromised
immune defenses. Pseudomonal lung abscesses usually require prolonged
courses of parenteral antibiotics. Carbapenems or -lactams are frequently
combined with aminoglycosides; oral fluoroquinolones are often effective
initially, but resistance is common with prolonged use. Aerosolized colistin and
aminoglycosides are sometimes used to augment other therapy, but the
 SURGERY
 Recent large-scale reviews indicate that, in general,
surgery is now reserved for ~10–12% of patients.
 The major indications for surgery are failure to
respond to medical management, suspected neoplasm,
and hemorrhage.
 Failure to respond to antibiotics is usually due to an
obstructed bronchus and an extremely large abscess
(>6 cm in diameter) or to infection involving relatively
resistant bacteria, such as P. aeruginosa.
 The usual procedure is lobectomy. An alternative
intervention that is becoming popular is percutaneous
drainage under CT guidance. Aspirate samples for
assay of possible pathogens should be carefully
collected
 RESPONSE TO THERAPY
 Patients with lung abscess usually show clinical improvement, with
decreased fever, within 3–5 days of initiation of antibiotic treatment.
 Defervescence can be expected within 5–10 days.
 Patients with fevers persisting for 7–14 days should undergo bronchoscopy
or other diagnostic tests to better define anatomic changes and
microbiologic findings.
 Cultures of expectorated sputum are not likely to be helpful at this
juncture except for detecting pathogens such as mycobacteria and fungi.
 The response to therapy apparent on serial chest radiographs is delayed
in comparison with the clinical course.
 In fact, infiltrates usually progress during the first 3 days of treatment in
approximately one-half of patients.
 Pleural involvement is relatively common and may develop in dramatic
fashion.
 The most common causes of failures of medical management include a
failure to drain pleural collections, an inappropriate choice of
antimicrobial therapy, an obstructed bronchus that prevents drainage, a
"giant" abscess, a resistant pathogen, or refractory lesions due to
immunocompromise.