Lung Abscess
Lung Abscess
Lung Abscess
CONSULTANT PULMONOLOGIST
• CLASSIFICATION
• PATHOPHYSIOLOGY
• PRESENTATION
• RISK FACTORS
• DIFFERENTIALS
• WORKUP
• TREATMENT
DEFINITION
‘Lung abscess is defined as a circumscribed area of pus or necrosis in the pulmonary parenchyma caused
by microbial infection.’
CLASSIFICATI
ON
PRIMARY SECONDARY
LUNG LUNG
ABSCESS ABSCESS
PRIMARY LUNG ABSCESS
• Primary lung abscesses result from direct infection of the pulmonary parenchyma in an otherwise
healthy person.
• Primary lung abscesses can also arise within an area of pneumonia caused by necrotizing
organisms (eg, s. Aureus).
SECONDARY LUNG ABSCESS
• 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.
PATHOGENESIS
Pathogenesis depends upon the cause. Some of the important mechanisms of lung abscess
formation are ;
1. Aspiration
2. Hematogenous spread
3. Direct extension
4. Bronchial obstruction
5. Superinfection or spread of airway infection
ASPIRATION
• Lung abscess is classically caused by aspiration of oropharyngeal secretions especially in patients with dental, gingival, or
periodontal infection or paranasal sinusitis.
• 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.
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
• bronchial stenosis or
may result in postobstructive pneumonia that progresses to abscess formation presumably due to impaired drainage of local
pulmonary secretions.
SUPERINFECTION
• Flares of bronchiectasis can lead to parenchymal infection that evolves into a lung abscess in a
minority of patients.
• The mechanism is likely multifactorial and includes poor drainage and impaired clearance of
microbiologic flora from the lower airways.
RISK FACTORS
• Periodontal disease
• Alcoholism
• Coma
• Drug abuse
• Seizure disorder
• Reflux disease
• Neuromuscular diseases
• Stroke
DIFFERENTIAL DIAGNOSIS
Common Uncommon
Bacteria
Bacteria
Pseudomonas aeruginosa
Rhodococcus equi
Enterobacteriaceae
Nocardia spp
Legionella spp
Mycobacteria
Anaerobic bacteria and microaerophilic streptococci (eg, Streptococcus milleri)
M. avium complex
Staphylococcus aureus
Mycobacteria Other nontuberculous mycobacteria
M. tuberculosis
Fungi
M. kansasii
Fungi
Agents of mucormycosis
Cryptococcus spp Blastomyces dermatitidis
Aspergillus spp
Pneumocystis jirovecii (formerly P. carinii)
Histoplasma capsulatum
CLINICAL FEATURES
Symptoms evolve over weeks to months.
• Fever and chills (80 %)
• Dyspnea (10 %)
• Hemoptysis (10 %)
• Night sweats
• Fatigue
WORKUP
• CBC
R.M.L abscess
CXR
CT SCAN
TREATMENT
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
• The optimal total duration of therapy (IV plus oral) is unknown; reported ranges include 21 to 48
days.
• Some experts treat for three weeks as a standard and others treat based upon the response.
FAILURE OF ANTIMICROBIAL THERAPY
1. NEEDLE OR CATHETER DRAINAGE
• Transthoracic (percutaneous) catheter drainage
• Transbronchoscopic catheter drainage