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Lung Abscess

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LUNG ABSCESS

DR. MOHAMMAD ASIM

CONSULTANT PULMONOLOGIST

NORTHWEST GENERAL HOSPITAL AND RESEARCH


CENTER
LEARNING OBJECIVES
• DEFINITON

• 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.

• 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 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

syndrome [ie, jugular vein suppurative thrombophlebitis]). 


DIRECT EXTENSION

•  A lung abscess may develop by direct extension of an empyema, subphrenic, or mediastinal

abscess or a tracheo-esophageal or broncho-esophageal fistula.


BRONCHIAL OBSTRUCTION

Endobronchial obstruction from a

• bronchogenic or mediastinal mass (eg, aneurysm, lymphadenopathy, tumor)

• bronchial stenosis or

• inhaled foreign body

may result in postobstructive pneumonia that progresses to abscess formation presumably due to impaired drainage of local

pulmonary secretions.
SUPERINFECTION

• 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.

• 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

What do you think?


• Empyema • Pneumonia
• Hydatid cyst • Pulmonary embolism with infarction
• Infective endocarditis • Cryptogenic organizing pneumonia
• Small cell lung cancer • Sarcoidosis
• Non small cell lung cancer • Rheumatoid nodules
• Foreign body aspiration • Tuberculosis
• Pulmonary Langerhans histiocytosis • Granulomatosis with Polyangiitis
ETIOLOGY

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 %)

• Productive cough (often putrid, sour-tasting; 55 to 90 %)

• Dyspnea (10 %)

• Chest pain (20 to 35 %)

• Hemoptysis (10 %)

• Night sweats

• Weight loss and anorexia

• Fatigue
WORKUP

• CBC

• Blood C/S both aerobic and anaerobic

• Sputum for gram stain, culture and sensitivity


CXR

R.M.L abscess
CXR
CT SCAN
TREATMENT

ANTIBIOTICS

1. Beta lactamase inhibitors (ampicillin-sulbactam) + Carbapenems (meropenem, imipenem)

2. Penicillin allergy : Clindamycin + Levofloxacin + Metronidazole

3. MSSA : Cefazolin, Nafcillin or Oxacillin

4. MRSA : Vancomycin or Linezolid


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

• 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

2. TREATING ENDOBRONCHIAL OBSTRUCTION 


• Rigid / flexible bronchoscopy for foreign body
• Lobectomy for tumor
• Endobronchial balloon/stent/laser for bronchial stenosis
SURGICAL INTERVENTION 
Mostly done when complications (hemorrhage, bronchopleural fistula) develop.
Procedures include :

1. LOBECTOMY – Large abscesses

2. PNEUMONECTOMY – Large abscess

3. SEGMENTECTOMY – Small abscess

4. WEDGE RESECTION – Peripheral small abscess

5. VATS – Procedure of choice


VIDEO ASSISTED THORACOSCOPIC SURGERY
THANKYOU!
ANY QUESTIONS?

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