31.

Acute Lung Abcess

Definition of the idea
A lung abscess is a localized cavity of pus resulting from necrosis of lung tissue
(infection→thrombosis of segmental artery + vein →tissue necrosis),surrounded by
pneumonitis

Classification
Etiologic classfn:
Bacterial Non bacterial
1.Aerobic 1. Fungal
2. Anaerobic 2. Viral
3.Mixed 3. Atypical mo

Pathogenetic:
1.Bronchogenetic
• Aspiration
• Obturation
• Metapneumonic
2. Hematogenous
3. Traumatic
4. Lymphogenous
5. Contact

❖ Acc to number
• Single
• Multiple
- unilateral
- bilateral
❖ Acc to course
• Acute
• Chronic
-phase remission
-phase of excacerbation
❖ Acc to connection with bronchus
• Drained
-complete
- incomplete
• Not drained
❖ Acc to localization
• Central
• Peripheral
-cortical
-subpleural

Etiology & Pathogenesis

1. Aspiration pneumonia (50%)- aaspiration of infected material from upper airway
 eg. In unconscious pt (alcoholicstupor,coma,general anaesthesia,excessive
sedation)

Classic sites → post. Superior segment of R upper lobe

→ sup. Segment of left lower lobe

2. Primary necrotizing pneumonia – klebsiella pneumonia,staphylococcus

aureus,Actinomycetes Isareli,Strept
milleria,leigenella,H.Influenza,Mycobacterium also in immunocompromised –
Norcardia,Cryptocceus,Aspergillus<Blastomycosis,Histoplasmosis,Coccidomyco
sis
*aerobic- (strep,staph,pneumococci)
–anaerobic (fusobacterium,Deptostreptococci,bacteroides)

3. Bronchial obstruction secondary to neoplasm (10-20%)

4. Septic emboli
5. Pulmonary infacrtion oinfection
6. Chronic respiratory sepsis –sinusiti,tonsillitis,dental infection
7. Penetrating lung injury

Clinical picture
1. Period of abcess formation b4 drainage – Acute onset
• Persistent and spiking fever (40º),with chills + malaise,anorexia
• Pain on affected side (dull)
• Dyspnoea

2. After drainage
• Sudden dec in fever up to 37-38º C
• Improvement of subjective symptoms
• Productive cough with copius fetid sputum expectoration (3 layers of
sputum=foam,serous,pus)

Physical signs
1. if peripheral
• dull sound on percussion (1) + pain
• tympanic sound (2)

2. Auscultation
• Fine/medium moist cracles
• Large – tympany/amphoric sounds

Diagnosis

1. Sputum examination – 3layers –foam,serous liquid,pus with fetid odor

- maybe with blood streaks
- may contain gangrenous lung tissue
 - microscopic- fibrin,leukocytes,RBCs etc + microorganism for
antibiotic rxn
- not expectorated sputum since it is contaminated with oral MO so
(transtracheal aspiration,transthoracic,fibroscopic aspiration)

2. Chest X-Ray 1- homogenous shadow –consolidation

2- thick walled,large (>6cm) cavity with air-fluid level

3. CT scan for detection of tumor/foreign body

4. Pulmonary angiography – PE
5. Ultrasound
6. MRI
7. Radionucleide scanning
8. Diagnostic thoracocentesis,thoracosopy,thoracotomy
9. Bronchoscopy with biopsy – to rule out carcinoma
10. Bronchoalveolar lavage
11. Transbronchial lung biopsy
12. submucosal + transbronhial needle aspiration
13. Percutaneous ttansthoracic needle aspiration
14. Tracheal aspiration

Definition of the idea.

Lung abscess: A localized cavity with pus, resulting from necrosis of lung tissue, with
surrounding pneumonitis.
A lung abscess may be putrid (due to anaerobic bacteria) or nonputrid (due to anaerobes
or aerobes). "Gangrene of the lung" denotes a similar though more diffuse and extensive
process in which necrosis predominates.

Classification.
Acc Etiology:
1 Bacterial (Aerobic , Anaerobic, Mixed)
2. Not bacterial (The elementary organisms , Fungus)
Acc Pathogenesis
1. Bronchogenic (With aspiration ,With obtiration, Metapneumonic)
2. Hematogenous (embolic).
3 Traumatic
4. Lymphogenous.
5. Contact.
Acc Localization:
1.Central
2 Peripheric (cortical , subpleural)
Acc Spreading:
1. Singular.
2. Multiple(Unilateral, Bilaterial)
Acc Character of the clinical features
1. Acute
 2. Chronic:( In phase of the remission, In phase of the exacerbation)
Acc Connection with the bronchus:
1. It is not drained.
2. It is drained:( There is enough, There is not enough)
Acc Complications:
• Empyema of the pleura
• Bleeding.
• Defeat of another mild
• Phlegmon of the thoracal wall.
• Bacterial shock
• Sepsis

Etiology and pathogenesis.

Lung abscesses are usually due to infected material from the upper airway aspirated when
a patient is unconscious or obtunded from alcohol, other drugs, CNS disease, general
anesthesia, coma, or excessive sedation. The causative organisms are usually
anaerobes. Lung abscesses are often associated with periodontal disease, in which
anaerobes are prevalent. Bacteria cultured from lung abscesses include common and
nasopharyngeal flora, particularly anaerobes, and less often, aerobic bacteria or fungi.
Bronchogenic carcinoma is an occasional underlying cause in older smokers.
Pneumonia due to Klebsiella pneumoniae (Friedländer's bacillus), Staphylococcus
aureus, Actinomyces israelii, -hemolytic streptococcus, Streptococcus milleri (and
other aerobic or microaerophilic streptococci), Legionella sp, or Haemophilus
influenzae is sometimes complicated by abscess formation. Lung abscess in the
compromised host is usually due to Nocardia sp, Cryptococcus sp, Aspergillus sp,
Phycomycetes sp, atypical mycobacteria (primarily Mycobacterium avium-
intracellulare or M. kansasii), or gram-negative bacilli. Blastomycosis, histoplasmosis,
and coccidioidomycosis may also cause acute or chronic lung abscesses. Less
common causes of lung abscess include septic pulmonary emboli, secondary infection
of pulmonary infarcts, and direct extension of amebic or bacterial abscesses from the
liver through the diaphragm into the lower lobe of the lung.
Single lung abscesses are most common. Multiple abscesses usually are unilateral; they
may develop simultaneously or spread from a single focus. In abscesses due to
aspiration, the superior segment of a lower lobe and the posterior segment of an upper
lobe are affected most often. A solitary abscess secondary to bronchial obstruction or
to an infected embolus starts as necrosis of a major portion of the affected
bronchopulmonary segment. The base of the segment is usually next to the chest wall,
and the pleural space in the area is often obliterated by inflammatory adhesions.
Embolic spread of infection, most often due to S. aureus with tricuspid endocarditis in
IV drug abusers, has become more common and is usually characterized by multiple
lung lesions in noncontiguous sites. Suppurative venous thrombophlebitis due to
aerobic or anaerobic bacteria may also cause embolic lung abscesses.
An abscess usually ruptures into a bronchus, and its contents are expectorated, leaving a
cavity filled with fluid and air. Occasionally, an abscess ruptures into the pleural
cavity, resulting in an empyema, sometimes with bronchopleural fistula. Similarly, the
rupture of a large abscess into a bronchus or vigorous attempts at drainage may cause
 widespread bronchial dissemination of pus with diffuse pneumonia and a condition
resembling adult respiratory distress syndrome.

Clinical picture.
There are two periods of development this disease.
The first period - before break of pus in the bronchi.

Signs:
Body temperature about 40 C
Stethalgias on the side of defeat
Backlog of the struck side in the act of respiration
Morbidity at the palpation of the struck side

The second period -

The second period begins after break of an abscess in bronchus (draining bronchus).
Signs:
Fast downstroke of temperature (37,5-38 C)
A plenty of the sputum. The sputum is parted on three layers
1. Bottom Layer - pus
2. Average Layer - serous liquid
3. Top Layer - foam.
Sometimes there is the impurity of blood.
Onset may be acute or insidious. Early symptoms are often those of pneumonia, ie,
malaise, anorexia, sputum-producing cough, sweats, and fever. Severe prostration and
a temperature of 39.4° C (103° F) or higher may be present. Fever, anorexia,
weakness, and debility are sometimes minimal if the infection is limited or indolent.
Unless the abscess is completely walled off, the sputum is purulent and may be blood-
streaked. An abscess may not be suspected until it perforates a bronchus, when a large
amount of purulent sputum, putrid or not, may be expectorated over a few hours or
several days. The sputum may contain gangrenous lung tissue. A putrid (penetrating
and foul) odor is diagnostic of anaerobic bacterial causation. Putrid sputum occurs in
30 to 50% of all patients with lung abscess, but about 40% of patients with abscesses
due to anaerobes do not have a putrid sputum, so its absence does not exclude this
diagnosis. Chest pain, if present, usually indicates pleural involvement.
Physical signs include a small area of dullness, indicating localized pneumonic
consolidation, and usually suppressed (rather than bronchial) breath sounds. Fine or
medium moist crackles may be present. If the cavity is large there may be tympany
and amphoric breath sounds.
If the abscess becomes chronic, weight loss, anemia, and hypertrophic pulmonary
osteoarthropathy may occur. Physical examination of the chest may be negative in the
chronic phase, but rales and rhonchi are usually present.

Diagnosis.
Methods of Diagnostics:
- Chest Imaging
• conventional chest x-ray
 • CT with or without contrast or high-resolution techniques
• angiography of the pulmonary or bronchial circulation using contrast materials or
digital subtraction
• ultrasonography
• radionuclide scanning
• MRI.
- Diagnostic thoracentesis
- Thoracoscopy
- Bronchoscopy
- Ancillary procedures:
• Bronchoalveolar lavage
• Transbronchial lung biopsy
• Submucosal and transbronchial needle aspiration
- Percutaneous Transthoracic Needle Aspiration
- Thoracotomy
- Tracheal Aspiration

Chest x-rays early in the course may show a segmental or lobar consolidation, which
sometimes becomes globular as pus distends it.
After an abscess ruptures into a bronchus, a cavity with a fluid level appears on x-ray. If
chest x-rays suggest an underlying tumor or foreign body or if the presentation is
atypical, CT scanning may provide better anatomic definition.
Sputum should be examined by smear and culture for bacteria, fungi, and mycobacteria.
Expectorated sputum is not appropriate because the mouth normally contains anaerobic
organisms that contaminate the specimen during passage through the upper airways. The
attribution of disease to anaerobes usually requires a specimen obtained by transtracheal
aspiration, transthoracic aspiration, or fiberoptic bronchoscopy with a protected brush and
quantitative cultures, but these procedures are not performed often. Such invasive
procedures should be reserved for cases that have an atypical presentation or that are
unresponsive to antibiotics; however, once antibiotics are initiated, there is no reliable
method for obtaining specimens useful for bacterial culture. Bronchoscopy is
unnecessary if response to antibiotics is adequate and if a foreign body or tumor is not
suspected.