Chapter 16

Lung Abscess
EDA

PM
AFC

RB

B
A
Figure 16-1. Lung abscess. A, Cross-sectional view of lung abscess. AFC, Air-fluid cavity;
RB, ruptured bronchus (and drainage of the liquified contents of the cavity); EDA, early
development of abscess; PM, pyogenic membrane. Consolidation (B) and excessive bronchial
secretions (C) are common secondary anatomic alterations of the lungs.
Slide 1

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Anatomic Alterations of the Lungs

Slide 2

Alveolar consolidation

Alveolar-capillary and bronchial wall destruction

Tissue necrosis

Cavity formation

Fibrosis and calcification of the lung parenchyma

Bronchopleural fistulae

Atelectasis

Excessive airway secretions and empyema

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Etiology

Slide 3

Pneumonia caused by aspiration (most common)

Klebsiella

Staphylococcus

Predisposing factors for aspiration

Alcohol abuse

Seizure disorders

General anesthesia

Head trauma

Cerebrovascular accident

Swallowing disorders

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Etiology
(Less frequent causes)

Slide 4

Aerobic organisms

Streptococcus pyogenes

Klebsiella pneumoniae

Escherichia coli

On rare occasions

Streptococcus pneumoniae

Pseudomonas aeruginosa

Legionella pneumophila
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Etiology
(Other organisms that may lead to a lung abscess)

Mycobacterium tuberculosis

Fungal organisms

Slide 5

Histoplasma capsulatum

Coccidioides immitis

Blastomyces

Aspergillus fumigatus

Parasites

Paragonimus westermani

Echinococcus

Entamoeba histolytica

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Etiology
Lung abscess may also develop from:

Slide 6

Bronchial obstruction

Vascular obstruction

Interstitial lung disease

Bullae or cysts

Penetrating chest wounds

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Overview of the Cardiopulmonary

Clinical Manifestations Associated
with LUNG ABSCESS

The following clinical manifestations result from

the pathophysiologic mechanisms caused
(or activated) by Alveolar Consolidation (see
Figure 9-8), and when the abscess is draining,
by Excessive Bronchial Secretions (see
Figure 9-8)the major anatomic alterations of
the lungs associated with chronic bronchitis
(see Figure 16-1).

Slide 7

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Clinical Data Obtained at the

Patients Bedside
Vital signs

Slide 8

Increased respiratory rate

Increased heart rate, cardiac output,

blood pressure

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Clinical Data Obtained at the

Patients Bedside

Slide 9

Chest pain/decreased chest expansion

Cyanosis

Cough, sputum production, and hemoptysis

Chest assessment findings

Increased tactile and vocal fremitus

Dull percussion note

Bronchial breath sounds

Diminished breath sounds

Whispered pectoriloquy

Pleural friction rub

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Figure 2-11. A short, dull, or flat percussion note is typically produced over areas
of alveolar consolidation.
Slide 10

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Figure 2-16. Auscultation of bronchial breath sounds over a consolidated lung

unit.
Slide 11

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Figure 2-19. Whispered voice sounds auscultated over a normal lung

are usually faint and unintelligible.
Slide 12

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Clinical Data Obtained from

Laboratory Tests and Special
Procedures

Slide 13

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Pulmonary Function Study:

Expiratory Maneuver Findings
FVC

FEVT

FEF25%-75%

N or

N or

PEFR
N

Slide 14

MVV
N or

FEF50%
N

FEF200-1200
N
FEV1%
N or

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Pulmonary Function Study:

Lung Volume and Capacity Findings
VT

RV

FRC

TLC

N or

IC

ERV

VC

RV/TLC%

Slide 15

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Arterial Blood Gases

Mild to Moderate Lung Abscess

Slide 16

Acute alveolar hyperventilation with

hypoxemia

pH

PaCO2

HCO3 (Slightly)

PaO2

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Time and Progression of Disease

Disease Onset

Alveolar Hyperventilation

100
90

PaO2 or PaCO2

80

Point at which PaO22

declines enough to
stimulate peripheral
oxygen receptors

70
60

PaO2

50
40
30
20

PaC
O

10
0
Figure 4-2. PaO2 and PaC02 trends during acute alveolar hyperventilation.
Slide 17

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Arterial Blood Gases

Severe Lung Abscess

Slide 18

Acute ventilatory failure with hypoxemia

pH

PaCO2

HCO3 (Slightly)

PaO2

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Time and Progression of Disease

Disease Onset

Alveolar Hyperventilation

Acute Ventilatory Failure

100
90

Pa02 or PaC02

80
70
60

Point at which PaO22

declines enough to
stimulate peripheral
oxygen receptors

Point at which disease

becomes severe and patient
begins to become fatigued

O2
C
a

50
40
30

Pa
O

20
10
0
Figure 4-7. PaO2 and PaCO2 trends during acute ventilatory failure.
Slide 19

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Oxygenation Indices
QS/QT

D O2

V O2

Normal

O2ER

Normal

SvO2

Slide 20

C(a-v)O2

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Abnormal Laboratory Tests

and Procedures
Sputum examination

Gram-positive organism

Slide 21

Streptococcus

Anaerobic organisms

Peptococcus

Peptostreptococcus

Bacteroides

Fusobacterium
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Radiologic Findings
Chest radiograph

Slide 22

Increased density

Cavity formation

Cavity with air-fluid levels

Fibrosis

Pleural effusion

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Figure 16-2. Reactivation tuberculosis with a large cavitary lesion containing an air-fluid level in
the right lower lobe. Smaller cavitary lesions are seen in other lobes. (From Armstrong P et al:
Imaging of diseases of the chest, ed 2, St. Louis, 1995, Mosby.)
Slide 23

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General Management of
Lung Abscess
Respiratory care treatment protocols

Slide 24

Oxygen therapy protocol

Bronchopulmonary hygiene therapy protocol

Hyperinflation therapy protocol

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General Management of
Lung Abscess
Medications and procedures commonly
prescribed by the physician

Slide 25

Antibiotics

Surgery

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Classroom Discussion

Case Study: Lung Abscess

Slide 26

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