Transcript Chapter 7 Body Systems - Kingwood Application Server

Chapter 16
Lung Abscess
EDA
PM
AFC
C
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
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Tissue necrosis
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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
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Streptococcus pyogenes
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Klebsiella pneumoniae
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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)
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Mycobacterium tuberculosis
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Fungal organisms

Slide 5
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Histoplasma capsulatum
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Coccidioides immitis
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Blastomyces

Aspergillus fumigatus
Parasites

Paragonimus westermani
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Echinococcus

Entamoeba histolytica
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Etiology
Lung abscess may also develop from:
Slide 6

Bronchial obstruction
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Vascular obstruction
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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
Patient’s Bedside
Vital signs
Slide 8
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Increased respiratory rate

Increased heart rate, cardiac output,
blood pressure
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Clinical Data Obtained at the
Patient’s Bedside
Slide 9
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Chest pain/decreased chest expansion
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Cyanosis
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Cough, sputum production, and hemoptysis
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Chest assessment findings
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Increased tactile and vocal fremitus
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Dull percussion note
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Bronchial breath sounds
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Diminished breath sounds
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Whispered pectoriloquy
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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
Slide 14
FVC

FEVT
N or 
FEF25%-75%
N or 
FEF200-1200
N
PEFR
MVV
FEF50%
FEV1%
N
N or 
N
N or 
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Pulmonary Function Study:
Lung Volume and Capacity Findings
VT
RV
FRC
TLC
N or 



VC

Slide 15
IC

ERV

RV/TLC%
N
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Arterial Blood Gases
Mild to Moderate Lung Abscess

pH

Slide 16
Acute alveolar hyperventilation with
hypoxemia
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 PaO2
declines enough to
stimulate peripheral
oxygen receptors
70
60
PaO2
50
40
30
20
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

Acute ventilatory failure with hypoxemia
pH

Slide 18
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
Point at which PaO2
declines enough to
stimulate peripheral
oxygen receptors
Point at which disease
becomes severe and patient
begins to become fatigued
60
50
40
30
20
10
0
Figure 4-7. PaO2 and PaCO2 trends during acute ventilatory failure.
Slide 19
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Oxygenation Indices
QS/QT
DO2
VO2


Normal
O2ER

Slide 20
C(a-v)O2
Normal
SvO2

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Abnormal Laboratory Tests
and Procedures
Sputum examination

Gram-positive organism


Slide 21
Streptococcus
Anaerobic organisms

Peptococcus

Peptostreptococcus
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Bacteroides

Fusobacterium
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Radiologic Findings
Chest radiograph
Slide 22
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Increased density
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Cavity formation
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Cavity with air-fluid levels
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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
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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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