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.
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Anatomic Alterations of the Lungs

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

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)

Aerobic organisms

Streptococcus pyogenes Klebsiella pneumoniae Escherichia coli

On rare occasions

Streptococcus pneumoniae Pseudomonas aeruginosa

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

Mycobacterium tuberculosis

Fungal organisms

Histoplasma capsulatum Coccidioides immitis Blastomyces Aspergillus fumigatus

Parasites

Paragonimus westermani Echinococcus Entamoeba histolytica

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Etiology
Lung abscess may also develop from:

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).

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Clinical Data Obtained at the Patients Bedside

Vital signs

Increased respiratory rate Increased heart rate, cardiac output, blood pressure

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Clinical Data Obtained at the Patients Bedside

Chest pain/decreased chest expansion Cyanosis Cough, sputum production, and hemoptysis Chest assessment findings

Increased tactile and vocal fremitus Dull percussion note

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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.
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Figure 2-16. Auscultation of bronchial breath sounds over a consolidated lung unit.
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Figure 2-19. Whispered voice sounds auscultated over a normal lung are usually faint and unintelligible.
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Clinical Data Obtained from Laboratory Tests and Special Procedures

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Pulmonary Function Study: Expiratory Maneuver Findings

FVC PEFR FEVT N or MVV FEF25%-75% N or FEF50% FEF200-1200 N FEV1%

N or

N or

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Pulmonary Function Study: Lung Volume and Capacity Findings

VT N or RV FRC TLC

VC

IC

ERV

RV/TLC%

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Arterial Blood Gases

Mild to Moderate Lung Abscess

Acute alveolar hyperventilation with hypoxemia

PaCO2 HCO3 (Slightly) PaO2

pH

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Time and Progression of Disease Disease Onset

100 90 80 Point at which PaO2 declines enough to stimulate peripheral oxygen receptors

Alveolar Hyperventilation

PaO2 or PaCO2

70 60 50 40 30 20 10 0

PaO2

Figure 4-2. PaO2 and PaC02 trends during acute alveolar hyperventilation.
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Arterial Blood Gases

Severe Lung Abscess

Acute ventilatory failure with hypoxemia

pH

PaCO2

HCO3 (Slightly)

PaO2

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Time and Progression of Disease

Disease Onset
100 90 80 Pa02 or PaC02 70 60 50 40 30 20 10 0 Figure 4-7. PaO2 and PaCO2 trends during acute ventilatory failure.
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Alveolar Hyperventilation

Acute Ventilatory Failure

Point at which PaO2 declines enough to stimulate peripheral oxygen receptors

Point at which disease becomes severe and patient begins to become fatigued

Oxygenation Indices
QS/QT DO2 VO2 Normal C(a-v)O2 Normal

O2ER

SvO2

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Abnormal Laboratory Tests and Procedures

Sputum examination

Gram-positive organism

Streptococcus

Anaerobic organisms

Peptococcus

Peptostreptococcus
Bacteroides Fusobacterium
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Radiologic Findings
Chest radiograph

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.)
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General Management of Lung Abscess

Respiratory care treatment protocols

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

Antibiotics Surgery

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Classroom Discussion
Case Study: Lung Abscess

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