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    Lung Abscess Presentation

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    Consolidation and Excessive Bronchial Secretions are common secondary anatomic alterations of the lungs. Mycobacterium tuberculosis, streptococcus pneumoniae and Pseudomonas aeruginosa are the most common causes. A lung abscess may also develop from: bronchial obstruction Vascular obstruction Interstitial lung disease Bullae or cysts Penetrating chest wounds.

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    Lung Abscess Presentation

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    mirayub
    406 views26 pages
    Consolidation and Excessive Bronchial Secretions are common secondary anatomic alterations of the lungs. Mycobacterium tuberculosis, streptococcus pneumoniae and Pseudomonas aeruginosa are the most common causes. A lung abscess may also develop from: bronchial obstruction Vascular obstruction Interstitial lung disease Bullae or cysts Penetrating chest wounds.

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    Consolidation and Excessive Bronchial Secretions are common secondary anatomic alterations of the lungs. Mycobacterium tuberculosis, streptococcus pneumoniae and Pseudomonas aeruginosa are the most common causes. A lung abscess may also develop from: bronchial obstruction Vascular obstruction Interstitial lung disease Bullae or cysts Penetrating chest wounds.

    Copyright:

    Attribution Non-Commercial (BY-NC)
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    406 views26 pages

    Lung Abscess Presentation

    Uploaded by

    mirayub
    Consolidation and Excessive Bronchial Secretions are common secondary anatomic alterations of the lungs. Mycobacterium tuberculosis, streptococcus pneumoniae and Pseudomonas aeruginosa are the most common causes. A lung abscess may also develop from: bronchial obstruction Vascular obstruction Interstitial lung disease Bullae or cysts Penetrating chest wounds.

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    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 Copyright 2006 by Mosby, Inc.

    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

    Slide 2

    Copyright 2006 by Mosby, Inc.

    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
    Copyright 2006 by Mosby, Inc.

    Slide 3

    Etiology
    (Less frequent causes)

    Aerobic organisms

    Streptococcus pyogenes Klebsiella pneumoniae Escherichia coli

    On rare occasions

    Streptococcus pneumoniae Pseudomonas aeruginosa

    Slide 4

    Legionella pneumophila
    Copyright 2006 by Mosby, Inc.

    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


    Copyright 2006 by Mosby, Inc.

    Slide 5

    Etiology
    Lung abscess may also develop from:

    Bronchial obstruction Vascular obstruction Interstitial lung disease Bullae or cysts Penetrating chest wounds

    Slide 6

    Copyright 2006 by Mosby, Inc.

    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

    Copyright 2006 by Mosby, Inc.

    Clinical Data Obtained at the Patients Bedside


    Vital signs

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

    Slide 8

    Copyright 2006 by Mosby, Inc.

    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


    Slide 9

    Bronchial breath sounds


    Diminished breath sounds Whispered pectoriloquy Pleural friction rub
    Copyright 2006 by Mosby, Inc.

    Figure 2-11. A short, dull, or flat percussion note is typically produced over areas of alveolar consolidation.
    Slide 10 Copyright 2006 by Mosby, Inc.

    Figure 2-16. Auscultation of bronchial breath sounds over a consolidated lung unit.
    Slide 11 Copyright 2006 by Mosby, Inc.

    Figure 2-19. Whispered voice sounds auscultated over a normal lung are usually faint and unintelligible.
    Slide 12 Copyright 2006 by Mosby, Inc.

    Clinical Data Obtained from Laboratory Tests and Special Procedures

    Slide 13

    Copyright 2006 by Mosby, Inc.

    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

    Slide 14

    Copyright 2006 by Mosby, Inc.

    Pulmonary Function Study: Lung Volume and Capacity Findings


    VT N or RV FRC TLC

    VC

    IC

    ERV

    RV/TLC%

    Slide 15

    Copyright 2006 by Mosby, Inc.

    Arterial Blood Gases


    Mild to Moderate Lung Abscess

    Acute alveolar hyperventilation with hypoxemia


    PaCO2 HCO3 (Slightly) PaO2

    pH

    Slide 16

    Copyright 2006 by Mosby, Inc.

    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.
    Slide 17 Copyright 2006 by Mosby, Inc.

    Arterial Blood Gases


    Severe Lung Abscess

    Acute ventilatory failure with hypoxemia

    pH

    PaCO2

    HCO3 (Slightly)

    PaO2

    Slide 18

    Copyright 2006 by Mosby, Inc.

    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.
    Slide 19 Copyright 2006 by Mosby, Inc.

    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

    Slide 20

    Copyright 2006 by Mosby, Inc.

    Abnormal Laboratory Tests and Procedures


    Sputum examination

    Gram-positive organism

    Streptococcus

    Anaerobic organisms

    Peptococcus

    Peptostreptococcus
    Bacteroides Fusobacterium
    Copyright 2006 by Mosby, Inc.

    Slide 21

    Radiologic Findings
    Chest radiograph

    Increased density Cavity formation Cavity with air-fluid levels Fibrosis Pleural effusion

    Slide 22

    Copyright 2006 by Mosby, Inc.

    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 Copyright 2006 by Mosby, Inc.

    General Management of Lung Abscess


    Respiratory care treatment protocols

    Oxygen therapy protocol Bronchopulmonary hygiene therapy protocol Hyperinflation therapy protocol

    Slide 24

    Copyright 2006 by Mosby, Inc.

    General Management of Lung Abscess


    Medications and procedures commonly prescribed by the physician

    Antibiotics Surgery

    Slide 25

    Copyright 2006 by Mosby, Inc.

    Classroom Discussion
    Case Study: Lung Abscess

    Slide 26

    Copyright 2006 by Mosby, Inc.

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