Copyright © 2006 by Mosby, Inc. Slide 1 Chapter 16 Lung Abscess Figure 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. A AFC RB EDA PM B C
Copyright © 2006 by Mosby, Inc. Slide 2 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
Copyright © 2006 by Mosby, Inc. Slide 3 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 4 Etiology (Less frequent causes) Aerobic organisms Streptococcus pyogenes Klebsiella pneumoniae Escherichia coli On rare occasions Streptococcus pneumoniae Pseudomonas aeruginosa Legionella pneumophila
Copyright © 2006 by Mosby, Inc. Slide 5 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 6 Etiology Lung abscess may also develop from: Bronchial obstruction Vascular obstruction Interstitial lung disease Bullae or cysts Penetrating chest wounds
Copyright © 2006 by Mosby, Inc. Slide 7 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).
Copyright © 2006 by Mosby, Inc. Slide 8 Clinical Data Obtained at the Patient’s Bedside Clinical Data Obtained at the Patient’s Bedside Vital signs Increased respiratory rate Increased heart rate, cardiac output, blood pressure
Copyright © 2006 by Mosby, Inc. Slide 9 Clinical Data Obtained at the Patient’s Bedside 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
Copyright © 2006 by Mosby, Inc. Slide 10 Figure A short, dull, or flat percussion note is typically produced over areas of alveolar consolidation.
Copyright © 2006 by Mosby, Inc. Slide 11 Figure Auscultation of bronchial breath sounds over a consolidated lung unit.
Copyright © 2006 by Mosby, Inc. Slide 12 Figure Whispered voice sounds auscultated over a normal lung are usually faint and unintelligible.
Copyright © 2006 by Mosby, Inc. Slide 13 Clinical Data Obtained from Laboratory Tests and Special Procedures
Copyright © 2006 by Mosby, Inc. Slide 14 Pulmonary Function Study: Expiratory Maneuver Findings FVC FEV T FEF 25%-75% FEF N or N or N PEFR MVV FEF 50% FEV 1% N N or N N or FVC FEV T FEF 25%-75% FEF N or N or N PEFR MVV FEF 50% FEV 1% N N or N N or
Copyright © 2006 by Mosby, Inc. Slide 15 Pulmonary Function Study: Lung Volume and Capacity Findings V T RV FRC TLC N or VC IC ERV RV/TLC% N V T RV FRC TLC N or VC IC ERV RV/TLC% N
Copyright © 2006 by Mosby, Inc. Slide 16 Arterial Blood Gases Mild to Moderate Lung Abscess Acute alveolar hyperventilation with hypoxemia pH PaCO 2 HCO 3 - PaO 2 (Slightly) pH PaCO 2 HCO 3 - PaO 2 (Slightly)
Copyright © 2006 by Mosby, Inc. Slide 17 Time and Progression of Disease Pa CO Alveolar Hyperventilation Point at which PaO 2 declines enough to stimulate peripheral oxygen receptors Pa O 2 Disease Onset Pa O 2 or Pa CO 2 Figure 4-2. PaO 2 and PaC0 2 trends during acute alveolar hyperventilation.
Copyright © 2006 by Mosby, Inc. Slide 18 Arterial Blood Gases Severe Lung Abscess Acute ventilatory failure with hypoxemia pH PaCO 2 HCO 3 - PaO 2 (Slightly) pH PaCO 2 HCO 3 - PaO 2 (Slightly)
Copyright © 2006 by Mosby, Inc. Slide 19 Time and Progression of Disease Pa O Alveolar Hyperventilation Point at which PaO 2 declines enough to stimulate peripheral oxygen receptors Pa CO 2 Acute Ventilatory Failure Disease Onset Point at which disease becomes severe and patient begins to become fatigued Pa 0 2 or Pa C0 2 Figure 4-7. PaO 2 and PaCO 2 trends during acute ventilatory failure.
Copyright © 2006 by Mosby, Inc. Slide 20 Oxygenation Indices Q S /Q T D O 2 V O 2 C(a-v) O 2 Normal Normal O 2 ER Sv O 2 Q S /Q T D O 2 V O 2 C(a-v) O 2 Normal Normal O 2 ER Sv O 2
Copyright © 2006 by Mosby, Inc. Slide 21 Abnormal Laboratory Tests and Procedures Sputum examination Gram-positive organism Streptococcus Anaerobic organisms Peptococcus Peptostreptococcus Bacteroides Fusobacterium
Copyright © 2006 by Mosby, Inc. Slide 22 Radiologic Findings Chest radiograph Increased density Cavity formation Cavity with air-fluid levels Fibrosis Pleural effusion
Copyright © 2006 by Mosby, Inc. Slide 23 Figure 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.)
Copyright © 2006 by Mosby, Inc. Slide 24 General Management of Lung Abscess Respiratory care treatment protocols Oxygen therapy protocol Bronchopulmonary hygiene therapy protocol Hyperinflation therapy protocol
Copyright © 2006 by Mosby, Inc. Slide 25 General Management of Lung Abscess Medications and procedures commonly prescribed by the physician Antibiotics Surgery
Copyright © 2006 by Mosby, Inc. Slide 26 Classroom Discussion Case Study: Lung Abscess