Lung Abscess PDF

Pneumonia Lung Abscess Lung Abscess Anatomic Alterations  Definition  Necrosis of lung tissue  Early presentation looks like pneumonia  Neutrophils & macrophages go to work  Alveoli become consolidated  May lead to localized air/fluid-filled cavity  Fluid is pu...

Pneumonia Lung Abscess Lung Abscess Anatomic Alterations  Definition  Necrosis of lung tissue  Early presentation looks like pneumonia  Neutrophils & macrophages go to work  Alveoli become consolidated  May lead to localized air/fluid-filled cavity  Fluid is purulent exudate  Liquefied white blood cells  Protiens  Tissue debris Anatomic Alterations  Main pathology:  Alveolar consolidation  Alveolar cap./ bronchial wall destruction  Tissue necrosis – cavity formation  Fibrosis & calcification of parenchyma  Bronchopleural fistula & empyema  Atelectasis & excessive airway secretions Etiology  Most common:  Pneumonia caused by aspiration, Kliebsiella, Staphylococcus & anerobic organisms.  Poor oral hygiene leads to anerobic organisms  Predisposing factors that lead to aspiration:  Alcohol abuse Seizure disorder  General anesthesia head trauma  CVA swallowing disorders Etiology  Infections are typically from more than one organism.  Development of abscess may be from:  Bronchial obstruction  Cavitating infection (distal from carcinoma or aspirated foreign body  Vascular obstruction  Septic embolism  Infected bullae or cysts  Penetrating chest wounds (infected) Etiology  Commonly found in:  Superior segments of lower lobes  Posterior segments of upper lobes.  Effect of gravity & dependent area of aspiration (right lung more than left) Clinical Data  Physical Exam  Increased respiratory rate  Hypoxemia – stimulates Peripheral chemos.  ↓ CL causes ↑ respiratory rate  Stimulation of J receptors  Pain/anxiety/fever  Inflammatory Stage  Nonproductive cough vigorous cough  Abscess → cavity → ruptures  Produces foul-smelling brown/gray sputum Clinical Data  Increased: Heart rate, blood pressure & cardiac output  Review hypoxia’s effect on the above  Chest pain/decreased chest excursion  Cyanosis  Cough/sputum production  Cavity rupture into bronchus  foul-smelling, brown or gray color, green or yellow (nonputrid), blood-streaked or Frank hemoptysis may be present. Clinical Data  Chest Assessment:  ↑ tactile & vocal fremitus  Crackles & rhonchi  Over the abscess:  Dull percussion note  Bronchial breath sounds  Diminished breath sounds  Whispering pectoriloquy  Pleural friction rub (if near pleural surface) Clinical Data  PFT data:  Reduction in volumes  Most flows are normal  ABG  Acute alveolar hyperventilation with hypoxemia (mild-moderate abscess)  Acute ventilatory failure (severe abscess)  Oxygenation indices  ↑ shunt, ↑ O2 ER, ↓ diffusion, ↓ SvO2  Normal VO2 & O2 content Clinical Data  Sputum  Gram positive & anerobic organisms  Radiologic Findings  Increased opacity  Cavity formation  Air-fluid formation  Fibrosis & calcification  Pleural effusion  Localized consolidation (early) Management  Medications  Antibiotics  Sensitivity  Surgery – drainage  O2 per protocol – treat hypoxia  Bronchial hygiene – move mucus  Bronchoscopy if indicated  Hyperinflation therapy protocol Pneumonia 1. Anatomic Alterations/Etiology & Epi. 1. Through Community-Acquired Pneumonia 2. Community-Acquired Atypical Pneumonia 1. Through Other Causes 3. Clinical Data 4. Management 1. Including Appendix III (antibiotics) 2. Utilize Case Study Discussion to cover