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- Hypersensitivity Lung Diseases
Differential Diagnosis in AdultsCOPD, heart failure, multiple small pulmonary emboli occasionally cause wheezing, hypersensitivity pneumonitis (more constitutional symptoms, not wheeze, except in allergic bronchopulmonary aspergillosis), bronchial obstructions (malignancy, aortic aneurysm, endobronchial TB, or sarcoidosis) occasionally present with wheezing, upper airway obstruction due to vocal cord dysfunction (can be diagnosed w/ bronchoscopy) More rare carcinoid syndrome, Churg-Strauss syndrome, and eosinophilic pneumonias such as tropical eosinophilia and other parasitic infestations like Strongyloides stercoralis (steroids can cause hyperinfection syndrome) Churg-Straus Angiitis (see vasculitides) Hypersensitivity Lung DiseasesHypersensitivity pneumonitis / dust from actinomycetes, fungus, avian proteins Acute onset: cough, dyspnea, fever, chills, myalgias / 4 to 8 hrs Subacute onset: dyspnea on exertion and dry cough over weeks to months Chronic: dyspnea, weight loss, anorexia Complications: chronic hypoxemia, clubbing, pulmonary hypertension, pulmonary fibrosis Diagnosis: CXR may or may not show reticulonodular infiltrates HRCT shows ground-glass infiltrates in lower lobes / may see centrilobular infiltrates as well / chronic disease may have patchy emphysema Labs: IgG present, but not specific; peripheral eosinophilia not a feature; may see lymphopenia and neutrophilia / tissue histology with loose, noncaseating granulomas Treatment: remove from exposure / bronchodilators and antihistamines are not effective; steroids may help in severe cases; try moderate dose then rapid taper Eosinophilic Asthmas
Chronic Obstructive Pulmonary Disease (COPD) Emphysema: abnormal permanent enlargement of the airspaces distal to the terminal bronchioles with destruction of their walls and without obvious fibrosis Risk factors: cigarette smoking, air pollution, hyperresponsive airways,  1-Antitrypsin deficiency
Classification (not much clinical utility): panacinar emphysema (PAE) – increased compliance centrilobular emphysema (CLE) – most common form in smokers / affects upper, posterior > bases / decreased compliance distal acinar emphysema (paraseptal or subpleural emphysema) subpleural or along fibrous interlobular septa / rest of the lung often spared, so lung function may be well preserved despite many foci of locally severe disease / often in apices / can cause spontaneous pneumothorax in young persons and may produce giant bullae (bullae = airspaces ≥ 1 cm, may become huge, rarely large enough to compress lung tissue and severely impair lung function) Findings: barrel chest (increased AP diameter (TLC), but VC drops because RV increases) dyspnea, decreased breath sounds, hyperresonance, pink puffers / tachycardia / decreased I/E ratio / smoking (centroacinar, usually upper lobes) / increased risk for mucoid strain of Pseudomonas (fluoroquinolones for outpatient) / hemoptysis: first rule out lung cancer, but simple mucosal erosion more common Complications acute bronchitis (see below) acute respiratory failure in COPD is defined as an exacerbation accompanied by a PaO2 < 50 mm Hg or a PaCO2 > 50 mm Hg. PaCO2 rarely rises above 80 mm Hg unless patient has received O2 therapy. Mental state ranges from alert, anxious, agitated, and distressed to somnolent, stuporous, or comatose. Cyanosis is usually present unless the patient is receiving O2 therapy. Diaphoresis and a hyperdynamic circulation are typical. Breathing is labored, and the accessory respiratory muscles are in full use. pneumothorax should be suspected in any patient whose pulmonary status suddenly worsens cor pulmonale (see other) Diagnosis CXR: exclude Tb, lung cancer / overdistention of the lungs (low, flat diaphragm) / widening of the retrosternal airspace in lateral view, increase in angle formed by the sternum and diaphragm from acute to ≥ 90° / heart shadow tends to be long and narrow / excessively rapid tapering of the vascular shadows is a sign of emphysema but may be difficult to identify unless accompanied by obviously hyperlucent lungs / RVH may or may not be apparent / may see prominent hilar vascular shadows / bullae reflect local severe disease (may not correlate with overall disease) / presence of diffuse (acute) infiltrate makes it easier to see changes of emphysema (air spaces and lack of apical vascularity) HRCT: shows all of these things in more detail [pic] PFT: FEV1 and the FEV1/FVC fall progressively as the severity of COPD increases / ABG: usually takes FEV1 < 50% predicted or < 1.5 L in order to cause hypercapnea (chronic CO2 retainer) EKG may show RAD, echo can estimate PAH Treatment: Specific therapy: eliminate risk factors, smoking cessation Drugs: bronchodilators (long-acting inhaled B-agonists or LABAs) anticholinergics (ipratropium; tiotropium) (mostly stays in lungs) corticosteroids (can sometimes have a role; no simple guidelines; current trend is inhaled steroids help QOL/fewer exacerbations for FEV1 < 50%) B-agonists (with no cardiac problems) DO NOT give B-blockers (can cause cor pulmonale) or digitalis (causes problems) antibiotics for acute COPD exacerbations (sometimes prophylactically) Trends: current thinking is to get best QOL (fewer exacerbations, etc.) is to use combination tiotropium + LABA 1/07; GOLD guidelines for FEV1 < 80%) Immunizations Oxygen Supplementation: maintain O2 saturation above 90% (corresponds to p O2 of 60) / be careful not to give too high oxygen (don’t try to correct O2 too rapidly, take several days) / Medicare pays if P02 < 55 on RA Problems with O2 use: removal of respiratory drive in pts with baseline C O2 retention too high O2 messes up VQ mismatch Haldane effect – ionized to gaseous form of C O2? Phlebotomy for polycythemia Lung volume reduction surgery: remove bad areas to relieve good areas Pulmonary rehabilitation programs Treatment of 1-antitrypsin deficiency (medical and single lung transplant)
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