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130 CHRONIC BRONCHITIS, EMPHYSEMA, AND ACUTE OR CHRONIC RESPIRATORY FAILURE

130 CHRONIC BRONCHITIS, EMPHYSEMA, AND ACUTE OR CHRONIC RESPIRATORY FAILURE
Harrison’s Manual of Medicine

130

CHRONIC BRONCHITIS, EMPHYSEMA, AND ACUTE OR CHRONIC RESPIRATORY FAILURE

Natural History
Clinical Manifestations
Acute Respiratory Failure
Bibliography

Natural History
Chronic obstructive pulmonary disease (COPD) is a progressive disorder even when contributing factors are eliminated and aggressive therapy is instituted. Progression is inevitable, since loss of elastic tissue is a normal part of the aging process. In normal individuals, forced expiratory volume in 1 s (FEV1) reaches lifetime peak around 25 years and declines on average approx 35 milliliters per year thereafter. Annual loss among susceptible individuals with COPD is 50– 100 mL/year. Greater rates of decline are associated with mucus hypersecretion (men) and with airway hyperreactivity. Symptoms occur only in association with moderate or severe COPD. Typically, dyspnea occurs when FEV1 falls below ~40% of predicted. Hypercarbia is most common after FEV1 has fallen to <25% of predicted. Some pts whose symptoms are out of proportion to the decrease in FEV1 have marked reductions in diffusing capacity for carbon monoxide.
Clinical Manifestations
HISTORY   Pts with COPD usually have an exposure to tobacco of ³20 pack years. Onset is typically in the fifth decade or later. Exertional dyspnea and productive cough are typical early symptoms. Functional limitation may correlate poorly with reduction in FEV1. Sputum volume is usually small; production of >60 mL/d should prompt investigation for bronchiectasis. Weight loss is common in advanced disease. Hypoxemia and hypercarbia may result in fluid retention, morning headaches, sleep disruption, erythrocytosis, and cyanosis. Exacerbations are more frequent as disease progresses and are most often triggered by respiratory infections, often with a bacterial component. They may also be precipitated by left ventricular failure, cardiac arrhythmia, pneumothorax, pneumonia, and pulmonary thromboembolism.
PHYSICAL FINDINGS   These correlate poorly with disease severity. Exam may be normal early. As disease progresses, signs of hyperinflation become more prominent. Mid-inspiratory crackles may reflect disease of moderate-size airways. Pursed-lip breathing may reduce dyspnea and dynamic hyperinflation. Wheezing is an inconstant finding and does not predict degree of obstruction or response to therapy.
RADIOGRAPHIC FINDINGS   Plain CXR may show hyperinflation, emphysema, and pulmonary hypertension. Local radiolucencies (>1 cm) may indicate bullae. CT scan has greater sensitivity for emphysema but is not necessary for diagnosis.
PULMONARY FUNCTION TESTS   Objective documentation of airflow obstruction is essential for diagnosis of COPD. Forced vital capacity (FVC) is typically decreased, but FEV1 is decreased more so that the ratio of FEV1/ FVC is reduced. Exhalation may be incomplete even after a 10-s forced attempt. The American Thoracic Society grades COPD by FEV1: stage I, mild disease FEV1 ³ 50% predicted; stage II, moderate disease, FEV1 35–49% predicted; stage III, severe disease, FEV1 < 35% predicted. Reversibility of obstruction is determined by a trial of inhaled bronchodilators.

TREATMENT
Smoking Cessation Elimination of tobacco has been convincingly shown to prolong survival in patients with COPD. Although lost lung function is not regained, the rate of decline in FEV1 reverts rapidly to that of nonsmokers. Use of nicotine replacement therapy (patch, gum) can increase rates of cessation in motivated pts. Oral bupropion (150 mg bid) produces significant additional benefit.
Bronchodilators(Table 130-1) These do not influence longevity in pts with COPD but may significantly reduce symptoms. Short- and long-acting b-adrenergic agonists, anticholinergics, and theophylline derivatives may all be used. Although oral medications are associated with greater rates of adherence, inhaled medications generally have fewer side effects. Pts with mild disease can usually be managed with an inhaled short-acting b agonist such as albuterol. Anticholinergic therapy, e.g., inhaled ipatroprium, may be added to more symptomatic pts with moderate disease. Long-acting b agents, e.g., inhaled salmeterol or oral sustained-release albuterol, should be added in pts with severe disease. The narrow toxic-therapeutic ratio of theophylline compounds limits their use.

Table 130-1 Recommended Bronchodilator Therapy for Chronic Obstructive Pulmonary Disease

Glucocorticoids Unlike pts with asthma, patients with COPD respond unpredictably to glucocorticoids. Approximately 10% of pts will have a significant response as assessed by symptoms and FEV1. Responders cannot be predicted by clinical characteristics. Systemic steroids have substantial side effects, so their use should be restricted. The role of inhaled steroids is uncertain, but some evidence suggests they may reduce the severity of exacerbations. However, they do not slow progression of disease.
Oxygen Long-term domicilary O2 therapy has been shown to reduce symptoms and improve survival in pts who are chronically hypoxemic, if they have stopped smoking. Documentation of the need for O2 requires a measurement of PaO2 or oxygen saturation (SaO2) after a period of stability. Pts with a PaO2 £ 55 mmHg or SaO2 £ 88% should receive O2 to raise the SaO2 ³ 90%. O2 is also indicated for pts with PaO2 of 56–59 mmHg or SaO2 £ 89% if associated with signs and symptoms of pulmonary hypertension or cor pulmonale. O2 may also be prescribed for selected pts who desaturate with exercise or during sleep.
Transplantation Lung transplantation should be considered for pts with severe COPD whose FEV1 is < 25% predicted despite maximal therapy, particularly if associated with hypoxemia and cor pulmonale.
Lung Volume Reduction Surgery This procedure, which removes emphysematous lung tissue to allow expansion of the remaining pulmonary parenchyma, is currently being studied in pts with disabling dyspnea. Indications and potential for long-term benefit remain controversial.
MILD EXACERBATIONS
These may be managed with bronchodilators, antibiotics, and short courses of systemic glucocorticoids. Short-acting b-adrenergic agonists such as albuterol may be used up to every 1–2 h by metered dose inhaler (MDI). Anticholinergics such as ipatroprium by MDI should not be used more frequently than every 4–6 h, however. With increased sputum volume or change in character, antibiotic therapy should be administered. Trimethoprim-sulfamethoxazole, doxycycline, and amoxicillin are all acceptable choices. Evidence for effectiveness of systemic glucocorticoids in outpatient management of exacerbations is lacking, but usual practice is to administer 20–40 mg of prednisone daily for 7–10 days.

Acute Respiratory Failure
Diagnosis is made on the basis of decrease in PaO2 by 10–15 mmHg from baseline or increase in PaCO2 associated with a pH £ 7.30.

TREATMENT
Precipitating factors should be sought, especially the presence of left ventricular failure. Clinical signs of CHF are often difficult to identify, so empirical therapy with a diuretic (furosemide 10–60 mg IV) is appropriate if peripheral edema is present.
Bronchodilators Administer short-acting b-adrenergic agonists by inhalation (e.g., albuterol q1–2h; may be administered as frequently as q20mins initially). Because absorption is unpredictable when pts are in distress, dosing should be dictated by side effects. Addition of anticholinergics is likely of benefit (ipatroprium q4–6h).
Glucocorticoids Evidence is convincing that systemic steroids may hasten resolution of symptoms. Dosing is not well worked out, but 30–60 mg of prednisone daily (or IV equivalent) is standard, with a total course of 14 days.
Oxygen Supplemental O2 should be administered to maintain SaO2 ³ 90%. Delivery systems include nasal prongs 1–2 1pm or 24% Venturi mask.
Ventilatory Support Numerous studies suggest noninvasive mask ventilation can improve outcomes in acute exacerbations. Pts with marked respiratory distress (respiratory rate > 30 breaths/min) should have a trial of mask ventilation. Success is indicated by a reduction in respiratory rate to < 25 breaths/min after 30–60 min. Progressive hypercarbia, refractory hypoxemia, or alteration in mental status that compromises ability to comply with therapy may necessitate endotracheal intubation.

Bibliography

For a more detailed discussion, see Honig EG, Ingram RH Jr: Chronic Bronchitis, Emphysema, and Airways Obstruction, Chap. 258, p. 1491, in HPIM-15.

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