Chronic Obstructive Pulmonary Disease

• Chronic obstructive pulmonary disease (COPD) is defined as progressive, chronic airflow obstruction due to chronic bronchitis, emphysema, or both. The majority of patients have components of both, although one of these entities will frequently dominate the clinical picture.
• Emphysema—airspace enlargement distal to the terminal bronchioles due to destruction of alveolar septa.
• Chronic bronchitis—chronic airway inflammation and bronchospasm. Clinically defined as productive cough lasting for at least 3 mo over 2 consecutive years.
• Although COPD is irreversible, patients with acute exacerbations do have reversible bronchospastic and inflammatory components.

  Etiology and Risk Factors

• Cigarette smoking, including passive exposure to cigarette smoke, is by far the leading cause.
• Occupational exposures and hereditary a-1 antitrypsin deficiency are less common.

  Diagnosis

• Clinical diagnosis is based on the presence of dyspnea, wheezing, and/or cough in a patient with a history of causative exposure and chronic, progressive symptoms. Patients usually present in the fifth or sixth decades of life. Alpha-1 antitrypsin deficiency should be suspected in any patient younger than 40 yr old with signs and symptoms of COPD.
• Presentation may separated into two syndromes, depending on the predominate pathologic process.
• "Pink puffer" (emphysema dominant) Patient is barrel-chested with thin build.
• Cough is nonproductive or has scant sputum only. Exam remarkable for decreased breath sounds.
• Hypoxemia and hypercarbia occur only in end-stage disease.
• CXR shows hyperinflation, flattened diaphragms, and a small heart.
• "Blue bloater" (bronchitis dominant)
• Patient is overweight with stocky build.
• Patients have prominent, productive cough with wheezes and rhonchi on examination.
• Patients usually retain CO2. Hypoxemia and hypercarbia occur early in disease.
• CXR shows increased vascular markings and a large heart.
• Patients may present with varying degrees of respiratory difficulty. Dyspnea, worsening cough, and chest tightness are common complaints.
• Physical examination is similar to asthma with varying degrees of audible wheezing, decreased breath sounds, and prolonged expiratory phase. Patients may also have other signs such as a barrel chest and stigmata of chronic pulmonary disease such as clubbing.
• Diagnostic Studies
• Pox and ABG—All COPD patients should have continuous Pox monitoring.
• Unlike patients with asthma, many with COPD have baseline oxygen saturations well below 95%. ABG is helpful in critically ill patients and those requiring mechanical ventilation. Note that COPD patients often have an elevated pCO2 at baseline. In these patients, ventilator insufficiency is indicated by a decreased pH in conjunction with a high pCO2. ABG may be helpful in assessing the severity of an exacerbation if a baseline pCO2 is available in the patient’s chart.
• PEFR is sometimes used to monitor the effects of maintenance therapy in patients with mild to moderate disease but is of little use in the ED.
• CXR—The EP should consider CXR in most patients with COPD exacerbation, the exception being those with mild exacerbation and prompt response to therapy.
  CXR is helpful in diagnosing an underlying source of for acute symptoms including PTX and pulmonary infiltrates.
• Laboratory testing—As with asthma, routine laboratory evaluation contributes little to management (see "Asthma"). If a CBC is obtained, the EP may note polycythemia secondary to chronic hypoxia. The EP may consider electrolytes, renal function studies, and/or cardiac enzymes as indicated by presentation and comorbidities.
• EKG—Patients in moderate to severe distress require continuous EKG monitoring. The 12-lead EKG often has findings consistent with right heart strain. An
  EKG should be obtained in those patients with chest pain, severe hypoxia, suspected dysrrhythmia or acute coronary syndrome.
• Differential Diagnosis
• The diagnosis of COPD is usually not difficult. However, the EP should determine the cause of the acute exacerbation. Respiratory infections, allergen exposure, continued cigarette smoking, air pollution, and patient noncompliance are common causes.
• Acute PTX, lobar atelectasis, and PE are the most potentially deadly causes of exacerbation. Unfortunately, PTX and PE can be difficult to diagnose in the COPD patient but should be suspected in all patients with exacerbation especially those with acute onset of symptoms.
• Pneumonia occurs frequently in patients with COPD. This diagnosis should be considered based on clinical findings since CXR may or may not reveal an infiltrate.

Treatment

• To a large degree, this mirrors therapy for asthma (see "Asthma") with some variations as discussed below. The most important aspect of therapy is to initiate rapid intervention for those patients with acute or impending respiratory failure.
• Respiratory support
• Concern exists that aggressive oxygen therapy may thus worsen hypercarbia by suppression of hypoxic respiratory drive. This concern is somewhat theoretical and less important in the ED where ventilator support is immediately available. A safe approach in the nonintubated patient is to titrate oxygen to achieve saturation between 90-92%.
• Application of NPPV, endotracheal intubation, and ventilator management in COPD patients is similar to use as described in "Asthma" section.
• Medications
• Beta2 agonists—The EP should follow the same dosing recommendations as previously described but should keep in mind that many patients with COPD are elderly and have cardiovascular comorbid disease. As a result, administration of ß2 agonists is more likely to be limited by adverse side effects.
• Inhaled Anticholinergics—these agents are very effective in COPD both alone and in conjunction with ß2 agonists. Ipratropium should be used in all patients with COPD exacerbation. Dosing is the same as for asthma.
• Corticosteroids, methylxanthines, and magnesium—Indications and dosing are discussed in the asthma section.
• Antibiotics
• Although the role of bacterial infection in acute bronchitis is controversial, antibiotic therapy has been shown to improve outcomes for patients with purulent sputum and severe COPD exacerbation.
• Trimethoprim-sulfmethoxazole, doxycycline, amoxicillin-clavulanate, azithromycin, or clarithromycin are appropriate choices for both acute bronchitis and outpatient pneumonia therapy.
• Empiric inpatient pneumonia treatment is with second or third generation cephalosporin and possibly a macrolide to cover atypical organisms. If possible, sputum cultures should be obtained for all admitted patients to guide future antibiotic therapy.

  Disposition

• Patients who respond rapidly to therapy and return to baseline in the ED can be discharged with close outpatient follow-up. However, many patients with COPD exacerbation require admission. This is due to the relatively smaller reversible component of airway disease that exists in COPD. The EP should also maintain a low threshold for admission for those with pneumonia. Intubated patients and those at risk for decompensation require ICU admission.
• All discharged patients should receive appropriate therapy including bronchodilators ± anticholinergics, corticosteroids, and antibiotics.

Suggested Reading

1. Madison MJ, Irwin RS. Chronic obstructive pulmonary disease. Lancet 1998; 352:467-473.
2. Advanced Cardiac Life Support Textbook. Dallas, TX: American Heart Association, 1994.
3. Gammon RB, Strickland JH, Kennedy JI et al.: Mechanical ventilation: A review for the internist. Amer J Med 1995; 99:553-562.
4. McFadden ER. Asthma. In: Isselbacher KJ, ed. Harrison’s Textbook of Medicine 13th Ed. New York: McGraw-Hill, 1994.
5. Honig EG, Ingram RH. Chronic bronchitis, emphysema, and airways obstruction. In: Isselbacher KJ, ed. Harrison’s Textbook of Medicine. 13th Ed. New York: McGraw-Hill, 1994.
6. Mandavia DP, Dailey RH. Chronic obstructive pulmonary disease. In: Rosen Frakes MA, Richardson LE, eds. Magnesium therapy in certain emergency conditions. Am J Emerg Med 1997; 15:182-187.
7. West JB. Respiratory physiology-the essentials, 4th ed. Baltimore: Williams & Wilkins, 1990.
8. Emond SD, Camargo CA, Nowak RM. 1997 National Asthma Education and Prevention Program guidelines: A practical summary for emergency physicians. Ann Emerg Med 1998; 31(5):579-594.
9. Brenner B, Kohn MS. The acute asthmatic patient in the ED: To admit or discharge. Am J Emerg Med 1998; 16(1):69-75.
10. Panacek EA, Pollack CV. Medical management of severe acute asthma. In: Brenner BE, ed. Emergency Asthma. New York: Marcel Dekker Inc., 1999.
11. Stedman’s Medical Dictionary. In: William R. Henyl, ed. Baltimore: William & Wilkens, 1990.