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1
Question:

A 69-year-old man comes to the emergency department due to severe shortness of breath for the past 24 hours.  The patient has used an albuterol inhaler many times without relief.  He reports one day of low-grade fever that resolved with acetaminophen.  The patient has a 60-pack-year history.  Temperature is 37.2 C (99 F), pulse is 112/min, blood pressure is 150/90 mm Hg, and respirations are 22/min.  He is using accessory muscles of respiration and is too dyspneic to speak in full sentences.  Lung examination shows prolonged expiration with end-expiratory wheezing bilaterally.  Chest x-ray reveals hyperlucency of the lung tissue, a large right upper lobe bulla, and no airspace infiltrates.  Results of arterial blood gas testing performed on room air are as follows:

pH7.27
pCO272 mm Hg
pO250 mm Hg
HCO332 mEq/L

Respiratory viral panel is negative.  Antibiotic therapy and noninvasive positive pressure ventilation are initiated.  Which of the following medications is most strongly indicated at this time?

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Explanation:

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This patient with a long smoking history, radiographic emphysema (bulla, hyperlucent lung tissue), and expiratory airflow limitation (prolonged expiration, wheezing) likely has chronic obstructive pulmonary disease (COPD).  Arterial blood gas analysis shows acute-on-chronic respiratory acidosis.  In addition to his increased dyspnea, these features are consistent with an acute exacerbation of COPD (AECOPD).

The pathophysiology of AECOPD involves increased lower respiratory tract inflammation, often in response to an underlying infectious trigger (~70% of cases).  Management of AECOPD addresses the infectious and inflammatory processes:

  • Antibiotics, which are given to select patients, offer empiric coverage of commensal bacterial flora (eg, Haemophilus influenzae) to reduce bacterial burden and dampen the attendant inflammatory response.

  • Systemic glucocorticoids (eg, prednisone, methylprednisolone), which are given to all patients, reduce airway inflammation to lessen bronchial wall edema and secretions and improve expiratory airflow.  A typical treatment duration is 5-7 days; oral and intravenous administration is considered equivalent, but the latter may be required for patients who are too dyspneic to swallow.

Systemic glucocorticoids should be administered even when there is an underlying infectious trigger because respiratory dysfunction is mostly driven by the infection-elicited inflammatory response rather than the pathogen itself.

(Choices A and B)  Inhaled corticosteroids (eg, fluticasone) and long-acting beta agonists (eg, salmeterol) are used for long-term control of asthma, but they have no role in treatment of AECOPD.

(Choice C)  Intravenous magnesium sulfate is a smooth muscle relaxant that produces bronchodilation to treat severe asthma exacerbations.  It has minimal effect in AECOPD, which involves expiratory small airway collapse (emphysema) and mucus hypersecretion (chronic bronchitis), rather than intense smooth muscle constriction.

(Choices E)  Nebulized epinephrine is used for treatment of croup, wherein it produces mucosal vasoconstriction to reduce laryngeal or epiglottic edema.  Upper airway edema is not a significant component of AECOPD.

(Choice F)  Nebulized hypertonic saline is sometimes used to thin respiratory secretions in patients with significant mucostasis (eg, bronchiectasis).  It can be a supportive adjunct for AECOPD associated with tenacious secretions (absent in this patient); however, it does not alter outcomes or recovery.

(Choice G)  Oral furosemide is indicated for patients with decompensated heart failure, which is characterized by orthopnea, wet inspiratory crackles, and vascular congestion or pulmonary edema on chest x-ray.

(Choice H)  Roflumilast, a phosphodiesterase-4 inhibitor with anti-inflammatory properties, is used for AECOPD prophylaxis in patients with frequent exacerbations; however, it has no role in acute treatment.

Educational objective:
Patients with acute exacerbations of chronic obstructive pulmonary disease should be treated with systemic glucocorticoids, even in the setting of an infectious trigger, to inhibit the cascade of airway inflammation.