A 74-year-old man is evaluated in the outpatient clinic due to a two-month history of prog… — USMLE Step 2 CK

A 74-year-old man is evaluated in the outpatient clinic due to a two-month history of progressively worsening exertional dyspnea and a persistent, dry cough. He has a known history of ischemic cardiomyopathy with a left ventricular ejection fraction of $35\%$ , moderate chronic obstructive pulmonary disease, and recurrent symptomatic ventricular tachycardia. His current daily medications include aspirin, metoprolol succinate, lisinopril, empagliflozin, inhaled tiotropium, and amiodarone, which was initiated eight months ago for arrhythmia control. His temperature is $37.4^\circ\text{C}$ ( $99.3^\circ\text{F}$ ), blood pressure is $128/78\text{ mm Hg}$ , pulse is $64/\text{min}$ , and respiratory rate is $22/\text{min}$ . Pulse oximetry shows an oxygen saturation of $91\%$ on room air. Jugular venous pressure is measured at $6\text{ cm H}_2\text{O}$ . Cardiopulmonary examination reveals regular heart sounds with no murmurs, gallops, or rubs. Auscultation of the lungs reveals fine, bilateral inspiratory crackles most prominent at the bases, without any wheezing. There is no lower extremity edema. Laboratory studies show a white blood cell count of $8,500/\mu\text{L}$ and a B-type natriuretic peptide level of $145\text{ pg/mL}$ . A high-resolution computed tomography scan of the chest demonstrates diffuse, bilateral ground-glass opacities and thickened interlobular septa. Which of the following is the most appropriate next step in the management of this patient?

Discontinue amiodarone and initiate oral prednisoneAnswer
B
Administer intravenous furosemide and obtain an echocardiogram
C
Prescribe oral azithromycin and increase the frequency of inhaled tiotropium
D
Discontinue lisinopril and observe the patient for symptom improvement
E
Perform urgent diagnostic bronchoscopy with bronchoalveolar lavage

Answer

The most appropriate next step is to discontinue amiodarone and initiate oral prednisone.

The patient presents with classic signs of amiodarone-induced pulmonary toxicity (APT), which occurs in up to 5% of patients on chronic amiodarone therapy. The presentation typically involves the insidious onset of dyspnea, dry cough, and low-grade fever. Physical examination classically reveals focal or diffuse fine crackles. High-resolution CT scanning is the most sensitive imaging modality and typically shows diffuse ground-glass opacities and thickened interlobular septa. A normal BNP level and JVP effectively rule out cardiogenic pulmonary edema as the cause of his respiratory failure. The definitive initial management for suspected APT is the immediate discontinuation of amiodarone. In patients with significant hypoxemia or extensive lung involvement, systemic corticosteroids (e.g., oral prednisone) are strongly indicated to reduce inflammatory damage.

Step-by-Step Solution

Analyze the patient's presenting symptoms and medication history.

The patient has a two-month history of dyspnea and dry cough, and has been taking amiodarone for eight months.

Establishing the timeline of symptoms relative to medication initiation is crucial for identifying drug-induced toxicities.

Evaluate for alternative cardiopulmonary causes of dyspnea.

Normal jugular venous pressure, absence of edema, and a low BNP level rule out acute decompensated heart failure. The lack of wheezing and presence of restrictive imaging patterns rule out a COPD exacerbation.

The patient has known heart failure and COPD, so these must be actively excluded using clinical and laboratory data.

Synthesize the physical exam and imaging findings.

Fine bilateral inspiratory crackles and diffuse ground-glass opacities on HRCT strongly indicate interstitial lung disease.

To correlate the clinical presentation with a specific pathophysiological process.

Determine the definitive management.

The diagnosis is amiodarone-induced interstitial pneumonitis. The immediate action is to stop amiodarone and start systemic corticosteroids.

Withdrawal of the toxic agent halts disease progression, and corticosteroids accelerate the resolution of pulmonary inflammation.

Key Concept

Amiodarone-induced pulmonary toxicity typically presents with progressive dyspnea, nonproductive cough, and bilateral interstitial infiltrates; the cornerstone of management is immediate discontinuation of the drug and systemic corticosteroids.

Estimated Time:1m 30s

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