A 65-year-old man with known ischemic cardiomyopathy comes to the office due to 2 weeks of progressive shortness of breath and nonproductive cough. One week ago, he was instructed to increase his furosemide dose, but it did not seem to help. He has had no chest pain or orthopnea. He takes all of his medications as directed and comes to all of his clinic visits. The patient had a myocardial infarction 5 years ago and has severe left ventricular systolic dysfunction with an ejection fraction of 20%. He has an automatic implantable cardioverter-defibrillator (AICD). Six months ago, he was hospitalized with recurrent AICD shocks due to ventricular tachycardia; he was successfully treated with antiarrhythmic therapy, which he is currently still taking. He is afebrile. His blood pressure is 122/70 mm Hg and his pulse is 68/min and regular. His mucous membranes are moist. His jugular veins are flat while he is in a seated position. Bilateral inspiratory crackles are heard on lung auscultation. There are no cardiac murmurs. There is no significant peripheral edema. Chest x-ray reveals bilateral lung infiltrates involving primarily the middle lung fields. Which of the following is the most likely cause of this patient's current symptoms?
Major side effects of amiodarone | |
Cardiac |
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Pulmonary |
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Endocrine |
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Gastrointestinal/ |
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Ocular |
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Dermatologic |
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Neurologic |
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This patient's clinical presentation - progressive dyspnea, nonproductive cough, bilateral inspiratory crackles, and chest radiograph findings - is consistent with amiodarone-induced interstitial pneumonitis. Chest x-ray further supports the diagnosis with the presence of localized or diffuse reticular or ground-glass opacities (which can be migratory). Pulmonary function tests would reveal a restrictive pattern with a reduced diffusion capacity of carbon monoxide (DLCO).
Amiodarone is a class III antiarrhythmic drug often used for management of ventricular arrhythmias in patients with coronary artery disease and ischemic cardiomyopathy. It can cause several potential adverse effects, and monitoring of several parameters (eg, TSH) is recommended. Some manifestations of pulmonary toxicity due to amiodarone include chronic interstitial pneumonitis (usually within months of therapy), organizing pneumonia, acute respiratory distress syndrome, diffuse alveolar hemorrhage, pulmonary nodules, and solitary masses.
(Choice A) Advanced or worsening heart failure is unlikely to explain this patient's dyspnea given the flat jugular veins, absence of peripheral edema, and lack of improvement with higher diuretic doses.
(Choice C) Diuretic toxicity or overdose typically results in intravascular volume depletion with signs of dehydration (dry mucous membranes). Electrolyte imbalances (eg, hypokalemia, hypomagnesemia) can develop and sometimes manifest as palpitations. Bilateral infiltrates would not be expected.
(Choice D) Tricuspid valve insufficiency causes a holosystolic murmur along the lower left sternal border and signs of right heart failure with prominent jugular pulsations, hepatomegaly, and peripheral edema.
(Choice E) Viral pneumonia is one of the differential diagnoses in patients with amiodarone lung toxicity. However, the lack of fever (although fever can occur with amiodarone lung toxicity), time course of symptoms after initiation of antiarrhythmic therapy, and radiographic findings all make interstitial pneumonia due to amiodarone use more likely.
Educational objective:
Pulmonary toxicity is a serious adverse effect of long-term amiodarone use and can occur months to several years after the initiation of therapy. Interstitial pneumonitis due to amiodarone presents with progressive dyspnea, nonproductive cough, and new reticular or ground-glass opacities on chest radiograph.