Images in Clinical Medicine

Amiodarone-Induced Pulmonary Toxicity

Brian Olshansky, M.D.

N Engl J Med 1997; 337:1814December 18, 1997

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Figure 1 Osteomyelitis of a toe developed in a 59-year-old man with diabetes, coronary artery disease, and a cardioverter–defibrillator, which had been implanted three years earlier. The infection, which was caused by group B streptococcus, spread to the cardioverter–defibrillator. Computed tomography of the chest revealed no abnormalities (Panel A). The grossly infected cardioverter–defibrillator and epicardial patches were removed, and the patient was treated with amiodarone at a dose of 400 mg per day. Two months later, cough and dyspnea developed and the partial pressure of oxygen plummeted. The measured diffusing capacity of carbon monoxide dropped below 20 percent of the predicted value, and the patient became dependent on oxygen. No infectious cause could explain the new infiltrates seen on a chest film. Computed tomography showed amiodarone-induced pulmonary toxicity (Panel B). The results of right ventricular catheterization were normal. The serum amiodarone level was 2.3 mg per liter. Within two weeks after the initiation of a six-week course of oral prednisone without antibiotics, the chest film cleared, the diffusing capacity of carbon monoxide doubled, the oxygen saturation value normalized, and dyspnea resolved. Eight months after the resolution of the osteomyelitis, the patient had no dyspnea, was not receiving amiodarone or oxygen, had resumed his normal activities, and had had no recurrence of ventricular tachycardia. Seven months later a new cardioverter–defibrillator was implanted without thoracotomy.

Brian Olshansky, M.D.
Loyola University Medical Center, Maywood, IL 60153

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