Amiodarone-Induced Central Nervous System Toxicity in the Frail Geriatric Patient: A Case Report and Review of the Literature
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The Case
A 91-year-old female was admitted to a transitional care unit after being discharged from a hospitalization for atrial fibrillation (AF) with rapid ventricular response. She initially presented to the hospital in mild acute heart failure and, following a transesophageal echocardiogram, underwent direct current (DC) cardioversion to sinus rhythm. Following DC cardioversion, however, she reverted to AF and was started on amiodarone at a dosage of 400 mg once daily. After a day on this medication she converted to sinus rhythm. Two days later, she was discharged to the transitional care unit on a reduced maintenance dosage of amiodarone of 200 mg once daily. She had no other medication changes at that time.
Five days after admission to the transitional care unit, the patient developed light-headedness, lethargy, and increased confusion over her baseline.
Her past medical history was significant for ischemic heart disease, prior coronary bypass surgery, hypertension, hyperlipidemia, hypothyroidism, mild dementia, and osteoarthritis. She also had a diagnosis of 3+ mitral regurgitation, which was felt during the hospitalization to be contributing to the heart failure. A cardiac surgery consultation in the hospital recommended attempting to convert her to sinus rhythm to see if that would help control her heart failure, and thereby obviate the need for valvular surgical repair.
Medications on admission to the transitional care unit, which were unchanged at the time the patient developed the new symptoms, were amiodarone 200 mg once daily, warfarin 2.5 mg once daily, furosemide 20 mg once daily, metoprolol 12.5 mg twice daily, aspirin 325 mg once daily, pravastatin 40 mg at bedtime, levothyroxine 125 mcg once daily, and donepezil 10 mg once daily.
On examination, the patient was noted to be oriented to person only; she was usually oriented to person, place, and month. She was slow to respond to queries and appeared sleepy. Blood pressure was 110/74, pulse was 44 and regular, respirations were 12 and relaxed, and temperature was 96.8 degrees F. Pulse oximetry was 96% on room air. Lungs were clear to auscultation, and cardiac exam revealed a 3/6 holosystolic blowing murmur heard loudest at the apex.
Laboratory study results were complete blood count and basic metabolic panel within normal limits, and thyroid-stimulating hormone (TSH) level was elevated at 11.4 mIU/L.
Amiodarone was discontinued, and dosages of the remaining medications were retained. Over the next five days, the patient's cognitive status gradually returned to baseline. Heart rate rose to 60-65 beats per minute and remained stable.
Introduction
Amiodarone is a unique and complex cardiac antiarrhythmic medication that is indicated for the treatment of recurrent ventricular fibrillation, hemodynamically unstable ventricular tachycardia, and rhythm control of AF. Amiodarone is a class III antiarrhythmic drug, indicating that it prolongs the QT interval; it also slows heart rate and AV nodal conduction and prolongs refractoriness.
Although amiodarone is a highly effective antiarrhythmic medication, it carries considerable risks of serious adverse reactions, including pulmonary disorders, particularly fibrosis and pneumonitis; thyroid disturbances; dermatologic, gastrointestinal, and neurologic adverse reactions; multiple eye disorders and, rarely, blindness; and elevation of hepatic enzymes.1-10
The structure and pharmacology of the drug provide insight into some of these adverse effects. Amiodarone consists of a benzene ring containing two iodine molecules. Doses of 100 to 600 mg daily provide 37 to 222 mg of iodine.11 These amounts are much greater than the recommended daily allowance of 0.15 mg of iodine. This large iodine load can lead to increased incidence of both hypo- and hyperthyroidism in patients taking amiodarone.
References
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