While very effective as an antiarrhythmic, amiodarone therapy is also associated with a wide array of adverse side effects involving the cornea, lungs, liver, skin, and thyroid. Although the majority of amiodarone therapy ‘s adverse effects on these organs result from deposition of the drug in the parenchyma, its effect on the thyroid gland is quite unique.
Amiodarone has become a popular drug in the intensive care unit (ICU) because of its utility in the management of a broad spectrum of ventricular and atrial arrhythmias.
As a class III antiarrhythmic agent, its mechanism of action is to delay repolarization and increase the duration of the action potential through inhibition of myocardial potassium ion channels.
Amiodarone bears a structural resemblance to the thyroid hormones thyroxine (T4) and triiodothyronine (T3), while containing approximately 37% iodine by weight.
Metabolism of amiodarone therapy causes deiodination, which results in the release of up to 50- to 100-fold excess iodine compared with normal daily intake. amiodarone therapy induced thyroid dysfunction results from this massive increase in total iodine, as well as alterations in hormone metabolism caused by the drug.
While amiodarone therapy can cause either hyper- or hypo-thyroidism, it typically induces hypothyroidism in iodine-sufficient areas such as the United States where the incidence is estimated to range up to 30%. In particular, patients with preexisting thyroid autoimmunity are at increased risk for the development of hypothyroidism while receiving the drug.
The acute effects observed after initiating therapy is an increase in thyroid-stimulating hormone (TSH) levels by 20% to 50%, with a decrease in serum T3 levels by 15% to 20% within the first 2 weeks of therapy. amiodarone therapy blocks the peripheral conversion of T4 to T3 and inhibits the entry of these hormones into peripheral tissue.
The resulting symptoms of hypothyroidism include cold intolerance, dry skin, weight gain, and fatigue. In the ICU, signs of hypothyroidism may also manifest when a patient is having difficulty weaning from mechanical ventilation.
Once patients are diagnosed, treatment with levothyroxine should be initiated and amiodarone therapy may be continued if a suitable replacement antiarrhythmic is not available.
Before starting patients in the ICU on amiodarone therapy, a careful examination of the thyroid should be performed along with baseline measurements of serum TSH, free T4, T3, and thyroid peroxidase and thyroglobulin antibodies.
This will help detect underlying thyroid dysfunction and identify patients who may be more predisposed to develop thyroid dysfunction while on amiodarone therapy. Thyroid function should thereafter be checked every 3 to 6 months while patients are continued on therapy.