Severe hypothyroidism and atrial fibrillation — a therapeutic dilemma

A 76-year-old man with advanced Parkinson’s disease and long-standing hypothyroidism had his thyroid replacement therapy carefully monitored by his physician. A few months ago his dose was reduced from daily to just six days a week because his thyroid-stimulating hormone level was a bit low. Some weeks later he developed congestive heart failure, most likely unrelated to the change in thyroid dose because he was euthyroid when admitted to the hospital. He was discharged after a few days but readmitted within a week because of worsening symptoms of CHF. On this occasion the response was slow, and he required intubation. There was great difficulty in weaning him off the ventilator, and a tracheotomy was performed. (Hypothyroidism should always be considered in patients difficult to wean off a respirator.) He had difficulty eating, and a feeding tube was needed to maintain adequate nutrition. He subsequently developed atrial fibrillation, and amiodarone therapy was started. Improvement was slow, and he was transferred to another hospital where initial laboratory studies revealed severe hypothyroidism with free thyroxine of 0.4 and TSH, 54.

The cardiologist appropriately wanted to continue amiodarone, but what to do about his thyroid replacement? The old maxim for thyroid replacement in hypothyroid patients with heart disease is “start low and go slow." That begs the question as to whether there is time to go slow with thyroid replacement in this critically ill gentleman. After extensive and amicable discussion with the cardiologist we settled on 50 mcg T₄ with both of us acknowledging that the data on which to base our decision is really quite weak.

I did a PubMed search and found an excellent review article,* but not surprisingly, it did not address the specific question in hand. In one paragraph the researchers discussed thyroid replacement in hypothyroid patients with arrhythmia and cited an article discussing dosing. I quickly went to the reference list only to discover that the citation was from a paper published in 1961. Back to PubMed, but still nothing that could really help in determining the right dose.

The next issue to address was how to give the replacement hormone. Usually in severe hypothyroidism replacement is given intravenously, but how would that affect our dosing decisions? The patient had a feeding tube, and it would be easy to give the crushed tablets through that. One problem — he was already receiving several medications through that feeding tube, and adding T₄ to that mix would almost certainly impede its absorption. To ensure maximum absorption of T₄ it is best taken between meals and without any other medications — yet another chore for the busy ICU nursing staff. The patient has tolerated the 50 mcg dose IV, and his overall condition has slowly improved.

PS: To my knowledge there is no concern that amiodarone will affect thyroid function in this patient whose thyroid gland has been nonfunctional for many years.

For more information:

*Klein I, Ojamaa K. Mechanism of disease: thyroid hormone and the cardiovascular system. N Engl J Med. 2001 ;344:501-509.