Final Diagnosis -- Thyrotoxicosis in an 11 year-old girl with Averted Thyroid Storm Following Radio-pharmaceutically Induced Therapeutic Lysis of Thyroid Gland


Thyroid storm is diagnosed on the basis of symptoms. Although laboratory tests indicate thyrotoxicosis (by elevated thyroid hormone levels) there is nothing to distinguish thyroid storm from ordinary hyperthyroidism.

Much of the treatment protocol for thyroid storm is aimed at Graves' disease and other hyper-thyroid forms of thyrotoxicosis. Beta-blockade, antipyretics, hydration, and supportive care including steroids will be beneficial regardless of the etiology of thyroid storm. Corticosteroids are also known to inhibit the extra-thyroidal conversion of FT4 to FT3 (17, 18). There is also some thought that hydrocortisone may act as a membrane stabilizing agent, thus potentially further contributing to a decrease in the levels of circulating thyroid hormone (19). One could postulate a similar effect from lithium. Cholestyramine may also help lower thyroid hormone levels irrespective of thyrotoxic etiology via interruption of enterohepatic recirculation. (Insert here a brief note on the prophylaxis for thyroid storm in patients undergoing RAI treatment for hyperthyroidism and thyrotoxicosis).


Patient follow/up:

The elevated thyroid hormone levels in this patient after RAI were expected at the peak of the destruction of thyroid cells by 131I. The patient received appropriate pharmaceutical regimen to block the effects of markedly elevated circulating thyroid hormones following RAI thyroid ablation. Due to the fact that the patient did not manifest any symptoms suggestive of a thyroid storm, a diagnosis of thyrotoxicosis following the RAI treatment is favored.

The markedly elevated free T4, total T4 as well as total T3 concentrations are confirming laboratory findings, but do not by themselves indicate a thyroid storm. The markedly elevated thyroid hormone levels and suppressed TSH support the diagnosis of thyroid tissue lysis due to radio-iodine administration with potential for thyroid storm. However, being aware of this possibility in this adolescent patient who was treated with the radio-pharmaceutical approach for Grave's thyrotoxicosis after failing medical management, the endocrinologist did prophylactically administer beta blockers specifically to prevent the effect of thyroid hormones released from the tissues undergoing lysis.

After approximately one month from RAI the patient was started on thyroid hormone supplementation (Levoxyl) at 37.5 mcg daily and she was also taken off the atenolol.

In terms of review of systems, the patient reports that sleep, appetite, and energy all were at a normal level, as well as the school performance. The last battery of tests done at approximately 6 weeks after the RAI shows the following results: TSH, 7.14 mIU/L, Free T4, 0.5 ng/mL, Total T3, 79 ng/dL, Free T3, 2.3 pg/mL.

The patient was judged to be biochemically under-treated with replacement thyroid hormone and the Levoxyl dose was increased from 37.5 mcg daily to 75 mcg daily.


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Contributed by Anca V. Florea, MD and Mohamed A. Virji, MD, PhD

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