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Batten down the hatches for thyroid storm



Management of thyroid storm

There is usually a precipitating event that drives the transition from smoldering thyrotoxicosis to thyroid storm.

“The big thing is to look for and treat the underlying precipitating event,” the endocrinologist stressed.

It’s often a systemic insult: severe infection, trauma, surgery, an acute MI, diabetic ketoacidosis, pulmonary embolism, or perhaps having just gone through labor. Iodine exposure in the form of IV contrast or taking amiodarone, which contains 37% iodine by weight, can also fan thyrotoxicosis into thyroid storm. Abrupt discontinuation of antithyroid medication is another common cause.

Fluid and electrolyte replacement, oxygen if appropriate, cooling blankets, and other supportive measures are also important.

Medical management targets multiple steps in thyroid hormone production and action to quell thyroid storm. The first order of business is to inhibit synthesis of new thyroid hormone by prescribing a thioamide. Dr. Mayer favors propylthiouracil over methimazole for this purpose because, not only does it block the thyroid gland from synthesizing new hormone, it also reduces conversion of T4 to T3. Propylthiouracil is usually given orally as a 500- to 1,000-mg loading dose, then 250 mg every 4 hours. The drug can also be given rectally or by nasogastric tube.

One hour or more after starting the thioamide, inorganic iodine is started to inhibit release of preformed hormone from the thyroid gland. Five drops of saturated solution of potassium iodide given every 6 hours is the recommended dose; it provides 764 mg of iodide per day. Lugol’s solution dosed at four to eight drops every 6-8 hours is an effective alternative.

Simultaneous with starting the patient on inorganic iodine, a low-dose beta blocker is introduced to control adrenergic symptoms.

“Propranolol is first line because it also decreases T4 to T3 conversion and it’s noncardioselective, so it’s better than a cardioselective beta blocker at reducing sympathetic tone-related symptoms, such as agitation, fever, and psychosis,” the endocrinologist explained.

At the same time that propranolol at 60-80 mg is given orally every 4 hours and iodine are started, the patient is placed on glucocorticoids as another means of reducing peripheral conversion of T4 to T3. The options are intravenous hydrocortisone at 100-300 mg/day in divided doses or dexamethasone at 2 mg every 6 hours.

Aspirin and NSAIDs should be avoided as antipyretics because they can actually raise T3 and T4 levels. Acetaminophen is the right fever-lowering agent in the setting of thyroid storm.

Dr. Mayer has occasionally had to reach for one of several backup therapies. Prescribing a bile acid sequestrant – 20-30 g/day of cholestyramine or colestipol – will trap thyroid hormone in the intestine, preventing it from recirculating.

“Be careful to dose it away from the other medications,” she cautioned.

Also, therapeutic plasmapheresis is effective at rapidly removing circulating thyroid hormone in patients who don’t show early clinical improvement in response to multipronged medical therapy.

Dr. Mayer offered a couple of final tips to hospitalists regarding thyroid storm: Know who directs plasmapheresis at your hospital, and keep the American Thyroid Association management guidelines handy (Thyroid. 2016 Oct;26[10]:1343-421).

She reported receiving funding from both NovoNordisk and Astra Zeneca.


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