Treatment

Initial treatment of thyroid storm consists of stabilization, airway protection, oxygenation, intravenous fluids, and monitoring. Specific therapy is outlined in Table 206-6. b blockers are used to treat the severe adrenergic symptoms. Utilizing propranolol has the additional benefit of inhibiting peripheral conversion of T 4 to T3. If there is a contraindication to propranolol administration (e.g., asthma, congestive heart failure, or chronic obstructive pulmonary disease), a selective b ! medication (e.g., esmolol) may be substituted. Guanethidine (inhibits norepinephrine release at the sympathetic junction) or reserpine (depletes stored catecholamines both centrally and peripherally including the adrenal medulla) may be considered as alternative therapy. An additional treatment goal is to decrease synthesis of hormone by the administration of PTU or MMI. PTU also decreases T4 to T3 conversion. After PTU administration has been initiated, treatment is directed toward decreasing the release of preformed thyroid hormone by the administration of iodine. It is important to not administer iodine until the synthetic pathway has been blocked. Otherwise, the addition of iodine will promote further hormone production. Various iodine-containing preparations, including iodine-containing radiographic contrast material (iopodate [Oragrafin] and ipanoate [Telepaque]) have been utilized for this purpose. Administration of lithium should be considered in patients with a prior history of iodine allergies. Note that many of the drugs used to treat thyroid storm are oral preparations and subsequently may need to be administered via orogastric tube. In cases where clinical deterioration occurs despite appropriate therapy, direct removal of circulating thyroid hormone has been accomplished by exchange transfusion,9 plasma transfusion,10 plasmapheresis, and charcoal plasmaperfusion.11 Other therapeutic goals include treatment of hyperthermia with cooling blankets, ice packs, and antipyretics (acetaminophen). Avoidance of salicylates has been recommended because of displacement of T 4 from TBG, thereby increasing free T4 levels. The empiric use of corticosteroids has been suggested to treat the potential adrenal insufficiency that may occur with such a hypermetabolic state.

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