A 34-year-old woman with a history of poorly controlled Graves disease presents to the emergency department with severe agitation, nausea, and vomiting. Her family reports she abruptly stopped taking all her medications two weeks ago. On examination, she is delirious, profusely diaphoretic, and tremulous. Her temperature is 40.2°C (104.4°F), blood pressure is 158/70 mm Hg, and heart rate is 155/min. An electrocardiogram demonstrates atrial fibrillation with a rapid ventricular response. Intravenous access is established. Arrange the following pharmacologic interventions in the required chronological sequence for the acute stabilization of this patient.
- 1Administer intravenous propranolol
- 2Administer oral propylthiouracil (PTU)
- 3Administer a saturated solution of potassium iodide
- 4Administer intravenous hydrocortisone
- 5Administer oral cholestyramine
Cevap
The required sequence for thyroid storm stabilization is: beta-blocker (propranolol), followed by a thionamide (propylthiouracil), followed at least an hour later by iodine (potassium iodide), with concurrent or subsequent glucocorticoids (hydrocortisone), and finally adjunctive bile acid sequestrants (cholestyramine).
Thyroid storm is a life-threatening hypermetabolic state that requires a strict pharmacological sequence. First, adrenergic overactivity must be neutralized with a beta-blocker like propranolol, which also provides some block of T4 to T3 conversion. Second, the synthesis of new thyroid hormone is stopped with a thionamide (PTU). Third, the release of pre-stored thyroid hormone is halted with iodine. Crucially, iodine must be administered at least 1 hour after the thionamide to prevent the iodine from being utilized to synthesize new hormone. Fourth, high-dose glucocorticoids are given to further block peripheral conversion of T4 to T3 and treat potential adrenal insufficiency. Finally, cholestyramine is given to prevent enterohepatic recycling.
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In the acute management of thyroid storm, iodine must never be given before a thionamide (PTU or methimazole) to prevent paradoxical worsening of thyrotoxicosis via the Jod-Basedow phenomenon.
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