Thyroid storm is a rare, life-threatening condition characterized by severe or exaggerated clinical manifestations of thyrotoxicosis. Although thyroid storm can develop in patients with longstanding untreated hyperthyroidism (Graves’ disease, toxic multinodular goiter, solitary toxic adenoma), it is often precipitated by an acute event such as thyroid or nonthyroidal surgery, trauma, infection, an acute iodine load, or parturition.
Patients with thyroid storm typically have an exaggeration of the usual symptoms of hyperthyroidism. The classical symptoms of thyroid storm include tachycardia, hyperpyrexia, central nervous system (CNS) dysfunction (agitation, delirium, psychosis, stupor, or coma), and gastrointestinal symptoms (nausea, vomiting, abdominal pain). Physical examination may reveal goiter, ophthalmopathy (in the presence of Graves’ disease), lid lag, hand tremor, and warm and moist skin. Thyroid function tests show hyperthyroidism (suppressed thyroid-stimulating hormone [TSH], elevated free thyroxine [T4] and triiodothyronine [T3]) generally comparable with that in patients with uncomplicated overt hyperthyroidism.
the mortality rate of thyroid storm is substantial (10 to 30 percent).
The diagnosis of thyroid storm is based upon the presence of severe and life-threatening symptoms (hyperpyrexia, cardiovascular dysfunction, altered mentation) in a patient with biochemical evidence of hyperthyroidism (elevation of free T4 and/or T3 and suppression of TSH). There are no universally accepted criteria or validated clinical tools for diagnosing thyroid storm. In one scoring system, a score of 45 or more is highly suggestive of thyroid storm, whereas a score below 25 makes thyroid storm unlikely.
The therapeutic options for thyroid storm are expanded from those used for uncomplicated hyperthyroidism, with additional drugs typically used, such as glucocorticoids and iodine solution (eg, saturated solution of potassium iodide [SSKI]), and standard drugs are given in higher doses and more frequently. In addition to specific therapy directed against the thyroid, supportive therapy in an intensive care unit (ICU) and recognition and treatment of any precipitating factors is essential since the mortality rate of thyroid storm is substantial (10 to 30 percent).
For patients with clinical features of thyroid storm, we begin immediate treatment with a beta blocker (propranolol 心得安/ 普萘洛尔 in a dose to achieve adequate control of heart rate, typically 60 to 80 mg orally every four to six hours), a thionamide (硫氨类化合物,1943年被发现,其主要作用机制是抑制甲状腺激素的合成, 这类药物常用的只要包括他巴唑(MMI)、丙基硫氧嘧啶(PTU)和卡比马唑), and glucocorticoids (hydrocortisone氢化可的松 , 100 mg intravenously every eight hours). One hour after a thionamide is given, we administer iodine (SSKI, 5 drops [20 drops/mL, 50 mg iodide/drop] orally every six hours or Lugol’s solution, 10 drops [20 drops/mL, 6.25 mg iodine/drop] every eight hours). Bile acid sequestrants (cholestyramine考来烯/消胆胺, 4 g orally four times daily) may also be of benefit in severe cases to decrease enterohepatic recycling of thyroid hormones.
For patients with life-threatening thyroid storm admitted to an ICU, we suggest propylthiouracil (PTU) (200 mg orally every four hours) rather than methimazole 他巴唑/甲硫咪唑 as initial therapy. PTU blocks T4-to-T3 conversion and results in lower serum T3 levels for the first several days of treatment. However, for severe, but not life-threatening, hyperthyroidism, methimazole(20 mg every six hours) may be preferred because of its longer half-life, lower risk of hepatic toxicity, and because it ultimately restores euthyroidism more quickly than PTU. Patients initially treated with PTU should be transitioned to methimazole before discharge from the hospital.
For patients with contraindications to thionamides who require urgent correction of hyperthyroidism, surgery is the treatment of choice.