Thyroid Storm
	Thyroid storm is a worrisome complication of hyperthyroidism, characterized by manifestations of severe hypermetabolism including fever, tachyarrhythmias, confusion, restlessness, tremulousness, and profuse sweating[2, 3]. Congestive heart failure frequently accompanies cardiac manifestations, and, as the disorder progresses, stupor, coma, and vascular collapse may supervene leading the patient to death. Thyroid storm occurs in patients with a preexisting thyrotoxicosis, either not recognized or not adequately treated, in whom a precipitating factor produces an abrupt release into the circulation of large quantities of stored thyroid hormones. Prior to the use of antithyroid drugs, thyroid surgery and radioiodine therapy were relatively common causes of thyroid storm. Infections, traumas, surgical distress, metabolic disorders, pulmonary and cardiovascular diseases are among the other factors which may precipitate a thyroid storm. Thyrotoxic crises have been reported following surreptitious ingestion of overdoses of thyroid hormones. Nowadays, early diagnosis and effective treatment of hyperthyroidism, and adequate preparation of patients undergoing thyroid surgery or radioiodine therapy, have rendered thyroid storm a rare event. However, less severe forms of thyrotoxic crisis are not exceptional, and may represent a medical emergency which requires prompt recognition and adequate treatment. Therapeutic guidelines are directed to: Treatment of underlying nonthyroidal illnesses by specific means, such as digoxin, diuretics, antibiotics, and intravenous fluids, as required; Normalization of body temperature by cooling blankets and/or pharmacological agents such as acetaminophen, chlorpromazine, or meperidine; Inhibition of the synthesis and release of thyroid hormones by thionamides (MMI, PTU), iodides (Lugol's solution, SSKI, intravenous sodium iodide) or iodinated contrast agents (iopanoic acid, sodium ipodate); Inhibition of the peripheral conversion of T4 to T3 by glucocorticoids, iodinated contrast agents, or PTU; Block of the peripheral effects of thyroid hormones by beta-adrenergic antagonists (propranolol, metoprolol, atenolol); Removal of excess thyroid hormones from the circulation by plasmapheresis, peritoneal dialysis, extracorporeal resin perfusion or charcoal plasmaperfusion. All drugs should be employed in maximal doses. Patients require continues monitoring of the electrocardiogram and an intravenous line to administer fluids and drugs. Alternatively drugs can be delivered by a nasogastric tube. Our protocol for treatment of patients with hyperthyroidism and thyroid crises is as follows: methimazole 40 mg every 12 h, Lugol's solution 20 drops orally every 6 h, propranolol 40 mg orally every 4 h, dexamethasone 2 mg intravenously every 6 h. Doses can be gradually reduced as general conditions improve. If the patient does not respond to this treatment, or presenting symptoms are too severe, direct removal of thyroid hormones from the circulation becomes necessary. In our experience plasmapheresis is an effective mean to achieve this goal. Plasmapheresis should also be used in thyrotoxic crises due to the surreptitious ingestion of thyroid hormones, or in patients whose thyrotoxicosis has been induced by long-lasting iodine substance.