Thyrotoxicosis management

Three main modalities of therapy should be considered for patients with thyrotoxicosis, namely, medical therapy, surgical thyroidectomy, and radioiodine. The choice between these therapies should be dictated by the clinical nature of the disease, the patient s general health, her desire for pregnancy or need to care for young children, and overall patient preference. Treatment is initially monitored by free thyroxine (T4) values, as suppression of thyroid-stimulating hormone (TSH) may persist for months despite adequate management. 

Propranolol is indicated in the management of a variety of cardiac rhythm abnormalities that are totally or partially due to enhanced adrenergic stimulation. In selected cases of sinus tachycardia caused by anxiety, pheochromocytoma, or thyrotoxicosis, (3-blockade will reduce the spontaneous heart rate. 

It is indicated in hypertension, angina pectoris, cardiac arrhythmia, post MI patients, adjunctive management of thyrotoxicosis and prophylaxis of migraine. 

Beta blockers without intrinsic sympathomimetic activity (eg, metoprolol, propranolol, atenolol) are effective therapeutic adjuncts in the management of thyrotoxicosis since many of these symptoms mimic those associated with sympathetic stimulation. Propranolol has been the 3 blocker most widely studied and used in the therapy of thyrotoxicosis. Beta blockers cause clinical improvement of hyperthyroid symptoms but do not typically alter thyroid hormone levels. Propranolol at doses greater than 160 mg/d may also reduce T3 levels approximately 20% by inhibiting the peripheral conversion of T4 to T3. 

Bartalena L, Wiersinga WM, Tanda ML, Bogazzi F, Piantanida E, Lai A, Martino E. Diagnosis and management of amiodarone-induced thyrotoxicosis in Europe results of an international survey among members of the European Thyroid Association. Clin Endocrinol (Oxf) 2004 61(4) 494-502. 

Franzese CB, Fan CY, Stack BC. Surgical management of amiodarone-induced thyrotoxicosis. Otolaryngol Head Neck Surg 2003 129 565-70. 

Beta blockers without intrinsic sympathomimetic activity are effective therapeutic adjuncts in the management of thyrotoxicosis since many of these symptoms mimic those associated with... 

Hypercalcemia causes central nervous system depression, including coma, and is potentially lethal. Its major causes (other than thiazide therapy) are hyperparathyroidism and cancer with or without bone metastases. Less common causes are hypervitaminosis D, sarcoidosis, thyrotoxicosis, milk-alkali syndrome, adrenal insufficiency, and immobilization. With the possible exception of hypervitaminosis D, these latter disorders seldom require emergency lowering of serum calcium. A number of approaches are used to manage the hypercalcemic crisis. 

Brennan MD, van Heerden JA, Carney JA. Amiodarone-associated thyrotoxicosis (AAT) experience with surgical management. Surgery 1987 102(6) 1062-7. 

Reserpine has been used in the management of mild to moderate hypertension, the treatment of agitated psychotic states, as adjunctive therapy, second-line, for treating thyrotoxicosis, and to decrease the number and severity of vasospastic attacks caused by Raynaud s phenomenon and similar peripheral vascular disorders. 

Serial measurement of Tg is most useful in detecting recurrence of DTC following surgical resection or radioactive iodine ablation. Tg determination is used as an adjunct to ultrasound and scanning. Assessment of serum Tg also aids in the management of infants with congenital hypothyroidism, All patients with hyperthyroidism should have elevated Tg low concentrations of Tg may be an indication that thyrotoxicosis factitia is present. 

Knighton JD, Crosse MM. Anaesthetic management of childhood thyrotoxicosis and the use of esmolol. Anaesthesia 1997 52 67-70. 

Answer E. Increased sympathetic activity is a major problem in hyperthyroidism and is best managed by use of beta blockers, which can offset cardiac stimulatory effects. Propranolol has an ancillary action in thyrotoxicosis in that it prevents conversion of T4 to T3 via its inhibition of 5 deiodinase. Amiodarone causes difficult-to-predict adverse effects on thyroid function and would not be appropriate in a patient with hyperthyroidism. Bretylium is an IV agent reserved for ventricular arrhythmias. Digoxin is not ideal because of its complex actions on the heart, which include both inhibition and stimulation. 

Propranolol has been shown to be effective in the management of angina pectoris, myocardial infarction, ventric-nlar and supraventricular arrhythmias, hypertension, aortic dissection, hypertrophic cardiomyopathy, mitral valve prolapse, thyrotoxicosis, migraine, tremor, and performance anxiety (stage fright). 

The management of amiodarone-induced thyrotoxicosis has been extensively reviewed [42 ]. For type 1 thyrotoxicosis, thionamides are the best treatment (possibly associated with potassium perchlorate) for type 2, glucocorticoids are the treatment of choice. However, if rapid restoration of euthyroidism is necessary, a short course of iopanoic acid followed by total thyroidectomy is an option. Radioactive iodine has a marginal role. The authors addressed some important controversies, practical problems, and unanswered questions. 

More about amiodarone-induced thyrotoxicosis and its management... 

Management Glucocorticoids are the first-line treatment in type 2 amiodarone-induced thyrotoxicosis, and thionamides play no role. In a matched retrospective cohort comparison of the ejficacy of a thionamide (methimazole) or a glucocorticoid (prednisone) for 40 days in type 2 amiodarone-induced thyrotoxicosis, in 42 patients, 23% of those who took prednisone were still thyrotoxic, compared with 86% of those who took methimazole [39 ]. When those who had taken methimazole were then given prednisone, 94% achieved euthyroidism within another 40 days. 

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