in the treatment of thyrotoxicosis. Although they alleviate many of the signs and symptoms, they have little effect on the fundamental disease process[ 166, 167]. Palpitations, excessive sweating, and nervousness improve, and tremor and tachycardia are controlled. Many patients feel much improved, but others are depressed by the drug and prefer not to take it. Improvement in myocardial efficiency and reduction in the exaggerated myocardial oxygen consumption have been demonstrated . Propranolol lowers oxygen consumption  and reverses the nitrogen wasting of thyrotoxicosis, although it does not inhibit excess urinary calcium and hydroxyproline loss . Propranolol is useful in symptomatic treatment while physician and patient are awaiting the improvement from antithyroid drug or 131-I therapy . Some patients appear to enter remission after using this drug alone for six months or so of therapy[ 169, 172]. It has been useful in neonatal thyrotoxicosis  and in thyroid storm . The drug must be used cautiously when there is evidence of severe thyrotoxicosis, or heart failure, but often control of tachycardia permits improved circulation. Beta blockade can induce cardiovascular collapse in patients with or without heart failure, and asystolic arrest (174a,b). Administration of beta blocker was shown by Ikram to reduce CO by 13% in patients with uncontrolled CHF, and apparently this reduction in CO can be near fatal in rare patients. Some surgical groups routinely prepare patients for thyroidectomy with propranolol for 20 – 40 days and add potassium iodide during the last week . The BMR and thyroid hormone level remain elevated at the time of operation, but the patient experiences no problems. We prefer conventional preoperativepreparation with thiocarbamides, with or without iodide, and would use propranolol as an adjunct, or if the patient is allergic to the usual drugs.
Propranolol is usually given orally as 20 – 40 mg every four to six hours, but up to 200 mg every six hours may be needed. In emergency management of thyroid storm (see also Chapter 12) or tachycardia, it may be given intravenously (1 – 3 mg, rarely up to 6 mg) over 3 – 10 minutes and repeated every four to six hours under electrocardiographic control. Atropine (0.5 – 1.0 mg) is the appropriate antidote if severe brachycardia is seen.
Reserpine and Guanethidine Drugs such as reserpine  and guanethidine  that deplete tissue catecholamines were used extensively in the past as adjuncts in the therapy for thyrotoxicosis, but fell into disuse as the value of beta -sympathetic blockade with propranolol became recognized. Glucocorticoids,
Ipodate, and Other Treatments As described elsewhere, potassium iodide acts promptly to inhibit thyroid hormone secretion from the Graves’ disease thyroid gland. PTU, propranolol, glucocorticoids , amiodarone, and sodium ipodate (Oragrafin Sodium) inhibit peripheral T4 to T3 conversion, and glucocorticoids may have a more prolonged suppressive effect on thyrotoxicosis . Orally administered resins bind T 4in the intestine and prevent recirculation . All of these agents have been used for control of thyrotoxicosis [ 184, 185]. Combined dexamethasone, potassium iodide, and PTU can lower the serum T3 level to normal in 24 hours, which is useful in severe thyrotoxicosis. Prednisone has been reported to induce remission of Graves’ disease, but at the expense of causing Cushing’s syndrome . Ipodate (0.5 – 1 g orally per day) acts to inhibit hormone release because of its iodine content, in addition to its action to inhibit T4 to T3 conversion. This dose of ipodate given to patients with Graves’ disease reduced the serum T3 level by 58% and the T 4level by 20% within 24 hours, and the effect persisted for three weeks[ 188, 189]. This dose of ipodate was more effective than 600 mg of PTU, which decreased the T3 level by only 23% during the first 24 hours, whereas the T4 level did not drop.Ipodate may prove to be a useful adjunct in the early therapy of hyperthyroidism, but will increase total body and thyroidal iodine. However, when the drug i