Treatment can't wait for lab results If you suspect that your patient has TS, draw blood for lab studies, including thyroid function tests, but start treatment right away. As you might expect, patients who have TS will have a low level of thyroid-stimulating hormone, and elevated T₃ and T₄ levels.⁴

The four equally important goals of therapy are to block the formation of new hormones in the thyroid gland, inhibit the action of hormones already formed, support vital functions, and identify and treat the precipitating event.⁴ You need to address the first three of these immediately and simultaneously; treating the underlying condition can wait until your patient is stabilized and out of danger.

Your first priority should be to ensure adequate oxygenation. If O₂ delivered via nasal cannula or mask is insufficient, be prepared to assist with endotracheal intubation and mechanical ventilation. You'll also need to insert an IV and a nasogastric tube so that you can administer antithyroid medications.

The mainstay of treatment for TS is drug therapy with antithyroid thioamide medications, also called thioureas. Typical adult dosages for these and other drugs commonly used to treat TS appear in the box on page 10.

First, you'll administer propylthiouracil (also called PTU) or methimazole (Tapazole).¹ Propylthiouracil is the preferred drug. In addition to preventing the production of more T₄ and T₃ in the thyroid, it blocks the conversion of T₄ to T₃ outside of the thyroid, resulting in a rapid reduction in the level of circulating hormone.⁵ Methimazole blocks the production of T₄ and T₃, but it does not prevent T₄ from converting to T₃, so it takes longer to reduce the level of circulating thyroid hormone. Because both drugs are available only in oral form, they must be administered by mouth or feeding tube.⁴

Neither of these drugs, however, blocks the in-between step—that is, the step prior to conversion, when stored T₄ and T₃ are released from the thyroid. To block their release, you'll need to wait at least an hour after giving propylthiouracil or methima-zole and administer inorganic iodide—either Lugol's solution or saturated solution of potassium iodide (Pima, SSKI).⁴ If you give the iodide too soon after the propylthiouracil or methimazole, the body will use the iodide to produce more T₄. The inorganic iodides are available only in an oral preparation.

TS can produce an increased stress response that depletes a patient's cortisol.⁴ If your patient has a cortisol deficiency, you will administer a glucocorticoid such as dexamethasone (Decadron) or hydrocortisone.⁴ These steroids add to the effects of propylthiouracil by blocking the conversion of T₄ to T₃ in peripheral tissue.⁴

You may also need to administer a beta-adrenergic blocking agent, either propranolol (Inderal) or the shorter-acting esmolol (Brevibloc Injection).⁴ Beta-blockers reduce symptoms caused by the heightened response to catecholamines, particularly tachycardia, tremor, and restlessness.⁴ Beta-blockers can work quickly—within 10 minutes of administration—and are effective, but because they can make certain types of heart failure worse, they should be used with caution in patients with CHF.¹

Supportive care is equally important Supporting your patient's vital functions during TS will call into play many of your critical care assessment skills. Continuous cardiac monitoring is essential; it will help you watch for the onset of life-threatening dysrhythmias and monitor your patient's response to treatment. A patient with severe tachycardia who doesn't respond to drugs may need vagal maneuvers like carotid massage, or cardioversion if vagal maneuvers aren't effective.

For critically ill patients with TS, especially those in CHF, hemodynamic monitoring may be indicated.⁴ You may need to assist with pulmonary artery catheter insertion, as well as measure cardiac output, pulmonary artery pressure, and other cardiac parameters. Because the rate at which your patient metabolizes and clears drugs may be markedly increased, don't be alarmed if you need to administer higher-than-usual doses of medications, such as diuretics, digoxin (Lanoxin), or agents used to treat CHF and dysrhythmias.⁴

You may find that your patient has a profound fluid deficit; if so, reversing dehydration and secondary electrolyte imbalance will require vigorous IV fluid replacement. You will probably give solutions that contain dextrose, as these will replace hepatic stores of glycogen, which are frequently depleted in TS.³ Of course, you will monitor for signs of fluid and electrolyte imbalance as you administer these solutions.

Treat hyperthermia with ice packs, fans, and cooling blankets, and administer acetaminophen, the antipyretic of choice for TS. Do not give aspirin or other salicylates; they can increase the level of circulating thyroid hormone.¹ Finally, be alert for and report any signs of bleeding, as propylthiouracil and methimazole may cause a drop in the platelet count—a rare but dangerous side effect.

Once your patient is stabilized, further diagnostic studies will reveal the cause of the TS. Additional tests may include a CBC, chest X-ray, liver function tests, scintigraphy, blood urea nitrogen measurement, radionuclide imaging, and thyroid antibody tests.^3,4 Any precipitating or underlying causes need to be treated aggressively to prevent TS from recurring. For example, if an infection was the trigger, the patient will need antibiotics. TS may be prompted by undiagnosed or inadequately treated thyroid disease, such as Graves' disease, the most common cause of hyperthyroidism. Graves' disease is treated with radioactive iodine, antithyroid medications, or thyroidectomy.⁶

With appropriate treatment for TS, your patient should show improvement within 24 hours.^3,5 Full recovery, however, may take up to a week. During that time, you will gradually taper the patient's medications.

Before the patient is discharged, you will need to teach him about thyroid storm and hyperthyroidism and assure him that his condition can be controlled. You should stress the importance of sticking to the prescribed medication regimen and make certain he schedules a follow-up appointment with his primary care provider or endocrinologist. With proper therapy, your patient need not fear another life-threatening storm.

REFERENCES 1. Manifold, C. A. "Hyperthyroidism, thyroid storm, and Graves' disease." 2004. www.emedicine.com/emerg/topic269.htm (9 Dec. 2004).

2. Fisher, J. N. (2002). Management of thyrotoxicosis. South Med J, 95(5), 493.

3. Singhal, A., & Campbell, D. "Thyroid storm." 2003. www.emedicine.com/ped/topic2247.htm (16 Dec. 2004).

4. Dahlen, R. (2002). Managing patients with acute thyrotoxicosis. Crit Care Nurse, 22(1), 62.

5. Henneman, G. "Graves' disease: Complications." 2003. www.thyroidmanager.org/Chapter12/12-text.htm (16 Dec. 2004).

6. Schori-Ahmen, D. (2003). Defenses gone awry: Thyroid disease. RN, 66(6), 38.

The thyroid hormone feedback loopThe thyroid gland maintains homeostasis: It balances things like metabolic rate, tissue oxygen consumption, and the production of body heat. The gland secretes two hormones—triiodothyronine (T₃) and thyroxine (T₄), collectively referred to as thyroid hormone. They regulate protein, fat, and carbohydrate breakdown, thereby controlling the metabolic rate in all body cells.

The level of these hormones is controlled by a feedback loop that involves the thyroid gland, the hypothalamus, and the anterior portion of the pituitary gland. When T₃ and T₄ levels become low, the hypothalamus secretes thyrotropin-releasing hormone (TRH), which in turn signals the pituitary gland to increase the level of thyrotropin, or thyroid-stimulating hormone (TSH), in the bloodstream. TSH triggers the release of T₃ and T₄ from the thyroid gland. Once the level of thyroid hormone is high enough, the hypothalamus stops secreting TRH.

Normally, this feedback loop ensures that the level of circulating thyroid hormone is appropriate for metabolic needs. If this loop is disrupted by, say, an infection, a life-threatening excess of thyroid hormone—a thyroid storm—can occur.

Sources: 1. Dahlen, R. (2002). Managing patients with acute thyrotoxicosis. Crit Care Nurse, 22(1), 62. 2. Schori-Ahmen, D. (2003). Defenses gone awry: Thyroid disease. RN, 66(6), 38.

Drugs used to treat thyroid storm Drug therapy is the mainstay of treatment for thyroid storm. It typically consists of antithyroid medications, iodides, glucocorticoids, and beta-blockers. After administering an antithyroid drug, it's important that you wait at least an hour before giving an iodide; failure to do so could increase the level of circulating thyroid hormone (T₄ and T₃) and make the patient's condition worse.

Sources: 1. Ginsberg, J. (2003). Diagnosis and management of Graves' disease. CMAJ, 168(5), 575. 2. Dahlen, R. (2002). Managing patients with acute thyrotoxicosis. Crit Care Nurse, 22(1), 62. 3. Singhal, A., & Campbell, D. "Thyroid storm." 2003. www.emedicine.com/ped/topic2247.htm (9 Dec. 2004).