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    Thyroid storm: A medical emergency

    CE Center

    RN/Thomson AHC Home Study Program

    Thyroid storm: A medical emergency

    CE credit is no longer available for this article. (Expired April 2007)


    Originally posted April 2005


    SALLY BEATTIE DULAK, a member of the RN editorial board, is the principal of CV Health Promotions, a cardiovascular consultancy in Columbia, MO. The author has no financial relationships to disclose.

    Thyroid storm is relatively rare, but without early recognition and aggressive treatment, it's usually fatal. Would you know what to do to help your patient get through this crisis?

    Early recognition and treatment of hyperthyroidism have made thyroid storm (TS) less common than it once was. Nevertheless, when this extreme hypermetabolic state does occur and isn't treated promptly, it's often fatal. Only 1% - 2% of people with hyperthyroidism will develop TS,1 but the mortality rate for patients with untreated TS ranges from 50% - 90%.2,3 With early intervention, mortality drops to less than 20%.3

    Thyroid storm is caused by an excess of thyroid hormone in the blood. It develops abruptly and affects the body's thermoregulatory, cardiovascular, nervous, and GI systems, leading to multi-organ decompensation.4

    Because even the slightest delay in treatment could prove fatal, TS is diagnosed and treated entirely on the basis of clinical examination, without waiting for laboratory confirmation of hyperthyroidism.1 This means your ability to quickly recognize the impending signs of TS, and intervene accordingly, can literally make the difference between life and death.

    A "storm" of elevated thyroid hormones

    In order to understand TS, it helps to review the function of the thyroid gland. The thyroid is responsible for regulating the physiologic processes of all body systems. This is achieved by a feedback loop, which ultimately tells the thyroid gland how much triiodothyronine (T3) and thyroxine (T4)?collectively called thyroid hormone?to secrete in order to maintain homeostasis. (See the box) In TS, this feedback loop is disrupted. The disruption results in an excess of circulating thyroid hormone, which causes a marked increase in cellular function in all body tissues.

    You'll see TS in patients with undiagnosed hyperthyroidism or in those with known hyperthyroidism, such as Graves' disease, that's been inadequately treated.2 In these patients, infection is often the trigger. However, TS may also develop in hyperthyroidism patients following trauma, surgery (thyroid or other), severe emotional distress, stroke, congestive heart failure (CHF), diabetic ketoacidosis, or pulmonary embolism.3,4 TS can also occur in hyperthyroidism patients immediately postpartum or after taking or receiving drugs or dyes that contain iodine.3,4 Patients with hypothyroidism also run the risk of TS if they take an overdose of levothyroxine (Levoxyl, Synthroid others).

    Look for signs of decompensation

    Your ability to recognize the constellation of clinical features that accompanies TS is crucial to ensuring that aggressive treatment is not delayed. Patients typically present with high fever, above 101.3° F (38.5° C), though temperature may exceed 105.8° F (41° C).3,5 Skin may be warm, moist, and silky or smooth, and the patient may be sweating excessively.4 Heat intolerance is also a common symptom.1

    The cardiovascular system is particularly affected, as the body attempts to respond to the increased activity of the sympathetic nervous system. Tachycardia that exceeds 140 beats/min is very common and may be accompanied by ectopic beats and dysrhythmias, especially atrial fibrillation.4 Signs of high-output CHF and pulmonary edema may be apparent, especially in older patients with preexisting cardiac dysfunction. Blood pressure may be normal or high; however, without treatment for TS, hypotension can develop.3

    Because increased levels of thyroid hormone can affect the nervous system, patients experience changes in mental status.4 They may appear restless, nervous, and agitated, and may exhibit tremors. Agitation and confusion are common and may progress to delirium and coma, without prompt treatment.4

    Early in the course of TS, the patient may complain of abdominal pain.5 Nausea, vomiting, and diarrhea may be present as well, due to accelerated intestinal transport and decreased absorption in the GI tract.4

    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.


    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. http://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 loop

    The 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.

    Drugs used to treat thyroid storm

    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).

    Sally Beattie, RN, MS, CNS, GNP