Thyroid storm

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Thyroid storm
Other namesThyrotoxic crisis
Specialty Endocrinology   OOjs UI icon edit-ltr-progressive.svg
Differential diagnosis Sepsis, infectious disease [1]
Prognosis 8-25% mortality with treatment; 80-100% mortality if untreated

Thyroid storm is a rare but severe and life-threatening complication of hyperthyroidism. It occurs when an overactive thyroid leads to hypermetabolism, which can cause death from cardiac arrest or multiple organ failure. [2]


It is characterized by a high fever (temperatures often above 40 °C / 104 °F), fast and often irregular heart beat, elevated blood pressure, vomiting, diarrhea, and agitation. Hypertension with a wide pulse pressure occurs in early to mid crisis, with hypotension accompanying shock occurring in the late stage. [3] Heart failure and heart attack may occur. Death may occur despite treatment. [4] Most episodes occur either in those with known hyperthyroidism whose treatment has stopped or become ineffective, or in those with untreated mild hyperthyroidism who have developed an intercurrent illness (such as an infection). [4]

The primary treatment of thyroid storm is with inorganic iodine and antithyroid drugs (propylthiouracil or methimazole) to reduce synthesis and release of thyroid hormone. Temperature control and intravenous fluids are also mainstays of management. Beta blockers are often used to reduce the effects of thyroid hormone. [5] Patients often require admission to the intensive care unit. [6]

As a life-threatening medical emergency, thyroid storm has a mortality rate of up to 25% despite treatment. [1] [7] Without treatment, the condition is typically fatal, with a mortality rate of 80-100%. [8] Historically, the condition was considered untreatable, with hospital mortality rates approaching 100%. [9] [10]

Signs and symptoms

Thyroid storm is characterized by an acute onset of symptoms of hyperthyroidism (fast heart rate, restlessness, agitation) accompanied by other features such as fever (temperatures often above 40 °C/104 °F), hypertension, mental status changes, diarrhea, and vomiting. [11]

Individuals can exhibit varying signs of organ dysfunction. Patients may experience liver dysfunction, and jaundice (yellowing of the skin), which is considered a poor prognostic sign. Cardiac (heart) symptoms include abnormal heart rhythms, myocardial infarction (heart attack), and congestive heart failure, which may lead to cardiovascular collapse. Mortality can be as high as 20–30%. [12]

In some situations, individuals may not experience the classic signs of restlessness and agitation, but instead present with apathetic signs of weakness and confusion. [11]


The transition from hyperthyroidism to thyroid storm is typically triggered by a non-thyroidal insult including, but not limited to fever, sepsis, dehydration, myocardial infarction, and psychiatric diseases.[ vague ] [13] [14] Individuals are at higher risk of thyroid storm if their hyperthyroidism is incompletely treated or if their anti-thyroid drugs are discontinued. Many of these individuals have underlying primary causes of hyperthyroidism (Graves' disease, toxic multi-nodular goiter, solitary toxic adenoma, or amiodarone). However, thyroid storm can occur in individuals with unrecognized thyrotoxicosis experiencing non-thyroid surgery, labor, infection, or exposure to certain medications and radiocontrast dyes.[ citation needed ]

Precipitating factors [11] [15]
Severe infection
Diabetic ketoacidosis
Thyroid surgery
Non-thyroid surgery
Struma ovarii
Molar pregnancy
Trauma (i.e. hip fracture)
Myocardial infarction
Pulmonary embolism
Heart failure
Radioactive iodine treatment
Medication side effect (anesthetics, salicylate, pseudoephedrine, amiodarone)
Exposure to iodinated contrast
Withdrawal of antithyroid treatment
Emotional stress
Intense exercise


Thyroid vector.svg

The precise mechanism for the development of thyroid storm is poorly understood. In the human body, thyroid hormone may be free (biologically active T3/T4) or bound to thyroid binding hormone (biologically inactive) for transport. The release of thyroid hormone is tightly regulated by a feedback system involving the hypothalamus, pituitary gland, and thyroid gland. Hyperthyroidism results from a dysregulation of this system that eventually leads to increases in levels of free T3/T4. The transition from simple hyperthyroidism to the medical emergency of thyroid storm can be triggered by conditions (§ Causes) that lead to:

Increases in free thyroid hormone

Individuals with thyroid storm tend to have increased levels of free thyroid hormone, although total thyroid hormone levels may not be much higher than in uncomplicated hyperthyroidism. [15] The rise in the availability of free thyroid hormone can be the result of manipulating the thyroid gland. In an individual receiving radioactive iodine therapy, free thyroid hormone levels can acutely increase due to the release of hormone from ablated thyroid tissue.[ citation needed ]

Decrease in thyroid hormone binding protein

A decrease in thyroid hormone binding protein under the effects of stressors or medications may also cause a rise in free thyroid hormone. [5]

Increased sensitivity to thyroid hormone

Along with increases in thyroid hormone availability, it is suggested that thyroid storm is characterized by the body's heightened sensitivity to thyroid hormone, which may be related to sympathetic activation. [15]

Sympathetic activation

Sympathetic nervous system activation during times of stress may also play a significant role in thyroid storm. [5] Sympathetic activation increases production of thyroid hormone by the thyroid gland. In the setting of elevated thyroid hormone, the density of thyroid hormone receptors (esp. beta-receptors) also increases, which enhances the response to catecholamines. This is likely responsible for several of the cardiovascular symptoms (increased cardiac output, heart rate, stroke volume) seen in thyroid storm.[ citation needed ] [16]

Thyroid storm as allostatic failure

According to newer theories, thyroid storm results from allostatic failure in a situation where thyrotoxicosis hampers the development of non-thyroidal illness syndrome, [17] which would help to save energy in critical illness and other instances of high metabolic demand. [14]

Usually, in critical illness (e.g. sepsis, myocardial infarction and other causes of shock) thyroid function is tuned down to result in low-T3 syndrome and, occasionally, also low TSH concentrations, low-T4 syndrome and impaired plasma protein binding of thyroid hormones. This endocrine pattern is referred to as euthyroid sick syndrome (ESS), non-thyroidal illness syndrome (NTIS) or thyroid allostasis in critical illness, tumours, uraemia and starvation (TACITUS). Although NTIS is associated with significantly worse prognosis, it is also assumed to represent a beneficial adaptation (type 1 allostasis). In cases where critical illness is accompanied by thyrotoxicosis, this comorbidity prevents the down-regulation of thyroid function. Therefore, the consumption of energy, oxygen and glutathione remains high, which leads to further increased mortality. [17]

These newer theories imply that thyroid storm results from an interaction of thyrotoxicosis with the specific response of the organism to an oversupply of thyroid hormones. [13]


The diagnosis of thyroid storm is based on the presence of signs and symptoms consistent with severe hyperthyroidism. [15] Multiple approaches have been proposed to calculate the probability of thyroid storm based on clinical criteria, however, none have been universally adopted by clinicians. For instance, Burch and Wartofsky published the Burch-Wartofsky point scale (BWPS) in 1993, assigning a numerical value based on the presence of specific signs and symptoms organized within the following categories: temperature, cardiovascular dysfunction (including heart rate and presence of atrial fibrillation or congestive heart failure), central nervous system (CNS) dysfunction, gastrointestinal or liver dysfunction and presence of a precipitating event. [15] [18] A Burch-Wartofsky score below 25 is not suggestive of thyroid storm whereas 25 to 45 suggests impending thyroid storm and greater than 45 suggests current thyroid storm. [19] Alternatively, the Japanese Thyroid Association (JTA) criteria, derived from a large cohort of patients with thyroid storm in Japan and published in 2012, provide a qualitative method to determine the probability of thyroid storm. The JTA criteria separate the diagnosis of thyroid storm into definite versus suspected based on the specific combination of signs and symptoms a patient exhibits and require elevated free triiodothyronine (T3) or free thyroxine (T4) for definite thyroid storm. [20]

Burch-Wartofsky Point Scale [15]
TemperatureScoreHeart RateScoreSymptoms of Heart FailureScorePresence of Atrial FibrillationScoreSymptoms of CNS DysfunctionScoreGastrointestinal or Liver DysfunctionScorePresence of Precipitating EventScore
99.0 to 99.9590 to 1095None0Absent0None0None0None0
100.0 to 100.910110 to 11910Mild (i.e. pedal edema)5Present10Mild (e.g. showing signs of agitation)10Moderate (e.g. diarrhea, nausea, vomiting or abdominal pain)10Present10
101.0 to 101.915120 to 12915Moderate (i.e. bibasilar rales)10Moderate (e.g. delirium, psychosis, lethargy)20Severe (i.e. unexplained jaundice)20
102.0 to 102.920130 to 13920Severe (i.e. pulmonary edema)15Severe (e.g. seizure or coma)30
103 to 103.925Greater than or equal to 14025
Greater than or equal to 10430

Laboratory findings

As with hyperthyroidism, TSH is suppressed. Both free and serum (or total) T3 and T4 are elevated. [11] An elevation in thyroid hormone levels is suggestive of thyroid storm when accompanied by signs of severe hyperthyroidism but is not diagnostic as it may also correlate with uncomplicated hyperthyroidism. [15] [18] Moreover, serum T3 may be normal in critically ill patients due to decreased conversion of T4 to T3. [15] Other potential abnormalities include the following: [15] [18]


The main strategies for the management of thyroid storm are reducing production and release of thyroid hormone, reducing the effects of thyroid hormone on tissues, replacing fluid losses, and controlling temperature. [5] Thyroid storm requires prompt treatment and hospitalization. Often, admission to the intensive care unit is needed. [21] In cases of heart failure leading to hemodynamic collapse, cardiocirculatory support including VA-ECMO may be required. [22]

In high fever, temperature control is achieved with fever reducers such as paracetamol/acetaminophen and external cooling measures (cool blankets, ice packs). Dehydration, which occurs due to fluid loss from sweating, diarrhea, and vomiting, is treated with frequent fluid replacement. [21] In severe cases, mechanical ventilation may be necessary. Any suspected underlying cause is also addressed. [4]


Guidelines recommend the administration of inorganic iodide (potassium iodide or Lugol's iodine [6] [21] ) to reduce the synthesis and release of thyroid hormone. In high dosage, iodine may reduce the synthesis of thyroid hormone via the Wolff-Chaikoff effect and its release via the Plummer effect. [5] Some guidelines recommend that iodine be administered after antithyroid medications are started, because iodine is also a substrate for the synthesis of thyroid hormone, and may worsen hyperthyroidism if administered without antithyroid medications. [5]

Antithyroid medications

Antithyroid drugs (propylthiouracil or methimazole) are used to reduce the synthesis and release of thyroid hormone. Propylthiouracil is preferred over methimazole due to its additional effects on reducing peripheral conversion of T4 to T3, [5] however both are commonly used. If the etiology involves subacute thyroiditis, antithyroid medications are not always used, and its use is "controversial". [23] [24]


Cholestyramine is an oral bile acid sequestrant used to reduce levels of circulating thyroid hormone in thyrotoxic patients by interfering with the enterohepatic circulation and thyroid hormone recycling. Cholestyramine use is usually reserved for patients who are intolerant of the other antithyroid medications. [25]

Beta blockers

The administration of beta-1-selective beta blockers (e.g. metoprolol) is recommended to reduce the effect of circulating thyroid hormone on end organs. [4] [21] [6]

Propranolol at high doses is a common first-line treatment, as it reduces peripheral conversion of T4 to T3, which is the more active form of thyroid hormone. [26] [21] Non-selective beta blockers have been suggested to be beneficial due to their inhibitory effects on peripheral deiodinases. Some recent research suggests them to be associated with increased mortality. [27] Therefore, cardioselective beta blockers may be favourable. [14]


High levels of thyroid hormone result in a hypermetabolic state, which can result in increased breakdown of cortisol, a hormone produced by the adrenal gland. This results in a state of relative adrenal insufficiency, in which the amount of cortisol is not sufficient. [27] Guidelines recommend that corticosteroids (hydrocortisone and dexamethasone are preferred over prednisolone or methylprednisolone) be administered to all patients with thyroid storm. However, doses should be altered for each individual patient to ensure that the relative adrenal insufficiency is adequately treated while minimizing the risk of side effects. [27]


Plasmapheresis removes cytokines, antibodies, and thyroid hormones from the plasma. [28] It is usually reserved for severe refractory cases of thyroid storm as a bridge to surgery. [29]

Supportive care

Patients with thyroid storm are usually hospitalized and managed in the intensive care unit. Supportive measures include treatment of precipitating factors (e.g. infection), intravenous fluids, and cooling blankets and ice packs for persistent fever. Extracorporeal membrane oxygenation (ECMO) can been used as a bridging measure for refractory cardiorespiratory failure induced by thyroid storm. [30]

See also

Related Research Articles

<span class="mw-page-title-main">Hyperthyroidism</span> Thyroid gland disease that involves an overproduction of thyroid hormone

Hyperthyroidism is the condition that occurs due to excessive production of thyroid hormones by the thyroid gland. Thyrotoxicosis is the condition that occurs due to excessive thyroid hormone of any cause and therefore includes hyperthyroidism. Some, however, use the terms interchangeably. Signs and symptoms vary between people and may include irritability, muscle weakness, sleeping problems, a fast heartbeat, heat intolerance, diarrhea, enlargement of the thyroid, hand tremor, and weight loss. Symptoms are typically less severe in the elderly and during pregnancy. An uncommon but life-threatening complication is thyroid storm in which an event such as an infection results in worsening symptoms such as confusion and a high temperature; this often results in death. The opposite is hypothyroidism, when the thyroid gland does not make enough thyroid hormone.

<span class="mw-page-title-main">Thyroid</span> Endocrine gland in the neck; secretes hormones that influence metabolism

The thyroid, or thyroid gland, is an endocrine gland in vertebrates. In humans, it is in the neck and consists of two connected lobes. The lower two thirds of the lobes are connected by a thin band of tissue called the isthmus (pl.: isthmi). The thyroid gland is a butterfly-shaped gland located in the neck below the Adam's apple. Microscopically, the functional unit of the thyroid gland is the spherical thyroid follicle, lined with follicular cells (thyrocytes), and occasional parafollicular cells that surround a lumen containing colloid. The thyroid gland secretes three hormones: the two thyroid hormones – triiodothyronine (T3) and thyroxine (T4) – and a peptide hormone, calcitonin. The thyroid hormones influence the metabolic rate and protein synthesis and growth and development in children. Calcitonin plays a role in calcium homeostasis. Secretion of the two thyroid hormones is regulated by thyroid-stimulating hormone (TSH), which is secreted from the anterior pituitary gland. TSH is regulated by thyrotropin-releasing hormone (TRH), which is produced by the hypothalamus.

<span class="mw-page-title-main">Graves' disease</span> Autoimmune endocrine disease

Graves' disease, also known as toxic diffuse goiter, is an autoimmune disease that affects the thyroid. It frequently results in and is the most common cause of hyperthyroidism. It also often results in an enlarged thyroid. Signs and symptoms of hyperthyroidism may include irritability, muscle weakness, sleeping problems, a fast heartbeat, poor tolerance of heat, diarrhea and unintentional weight loss. Other symptoms may include thickening of the skin on the shins, known as pretibial myxedema, and eye bulging, a condition caused by Graves' ophthalmopathy. About 25 to 30% of people with the condition develop eye problems.

Thyroid-stimulating hormone (also known as thyrotropin, thyrotropic hormone, or abbreviated TSH) is a pituitary hormone that stimulates the thyroid gland to produce thyroxine (T4), and then triiodothyronine (T3) which stimulates the metabolism of almost every tissue in the body. It is a glycoprotein hormone produced by thyrotrope cells in the anterior pituitary gland, which regulates the endocrine function of the thyroid.

<span class="mw-page-title-main">Triiodothyronine</span> Chemical compound

Triiodothyronine, also known as T3, is a thyroid hormone. It affects almost every physiological process in the body, including growth and development, metabolism, body temperature, and heart rate.

<span class="mw-page-title-main">Propylthiouracil</span> Medication used to treat hyperthyroidism

Propylthiouracil (PTU) is a medication used to treat hyperthyroidism. This includes hyperthyroidism due to Graves' disease and toxic multinodular goiter. In a thyrotoxic crisis it is generally more effective than methimazole. Otherwise it is typically only used when methimazole, surgery, and radioactive iodine is not possible. It is taken by mouth.

<span class="mw-page-title-main">Thyroid disease</span> Medical condition

Thyroid disease is a medical condition that affects the function of the thyroid gland. The thyroid gland is located at the front of the neck and produces thyroid hormones that travel through the blood to help regulate many other organs, meaning that it is an endocrine organ. These hormones normally act in the body to regulate energy use, infant development, and childhood development.

<span class="mw-page-title-main">Carbimazole</span> Medication used for hyperthyroidism

Carbimazole (brand names Neo-Mercazole, Anti-Thyrox, etc.) is used to treat hyperthyroidism. Carbimazole is a pro-drug as after absorption it is converted to the active form, methimazole. Methimazole prevents thyroid peroxidase enzyme from iodinating and coupling the tyrosine residues on thyroglobulin, hence reducing the production of the thyroid hormones T3 and T4 (thyroxine).

<span class="mw-page-title-main">Toxic multinodular goitre</span> Medical condition

Toxic multinodular goiter (TMNG), also known as multinodular toxic goiter (MNTG), is an active multinodular goiter associated with hyperthyroidism.

<span class="mw-page-title-main">De Quervain's thyroiditis</span> Medical condition

De Quervain's thyroiditis, also known as subacute granulomatous thyroiditis or giant cell thyroiditis, is a member of the group of thyroiditis conditions known as resolving thyroiditis. People of all ages and genders may be affected.

Goitrogens are substances that disrupt the production of thyroid hormones. This triggers the pituitary to release thyroid-stimulating hormone (TSH), which then promotes the growth of thyroid tissue, eventually leading to goiter.

<span class="mw-page-title-main">Hypothalamic–pituitary–thyroid axis</span> Part of the neuroendocrine system

The hypothalamic–pituitary–thyroid axis is part of the neuroendocrine system responsible for the regulation of metabolism and also responds to stress.

An antithyroid agent is a hormone inhibitor acting upon thyroid hormones.

Euthyroid sick syndrome (ESS) is a state of adaptation or dysregulation of thyrotropic feedback control wherein the levels of T3 and/or T4 are abnormal, but the thyroid gland does not appear to be dysfunctional. This condition may result from allostatic responses of hypothalamus-pituitary-thyroid feedback control, dyshomeostatic disorders, drug interferences, and impaired assay characteristics in critical illness.

Myxedema coma is an extreme or decompensated form of hypothyroidism and while uncommon, is potentially lethal. A person may have laboratory values identical to a "normal" hypothyroid state, but a stressful event precipitates the myxedema coma state, usually in the elderly. Primary symptoms of myxedema coma are altered mental status and low body temperature. Low blood sugar, low blood pressure, hyponatremia, hypercapnia, hypoxia, slowed heart rate, and hypoventilation may also occur. Myxedema, although included in the name, is not necessarily seen in myxedema coma. Coma is also not necessarily seen in myxedema coma, as patients may be obtunded without being comatose.

<span class="mw-page-title-main">Thyroid hormones</span> Hormones produced by the thyroid gland

Thyroid hormones are any hormones produced and released by the thyroid gland, namely triiodothyronine (T3) and thyroxine (T4). They are tyrosine-based hormones that are primarily responsible for regulation of metabolism. T3 and T4 are partially composed of iodine, derived from food. A deficiency of iodine leads to decreased production of T3 and T4, enlarges the thyroid tissue and will cause the disease known as simple goitre.

<span class="mw-page-title-main">Iopanoic acid</span> Chemical compound

Iopanoic acid is an iodine-containing radiocontrast medium used in cholecystography. Both iopanoic acid and ipodate sodium are potent inhibitors of thyroid hormone release from thyroid gland, as well as of peripheral conversion of thyroxine (T4) to triiodothyronine (T3). These compounds inhibit 5'deiodinase (5'DID-1 and 5'DID-2) enzymes, which catalyse T4-T3 conversion in the thyroid cell, liver, kidney, skeletal muscle, heart, brain, pituitary. This accounts for the dramatic improvement in both subjective and objective symptoms of hyperthyroidism, particularly when they are used as an adjunctive therapy with thioamides (propylthiouracil, carbimazole). They can be used in the treatment of patients with severe thyrotoxicosis (thyroid storm) and significant morbidity (e.g., myocardial infarction, or stroke) for rapid control of elevated plasma triiodothyronine concentrations. The use of iopanoic acid for treatment of thyrotoxicosis has been discontinued in the United States.

Thyroid disease in pregnancy can affect the health of the mother as well as the child before and after delivery. Thyroid disorders are prevalent in women of child-bearing age and for this reason commonly present as a pre-existing disease in pregnancy, or after childbirth. Uncorrected thyroid dysfunction in pregnancy has adverse effects on fetal and maternal well-being. The deleterious effects of thyroid dysfunction can also extend beyond pregnancy and delivery to affect neurointellectual development in the early life of the child. Due to an increase in thyroxine binding globulin, an increase in placental type 3 deioidinase and the placental transfer of maternal thyroxine to the fetus, the demand for thyroid hormones is increased during pregnancy. The necessary increase in thyroid hormone production is facilitated by high human chorionic gonadotropin (hCG) concentrations, which bind the TSH receptor and stimulate the maternal thyroid to increase maternal thyroid hormone concentrations by roughly 50%. If the necessary increase in thyroid function cannot be met, this may cause a previously unnoticed (mild) thyroid disorder to worsen and become evident as gestational thyroid disease. Currently, there is not enough evidence to suggest that screening for thyroid dysfunction is beneficial, especially since treatment thyroid hormone supplementation may come with a risk of overtreatment. After women give birth, about 5% develop postpartum thyroiditis which can occur up to nine months afterwards. This is characterized by a short period of hyperthyroidism followed by a period of hypothyroidism; 20–40% remain permanently hypothyroid.

The sum activity of peripheral deiodinases is the maximum amount of triiodothyronine produced per time-unit under conditions of substrate saturation. It is assumed to reflect the activity of deiodinases outside the central nervous system and other isolated compartments. GD is therefore expected to reflect predominantly the activity of type I deiodinase.

<span class="mw-page-title-main">Amiodarone induced thyrotoxicosis</span> Form of hyperthyroidism

Amiodarone induced thyrotoxicosis (AIT) is a form of hyperthyroidism due to treatment with antiarrhythmic drug, amiodarone.


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