Introduction
What Is a Thyroid Crisis?
A thyroid crisis also called thyroid storm and thyrotoxic crisis, occurs when the thyroid gland produces a large amount of thyroid hormone in a shorter duration. It is a complication of hyperthyroidism. People with underlying conditions leading to hyperthyroidism, such as Grave's disease (an autoimmune disorder of the thyroid gland), or a toxic thyroid adenoma (benign conditions of the thyroid gland), are more prone to get thyroid crisis. A thyroid crisis is a life-threatening medical emergency. Women are more likely to experience thyroid crises than men. The average age of a person in which a thyroid crisis occurs is 42 to 43 years.
What Happens During a Thyroid Crisis?
The thyroid hormones affect several body organs and parts. In case of a thyroid crisis thyroid storm, one may feel:
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Extremely hot and sweaty.
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Pounding heartbeat with increased heart rate.
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Very agitated or anxious.
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Tremors.
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Stomach problems.
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Loss of control of the body.
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High fever.
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Confusion.
What Causes Thyroid Crisis?
A thyroid crisis can develop in the case of chronic untreated or undertreated hyperthyroidism. However, it can also be caused by a sudden event like the following:
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Abruptly stopping the antithyroid medication.
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Thyroid surgery or thyroidectomy.
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Non-thyroid surgery.
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Infection.
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Acute illnesses include diabetic ketoacidosis (DKA), drug reactions, or heart failure.
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Sudden inoculation of iodine in the body from an iodine contrast agent used for specific imaging procedures.
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Stroke - Brain damage due to insufficient blood supply to the brain.
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Giving birth.
How Is Thyroid Crisis Treated or Managed?
Thyroid crisis is managed or treated in various ways:
As soon as the thyroid storm is detected, the patient is treated in an acute medical unit (A.M.U.), high-dependency area, or intensive care unit (I.C.U.). Like other medical emergencies, the patient's airway, breathing, circulation, and disability are promptly assessed and treated.
1. Supportive Care:
A thyroid crisis can give rise to fluid loss because of fever, diaphoresis, vomiting, and diarrhea. Normal saline can be administered to combat fluid loss. In case of low blood sugar, intravenous fluids with dextrose may be given to replenish the glycogen stores.
2. The Inhibition of the Synthesis of New Thyroid Hormones:
Thionamides, like Methimazole or Propylthiouracil (PTU), are used to treat thyrotoxicosis. Thionamides reduce the production of new thyroid hormones and also have immunosuppressive effects.
Methimazole has a longer half‐life than Propylthiouracil; hence frequent administration is unnecessary. 40 to 100 mg of Methimazole is given orally as the loading dose, followed by 20 mg every four hours. The total daily dose of Methimazole is 120 mg. 40 mg of Methimazole can be given through the anus (rectal) and crushed in an aqueous solution. The mode of action of Methimazole for both oral and intravenous use is the same. In case of unavailability of Methimazole, Carbimazole is used. The initial dose is 40 to 60 mg, followed by a maintenance dose of between 5 and 20 mg daily.
The dose of Propylthiouracil for thyroid crisis is 600 to 1,000 mg orally, followed by 200 to 250 mg every four hours. The total daily dose ranges between 1200 and 1500 mg. The drug can be administered through a nasogastric tube or anally.
3. The Inhibition of the Release of Thyroid Hormone:
To stop thyroid hormone release, iodine-Lugol solution, potassium iodide, or Ipodate can be administered after one hour of Thionamide therapy. Iodine blocks the release of the stored hormone and decreases iodide transport and oxidation. At the same time, the Lugol solution that provides 8 mg iodine per drop can be given three to four times for 30 to 40 drops per day. Therefore, the treatment can be started with eight to ten drops.
The iodine-containing solution is not administered to patients with iodine overload, iodine-induced hyperthyroidism, or amiodarone‐induced thyrotoxicosis; instead, lithium or potassium perchlorate is used. In severe cases of thyroid crisis, lithium can also be used with Propylthiouracil or Methimazole. Lithium inhibits the release of the thyroid hormone and decreases thyroid hormone production. Lithium is administered around 300 mg every eight hours in a thyroid crisis.
4. Preventing the Conversion of Thyroxine to Triiodothyronine:
Propylthiouracil, Propranolol, and glucocorticoid block the conversion of the thyroid hormone T4 to T3. Glucocorticoids like Hydrocortisone or Dexamethasone are essential in managing thyroid crises, thereby increasing the survival rate. Treatments with glucocorticoids are recommended in case of severe thyrotoxicosis and low blood pressure.
5. Blockage of Beta‐Adrenergic Receptor:
To block beta-adrenergic receptors, Propranolol is intravenously administered slowly in one to two mg boluses and repeated every 10 to 15 minutes until the desired result is achieved.
6. The Identification of the Risk Factors:
The source of infection-causing fever in individuals with thyroid crisis is identified with blood, urine, throat, and sputum cultures. A chest X-ray is done to rule out chest infection. An electrocardiogram is carried out to rule out myocardial infarction (heart attack), ischemia (reduced blood flow), or arrhythmia (irregular heartbeat).
In a thyroid crisis due to diabetic ketoacidosis, myocardial infarction, pulmonary embolism, or other acute processes, the underlying condition is managed along with treating the crisis.
Management:
If the patient shows improvement with the therapy, a few treatment methods can be altered or stopped. For example, Iodine therapy can be discontinued, and glucocorticoid dosage and Thionamide therapy can be gradually reduced. The beta-Adrenergic blockage is needed if the patient is still thyrotoxic. Definitive therapy with radioactive iodine is not needed for several weeks or months after the treatment with iodine for thyroid crisis. A follow-up is required for such patients even after the resolution of the thyroid crisis to prevent its recurrence.
Conclusion
A thyroid crisis is a rare, life-threatening thyroid emergency with a high mortality rate. It occurs commonly with the underlying condition of Graves' thyrotoxicosis, but secondary conditions such as infection or myocardial infarction also make one vulnerable to the life-threatening condition. Early diagnosis and prompt intervention, and management are essential. Treatment is based on immediately blocking the thyroid hormone synthesis, preventing their further release from the thyroid stores, thus reducing the excess hormones. The risk factors leading to thyroid crisis should be promptly identified and treated. Maintenance is required with the proper follow-up to prevent a recurrence of the crisis.
