Thyroid Storm

Thyroid Storm

Thyroid storm or thyrotoxic crisis represents an acute, life-threatening and extreme exacerbation manifestation of thyrotoxicosis. It is a rare but life-threatening condition requiring immediate treatment, preferably in an intensive care unit. Although Graves' disease is the most common underlying disorder in thyroid storm, there is usually a precipitating event or condition that transforms the patient into life-threatening thyrotoxicosis. Thyroid storm in the past most frequently occurred after surgery for thyrotoxicosis, now an infrequent occurrence, because of earlier diagnosis and treatment of thyrotoxicosis, and better pre- and postoperative medical management. However acute exacerbation of thyrotoxicosis typically caused by concurrent illness, especially infections (pneumonia, upper respiratory tract infection, enteric infections), and trauma such as operation, still occur. Precipitants of thyroid storm in a patient with previously compensated thyrotoxicosis include abrupt cessation of antithyroid drugs, thyroid, or nonthyroidal surgery in a patient with unrecognized or inadequately treated thyrotoxicosis, rarely following radioactive iodine therapy, and a number of acute illnesses unrelated to thyroid disease. Its incidence is about 1-2% among patients with overt hyperthyroidism. A thyrotoxic crisis occurs predominantly in the elderly and is three to five times more common in women than in men. The overall mortality is 10-20%. Even though the pathogenesis is still not fully understood, an increased sensitivity to catecholamines appears to be an important mechanism, and a number of endogenous and exogenous stress factors that can provoke the onset of a thyrotoxic storm have been identified.


The diagnosis of a thyrotoxic crisis is made entirely on the clinical findings: thyrotoxicosis, abnormal central nervous function function, fever, tachycardia (usually above 130bpm), gastrointestinal tract symptoms, and evidence of impending or present cardiac failure. Most importantly, there is no difference in thyroid hormone levels between patients with "uncomplicated" thyrotoxicosis and those undergoing a thyroid storm. Precise criteria for thyroid storm have been defined and include fever, tachycardia, arrhythmias, congestive heart failure, hypotension, hyperpyrexia, agitation, delirium, psychosis, stupor and coma, as well as nausea, vomiting, diarrhea, and hepatic failure. Fever is typical and may be higher than 105.8 F (41 C). Patients may present with a true psychosis or a marked deterioration of previously abnormal behavior. There are no distinctive laboratory abnormalities.


American Thyroid Association guidelines have recommended a multimodality treatment approach to patients with thyroid storm, including beta-adrenergic blockade, antithyroid drug therapy, inorganic iodide, corticosteroid therapy, aggressive cooling with acetaminophen and cooling blankets, volume resuscitation, respiratory support and monitoring in an intensive care unit. Treatment of thyroid storm involves decreasing new hormone synthesis, inhibiting the release of thyroid hormone, and blocking the peripheral effects of thyroid hormone. This multidrug, therapeutic approach uses thionamides, iodine, beta-adrenergic receptor antagonists, corticosteroids in certain circumstances, and supportive therapy. Any delay in therapy, e.g. by awaiting additional laboratory results, must be strictly avoided, because the mortality rate may rise to 75%. Thus early thyroidectomy should be considered as the treatment of choice, if medical treatment fails to result in clinical improvement. Medical treatment is based on three principles: 1) counteracting the peripheral effects of thyroid hormones; 2) inhibition of thyroid hormone synthesis; and 3) treatment of systemic complications. These measures should bring about clinical improvement within 12-24 hours. If death occurs it is most likely to be cardiopulmonary failure, particularly in the elderly. After the critical illness of thyroid storm subsides, definitive treatment of the underlying thyrotoxicosis can be planned.

Specific therapy

Propranolol (20 to 200 mg orally every 6 hours, or 1 to 3 mg intravenously every 4 to 6 hours), Start with low doses
Antithyroid drugs (150 to 250 mg PTU or 15 to 25 mg methimazole, every 6 hours)
Potassium iodide (one hour after first dose of antithyroid drugs): 100 mg KI every 12 hours
Dexamethasone (2 mg every 6 hours)

Supportive Measures

Mild sedation
Fluid and electrolyte replacement
Nutritional support and vitamins as needed
Oxygen therapy
Nonspecific therapy as indicated
Cooling, aided by cooling blankets and acetaminopheno


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