Left untreated, thyroid storm is an acute, life-threatening complication of thyrotoxicosis or poorly managed hyperthyroidism. In its full state, mortality rates of thyroid storm are around 90% (Singhal & Campbell, 2004). Early recognition is essential. Common clinical presentation includes fever, tachycardia, neurologic abnormalities, and hypertension, which is followed by hypotension and shock, two late signs that are usually fatal. Diagnosis is primarily clinical, so it is imperative that hyperthyroidism be carefully monitored. Thyroid storm is a decompensated state of severe hypermetabolism (Singhal & Campbell). Fever changes to hyperpyrexia in thyroid storm, and body temperature can reach 109 ºF. Mild to moderate sinus tachycardia can intensify quickly to accelerated tachycardia, hypertension, high-output heart failure, and arrhythmias. Irritability and restlessness can cause severe agitation, delirium, seizures, and coma. Extremely high metabolism also increases oxygen and energy consumption (Jao, Chen, Lee, & Tai, 2004). Factors known to precipitate thyroid storm are infection, surgery, trauma, radioactive iodine treatment in patients with toxic nodular goiters, pregnancy, anticholinergic and adrenergic drugs, thyroid hormone ingestion, and diabetic ketoacidosis (American Association of Clinical Endocrinologists [AACE], 2002).
Thyroid storm is a clinical diagnosis of exclusion; thus, lab tests will not verify that a person has this condition. If a person has a known history of hyperthyroidism, then TSH, free T4, T3, and a complete blood count should be evaluated. Like the blood count, which may show a mild leukocytosis, liver function tests are also followed and may show nonspecific abnormalities (AACE, 2002). A chest radiograph may show cardiac enlargement due to congestive heart failure, and an electrocardiogram (ECG) may reveal atrial fibrillation or other arrhythmias (AACE, 2002).
Treatment of thyroid storm focuses on symptom control. The basics must be considered: hyperthermia is controlled with ice packs, cooling blankets, and acetaminophen (Franklyn, 1994). Beta-adrenergic blockers are used to minimize sympathomimetic symptoms and block the adrenergic sites, which are thought to be stimulated by hyperactive catecholamines released by the thyroid hormones (Osman, Gammage, Sheppard, & Franklyn, 2002). These drugs are the mainstay of therapy to control the autonomic effects of thyroid hormone. They also block peripheral conversion of T4 to T3, which is an important component of managing thyroid storm. Giving antithyroid medications blocks production of thyroid hormones and further reduces the peripheral conversion of T4 to T3 (Singhal & Campbell, 2004).
A second line of treatment is the use of the antithyroid medications propylthiouracil (PTU) and methimazole. Propylthiouracil inhibits synthesis of thyroid hormone by decreasing iodine production (which produces T4) and also inhibits peripheral conversion of T4 to T3. Methimazole, another antithyroid medication, works much like PTU, except it does not inhibit peripheral conversion of T4 to T3; however, it is about 10 times more potent. Fewer side effects are associated with methimazole, making it preferable to PTU. Neither drug is available in anything other than oral form (Singhal & Campbell, 2004). Important points to remember with these two drugs are (1) the concurrent use of potassium iodide may cause hypothyroidism, and (2) if either is used with anticoagulation, a bleeding diathesis may result.
These antithyroid medications may be complemented by glucocorticoid steroids, which assist in preventing conversion of T4 to T3. They have been found to significantly reduce mortality rates when used in thyroid storm in conjunction with antithyroid medications (Singhal & Campbell, 2004).
J Neurosci Nurs. 2007;39(1):40-42, 57. © 2007 American Association of Neuroscience Nurses
Cite this: Recognizing Thyroid Storm in the Neurologically Impaired Patient - Medscape - Feb 01, 2007.