Recognizing Thyroid Storm in the Neurologically Impaired Patient

Catherine Harris

J Neurosci Nurs. 2007;39(1):40-42, 57. 

In This Article

Pathophysiology

The thyroid, an endocrine gland found in the anterior neck, is normally not palpable. It regulates the rate of metabolism, growth, and function of other systems through a negative feedback system monitored by levels of thyroxine (T4), triiodothyronine (T3), and calcitonin (Bullock & Henze, 1999). Thyroxine is the predominant hormone, which converts to triiodothyronine in the peripheral system. Calcitonin is essential for decreasing calcium levels in the blood when there is too much circulating calcium (Bullock & Henze). The hypothalamus releases thyrotropin releasing hormone (TRH) to stimulate the pituitary to release thyroid stimulating hormone (TSH). Then, TSH stimulates the thyroid to release thyroxine to regulate the function of the cells in the body (Bullock & Henze). If any one of these mechanisms breaks down, the entire system malfunctions. Thyroxine is critical to metabolism and growth; children with thyroid dysfunction will not grow well or will have impaired brain development. In hyperthyroidism, TSH deficiency can be due to several causes. Recall the complex feedback mechanism: If the hypothalamus is damaged, it may in turn disrupt the pathway of TRH secretion from the pituitary. This disruption will directly affect TSH, which is under the influence of TRH. More commonly, TSH production does not stop, even though its levels are consistently low. The thyroid continues to produce thyroxine because the negative feedback mechanism no longer processes the signal to stop. Disturbances of normal homeostatic mechanisms can happen at any level: in the thyroid, the pituitary, or the peripheral tissues. The excessive release of thyroxine sustains a hypermetabolic state, thereby increasing the heart rate and temperature. Patients tend to sweat profusely, lose weight, and become fatigued from the hypermetabolic state (Bullock & Henze).

The signs and symptoms of hyperthyroidism affect the entire body (Becker et al., 1995). Patients may suffer nervousness, irritability, and agitation. They may experience heat intolerance, sweat profusely, or lose hair. Cardiovascular symptoms frequently seen are tachycardia, palpitations, angina, and a new-onset heart murmur called the Means-Lerman "scratch" murmur—a systolic scratchy sound, thought to result from rubbing of the pericardium against the pleura. There may be diarrhea, weight loss, hyperphagia, tongue tremors, and increased thirst. A hand tremor may also be seen, in addition to muscle atrophy, weakness, or paralysis. Neurological symptoms include fever, delirium, stupor, coma, and syncope. Long-standing hyperthyroidism can also cause osteoporosis.

Common causes of hyperthyroidism are toxic diffuse goiter (Graves disease), toxic adenoma, toxic multinodular goiter, and painful subacute thyroiditis. The most common cause is Graves disease (Franklyn, 1994), an autoimmune illness that creates autoimmune antibodies that directly attack the thyroid, activating the synthesis of thyroid hormone (Lee, 2005). The TSH level is low because the body recognizes the state of impairment but is unable to correct it.

The eyes may also start bulging (a condition called exophthalmos) as a result of an inflammatory process of tissue damage that is mediated by the response of B and T lymphocytes to autoantibodies produced in Graves disease (Yeung, 2005). Depending on the cause of hyperthyroidism, exophthalmos may or may not be present.

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