INTRODUCTION AND EPIDEMIOLOGY
Thyroid hormone affects virtually all organ systems and is responsible for increasing metabolic rate, heart rate, and ventricle contractility, as well as muscle and CNS excitability. The thyroid hormones are thyroxine (T4) and triiodothyronine (T3). The ratio of T4 to T3 released in the blood is 10:1. Peripherally, T4 is converted to the active T3, which is three to four times more potent than T4.
Hyperthyroidism is an excessive amount of thyroid hormones in the body. The terms hyperthyroidism and thyrotoxicosis are often used interchangeably. Hyperthyroidism is a clinical syndrome with a variety of signs and symptoms, and thyroid storm is its extreme manifestation.
Thyroid storm is an acute, severe, life-threatening hypermetabolic state caused either by excessive release of thyroid hormones causing adrenergic hyperactivity or an increased peripheral response to thyroid hormone in response to one or more precipitants. The most common underlying cause is Graves’ disease (85% of all hyperthyroidism cases in the United States). It is caused by thyroid-stimulating hormone (TSH) receptor antibodies that stimulate excess and uncontrolled thyroidal synthesis and secretion of thyroid hormones. It occurs most frequently in young women (10 times more common in women compared with men) at any age group.1 The mortality of thyroid storm is in the range of 8% to 25%.1,2 This chapter will focus primarily on the treatment of thyroid storm.
Primary hyperthyroidism is caused by the excess production of thyroid hormones from the thyroid glands or from external factors. Secondary hyperthyroidism is caused by the excess production of thyroid-releasing hormones or TSH in the hypothalamus and pituitary, respectively (Tables 229-1 and 229-2).
TABLE 229-1Common Causes of Primary and Secondary Hyperthyroidism ||Download (.pdf) TABLE 229-1 Common Causes of Primary and Secondary Hyperthyroidism
|Primary Hyperthyroidism |
|Graves’ disease (toxic diffuse goiter) || |
Most common of all hyperthyroidism (85% of all cases)
Associated with diffuse goiter, ophthalmopathy, and local dermopathy
|Toxic multinodular goiter ||Second most common cause of hyperthyroidism |
|Toxic nodular (adenoma) goiter ||An enlarged thyroid gland that contains a small rounded mass or nodules with overproduction of thyroid hormone |
|Thyroiditis ||Inflammation of the thyroid gland |
|Hashimoto’s thyroiditis ||Initially gland is overactive (hyperthyroidism) but is typically followed by a state of hypothyroidism |
|Secondary Hyperthyroidism |
|Thyrotropin-secreting pituitary adenoma ||Thyroid gland stimulated to produce hormones |
TABLE 229-2External Causes of Hyperthyroidism ||Download (.pdf) TABLE 229-2 External Causes of Hyperthyroidism
|Nonthyroidal Disease |
|Ectopic thyroid tissue (struma ovarii)/teratoma ||A rare form of mature teratoma that contains thyroid tissue |
|Metastatic thyroid cancer ||Production of extraglandular thyroid hormones |
|Human chorionic gonadotropin ||Stimulates thyroid hormone secretion |
|Drug Induced or Iodine Intake |
|Iodine ||Iodine-induced thyrotoxicosis (called Jod-Basedow phenomenon): After treatment of endemic goiter patients with iodine or ...|