The thyroid gland is a butterfly-shaped gland found slightly inferior to the cricoid cartilage and wrapping around the trachea, to which it is firmly attached, in the anterior and lateral mid-neck. It is composed of two lobes joined at the center by an isthmus, which altogether weigh approximately 20 g. As a hormone-secreting organ, the thyroid commands a significant blood supply, relying on an extensive capillary network, which is supplied by the superior and inferior thyroid arteries. The superior, middle, and inferior thyroid veins each drain their respective portions of the thyroid gland. Adrenergic and cholinergic systems innervate the gland. The superior and recurrent laryngeal nerves (RLN), branches of the vagus nerve, innervate the larynx and thyroid. Recurrent laryngeal nerve and external motor branch of the superior laryngeal nerve travel close to the gland, which poses a risk for nerve injury during thyroid surgery. The internal and external laryngeal nerves branch off from the superior laryngeal nerve, with the former supplying sensory and autonomic innervation to the upper larynx, and the latter providing motor innervation to the cricothyroid and transverse arytenoid muscles. The remaining muscles and lower larynx are innervated with motor and sensory fibers from the recurrent laryngeal nerve. Vocal cords (VC) are innervates by RLN. It is extremely important to monitor RLN function during thyroid surgery to prevent VC paralysis postoperatively. The intraoperative laryngeal EMG testing is used introperatively to reduce the rate of recurrent laryngeal nerve injury [1].

Thyroid gland produces thyroid hormones: triiodothyronine (T3) and thyroxine (T4) from a thyroglobulin precursor in the thyroid follicles. Thyroglobulin, an iodinated glycoprotein, comprises the bulk of the proteinaceous colloid that fills the follicular cells of thyroid gland. Twenty to forty follicles form a lobule, and these lobules, separated by connective tissue, come together to form the thyroid gland [2].

The production of normal levels of thyroid hormones (TH) is dependent on adequate dietary iodine intake. When present, iodine is reduced to iodide in the gastrointestinal tract, absorbed into the blood, and actively transported into the thyroid follicular cell in a process known as iodide trapping. From there, in a process termed organification, iodide is oxidized and incorporated with thyroglobulin into monoiodotyrosine (MIT) and diiodotyrosine (DIT), which are precursors to the hormonally active T4 and T3. The enzyme thyroid peroxidase (TPO) subsequently catalyzes the coupling of MIT and DIT molecules into T4 or T3 [1, 2].

Both hormones are reversibly bound to circulating plasma proteins for transport to peripheral tissues. Approximately 0.02% of the total T4 remains unbound to protein in the circulation, and is known as free T4 [2]. T3 binds to receptors in target cells with 15-fold greater affinity than T4, and is proportionately more active. T3 and T4 function is to regulate cellular metabolism by increasing carbohydrate and fat metabolism, metabolic rate, minute ventilation, heart rate, contractility, all the while maintaining water and electrolyte balance, as well as the normal activity of the central nervous system. All of these systemic effects begin at the cellular level, where thyroid hormones regulate the nuclear transcription of messenger RNA. T3 bids to a DNA domain called the thyroid response element, inducing a plethora of enzymes responsible for tissue metabolism, such as the ubiquitous Na, K-ATPase. Thyroid hormones modify cellular energy consumption and basal metabolic rate can increase as much as 60–100% as a consequence of increased TH levels. It drives additional glucose to be absorbed in the gastrointestinal tract, and stimulates glycogenolysis, gluconeogenesis, and insulin secretion, all the while promoting cellular glucose uptake [3, 4].

The production of thyroid hormones is regulated by the hypothalamic–pituitary axis, which continuously senses the concentration of T4 and T3 in the blood. In response to low thyroid hormone (TH), the hypothalamus releases thyrotropin releasing hormone (TRH), which in turn induces the anterior pituitary gland to release thyrotropin stimulating hormone (TSH). Somatostatin is released by the hypothalamus and inhibits the release of growth hormone (GH, somatotropin) and thyroid stimulating hormone (TSH) from the anterior pituitary. As previously stated, iodine is required to manufacture TH, and hypothyroid status may develop in an iodine-deficient patient [5].

Hyperthyroidism is condition that occurs due to excess production of TH. Thyrotoxicosis is the condition that occurs due to the presence of excess TH, and the term itself refers to any disorder of increased TH concentration of any cause and includes hyperthyroidism. Many etiologies of thyrotoxicosis exist, and Graves’ disease (multinodular goiter) is the most common cause of hyperthyroidism in the United States. Graves’ disease occurs more often in women with a female: male ratio of 5:1 and a population prevalence of 1–2%. Surgery in goiter cases is indicated for cosmetic reasons or for airway compromise via tracheal compression [2].

Along with Graves’, toxic adenoma and toxic multinodular goiter combine to make up 99% of the cases of hyperthyroidism in this country. Other common causes include the earlier stages of Hashimoto’s thyroiditis, exogenous TH abuse, and de Quervain’s subacute thyroiditis. Diagnoses that present with signs and symptoms similar to hyperthyroidism is condition that occurs due to excess production of TH and include other hypermetabolic states such as malignant hyperthermia, carcinoid, choriocarcinoma, hydatidiform mole, pheochromocytoma, struma ovarii, and certain drugs such as antipsychotic agents, anticholinergic agents, serotonin antagonists, sympathomimetic agents, and strychnine poisoning. Regardless of etiology, patients with hyperthyroidism are in a hypermetabolic state and display signs and symptoms to be discussed later [6, 7].

By system

To investigate any clinical suspicion for hyperthyroidism and thyrotoxicosis, there are several laboratory tests that are available. Free T4 and total T4 are commonly measured, and an elevation in either is indicative, but not confirmatory, of a hyperthyroid state. The current best test of TH action remains the TSH assay. Minute changes in thyroid function can result in dramatic swings in TSH secretion. The normal level of TSH in the body lies between 0.4 and 5.0 mU/L, and any TSH less than 0.03 mU/L accompanied by an elevation in T3 and T4 is diagnostic of overt hyperthyroidism. A thyroid storm patient, on the other hand, may experience TSH levels less than 0.01 mU/L. To contrast, the TSH of a patient with overt hypothyroidism can skyrockets to 400 mU/L or more [2].

Thyroid storm, the most feared complication of hyperthyroidism, is a sudden, life-threatening surge in the level of TH that overcomes a patient’s metabolic, thermoregulatory, and cardiovascular compensatory mechanisms. It typically occurs in an individual with untreated hyperthyroidism under a stress of infection, trauma, or surgery. Thyroid storm precipitated by stress of surgery usually occurs 6–18 h postoperatively, rather than intraoperatively. Other causes are withdrawal of antithyroid medication therapy, radioiodine therapy, cerebrovascular accident, diabetic ketoacidosis, myocardial or bowel infarction, pulmonary embolism, and pregnancy.

Typical findings in thyroid storm involve an exaggeration of the typical symptoms of hyperthyroidism, such as tachycardia and hyperpyrexia, anxiety, disorientation, delirium, chest pain, shortness of breath, heart failure, dehydration, and shock. Thyroid storm carries a high mortality rate, ranging from 10–30%. Diagnostic criteria for thyroid storm, established in 1993 by Burch and Wartofsky, are listed in Table 25.1 [4, 11].