To treat thyroid disease, it is essential to have a thorough knowledge of its embryology. The thyroid is derived from the primitive pharynx as well as the neural crest with the main body arising from epithelial cells of the endoderm and forming the follicles of the gland. Arising as a diverticulum from the floor of the primitive pharynx, the thyroid transforms into a bilobed structure and descends in the midline of the neck. This tract remains attached to the posterior inferior tongue as the thyroglossal duct, and its distal end may go on to form a pyramidal lobe. This serves as the embryologic basis for the formation of a thyroglossal duct cyst as well as nodules within the pyramidal lobe, and underscores the need to completely excise the thyroglossal tract through the hyoid bone to the level of the foramen cecum when the aforementioned cyst is present. It also requires the surgeon to systematically search for a pyramidal lobe when performing a total thyroidectomy because it is present in 30% to 40% of patients and will be the point of persistent or recurrent disease if not identified at the time of operation.1

The neural crest serves as the basis for the formation of the parafollicular cells (C cells). The C cells, which secrete calcitonin, migrate from the fourth and fifth branchial pouches. The combination of these two branchial pouches leads to the formation of the caudal pharyngeal complex, which serves as the precursor to the lateral thyroid lobes (ultimobranchial bodies). Eventually, the lateral lobes join the main body on each side as they descend from the buccal cavity. The C cells ultimately populate the entire gland. The fusion of the ultimobranchial body and the main thyroid body forms the tubercle of Zuckerkandl and can be seen as a slight nodular thickening at the junction of the superior and middle third on the posterior surface of the gland where the lateral lobes meet the main thyroid body.

During development, the third branchial pouch (source of the thymus) is gradually separated caudally. As the thymus, heart, and great vessels descend, it is drawn toward the superior mediastinum. The thymus dissociates, leaving the thyrothymic ligaments as vestigial remnants of their connection. The track of descent of the thymus and great vessels into the superior mediastinum forms the thyrothymic ligaments. Along this path, thyroid rests are formed when the endoderm from the fourth branchial pouch may be pulled down in the descent of the primitive thymus to form retrosternal thyroid components.2 As with the pyramidal lobe, care must be taken to search for these extensions of thyroid tissue to prevent persistence or recurrence of disease when total thyroidectomy is being performed.

General

The normal thyroid gland lies caudal to the larynx and encircles the anterior and lateral aspects of the first several rings of the trachea. It normally weighs approximately 20 g and is composed of right and left lateral lobes; the isthmus; and at times, a superior extension of it, the pyramidal lobe (which occurs more often on the left). The strap muscles (sternohyoid, sternothyroid, and superior belly of the omohyoid) cover the anterolateral surface of the gland. The oblique upper insertion of the sternothyroid muscle to the thyroid cartilage prevents the lateral lobes from medializing and encroaching onto the underlying thyrohyoid muscle. The upper pole of the lateral lobe is attached medially to the inferior constrictor complex and to the posterior aspect of the cricothyroid muscle. The ansa cervicalis formed from the descendens hypoglossi (C1) and the descendens cervicalis (C2 and C3) innervate the strap muscles and should be preserved whenever possible. The obliterated thyroglossal duct may go on to form a muscular band (levator glandulae superioris) connecting the pyramidal lobe to the hyoid bone.3

The entire thyroid gland is enveloped in a thin, fibrous pretracheal capsular fascia. Dissection of this fascia from the surface of the gland serves as the basis for the term “capsular dissection.” The fascia coalesces near the cricoid cartilage and upper tracheal rings on the posterior aspect of the thyroid gland to form the ligament of Berry.

Arterial Blood Supply

The superior pole of the gland is supplied by multiple branches of the superior thyroid artery as it originates from the external carotid artery and gives off terminal branches enveloping the superior pole of the gland in a variable course. Great care must be taken to expose the avascular space between the cricothyroid muscle and the superior pole of the gland. The branches of the superior thyroid artery should be ligated as close to the gland as possible to prevent inadvertent incorporation of the external branch of the superior laryngeal nerve. This nerve often runs in a similar path with the superior thyroid artery; its anatomic variations are well described by Cernea et al.4 In addition to exposing the avascular cricothyroid space, the lateral aspect of the superior pole needs to be dissected free of the overlying sternothyroid muscle. Inferolateral traction on the gland is crucial in exposing both of these planes of dissection to safely ligate the superior pole.

The inferior thyroid artery arises from the thyrocervical trunk and gives off terminal branches entering the posterolateral aspect of the thyroid at the junction of the upper and middle third of the gland. It is intimately associated with the recurrent laryngeal nerve and runs along a course that generally intersects the nerve as its branches terminate in the gland.

Venous Drainage

Venous drainage of the thyroid gland is variable and occurs through a variety of intercommunicating vessels. The venous network may be divided into three separate regions: the superior veins (draining the superior pole and adjacent to the superior thyroid arteries); the middle thyroid veins (which may be absent in some patients), traveling laterally from each lobe and emptying into the internal jugular vein; and the inferior thyroid veins, draining the inferior pole and adjacent to and coursing with the thyrothymic ligament.

Nerves

Three major components of the nervous system are encountered in thyroid surgery. At the superior pole of the thyroid is the external branch of the superior laryngeal nerve (EBSLN). It is a branch of the vagus nerve and is the motor nerve supplying the cricothyroid muscle. As previously noted, its close but variable course to the superior pole vessels place it at risk for injury during thyroidectomy.4 When effort is taken to identify it as it courses through the cricothyroid space, the nerve may be found in more than 90% of cases.

The recurrent laryngeal nerves (RLNs) ascend from the thoracic inlet along the right and left tracheoesophageal grooves. Compared with the nerve on the left, the nerve on the right courses in a more lateral to medial oblique path. The nerves may give off anterior or posterior branches before entering the larynx. There are many variations of the nerve and its relation to the ligament of Berry as well as the inferior thyroid artery; however, it can generally be encountered passing into the pharynx in a cleft just medial to the tubercle of Zuckerkandl.1 A nonrecurrent laryngeal nerve is rare (<1%); if present, it is usually found on the right. Left-sided nonrecurrent laryngeal nerves are extremely uncommon, although a recent case report noted a patient with a right aortic arch, an aberrant left innominate artery, and the absence of a ductus arteriosus.5 A nonrecurrent nerve tracks along the same course as the vagus and sweeps from lateral to medial in the jugulocarotid groove. It is most commonly associated with a retroesophageal aberrant subclavian artery (lusorian artery).

An additional set of nerves that deserves mention are the sympathetic–inferior laryngeal nerve anastomotic branch (SILABs), which run between the cervical sympathetic ganglia and the recurrent laryngeal nerve with fine direct anastomosis and then run onto the surface of the gland itself. The SILAB may be larger than the RLN and as such leads to confusion in identification of the RLN, thus placing it at risk for injury. SILABs may be divided with impunity during capsular dissection, but their visualization is necessary to ensure proper identification and preservation of the RLN.1

Thyroid nodules are common in the general population. They may be found by physical examination in approximately 7% of the general population; if ultrasonography is used, thyroid nodules may be found in more than half of the general population over 50 years of age.6,7 The prevalence of nodules increases with age and is generally higher in women than men. The principal concern of a thyroid nodule is malignancy. In 80% of cases, solitary nodules are most commonly benign and include colloid nodules, thyroid cysts, or thyroiditis. The remaining 10% to 15% of thyroid nodules are follicular lesions; approximately 5% of thyroid nodules are malignant.7 Because of the large incidence of thyroid nodules in the general population, a concise scheme to approach thyroid nodules is important. This strategy should incorporate the characteristics of the nodule as well as the clinical history of the patient.

Exposure to ionizing radiation has been shown to increase the risk of malignancy for a thyroid nodule to approximately 40%.8 Medullary thyroid cancers (MTCs) may be familial 20% of the time, occurring in the multiple endocrine neoplasia (MEN) syndromes, or may be sporadic. Familial non-MTCs are rare, and the diagnosis is made when thyroid cancers occur in two first-degree relatives. Some of the conditions associated with differentiated thyroid cancer include familial adenomatous polyposis (FAP), phosphatase and tensin homolog hamartoma tumor syndrome (PHTS), Carney complex, Werner syndrome, and papillary renal cell carcinoma.9Table 1-1 lists both high- and moderate-risk features that may be associated with thyroid cancer. A general rule to follow is that for any nodule associated with two or more high-risk characteristics, the malignancy rate may be greater than 70%. All nodules that are hard, fixed to adjacent structures, rapidly growing, or associated with lymphadenopathy should be removed.

Patients presenting with other traditional benign thyroid disease may be at higher risk of harboring a malignant nodule. Cold nodules found on radionuclide scanning in patients with Graves’ disease may be malignant 15% to 38% of the time depending on the nodule’s size and the patient’s gender. Complex cysts in thyroid disease may also have an associated malignancy approximately 17% of the time. In patients with goiter, the malignancy risk is actually higher in patients who have one or two nodules than in patients with more than three nodules. However, it must be noted that patients with goiter are not at an increased risk of malignancy compared with the general population. Finally, patients with a nodule of 4 cm or greater should undergo diagnostic thyroid lobectomy because fine-needle aspiration (FNA) biopsy in this group of patients has been shown to have up to a 34% false-negative rate; 40% of indeterminate lesions diagnosed on FNA were later found on histologic section to be malignant.10

A final population at an increased risk of malignancy is children with thyroid nodules. Thyroid nodules occur in children in an average of 1% of the population. The rate of malignancy varies among studies at between 20% and 50%. The rate of malignancy is similar for both palpable as well as nonpalpable nodules as it is in adults.