Thyroid Enlargement/Goiter
Thyroid Enlargement/Goiter: Excerpt from The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter
Stephen F. Wheeler and David E. Bybee
Goiter, an enlarged thyroid gland, is the most common thyroid abnormality. Goiter is termed endemic if it occurs in more than 10% of a population. Endemic goiter most commonly results from dietary iodine deficiency and is extremely rare in the United States. Sporadic goiter arises in nonendemic areas and from various causes (1). Mean thyroid gland weight in iodine-sufficient populations is 10 g, with 20 g representing the upper limit of normal (2).
Approach
A. Goiter types. Simple goiter, also referred to as diffuse, is present in approximately 5% of the population. Its incidence increases with age and it is three to five times more common in women than men. Simple goiter is usually accompanied by a normal metabolic state, although functional status can change with time. A palpable goiter may represent a solitary nodule or multiple nodules (multinodular goiter) (Chapter 14.7). The functional status of a goiter can be hypothyroid (Chapter 14.4), normal, or hyperthyroid [also referred to as toxic (Chapter 14.8)].
B. Etiology. Any process that impedes thyroid hormone synthesis or release can cause simple goiter. Inherited defects of thyroid-stimulating hormone (TSH) receptors and virtually all biochemical steps in thyroid hormone synthesis and release have been identified as causes of goiter. The resulting thyroid hyperplasia is initially dependent on elevated levels of TSH from the pituitary; however, because of increased thyroxine production by the enlarged gland, serum TSH levels in patients with established goiter are usually normal (3). Goitrogens, substances that interfere with thyroid hormone production and action, can cause sporadic goiter. This category includes certain drugs (thioamide derivatives, lithium, iodides, amiodarone and others) and foods (rutabagas, cabbage, turnips, soybeans, kelp and others) (1).
History
In simple goiter, patients are asymptomatic or, if the gland is sufficiently enlarged, they present with symptoms caused by mechanical pressure. Substernal goiters are frequently responsible for tracheal pressure symptoms, including dyspnea and inspiratory stridor. They can also obstruct the large cervical veins at the thoracic inlet, causing suffusion of the face, giddiness, and syncope (Pemberton’s sign). Esophageal compression can lead to dysphagia (Chapter 9.5). Hoarseness caused by compression of or traction on the recurrent laryngeal nerve is rare in simple goiter and suggests a malignancy (Chapter 6.3). Generalized thyroid pain suggests subacute thyroiditis, whereas sudden localized pain and swelling are consistent with hemorrhage into a nodule. Although simple goiters are usually euthyroid, typical symptoms of hypothyroidism or thyrotoxicosis should be sought. A family history of goiter and a personal history of residing in an endemic goiter area or ingesting goitrogens may be significant (1).
Physical examination
A. General examination. Look for typical vital and physical signs consistent with hypothyroidism or thyrotoxicosis. Pemberton’s sign can be induced by having the patient raise both arms above the head.
B. Thyroid examination. Inspect the neck below the thyroid cartilage from the front, using cross-lighting to accentuate shadows and masses. Full extension of the neck enhances visibility of the gland. Inspection from the side with measurement of any prominence of the normally smooth and straight contour between the cricoid cartilage and the suprasternal notch is useful. Palpitation is done using the technique with which the examiner is most experienced and skilled. Approach the patient from either the front or behind and palpate using the fingers or thumbs. If felt between the cricoid cartilage and the suprasternal notch, the thyroid isthmus can be used to help locate the gland. Palpation of the lobes can be improved by relaxation of the sternocleidomastoid; for example, the left lobe can be defined better by having the patient slightly flex and rotate the neck to the left. Other useful maneuvers include measuring the circumference of the neck or the dimensions of each lobe. Note the location, size, consistency, mobility, and tenderness of any nodules. Having the patient swallow during both inspection and palpation causes the thyroid to move and aids in developing a three-dimensional impression of gland shape and size. This maneuver can also make a low-placed gland accessible. Categorize thyroid size as “normal” or “goiter,” and subcategorize “goiter” as “small” (two or less times normal) or “large” (more than two times normal) (2).
Testing
A. Laboratory testing. The sensitive TSH (sTSH) assay is the single best test to evaluate thyroid status. Elevated sTSH is highly suggestive of hypothyroidism (Chapter 14.4). If sTSH is suppressed, an elevated free thyroxine index (FTI) or free thyroxine (fT4) measured directly, confirms thyrotoxicosis (Chapter 14.8). In a patient with a suppressed sTSH and a normal FTI or fT4, serum triiodothyronine (T3) should be measured to assess for possible T3 thyrotoxicosis.
B. Diagnostic imaging. Nuclear scans and ultrasound studies are not warranted in the routine evaluation of simple or multinodular goiter (4). Ultrasonography may be helpful in patients with equivocal findings on palpation. Symptoms suggestive of substernal mechanical pressure require evaluation, usually by computed tomography (CT) or magnetic resonance imaging (MRI).
C. Other tests. Fine needle aspiration biopsy (FNAB) should be performed in cases of a solitary or dominant nodule found by palpation. Pulmonary function tests are warranted with evidence of inspiratory impairment. Barium swallow is indicated to evaluate goiter-associated dysphagia.
Diagnostic assessment
The evaluation of goiter focuses on the history, thyroid palpation, and functional status of the gland. An asymptomatic patient with a simple or multinodular goiter associated with a normal metabolic state does not necessarily require further diagnostic studies or treatment. Periodic assessment, at least annually, to evaluate growth, function, and symptoms is warranted. A palpable solitary nodule or dominant nodule in a multinodular gland should be evaluated by FNAB or excisional biopsy (Chapter 14.7). Goiter with compressive symptoms requires CT or MRI evaluation and referral for probable surgery. Further assess a goiter associated with an abnormal metabolic state as outlined for hypothyroidism (Chapter 14.4) or thyrotoxicosis (Chapter 14.8). Thyroid hormone suppression of any goiter type is controversial, and the risks associated with subclinical hyperthyroidism must be included in the risk-to-benefit analysis (5).
References
1. Petrone LR. A primary care approach to the adult patient with nodular thyroid disease. Arch Fam Med 1996;5:92–100.
2. Siminoski K. Does this patient have a goiter? JAMA 1995;273:813–817.
3. Peter HJ, Burgi U, Gerber H. Pathogenesis of nontoxic diffuse and nodular goiter. In: Braverman LE, Utiger RD, eds. Werner and Ingbar’s the thyroid, 7th ed. Philadelphia: JB Lippincott, 1996:890–895.
4. Tan GH, Gharib H. Thyroid nodular disease: diagnostic evaluation and management [Letter]. Arch Intern Med 1997;157:575.
5. Gharib H, Mazzaferri EL. Thyroxine suppressive therapy in patients with nodular thyroid disease. Ann Intern Med 1998;128:386–394.
Book Source Details
- Book Title: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter
- Author(s): Robert B. Taylor (editor)
- Year of Publication: 2000
- Copyright Details: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, Copyright © 2000 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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