Non Toxic Goiter


A nontoxic goiter is a diffuse or nodular enlargement of the thyroid gland that does not result from an inflammatory or neoplastic process and is not associated with abnormal thyroid function. Endemic goiter is defined as thyroid enlargement that occurs in more than 10% of a population, and sporadic goiter is a result of environmental or genetic factors that do not affect the general population.


The histopathology varies with etiology and age of the goiter. Initially, uniform follicular epithelial hyperplasia (diffuse goiter) is present, with an increase in thyroid mass. As the disorder persists, the thyroid architecture loses uniformity, with the development of areas of involution and fibrosis interspersed with areas of focal hyperplasia. This process results in multiple nodules (multinodular or adenomatous goiter). On nuclear scintigraphy, some nodules are hot, with high isotope uptake (autonomous) or cold, with low isotope uptake, compared with the normal thyroid tissue (as demonstrated in the images below).

The development of nodules correlates with the development of functional autonomy and reduction in thyroid-stimulating hormone (TSH) levels. Clinically, the natural history of a nontoxic goiter is growth, nodule production, and functional autonomy. However, abnormally high thyroid function resulting in thyrotoxicosis occurs in a minority of patients. The risk of malignancy is the same in a patient with a nodular goiter as with a solitary nodule.


More than 2.2 billion people worldwide have some form of iodine deficiency disorder. Twenty-nine percent of the world’s population lives in a region that has iodine deficiency (primarily in Asia, Latin American, central Africa, and regions of Europe). Of those at risk, 655 million were known to have goiter. In the iodine-deficient regions of the world, goiter is more common than in the United States. The prevalence of goiter can be estimated based on the iodine intake of the population.

As reported by the World Health Organization (WHO), the United Nations Children’s Fund (UNICEF), and the International Council for the Control of Iodine Deficiency Disorders (ICCIDD), the absence of iodine deficiency (ie, median urine iodine >100 mg/dL) is associated with a goiter prevalence of less than 5%; mild iodine deficiency (ie, median urine iodine 50-99 mg/dL), with a goiter prevalence of 5-20%; moderate iodine deficiency (ie, median urine iodine 20-49 mg/dL), with a goiter prevalence of 20-30%; and severe iodine deficiency (ie, median urine iodine 20-49 mg/dL), with a goiter prevalence of greater than 30%.


Endemic goiters arising from iodine deficiency are associated with sometimes immense thyroid hypertrophy, hypothyroidism, and cretinism. Sporadic goiters are generally asymptomatic and found either by a clinician’s physical examination or by the patient’s observation of neck enlargement. Occasionally, the goiter may produce symptoms caused by pressure on anterior neck structures, including the trachea (wheezing, cough, globus hystericus [anterior neck pressure]), the esophagus (dysphagia), and the recurrent laryngeal nerve (hoarseness).

Rarely, the obstruction can be dangerous because of narrowing of the trachea and the development of tracheitis with edema and tracheomalacia, leading to severe narrowing of the airway with serious obstruction resulting in a respiratory emergency.


No convincing epidemiologic studies suggest that race plays an important role in the development of nontoxic goiter. Generally, the lower socioeconomic conditions in nonindustrialized countries resulting in iodine deficiency have a more important role than race does in the development of a goiter.


Diffuse and nodular goiter is more common in women than in men. According to the best estimate, the incidence of goiter in women is 1.2-4.3 times as great as that in men.


Sporadic goiter from dyshormonogenesis, a genetic error in proteins that are necessary for thyroid hormone synthesis, occurs during childhood. Endemic goiter due to iodine deficiency occurs during childhood, with the goiter’s size increasing with age. Other causes of sporadic goiter rarely occur before puberty and do not have a peak age of occurrence. Thyroid nodules increase in incidence with age.


The thyroid gland usually grows outward because of its location anterior to the trachea (see the image below). Occasionally, the thyroid wraps around and compresses the trachea and/or esophagus or extends inferiorly into the anterior mediastinum.

Growth pattern

Determining whether the goiter has been present for many years and whether a change has occurred in the recent past is important.

Recent or accelerated growth of a discrete nodule or thyroid lobe should raise the suspicion of malignancy.

Goiters associated with unilateral adenopathy should raise the suspicion of malignancy.

Goiters rarely are painful or grow quickly unless recent hemorrhage into a nodule has occurred.

Tracheal compression is generally asymptomatic until critical narrowing has occurred.

Patients develop a dry cough, dyspnea, and stridor, especially with exertion. In patients with intrathoracic goiter, the dyspnea and stridor may be nocturnal or positional (ie, occurring when the patient’s arms are raised) when the thoracic outlet is narrowed.

Hemorrhage into a nodule or cyst or development of bronchitis may acutely worsen the respiratory symptoms in a patient with tracheal narrowing.

The esophagus is more posterior in the neck, and a goiter occasionally extends posteriorly and causes solid food and pill dysphagia.

Compression of the recurrent laryngeal nerve by a goiter or invasion by a thyroid malignancy results in vocal cord dysfunction and may cause hoarseness. The superior laryngeal nerve controls the pitch of the voice. An expanding goiter may cause a change in the character of the voice, especially in individuals who use their voice extensively (eg, in certain occupations).

Compression of the venous outflow through the thoracic inlet by a mediastinal goiter results in facial plethora and dilated neck and upper thoracic veins.

Iodine intake

Obtain a careful diet history for iodine deficiency, iodine excess from medications (eg, amiodarone), health food store supplements, or seaweed.

History of radiation

Record any history of head and neck radiation exposure, especially during childhood, which significantly increases the risk of benign and malignant nodular thyroid disease and thyroid dysfunction (hypothyroidism and hyperthyroidism).[2, 1]

Family history

Family history is very important in the evaluation of the patient with goiter. Investigate inherited forms of dyshormonogenesis in the pediatric patient, as well as familial papillary carcinoma of the thyroid and familial forms of medullary thyroid cancer (multiple endocrine neoplasia and familial medullary carcinoma of the thyroid).


Pertinent physical findings are limited to the evaluation of the shape, asymmetry, size, and consistency of nontoxic goiters; ultrasonographic characteristics of individual nodules within the goiter; lymphadenopathy; and assessment of thyroid function.[2, 1]

The thyroid evaluation starts with inspection of the neck for thyroid enlargement. Often, the thyroid enlargement can be detected only when the patient swallows.

The thyroid isthmus is usually located at or just below the level of the cricoid cartilage of the trachea. The lobes of the thyroid extend laterally and, if enlarged, may extend posterior to the sternocleidomastoid muscles. Up to 80% of thyroid glands may have a pyramidal lobe extending superiorly from the isthmus.

Assess the gland for overall size; in the United States, the normal weight is 15-20 grams.

Assess the thyroid for asymmetry and determine whether a dominant nodule is present in an overall nodular goiter or whether a solitary nodule is present in an otherwise normal gland. Evaluate dominant nodules that are bigger than 1-1.5 cm or a solitary nodule of the same size by a thin-needle aspiration biopsy.[3] Diffuse or nodular goiters without a dominant nodule do not require a biopsy for evaluation.


Examine patients with dyspnea and cough, especially with exertion, for tracheal obstruction. Note any tracheal deviation from midline.

The patient’s voice is assessed for hoarseness.

Venous outflow obstruction of the head and neck can be elicited by the Pemberton maneuver by raising the patient’s arms above the head until they touch the sides of the head for 1 minute. A positive finding occurs with facial plethora or engorgement of the neck veins.

Physical assessment of thyroid dysfunction

Examine patients for signs of thyroid dysfunction.

Hypothyroidism is indicated by a sallow complexion, dysarthric speech, mental slowing, weight gain without change in appetite, cold intolerance, constipation, hypersomnia, and delayed relaxation of deep tendon reflexes.

Hyperthyroidism is indicated by tachycardia, atrial arrhythmia (eg, atrial fibrillation), diaphoresis, weight loss without change in appetite, heat intolerance, hyperdefecation, palmar erythema, lid lag, tremor, and brisk reflexes.


Carefully examine the neck to identify any lymphadenopathy.


The most common worldwide cause of endemic nontoxic goiter is iodine deficiency. However, in patients with sporadic goiter, the cause is usually unknown. Nontoxic goiters have many etiologies, including the following:

  • Iodine deficiency – Goiter formation occurs with moderately deficient iodine intake of less than 50 mcg/d. Severe iodine deficiency associated with intake of less than 25 mcg/d is associated with hypothyroidism and cretinism.
  • Iodine excess – Goiter formation due to iodine excess is rare and usually occurs in the setting of preexisting autoimmune thyroid disease.
  • Goitrogens

    • Drugs – Propylthiouracil, lithium, phenylbutazone, aminoglutethimide, iodine-containing expectorants
    • Environmental agents – Phenolic and phthalate ester derivatives and resorcinol found downstream of coal and shale mines
    • Foods – Vegetables of the genus Brassica (eg, cabbage, turnips, brussels sprouts, rutabagas), seaweed, millet, cassava, and goitrin in grass and weeds
  • Dyshormonogenesis – A defect in the thyroid hormone biosynthetic pathway is inherited.
  • Childhood head and neck radiation – Radiation exposure during childhood results in benign and malignant nodules.


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