Goiter Clinical Presentation

Updated: Mar 21, 2017
  • Author: James R Mulinda, MD, FACP; Chief Editor: Romesh Khardori, MD, PhD, FACP  more...
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Presentation

History

A goiter may present in various ways, including the following:

  • Incidentally, as a swelling in the neck discovered by the patient or on routine physical examination
  • A finding on imaging studies performed for a related or unrelated medical evaluation
  • Local compression causing dysphagia, dyspnea, stridor, plethora or hoarseness
  • Pain due to hemorrhage, inflammation, necrosis, or malignant transformation
  • Signs and symptoms of hyperthyroidism or hypothyroidism
  • Thyroid cancer with or without metastases
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Physical

The general examination for hyperthyroidism, hypothyroidism, and autoimmune stigmata is followed by systematic examination of the goiter.

A retrosternal goiter may not be evident on physical examination.

Examination of the goiter is best performed with the patient upright, sitting or standing. Inspection from the side may better outline the thyroid profile, as shown below. Asking the patient to take a sip of water facilitates inspection. The thyroid should move upon swallowing. See the image below.

Patient with a goiter. Prominent side-view outline Patient with a goiter. Prominent side-view outline.

Palpation of the goiter is performed either facing the patient or from behind the patient, with the neck relaxed and not hyperextended. Palpation of the goiter rules out a pseudogoiter, which is a prominent thyroid seen in individuals who are thin. Each lobe is palpated for size, consistency, nodules, and tenderness. Cervical lymph nodes are then palpated. The oropharynx is visualized for the presence of lingular thyroid tissue.

The size of each lobe is measured in 2 dimensions using a tape measure. Some examiners make tracings on a sheet of paper, which is placed in the patient's chart. Suitable landmarks are used and documented to ensure consistent measurement of the thyroid gland.

The pyramidal lobe often is enlarged in Graves disease.

A firm rubbery thyroid gland suggests Hashimoto thyroiditis, and a hard thyroid gland suggests malignancy or Riedel struma.

Multiple nodules may suggest a multinodular goiter or Hashimoto thyroiditis. A solitary hard nodule suggests malignancy, whereas a solitary firm nodule may be a thyroid cyst.

Diffuse thyroid tenderness suggests subacute thyroiditis, and local thyroid tenderness suggests intranodal hemorrhage or necrosis.

Cervical lymph glands are palpated for signs of metastatic thyroid cancer.

Auscultation of a soft bruit over the inferior thyroidal artery may be appreciated in a toxic goiter. Palpation of a toxic goiter may reveal a thrill in the profoundly hyperthyroid patient.

Goiters are described in a variety of ways, including the following:

  • Toxic goiter: A goiter that is associated with hyperthyroidism is described as a toxic goiter. Examples of toxic goiters include diffuse toxic goiter (Graves disease), toxic multinodular goiter, and toxic adenoma (Plummer disease).
  • Nontoxic goiter: A goiter without hyperthyroidism or hypothyroidism is described as a nontoxic goiter. It may be diffuse or multinodular, but a diffuse goiter often evolves into a nodular goiter. Examination of the thyroid may not reveal small or posterior nodules. Examples of nontoxic goiters include chronic lymphocytic thyroiditis (Hashimoto disease), goiter identified in early Graves disease, endemic goiter, sporadic goiter, congenital goiter, and physiologic goiter that occurs during puberty.

Autonomously functioning nodules may present with inability to palpate the contralateral lobe. Unilobar agenesis may also present like a single thyroid nodule with hyperplasia of the remaining lobe.

The Pemberton maneuver raises a goiter into the thoracic inlet when the patient elevates the arms. This may cause shortness of breath, stridor, or distention of neck veins.

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Causes

The different etiologic mechanisms that can cause a goiter include the following:

  • Iodine deficiency [2]
  • Autoimmune thyroiditis - Hashimoto or postpartum thyroiditis
  • Excess iodine (Wolff-Chaikoff effect) [7] or lithium ingestion, which decrease release of thyroid hormone
  • Goitrogens
  • Stimulation of TSH receptors by TSH from pituitary tumors, pituitary thyroid hormone resistance, gonadotropins, and/or thyroid-stimulating immunoglobulins
  • Inborn errors of metabolism causing defects in biosynthesis of thyroid hormones
  • Exposure to radiation
  • Deposition diseases/infiltrative disease
  • Thyroid hormone resistance (pituitary thyroid hormone resistance with resultant elevated TSH)
  • Subacute thyroiditis (de Quervain thyroiditis)
  • Silent thyroiditis
  • Riedel thyroiditis
  • Infectious agents
    • Acute suppurative - Bacterial
    • Chronic - Mycobacteria, fungal, and parasitic
  • Granulomatous disease
  • Thyroid malignancy
  • Low selenium levels: This may be associated with goiter prevalence. [8]
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