Hyperthyroidism and Thyrotoxicosis Clinical Presentation

Updated: Mar 15, 2018
  • Author: Stephanie L Lee, MD, PhD; Chief Editor: Romesh Khardori, MD, PhD, FACP  more...
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Presentation

History

The presentation of thyrotoxicosis is variable among patients. Thyrotoxicosis leads to an apparent increase in sympathetic nervous system symptoms. Younger patients tend to exhibit symptoms of sympathetic activation, such as anxiety, hyperactivity, and tremor, while older patients have more cardiovascular symptoms, including dyspnea and atrial fibrillation with unexplained weight loss. [1] The clinical manifestations of thyrotoxicosis do not always correlate with the extent of the biochemical abnormality.

Common symptoms of thyrotoxicosis include the following:

  • Nervousness

  • Anxiety

  • Increased perspiration

  • Heat intolerance

  • Hyperactivity

  • Palpitations

Generally, a constellation of information, including the extent and duration of symptoms, past medical history, and social and family history, in addition to the information derived from physical examination, help to guide the clinician to the appropriate diagnosis. For example, Graves disease is an autoimmune disease, and patients often have a family history or past medical history of autoimmune disease (eg, rheumatoid arthritis, vitiligo, pernicious anemia).

Patients with Graves disease often have more marked symptoms than patients with thyrotoxicosis from other causes, because thyroid hormone levels usually are the highest with this form of hyperthyroidism. The diagnosis of Graves disease should also be considered if any evidence of thyroid eye disease exists, including periorbital edema, diplopia, or proptosis.

Toxic multinodular goiters occur in patients who have had a known nontoxic goiter for many years or decades. Often, patients have emigrated from regions of the world with borderline- low iodine intake or have a strong family history of nontoxic goiter.

Subclinical hyperthyroidism, defined as a low thyroid-stimulating hormone (TSH) level with normal free thyroxine (FT4) and free triiodothyronine (FT3) levels, is associated with no or minimal clinical symptoms of thyrotoxicosis. However, certain conditions (eg, atrial fibrillation, osteoporosis, or hypercalcemia) may suggest the possibility of thyrotoxicosis. In fact, subclinical hyperthyroidism may be associated with a 3-fold increase in the risk of atrial fibrillation. The prevalence of subclinical hyperthyroidism may be as high as 2% in the general population.

The risk of atrial fibrillation may be elevated even in persons with high-normal thyroid function. In a report from the Netherlands on 1426 patients whose TSH levels were in the normal range (0.4-4.0 mIU/L), the hazard ratio for atrial fibrillation was 1.94 for the lowest versus the highest quartile of TSH, after a median follow-up of 8 years. [17]

Radiation exposure increases the risk of benign and malignant nodular thyroid diseases, especially with the higher radiation levels used in radiation therapy. External radiation therapy is associated with an increase in the incidence of autoimmune hyperthyroidism when the thyroid is in the radiation field.

The family history should include careful documentation of the following:

  • Autoimmune disease

  • Thyroid disease

  • Emigration from iodine-deficient parts of the world

Review a complete list of medications and dietary supplements. A number of compounds—including expectorants, amiodarone, iodinated contrast dyes, and health food supplements containing seaweed or thyroid gland extracts—contain large amounts of iodine that can induce thyrotoxicosis in a patient with thyroid autonomy. Rarely, iodine exposure can cause thyrotoxicosis in a patient with an apparently healthy thyroid.

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Physical Examination

The thyroid is located in the lower anterior neck. The isthmus of the butterfly-shaped gland generally is located just below the cricoid cartilage of the trachea, with the wings of the gland wrapping around the trachea. Physical examination often can help the clinician to determine the etiology of thyrotoxicosis.

Common signs of thyrotoxicosis include the following:

  • Tachycardia or atrial arrhythmia

  • Systolic hypertension with wide pulse pressure

  • Warm, moist, smooth skin

  • Lid lag

  • Stare

  • Hand tremor

  • Muscle weakness

  • Weight loss despite increased appetite (although a few patients may gain weight, if excessive intake outstrips weight loss)

  • Reduction in menstrual flow or oligomenorrhea

Thyroid examination

Thyrotoxicosis from Graves disease is associated with a diffusely enlarged and slightly firm thyroid gland. Sometimes, a thyroid bruit can be heard by using the bell of the stethoscope.

Toxic multinodular goiters generally occur when the thyroid gland is enlarged to at least 2 to 3 times the normal size. The gland often is soft, but individual nodules occasionally can be palpated. Because most thyroid nodules cannot be palpated, thyroid nodules should be documented by thyroid ultrasonography, but overactive thyroid nodules can be demonstrated only by nuclear thyroid imaging with radioiodine (I-123) or technetium (Tc99m) thyroid scan.

If the thyroid is enlarged and painful, subacute painful or granulomatous thyroiditis is the likely diagnosis. However, degeneration or hemorrhage into a nodule and suppurative thyroiditis should also be considered.

Ophthalmologic and dermatologic examination

Approximately 50% of patients with Graves thyrotoxicosis have mild thyroid ophthalmopathy. Often, this is manifested only by periorbital edema, but it also can include conjunctival edema (chemosis), injection, poor lid closure, extraocular muscle dysfunction (diplopia), and Proptosis (see the image below). Evidence of thyroid eye disease and high thyroid hormone levels confirms the diagnosis of autoimmune Grave disease.

Severe proptosis, periorbital edema, and eyelid re Severe proptosis, periorbital edema, and eyelid retraction from thyroid-related orbitopathy. This patient also had optic nerve dysfunction and chemosis (conjunctival edema) from thyroid-related orbitopathy.

In rare instances, Graves disease affects the skin through deposition of glycosaminoglycans in the dermis of the lower leg. This causes nonpitting edema, which is usually associated with erythema and thickening of the skin, without pain or pruritus (see the image below).

Bilateral erythematous infiltrative plaques on low Bilateral erythematous infiltrative plaques on lower extremities in 42-year-old man with Graves disease are consistent with pretibial myxedema. Myxedematous changes of skin usually occur in pretibial areas and resemble orange peel in color and texture.
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