Hyperthyroidism Clinical Presentation

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 more sympathetic activation, such as anxiety, hyperactivity, and tremor, while older patients have more cardiovascular symptoms, including dyspnea and atrial fibrillation with unexplained weight loss.^[3] 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
• Tremor
• Hyperactivity
• Palpitations
• Weight loss despite increased appetite
• Reduction in menstrual flow or oligomenorrhea

Common signs of thyrotoxicosis include the following:

• Hyperactivity
• Tachycardia or atrial arrhythmia
• Systolic hypertension
• Warm, moist, smooth skin
• Lid lag
• Stare
• Tremor
• Muscle weakness

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.

The frequency and severity of symptoms of thyrotoxicosis vary from person to person. Graves disease is an autoimmune disease, and a strong family history or past medical history of autoimmune disease, such as with rheumatoid arthritis, vitiligo, or pernicious anemia, often exists. The symptoms of Graves disease often are more marked, because thyroid hormone levels usually are the highest with this form of hyperthyroidism. Also consider the diagnosis of Graves disease 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 is associated with no clinical symptoms of thyrotoxicosis. However, certain conditions, such as 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 12% in the general population.

A report from the Netherlands on 1426 patients whose TSH levels were in the normal range (0.4-4.0 mU/L) found evidence, after a median follow-up of 8 years, of an increased risk of atrial fibrillation even in persons with high-normal thyroid function.^[4]

Radiation exposure, whether due to radiation therapy or to lower-level radiographic treatment, increases the risk of benign and malignant nodular thyroid diseases, with an observed increase in the incidence of autoimmune hyperthyroidism.

Recording a careful family history of autoimmune disease, thyroid disease, and emigration from iodine-deficient areas is important.

Review a complete list of medications. A number of compounds—including expectorants, amiodarone, health food supplements containing seaweed, and iodinated contrast dyes—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.

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.

Thyroid examination

Thyrotoxicosis due to Graves disease is associated with a diffusely enlarged and slightly firm thyroid gland. Sometimes, a thyroid bruit is audible using the bell of the stethoscope.

Toxic multinodular goiters occur when goiters generally are enlarged to at least 2 to 3 times normal size. The gland often is soft, but individual nodules occasionally can be palpated. With regard to toxic adenomas, these generally do not cause thyrotoxicosis in a patient until it is at least 2.5 cm in diameter.

If the thyroid is enlarged and painful, the diagnosis is likely subacute painful or granulomatous thyroiditis; however, also consider degeneration or hemorrhage into a nodule or suppurative thyroiditis.

Ophthalmologic and dermatologic examination

Graves thyrotoxicosis can be associated with mild thyroid ophthalmopathy in 50% of patients. Often, it is manifested only by periorbital edema, but it also can include conjunctival edema (chemosis), injection, poor lid closure, extraocular muscle dysfunction (diplopia), and proptosis. Evidence of thyroid eye disease and high thyroid hormone levels confirms the diagnosis of autoimmune Graves disease.

In rare instances, Graves disease affects the skin by deposition of glycosaminoglycans in the dermis of the lower leg. This causes nonpitting edema, usually associated with erythema and thickening of the skin, without pain or pruritus.

Signs of thyrotoxicosis

Usually, signs of thyrotoxicosis upon physical examination include sinus tachycardia or atrial fibrillation, systolic hypertension, excessive perspiration, palmar erythema and sweating, lid lag, extension tremor, hyperkinesis, large-muscle weakness, and soft, smooth skin.