Approach

Patients with toxic adenomas usually present with signs and symptoms of hyperthyroidism.

Clinical exam

In most cases nodules are larger than 3 cm before the development of overt thyrotoxicosis.[3] History may reveal that the patient has resided in an iodine-deficient region. There may be hyperphagia and weight loss, oligomenorrhea, sweating, heat intolerance, nervousness, palpitations, shortness of breath or hyperdefecation. Onset is often more insidious and symptoms less dramatic than for Graves disease.

Physical exam may show tachycardia, stare, lid lag, warm moist skin, tremor or generalized/proximal muscle weakness. Stigmata of Graves disease (exophthalmos or pretibial myxedema) are absent.

Patients may have a choking sensation, dysphagia or hoarseness.[21] Usually these are not caused by apparent thyroid disease, and esophageal, cardiac, pulmonary or local pathology must be excluded.

Tests

The initial screening test is a thyroid-stimulating hormone (TSH) level.[1][22]​ Do not order more tests until the results of the TSH test are available as a TSH value within the reference range excludes the majority of primary thyroid diseases.[23]​ If suppressed, thyroid hormone levels (triiodothyronine [T3]/thyroxine [T4]) should be measured. The preferred tests are free T4, and total T3 plus a measure of binding. Some patients may have normal levels of thyroid hormones (subclinical hyperthyroidism) or have elevation of T3 alone (T3 toxicosis).[1]

If biochemical hyperthyroidism is confirmed, a thyroid scan and uptake (thyroid scintigraphy) is the next step.[1]​[24]​​[25]​ In toxic adenoma, this shows a hot (i.e., hyperfunctioning) nodule with suppression of surrounding thyroid tissue.[1][Figure caption and citation for the preceding image starts]: Hyperfunctioning thyroid nodule suppressing contralateral gland on thyroid scan (SSN = suprasternal notch)Arem R. Recurrent transient thyrotoxicosis in multinodular goitre. Postgrad Med J. 1990 Jan;66(771):54-6 [Citation ends].com.bmj.content.model.Caption@5bba283f​ Hot nodules are almost always benign.

If a hot nodule is not confirmed, other causes of hyperthyroidism such as Graves disease should be considered.

Thyroid ultrasound should be obtained in all patients with known or suspected thyroid nodules.[24] Do not routinely order thyroid ultrasound as part of the initial investigations for hyperthyroidism if there is no palpable abnormality of the thyroid gland.[1]​[26]​​​ Cold (i.e., nonfunctioning) or warm (i.e., isofunctioning) nodules >1 cm in diameter or with suspicious ultrasonographic characteristics (such as more-tall-than-wide shape, irregular margins, microcalcifications, increased vascularity, or marked hypoechogenicity) should be considered for further evaluation such as fine needle biopsy.[21][24]

Routine laboratory tests (CBC and metabolic panel) are not helpful for diagnosis, but may show nonspecific anemia, leukocytosis, elevated aminotransferases, hypercalcemia or elevated alkaline phosphatase. Elevated alkaline phosphatase is generally of bony origin, due to increased bone turnover. Most patients with hyperthyroidism will have elevated transaminases prior to initiating treatment and levels typically improve with antithyroid drug therapy.[27] Baseline white blood cell count is useful prior to starting antithyroid drugs. Mild neutropenia should not be regarded as a contraindication to use of antithyroid drug therapy and hyperthyroidism typically normalizes the neutrophil count.[28] 

Thyroid peroxidase antibodies may occasionally be helpful in distinguishing toxic adenoma from autoimmune forms of thyrotoxicosis. TSH receptor antibodies may be required to distinguish toxic adenoma from Graves disease, for example, when a clinical diagnosis cannot be made and nuclear scan is contraindicated.

An ECG may be required for suspected dysrhythmia. Occasionally a noncontrast computed tomography (CT) scan of the neck is indicated to evaluate a large goiter with compressive symptoms, or as part of a preoperative evaluation before thyroidectomy.

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