Approach
The diagnosis of subacute thyroiditis is mainly based on clinical grounds, although imaging studies and laboratory investigation may sometimes be required to confirm the diagnosis.
Clinical evaluation
Patients often give a history of an abrupt onset of a viral-like illness, with a fever >100.4°F (38°C), myalgia, malaise, and pharyngitis, and accompanying symptoms of thyrotoxicosis, such as palpitations, tremor, and heat intolerance.[1] Neck pain can develop over several days to a few weeks, and progress to severe anterior neck pain, overlying the thyroid gland, that may migrate from one side of the neck to the other. The pain may radiate to the jaw or the ears and mimic an upper respiratory, a dental, or an ear infection.
On examination, the patient appears ill, often with a mild to moderate fever to >100.4°F (38°C); has tachycardia; and has an enlarged, firm, and very tender thyroid gland.
Sometimes, the thyrotoxic phase of the disease may reach its peak within 3 to 4 days, then subside and disappear within a week. However, more typically, its onset is gradual and extends over 1 to 2 weeks, after which the condition continues with a fluctuating intensity for 3 to 6 weeks. Occasionally, patients may present with fever of unknown origin or thyrotoxic symptoms but no pain or viral-like illness, or may be asymptomatic with high serum thyroid hormone levels. Rarely, patients may present with a firm thyroid but without fever or pain, or just with biochemical thyrotoxicosis.
Investigations
Serum thyroid function tests should be ordered in all patients suspected of subacute thyroiditis. During the initial 1- to 2-month thyrotoxic phase, serum T3 and T4 levels are high and the thyroid-stimulating hormone (TSH) is suppressed. If obtained, the I-123 thyroid uptake will be low. As the thyroiditis progresses to the hypothyroid phase, the serum T4 will be low while the TSH becomes elevated. Although it is not necessary to confirm, the I-123 thyroid uptake slowly rises during the hypothyroid phase. In the final recovery phase, most patients return to normal serum thyroid function, and normal I-123 is restored, although confirmation with this nuclear study is also unnecessary.
Serum TSH levels are usually suppressed, at <0.01 mIU/L, in patients during the thyrotoxic phase. However, patients present with a higher TSH if tested later during their hypothyroid or recovery phases of the disease. Occasionally, some patients do not have any symptoms during the thyrotoxic phase of the disease and present only during the hypothyroid phase.
The circulating thyroid hormones (serum total T4, total T3, free T3, free T4 index, or free T4) will be elevated in patients during the thyrotoxic phase. If the patient is moderately or highly thyrotoxic during this phase due to the thyroiditis, the T3:T4 ratio is generally <15 (as assessed by total T3:total T4) or <3.0 (as assessed by free T3:free T4).[2][17] In contrast, in hyperthyroidism from other causes in which there is new synthesis of thyroid hormone, such as Graves disease, there will be greater T3 production. Therefore, serum T3:T4 ratios are usually >15:1.
The radioactive iodine uptake test is the most reliable test during the thyrotoxic phase to confirm the diagnosis of subacute thyroiditis. In the thyrotoxic phase, the I-123 or 99mTc-pertechnetate study shows very low thyroidal uptake, typically <1% to 3% at 24 hours.[18] All other etiologies associated with thyroid pain, such as a cystic or hemorrhagic nodule or infection in the thyroid, would present with normal thyroid function, normal radioactive iodine uptake, and a thyroid scan showing a cold area corresponding with the cyst or infection.
Serum erythrocyte sedimentation rate (ESR) levels are nonspecific, but are likely to be elevated in most patients. In one series, serum C-reactive protein (CRP) was found to be significantly elevated (i.e., >10 mg/L) in 86% of patients with subacute thyroiditis, but not in patients with other thyrotoxic conditions, such as Graves disease, toxic nodular goiter, or amiodarone-induced thyrotoxicosis (type I and II).[19] Thus, serum CRP levels may help when the diagnosis of subacute thyroiditis is not clear based on laboratory and imaging studies.[20] A complete blood count may show mild anemia and elevation of white blood cell count.[15]
Serum thyroid peroxidase antibody titers (TPO Ab) are generally not useful to confirm or exclude this diagnosis. Usually the titer is within the reference range, or mildly elevated, in the patient at initial presentation of the thyrotoxic phase. With resolution of the subacute thyroiditis, the titers usually will regress to normal.
A fine needle aspiration biopsy is not routinely performed, as the diagnosis of subacute thyroiditis may be made based on the clinical presentation of thyroid pain, viral-like syndrome, biochemical thyrotoxicosis, and low radioiodine thyroid uptake.[15] However, cytology can be useful to confirm a clinical diagnosis in the setting of high iodine intake, such as in an individual who recently received iodinated contrast for radiologic scans, or in an individual who used an iodine-rich medication such as amiodarone. Multinucleated giant cells are nearly always found on cytology in a background of degenerated follicular epithelium cells, rare epithelioid granulomas, and mixed inflammatory cells.[21]
On ultrasonography, approximately 78% to 90% of patients with painful subacute thyroiditis have areas of poorly-defined heterogenous hypoechoic echotexture, with irregular margins in the areas of the thyroid gland that are painful.[1][22][23][24][25] Normal or decreased vascular flow by Doppler ultrasound may be able to help distinguish this condition from Graves disease, which typically displays generalized increased vascular flow with an heterogeneous, hypoechoic echotexture.[26] However, the sensitivity and specificity of ultrasound appearance is not well established, and ultrasound should not be used alone for the diagnosis of subacute thyroiditis. Ultrasound is not superior to a radioactive iodine uptake scan for the diagnosis of subacute thyroiditis because the appearance is not specific and can be similar to the sonographic appearance of chronic thyroiditis. New technology utilizing real-time ultrasound elastography demonstrated that lesions of subacute thyroiditis had an elevated elasticity score compared with benign nodules of a multinodular goiter, but could not be distinguished from malignant nodules, which also had elevated elasticity scores.[27]
[Figure caption and citation for the preceding image starts]: I-123 radioactive iodine scan showing absence of thyroid uptake in thyroiditis and thyrotoxicosis; arrow indicates sternal notch markerFrom the personal collection of Dr Stephanie Lee [Citation ends].
[Figure caption and citation for the preceding image starts]: Clinical course of subacute thyroiditis: measurements of serum TSH, serum T3 and T4, and I-123 thyroid uptakeCreated by Dr Stephanie Lee [Citation ends].
Use of this content is subject to our disclaimer