Approach

The diagnosis of subacute thyroiditis is mainly based on clinical suspicion. Laboratory investigation and imaging studies may sometimes be required to confirm the diagnosis.

Symptoms and signs

Patients often give a history of a relatively abrupt onset of a viral-like illness, with a fever >38°C (100.4°F), 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 (termed 'creeping thyroiditis').[27] JTA: guideline for the diagnosis of subacute thyroiditis (acute phase) Opens in new window​​ The pain may radiate to the jaw or the ears and mimic an upper respiratory, a dental, or an ear infection.[4][28]​ 

Clinical evaluation

On examination, the patient typically appears ill, has tachycardia, and has an enlarged, firm, and exquisitely tender thyroid gland.

The thyrotoxic phase of the disease may reach its peak within 3-4 days, then subside and disappear within a week. More typically, its onset is gradual and extends over 1-2 weeks, after which the condition continues with a fluctuating intensity for up to 3 months.[2] ATA: thyroiditis Opens in new window​​

Occasionally, patients may:[5]

  • present with fever of unknown origin or thyrotoxic symptoms, but no pain or viral-like illness

  • be asymptomatic, with high serum thyroid hormone levels

  • rarely, present with a firm thyroid but without fever or pain, or just with biochemical thyrotoxicosis.

Initial investigations

Laboratory tests include full blood count, C-reactive protein (CRP) and/or erythrocyte sedimentation rate (ESR), and thyroid function tests when acute thyroiditis is suspected.[28]

  • Full blood count: mild anaemia and elevation of the WBC count are common.[4][28] JTA: guideline for the diagnosis of subacute thyroiditis (acute phase) Opens in new window

  • CRP: non-specific marker of inflammation, raised

  • ESR: non-specific marker of inflammation, raised

  • Thyroid function tests: during the initial thyrotoxic phase, serum triiodothyronine (T3) and thyroxine (T4) levels are raised; thyroid-stimulating hormone (TSH) is suppressed (<0.01 mIU/L).[4][28]​ As the thyroiditis progresses to the hypothyroid phase, the serum T4 will be low while the TSH may be variable, but usually raised or normal. In the final recovery phase, most patients return to normal serum thyroid function.

Imaging studies

Include scintigraphy and ultrasonography.

Radioactive iodine uptake (RAIU)

Reliably confirms the diagnosis of subacute hypothyroiditis in the thyrotoxic phase. RAIU can be obtained if the clinical presentation and serum thyroid function tests are not sufficient for diagnosis.

In the thyrotoxic phase, scintigraphy demonstrates low thyroidal uptake (I-123 or 99mTc-pertechnetate), typically <1% to 3% at 24 hours.[4][9]​ Other aetiologies associated with thyroid pain, such as a cystic or haemorrhagic nodule or infection in the thyroid, would typically present with normal thyroid function, normal radioactive iodine uptake, and a thyroid scan showing a cold area corresponding with the cyst or infection.

Note that patients with potentially fatal acute suppurative thyroiditis may be biochemically thyrotoxic with low radioiodine uptake during the thyrotoxic phase.[29][30]

Thyroid ultrasound

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][4][28]​​​[31][32][33][34]​​​​ Normal or decreased flow may be evident on color Doppler ultrasound.[1]

Ultrasound is not sufficiently specific to confirm the diagnosis of subacute thyroiditis; findings can be similar to the sonographic appearance of chronic thyroiditis or suspicious thyroid nodules.[34]​ Ultrasound should not, therefore, be used alone for the diagnosis of subacute thyroiditis.

Ultrasound elastography demonstrates that subacute thyroiditis lesions may have an elevated baseline elasticity score compared with benign nodules of a multinodular goitre or chronic autoimmune thyroiditis.[35][36]​ However, this imaging modality was unable to distinguish between subacute thyroiditis and thyroid cancer in one study.[35]

Biopsy is rarely required

Biopsy is not routinely performed.[4]​ Diagnosis of subacute thyroiditis may be made premised on clinical history, physical examination, laboratory data and, if needed, RAIU.[4]

Cytology (fine needle aspiration biopsy) may be useful to confirm a clinical diagnosis in the setting of:

  • high iodine intake (e.g., a patient who recently received iodinated contrast for a radiologic scan [within the past 2 months, approximately])

  • recent use of an iodine-rich drug (e.g., amiodarone [within the past 6 months, approximately).

Saturation of the thyroid's capacity to absorb radioactive iodine in these scenarios can lead to falsely low uptake.

Cytological features consistent with subacute thyroiditis include multinucleated giant cells, degenerated follicular epithelium cells, epithelioid granulomas, and mixed inflammatory cells.[37][38][Figure caption and citation for the preceding image starts]: I-123 radioactive iodine scan showing absence of thyroid uptake in the thyrotoxic phase of subacute thyroiditis; arrow indicates sternal notch markerFrom the personal collection of Dr Stephanie Lee [Citation ends].com.bmj.content.model.Caption@56cc34b4[Figure caption and citation for the preceding image starts]: Clinical course of subacute thyroiditis: measurements of serum TSH, serum T4, and I-123 thyroid uptake during thyrotoxic, hypothyroid, and euthyroid phasesCreated by Dr Stephanie Lee [Citation ends].com.bmj.content.model.Caption@3fa94a43

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