Subacute Thyroiditis
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Direct answer
Subacute (de Quervain, granulomatous) thyroiditis is a virus-triggered, painful inflammation of the thyroid — fever, neck pain radiating to the jaw or ear, a tender diffuse goitre, and a transient thyrotoxicosis caused by hormone leaking from destroyed follicles rather than by overproduction. The discriminating pair of tests is a suppressed thyroid-stimulating hormone with raised free T4 PLUS a near-absent radioactive iodine uptake, because the leaking gland cannot trap iodine; erythrocyte sedimentation rate and C-reactive protein are high, and thyroid antibodies are typically negative. Management is symptomatic: non-steroidal anti-inflammatory drugs for mild pain, prednisolone 20-40 mg daily tapered over weeks for severe pain, and a short beta-blocker for thyrotoxic symptoms — antithyroid drugs such as carbimazole do nothing, since no synthesis is occurring. Expect the four-phase course: thyrotoxicosis for weeks, a brief euthyroid interval, possible hypothyroidism for months, then recovery.
What you must remember
- Diagnosis in two sentences: painful tender goitre with thyrotoxic biochemistry, high ESR/CRP, and LOW radioactive iodine uptake — contrast with Graves disease, where uptake is diffuse and high; a "thionamide-resistant thyrotoxicosis" is thyroiditis until this uptake logic is applied.
- De Quervain features: preceding upper respiratory infection, painful unilateral-dominant gland, pain referred to ear or jaw, fever; histology shows granulomas with giant cells — the pathology one-liner.
- Four-phase timeline: destructive thyrotoxicosis (2-8 weeks), euthyroid transition, hypothyroid phase (weeks to months, permanent in a minority), recovery — counsel patients accordingly.
- Treatment ladder: NSAIDs (indomethacin) for mild disease; prednisolone 20-40 mg daily with response within days, tapered over 2-6 weeks; propranolol 20-40 mg for adrenergic symptoms; NO carbimazole, no surgery, no radioiodine.
- Hashimoto contrast: painless goitre, raised anti-thyroid peroxidase antibodies, hypothyroidism the dominant phase (with transient "hashitoxicosis" in some), levothyroxine when permanent — the painless mirror image.
- Other family members: postpartum (lymphocytic) thyroiditis — thyrotoxic then hypothyroid phases within a year of delivery, treated symptomatically; drug-induced (amiodarone type 2, immune-checkpoint inhibitors, lithium); suppurative thyroiditis — hot, fluctuant gland with fever and high neutrophils, needing antibiotics and drainage, not steroids.
- Steroid principle: dramatic pain relief within 24-72 hours of prednisolone is itself characteristic; failure to respond should prompt reconsideration of suppurative disease or haemorrhage into a nodule.
- India angle: subacute thyroiditis is diagnosed late in busy clinics because the pain is attributed to pharyngitis; palpate the thyroid in every "sore throat with fever and palpitations" — a cheap clinical habit with a high diagnostic yield.
A month in the life of the gland
A 38-year-old woman presents with 10 days of left-sided neck pain shooting to the ear, fever, palpitations and tremor after an upper respiratory infection. The left thyroid lobe is exquisitely tender; pulse 104 with fine tremor; free T4 high with TSH suppressed below 0.01 mIU/L; ESR 82 mm/hour. The clinical fork is overproduction versus destruction: a radioactive iodine uptake scan (or technetium pertechnetate, cheaper and widely available in India) shows virtually no uptake — destruction, not Graves disease. Management is NSAIDs with propranolol 20 mg thrice daily; because night pain keeps her awake, prednisolone 30 mg daily is added and tapered over four weeks. Carbimazole is explicitly withheld — the gland is a leaking warehouse, not an overactive factory, an explanation that doubles as viva practice.
Six weeks later she returns fatigued and gaining weight: TSH now 14 mIU/L with low free T4 — the hypothyroid phase. Levothyroxine starts at a low dose with review in three to six months, because most patients recover and stop it; a small proportion with persistent TSH elevation at a year remain permanently hypothyroid. Walking one patient through all four phases converts the textbook table into a remembered timeline — exactly what the exam stem asks you to reproduce.
Where students slip
The most expensive error is treating destructive thyrotoxicosis with carbimazole: it cannot help (no hormone synthesis) and speeds the arrival of hypothyroidism; the question-writer plants a tender gland plus low uptake and waits for the wrong prescription. Second, the painless-versus-painful axis: de Quervain hurts, Hashimoto and postpartum do not, suppurative hurts with fever and needs drainage. Third, the uptake rule: high uptake means synthesis (Graves, toxic nodular), low uptake means leak (thyroiditis, exogenous intake, struma ovarii). Fourth, a thyrotoxic patient becoming hypothyroid on no therapy is the natural history, not a mistreatment. Finally, a tender gland with normal ESR should push suspicion towards haemorrhage or malignancy, not de Quervain.
Frequently asked questions
How does radioactive iodine uptake differentiate Graves disease from subacute thyroiditis?
Uptake is diffusely increased in Graves disease (active synthesis) and near-absent in subacute thyroiditis (destruction with hormone leak).
What is the treatment of painful subacute thyroiditis?
Non-steroidal anti-inflammatory drugs for mild pain, prednisolone 20-40 mg daily tapered over weeks for severe pain, and propranolol for thyrotoxic symptoms — antithyroid drugs are ineffective.
What histology defines de Quervain thyroiditis?
Granulomatous inflammation with multinucleated giant cells within the thyroid parenchyma, following a viral trigger.
What is the natural course of subacute thyroiditis?
A thyrotoxic phase of several weeks, a transitional euthyroid period, a hypothyroid phase lasting months, and recovery in the majority of patients.
How does postpartum thyroiditis present?
Painless thyrotoxicosis followed by hypothyroidism within a year of delivery, typically with positive thyroid antibodies and low radioactive iodine uptake during the toxic phase.