Thyroiditis & Goitre

Meet the patient

Two women sit in your endocrine clinic on the same morning, and they look alike — until you touch the neck. [1][2]

Patient A is a 34-year-old, eight weeks after a flu-like illness, now with a painful anterior neck she cannot bear to have her collar touch, pain shooting to her jaw and ear, low-grade fever, palpitations and a tremor. Her TSH is suppressed, her free T4 is high, and her ESR is 68 mm per hour. This is subacute (de Quervain) thyroiditis — the painful thyroiditis, post-viral, self-limiting, low radioactive iodine uptake, treated with NSAIDs or a short course of prednisolone and a beta-blocker for the thyrotoxic phase. [1][10]

Patient B is a 29-year-old, four months postpartum, with palpitations and weight loss for two weeks followed by crushing fatigue, dry skin and low mood that everyone — including her — has blamed on the baby. Her thyroid is painless and slightly firm, her TSH is suppressed then rises, her anti-TPO is positive. This is postpartum thyroiditis — painless, transient, anti-TPO-positive, and easily missed because the symptoms masquerade as new-mother exhaustion. [6]

Hold these two side by side and the whole topic slots into place. The exam question they pose is the one this page exists to answer: is this thyrotoxicosis a leak or a fire — and why does the answer change everything I prescribe? [1]

Leak or fire? — the one test that splits thyrotoxicosis

Low radioactive iodine uptake means the gland is leaking, not making; high uptake means it is overproducing. That single distinction resolves almost every thyrotoxicosis MCQ and SAQ, because the two arms are treated in opposite ways. [1][2]

In all the destructive thyroiditides, inflammation ruptures follicles and dumps preformed T4 and T3 into the circulation. The gland is not synthesising anything — the same inflammation has shut synthesis down — so it does not trap iodine, and the radioactive iodine uptake (RAIU) is low. In Graves disease the TSH-receptor antibody drives the gland to actively synthesise, so uptake is high and diffuse; in toxic multinodular goitre and toxic adenoma autonomous nodules make excess hormone, so uptake is high and focal or patchy. [1][2]

This is the face-off that earns marks: [1]

[1]

The classic trap: every registrar reaches for carbimazole the moment the TSH comes back suppressed. In a destructive thyroiditis there is no synthesis to block — the hormone is already out of the gland and circulating — so antithyroid drugs do nothing useful and add needless risk. Beta-blocker for symptoms; let the leak resolve. [1]

Everyone forgets: the amiodarone patient breaks this rule. The huge iodine load suppresses uptake in both type 1 and type 2, so RAIU cannot tell them apart there — reach for colour-flow Doppler (vascular in type 1, flat in type 2) and interleukin-6 instead. [7]

Etymology for viva gold: Jod-Basedow is German Jod (iodine) plus Karl von Basedow, the German physician who described what the English-speaking world calls Graves and the French call Basedow — one disease, three national claimants. Wolff-Chaikoff is simply the two investigators who, in 1948, showed that a big iodine load transiently shuts down hormone synthesis — the gland's protective flinch before it escapes. [7]

The mantra for the whole topic: low uptake, beta-blocker; high uptake, antithyroid. Say it before you reach for the prescription, every single time. [1]

Three thyroiditides that look alike — name the discriminator

Three goitres walk into your clinic; one discriminator each tells them apart. Combine the bedside feel, the antibody pattern and the inflammatory markers and the diagnosis resolves before the scan returns. [1][6][10]

This is the four-way table examiners love, with the discriminating line beneath each name: [1]

[1]

The one-line discriminator each: Hashimoto — painless, anti-TPO, lifelong hypothyroid, risk of lymphoma; Subacute — painful, high ESR, post-viral, self-limiting; Postpartum or silent — painless, anti-TPO, transient, recurs; Amiodarone — check the drug chart, two types, treated oppositely. [1]

Hashimoto — the commonest one, and the one you treat for life

Hashimoto is organ-specific autoimmunity: anti-TPO, a firm rubbery goitre, and a slow slide into permanent hypothyroidism. It is the commonest cause of hypothyroidism and of goitre in iodine-sufficient regions, the form you will see every week of your career, and the reason most of your levothyroxine prescriptions exist. [3][5]

The histology is the story: CD8-positive T-cell-driven lymphocytic infiltration with germinal centres, Hurthle (oxyphil) cell metaplasia and fibrosis, with anti-thyroid peroxidase and anti-thyroglobulin antibodies fixing complement and driving antibody-dependent cytotoxicity. Early, the gland is firm, rubbery, goitrous and lobulated (infiltrated and hyperplastic under TSH drive); late, it is atrophic as fibrosis wins. Anti-TPO is positive in over 90 percent and predicts both onset and progression to permanent failure. [3][4]

The presentation is a painless, firm, diffusely enlarged goitre — often with a pyramidal lobe and a coarse lobulated surface — and gradual hypothyroidism: fatigue, cold intolerance, weight gain, constipation, dry skin, bradycardia, delayed reflexes, menorrhagia, and in severe disease periorbital puffiness and a serous effusion. It predominates in women 5 to 10 times, peaks between 30 and 50 years, clusters with other autoimmunity (type 1 diabetes, coeliac disease, pernicious anaemia, vitiligo, Addison disease), and links to HLA-DR3 and DR5 and Down and Turner syndromes; excess iodine intake can trigger it in susceptible people. [3][4]

The classic trap — hashitoxicosis. A minority of Hashimoto patients walk in thyrotoxic at the very start, from the initial burst of hormone release as follicles first rupture. It looks exactly like Graves — palpitations, tremor, weight loss — but there are no eye signs, the RAIU is low, and the antithyroid drugs you might reach for will do nothing. Give a beta-blocker for symptoms, then watch the patient slide into the hypothyroid phase they will occupy for life. [3]

Treatment is lifelong levothyroxine at about 1.6 mcg per kg per day — roughly 100 to 150 mcg for an average adult — titrated to a normal TSH, rechecked 6 to 8 weeks after each dose change. Start low at 25 mcg and titrate slowly in the elderly or the cardiac patient, because a sudden flood of thyroxine can precipitate angina or atrial fibrillation. A small euthyroid goitre with a normal TSH can simply be watched. [3][5]

Everyone forgets — the lymphoma risk. Long-standing Hashimoto is the substrate for primary thyroid B-cell lymphoma, presenting as a rapidly enlarging goitre in a known Hashimoto patient. Any dominant or rapidly growing nodule in this background gets urgent fine-needle aspiration. [3][8]

Etymology for viva gold: the disease carries Hakaru Hashimoto's name — the Japanese surgeon who, in 1912, described "struma lymphomatosa" in Berlin. He died believing the paper had been ignored; it took forty years for the German-speaking world to catch up and attach his name to the commonest thyroiditis on earth. [3]

Subacute (de Quervain) — the painful one, and the one you must not miss

Subacute thyroiditis is the commonest cause of a painful thyroid: tender goitre, fever, high ESR, post-viral, low RAIU, self-limiting. It is unmistakable once seen, and misdiagnosed as pharyngitis or Graves when not. [1][10]

The picture is a painful, exquisitely tender goitre with pain radiating to the jaw or ear (referred otalgia is the classic clue), fever, malaise and fatigue, a preceding viral upper respiratory infection, and a transient thyrotoxic phase that evolves into a hypothyroid phase before recovery over weeks to months. The tenderness is so marked the patient cannot tolerate a collar or turn the head. Histology is granulomatous — follicular destruction with macrophages and multinucleated giant cells reacting to extravasated colloid. [1][10]

The triggers are the viruses you already know — coxsackievirus, mumps, echovirus, influenza, and increasingly SARS-CoV-2 infection and vaccination — and the demographic is women aged 20 to 50, with an annual incidence of about 12 per 100,000. [1][10]

The single test that nails it: a markedly raised ESR (often over 50 mm per hour). Inflammatory markers are the key discriminator — high in subacute, normal in every other thyroiditis — and it is the favourite exam split between subacute and Hashimoto. [1]

Management is NSAIDs first-line (ibuprofen 400 to 600 mg three times daily, or naproxen 500 mg twice daily) for pain and inflammation, escalating to a short course of oral prednisolone 40 mg daily, tapered over 2 to 4 weeks, if pain is severe or NSAIDs fail — and the rapid response to steroids itself helps confirm the diagnosis. A beta-blocker covers the thyrotoxic phase; levothyroxine only if the hypothyroid phase is symptomatic and prolonged. [1][10]

Etymology for viva gold: Fritz de Quervain was the Swiss surgeon who distinguished this granulomatous form in 1904 — and whose name also attaches to the commonest wrist tenosynovitis. Two eponyms, one career. [1]

Postpartum and silent — the painless transient one you will miss

Postpartum and silent thyroiditis are painless, anti-TPO-positive, and run the classical triphasic curve — transient thyrotoxicosis, then hypothyroidism, then recovery — except in the 20 to 30 percent who never recover. They masquerade as new-mother exhaustion or "just anxiety". [6]

The presentation is a painless, slightly firm goitre with the classical sequence: transient thyrotoxicosis (palpitations, anxiety, weight loss, heat intolerance) followed by hypothyroidism (fatigue, depression, dry skin, weight gain). Postpartum thyroiditis occurs within 12 months of delivery, typically 1 to 6 months postpartum; silent (sporadic) thyroiditis is the same process outside the puerperium. [6]

The numbers examiners ask: postpartum thyroiditis hits roughly 5 to 10 percent of all pregnancies, rising to 30 to 50 percent in women anti-TPO-positive in early pregnancy, recurs in about 70 percent of subsequent pregnancies, and leaves 20 to 30 percent permanently hypothyroid. Anti-TPO positivity in early pregnancy is the predictor — screen for it. [6]

Management is a beta-blocker at the lowest effective dose for the shortest time for the thyrotoxic phase, levothyroxine if the hypothyroid phase is symptomatic, prolonged, or the woman is breastfeeding, and TSH monitoring for 6 to 12 months to catch the permanent-failure minority. The under-recognised hypothyroid phase is a quiet contributor to postnatal depression. [6]

Amiodarone — two diseases hiding in one tablet

Amiodarone is 37.5 percent iodine by weight and structurally resembles T4: a 200 mg maintenance dose delivers roughly 75 mg of organic iodine, a several-hundred-fold excess over the 150 mcg daily requirement. That iodine load causes both hypothyroidism and thyrotoxicosis, and the two thyrotoxic forms are treated in opposite ways. [1][7]

About 15 to 20 percent of amiodarone-treated patients develop some thyroid dysfunction. The two opposing effects are the Wolff-Chaikoff effect — acute iodine excess transiently blocks hormone synthesis (a protective escape normally follows; if it does not, hypothyroidism results, especially in anti-TPO-positive patients) — and the Jod-Basedow phenomenon, in which excess iodine fuels excess synthesis in an autonomously functioning gland (an underlying nodule or Graves), causing thyrotoxicosis. [7]

The classic trap — amiodarone type 1 versus type 2. They look similar at the bedside but are mechanistic opposites and need opposite treatment: [7]

[7]

Everyone forgets: because the iodine load suppresses uptake in both types, RAIU cannot separate them — reach for colour-flow Doppler and interleukin-6. Mixed forms exist and need both a thionamide with perchlorate and steroids. Amiodarone-induced hypothyroidism is simply replaced with levothyroxine and the drug need not be stopped; stopping amiodarone is a cardiologist-led decision, never an automatic one. Check baseline thyroid function and anti-TPO before starting the drug, then every 6 months while on it. [7]

The rare ones that bite — suppurative, Riedel, radiation, drugs

Acute suppurative thyroiditis is the bacterial abscess you must not miss, and Riedel is the woody fibrosis you must not cut. Both are rare, and both punish delay. [1]

Acute suppurative (infectious) thyroiditis is rare because the thyroid is remarkably resistant to infection — its capsule, rich vascularity and high iodine content make it hostile to bacteria. It affects children and the immunocompromised, is seeded via a pyriform sinus fistula (left-sided, a remnant of the third or fourth pharyngeal pouch) or haematogenously, is caused by Staphylococcus aureus, streptococci and anaerobes, and presents as a tender, fluctuant, warm, erythematous swelling with high fever and systemic sepsis — usually localised to the left lobe. Treat with IV antibiotics and surgical or image-guided drainage, then find and electively excise the fistula to prevent recurrence. [1][2]

Riedel thyroiditis is a fibrosing, IgG4-related disease in which dense fibrous tissue replaces the gland and invades beyond the capsule into strap muscles, trachea, oesophagus, the recurrent laryngeal nerve and even vascular structures — it may be part of multifocal IgG4-related disease (autoimmune pancreatitis, retroperitoneal fibrosis). The gland is stony-hard and fixed, the morbidity is from fibrosis not autoimmunity, and the treatment is glucocorticoids (prednisolone 30 to 40 mg daily) and tamoxifen 20 mg daily (anti-fibrotic via TGF-beta) — surgery only for severe compression, and the dissection is technically brutal in the woody plane. Check calcium for parathyroid infiltration. [9]

Radiation thyroiditis (after radioactive iodine therapy or external neck radiotherapy) and trauma or palpation thyroiditis cause a self-limiting thyrotoxic leak and need only a beta-blocker if symptomatic. Lithium impairs hormone release and raises goitre and hypothyroidism risk; interferon-alpha, interleukin-2, tyrosine-kinase inhibitors (sunitinib, sorafenib) and immune checkpoint inhibitors (pembrolizumab, nivolumab, ipilimumab) all trigger autoimmune or destructive thyroiditis in a meaningful minority — manage as for Hashimoto or silent thyroiditis and continue the immunotherapy with endocrine input where possible. [1]

The goitre — diffuse or nodular, toxic or not

A goitre is simply an enlarged thyroid; classify it on two axes — function (TSH) and structure (diffuse versus nodular) — and the management follows. The epidemiology splits the world: in iodine-sufficient regions autoimmune Hashimoto dominates; worldwide, iodine deficiency still leads. [1][5]

A goitre (from Latin guttur, throat) is defined either by palpation or by imaging volume above the upper normal — about 18 mL in women and 25 mL in men. It is classified by morphology (diffuse versus nodular, uni- or multinodular), by function (toxic versus non-toxic), and by epidemiology (endemic — iodine deficiency in a region — versus sporadic). [5]

The WHO grades goitre clinically: grade 0 (no goitre), grade 1 (palpable but not visible with the neck in normal position), grade 2 (visible at normal posture). A region is endemic when goitre prevalence exceeds 10 percent in school-age children. A retrosternal (substernal) goitre extends below the thoracic inlet and is a surgical concern because of the rigid bony thoracic inlet. [5]

The numbers examiners reach for first: [1]

[1]

Endemic goitre from iodine deficiency is the leading worldwide cause: the gland, unable to iodinate thyroglobulin adequately, falls under TSH hyperstimulation and undergoes diffuse then nodular hyperplasia, and over decades a simple diffuse goitre evolves into a multinodular one that may become autonomous and toxic. Universal salt iodisation (ICMR and NIDDCP programmes) is the public-health cornerstone and has eliminated endemic cretinism across much of India and the developing world. [5]

A diffuse non-toxic goitre is driven by iodine deficiency, Hashimoto, Graves, the physiological goitre of puberty and pregnancy (high hCG acts on the TSH receptor), dyshormonogenesis, or simple colloid goitre. A multinodular goitre is nodular hyperplasia — toxic when autonomous nodules suppress TSH, compressive when it grows into the thoracic inlet. The three thyrotoxic goitres split like this: [1][2]

[1]

Read the bedside feel of the neck — the feel predicts the diagnosis

Palpation is the bedside test that predicts the diagnosis before any bloods return. Examine from in front: inspect for swellings, then ask the patient to swallow — a thyroid swelling moves up with swallowing, distinguishing it from thyroglossal and other neck swellings. [2][3]

• A firm, rubbery, diffuse, non-tender gland with a lobulated surface suggests Hashimoto.
• An exquisitely tender, firm gland with overlying warmth suggests subacute thyroiditis (gently palpate — the patient will wince; pain may radiate to the ear).
• A stony-hard, fixed mass invading adjacent structures, not moving well on swallowing, suggests Riedel thyroiditis or malignancy.
• A soft, smooth, diffuse swelling with a bruit suggests Graves.
• A nodular gland with multiple lumps suggests multinodular goitre.
• A fluctuant, warm, erythematous tender swelling in an unwell child suggests acute suppurative thyroiditis. [1]

Pemberton's manoeuvre is the bedside sign for a retrosternal goitre. Ask the patient to raise both arms above the head until they touch the ears and hold the position; facial plethora, distension of the neck veins, stridor or distress within 30 to 60 seconds indicates a retrosternal goitre causing thoracic-inlet obstruction — a positive Pemberton sign mandates cross-sectional imaging and surgical referral. [2]

Look specifically for the signs that separate Graves from thyroiditis — exophthalmos (proptosis), lid retraction and lid lag, and ophthalmoplegia — and for tracheal deviation (best felt at the suprasternal notch), cervical lymphadenopathy (a red flag for malignancy) and hoarseness (recurrent laryngeal nerve involvement — also a malignancy red flag). A compressive goitre causes dysphagia, stridor, dyspnoea, a choking sensation lying flat, a Pemberton sign, and occasionally superior vena cava obstruction. [2][8]

First-line investigations — TSH, anti-TPO, ESR, RAIU

Thyroid function tests interpreted by phase are the first line; anti-TPO, ESR and RAIU are the discriminators. The TFT pattern depends on where in the triphasic curve the patient sits. [1][5]

• Thyrotoxic phase — suppressed TSH (below 0.1 mIU per L) with raised free T4 and free T3 (hormone leaking from the damaged gland). The TSH is the most sensitive marker.
• Hypothyroid phase — raised TSH with low free T4 (the gland store is exhausted and synthesis is impaired).
• Recovery — TFTs normalise as the gland regenerates. In Hashimoto the patient lands in the hypothyroid phase and stays there. [1]

Antibodies split the autoimmune forms: anti-TPO is positive in Hashimoto (over 90 percent), postpartum and silent thyroiditis and predicts permanent hypothyroidism, whereas TSH-receptor antibodies (TRAb) are the hallmark of Graves and are negative in thyroiditis. A TRAb level is the single most useful test to separate Graves from a destructive thyroiditis when RAIU is not available. [3][6]

Inflammatory markers are the key clue in subacute disease: ESR and CRP are markedly raised in subacute (de Quervain) thyroiditis — ESR often over 50 mm per hour — and normal in every other thyroiditis. This is the favourite discriminator in exams. [1][10]

Radioactive iodine uptake (RAIU, iodine-123 or technetium-99m scan) is the decisive discriminator: low in all destructive thyroiditides (subacute, postpartum, silent, amiodarone type 2, radiation and trauma) and high and diffuse in Graves, high and focal or patchy in toxic multinodular goitre or toxic adenoma. In amiodarone thyrotoxicosis the iodine load suppresses uptake in both types, so reach for colour-flow Doppler and interleukin-6 instead. [1][2]

Thyroid ultrasound shows heterogeneous hypoechogenicity in Hashimoto (often pseudo-nodular with increased vascularity), a swollen hypoechoic gland in subacute thyroiditis, and characterises nodules by TI-RADS. Fine-needle aspiration is indicated for a dominant or suspicious nodule (TI-RADS-guided), a rapidly enlarging goitre, or a dominant nodule in long-standing Hashimoto (to exclude lymphoma or papillary cancer) — it is not needed for a classic tender subacute thyroiditis. [3][8]

Cross-sectional imaging (CT or MRI) defines a retrosternal goitre's extent, tracheal compression and great-vessel relationship before surgery, and maps fibrosis in Riedel. Laryngoscopy checks vocal-cord function before any thyroid surgery; calcium is checked in Riedel for parathyroid infiltration. [2][9]

Thyroid storm is a clinical diagnosis, supported by the Burch-Wartofsky point score (BWPS), where a score of 45 or above is highly suggestive of storm, 25 to 44 impending, below 25 unlikely — points for thermoregulatory, CNS, gastrointestinal-hepatic, cardiac and precipitant dysfunction on a background of decompensated thyrotoxicosis. [1][2]

The management ladder — treat the type and the phase

In destructive thyroiditis the thyrotoxic phase is treated with a beta-blocker; the hormone is leaking, not being made. Synthetic thyrotoxicosis (Graves, toxic multinodular goitre, toxic adenoma) needs antithyroid drugs, radioiodine or surgery. [1][2]

[1]

The type-and-phase ladder, drug by drug: [1]

• Destructive thyroiditis, thyrotoxic phase — propranolol 20 to 40 mg orally every 6 to 8 hours, titrated to heart rate for symptom control. Antithyroid drugs are not used — the hormone is leaking, not synthesising, so they are useless and add needless risk.
• Subacute (de Quervain) — NSAIDs (ibuprofen 400 to 600 mg three times daily, or naproxen 500 mg twice daily) first-line; oral prednisolone 40 mg daily, tapered over 2 to 4 weeks, if pain is severe or NSAIDs fail; beta-blocker for the thyrotoxic phase; levothyroxine only if the hypothyroid phase is symptomatic and prolonged. [1][10]
• Hashimoto — lifelong levothyroxine at about 1.6 mcg per kg per day (100 to 150 mcg for an average adult), titrated to a normal TSH (recheck at 6 to 8 weeks after each change), started low at 25 mcg and titrated slowly in the elderly or cardiac patient; a small euthyroid goitre can be observed. [3][5]
• Postpartum and silent — beta-blocker at the lowest effective dose for the thyrotoxic phase; levothyroxine if the hypothyroid phase is symptomatic, prolonged, or the woman is breastfeeding; monitor TSH for 6 to 12 months. [6]
• Acute suppurative — IV antibiotics covering S. aureus, streptococci and anaerobes (flucloxacillin or vancomycin plus metronidazole, tailored to culture), and surgical or image-guided drainage; excise the pyriform sinus fistula electively. [1][2]
• Amiodarone type 1 — carbimazole 40 to 60 mg daily (or high-dose PTU) plus potassium perchlorate 250 mg four times daily; type 2 — prednisolone 40 to 60 mg daily tapered over weeks; mixed forms need both. Amiodarone hypothyroidism is replaced with levothyroxine and the drug need not be stopped. [7]
• Riedel — glucocorticoids (prednisolone 30 to 40 mg daily) and tamoxifen 20 mg daily; surgery only for severe compression. [9][1]

For the goitre itself, the ladder runs from observation to surgery: [2][8]

• An asymptomatic, non-toxic diffuse goitre with normal TSH and no suspicious nodule is observed with periodic ultrasound. Suppressive levothyroxine is controversial and not routinely recommended — it does not reliably shrink a non-toxic goitre and risks iatrogenic thyrotoxicosis and bone loss.
• A toxic multinodular goitre is treated with radioactive iodine (preferred in older or unfit patients) or surgery (near-total or total thyroidectomy) for large compressive goitres, those with a suspicious nodule, or younger patients; a brief thionamide course before radioiodine reduces the small risk of storm.
• A compressive or retrosternal goitre (dysphagia, stridor, Pemberton sign, tracheal narrowing) is referred for surgery.
• A solitary nodule is worked up by ultrasound and TI-RADS with FNA if indicated, and managed by the Bethesda cytology category — benign observe, indeterminate molecular testing or diagnostic lobectomy, malignant thyroidectomy. Percutaneous ethanol injection is an option for recurrent benign cystic nodules.
• Iodine supplementation is the definitive and preventive treatment for endemic iodine-deficiency goitre. [2][8]

Thyroid storm — the resuscitation scenario

Thyroid storm is the decompensation of thyrotoxicosis: hyperpyrexia, atrial fibrillation, heart failure, agitation or coma — an ICU emergency with mortality historically 20 to 30 percent. It is a clinical diagnosis, supported by the Burch-Wartofsky score. [1][2]

Recognise it from hyperpyrexia (often over 40 degrees C), severe tachycardia or atrial fibrillation, high-output or established heart failure, agitation, delirium or coma, and vomiting, diarrhoea or jaundice in a thyrotoxic patient, usually with a precipitant — infection, surgery, an iodine load (contrast or amiodarone), antithyroid-drug withdrawal, trauma, diabetic ketoacidosis, parturition, or stroke. [1]

Admit to ICU and give the bundle, in the order that matters — each drug blocks a different step in synthesis, release and peripheral action: [1][2]

• Supportive — oxygen, IV fluids (dextrose-saline, as glycogen stores are depleted), active cooling with cooling blankets and paracetamol (avoid aspirin, which displaces thyroid hormone from binding proteins), and treat the precipitant.
• Block synthesis — a thionamide. Propylthiouracil (PTU) is preferred because it also blocks peripheral T4-to-T3 conversion: a loading dose of 500 to 1000 mg, then 250 mg orally or by nasogastric tube every 4 hours. Carbimazole or methimazole 60 to 80 mg daily is an alternative but does not block conversion.
• Block release — iodine, at least 1 hour AFTER the thionamide, so the thionamide blocks organification first and the iodine cannot be used as fuel: Lugol's iodine 8 drops (about 0.5 mL) orally every 6 hours, or saturated solution of potassium iodide 5 drops every 6 hours.
• Block T4-to-T3 conversion and support the adrenal axis — glucocorticoids: hydrocortisone 100 mg IV every 8 hours (or dexamethasone 2 mg every 6 hours).
• Block adrenergic symptoms — beta-blocker: propranolol 60 to 80 mg orally every 4 to 6 hours (also blocks peripheral T4-to-T3 conversion; use IV esmolol with caution in asthma or heart failure). Cholestyramine 4 g four times daily can be added for refractory cases. [1][2]

The order is the exam answer: beta-blocker then thionamide, wait at least 1 hour, then iodine, then glucocorticoid — with supportive care and precipitant treatment throughout. Plasma exchange and thyroidectomy are salvage options for refractory storm. [1]

Complications and the preventable-harm list

Untreated thyrotoxicosis of any cause drives atrial fibrillation, thromboembolic stroke, high-output then dilated (thyrotoxic) heart failure, osteoporosis, weight loss and proximal myopathy — and at the extreme, thyroid storm. A large goitre compresses the airway, oesophagus and great veins, and any dominant nodule may harbour papillary carcinoma or, in long-standing Hashimoto, a primary thyroid B-cell lymphoma. [1][3][8]

The classic pitfalls that lose marks and harm patients: [1][2]

1. Giving antithyroid drugs to the thyrotoxic phase of thyroiditis — the gland is leaking, not synthesising; use a beta-blocker.
2. Missing subacute thyroiditis by not checking the ESR or not eliciting tenderness; it is then mislabelled pharyngitis or Graves.
3. Mislabelling amiodarone type 2 (destructive) as type 1 and treating with thionamides when steroids are needed — and vice versa.
4. Failing to biopsy a dominant or rapidly enlarging nodule, missing lymphoma or papillary cancer.
5. Treating a painless thyroiditis like Graves with antithyroid drugs or radioiodine.
6. Forgetting that RAIU is the single test that separates destructive thyroiditis from Graves.
7. Missing retrosternal extension by not performing Pemberton's manoeuvre, and sending a patient with tracheal compression for surgery without cross-sectional imaging. [1][2]

Most destructive thyroiditis is self-limiting — subacute, postpartum and silent recover within weeks to months, though subacute occasionally and postpartum in 20 to 30 percent leave permanent hypothyroidism. Hashimoto is lifelong but excellent once levothyroxine is established; thyroid storm carries high mortality even with treatment and mandates ICU. Disposition: outpatient with serial TSH for stable thyroiditis; surgical referral for compressive or retrosternal goitre, a suspicious nodule, or Riedel with compression; ICU for storm; inpatient for acute suppurative thyroiditis. [1][6]

Special populations

• Postpartum women — screen anti-TPO-positive women; postpartum thyroiditis develops in 5 to 10 percent of all women (up to 50 percent of those anti-TPO-positive); monitor TSH at 3 and 6 months postpartum as 20 to 30 percent become permanently hypothyroid; it recurs in about 70 percent of subsequent pregnancies. [6]
• Amiodarone-treated patients — check baseline thyroid function and anti-TPO before starting, then every 6 months; thyrotoxicosis can destabilise the underlying arrhythmia or cardiomyopathy, so it warrants prompt, type-specific treatment. [7]
• Iodine-deficient populations — endemic goitre and cretinism; universal salt iodisation is the public-health cornerstone, and adequate iodine in pregnancy and early childhood prevents the irreversible neurodevelopmental harm of endemic cretinism. [5]
• The elderly with toxic MNG — may present apathetically with atrial fibrillation, weight loss, heart failure and depression rather than agitation; treat cautiously with beta-blockade and radioactive iodine, often after a brief thionamide course to render them biochemically safer. [2]
• Pregnancy — radioactive iodine is absolutely contraindicated; a symptomatic thyrotoxic phase of thyroiditis is managed with the lowest effective beta-blocker for the shortest time, and overt hypothyroidism is treated with levothyroxine to trimester-specific TSH targets (first-trimester TSH below 2.5 mIU per L). Physiological goitre of pregnancy needs no treatment. [6]
• Children — acute suppurative thyroiditis is over-represented; think of a pyriform sinus fistula and arrange imaging for elective excision after the acute episode. Congenital dyshormonogenetic goitre presents with a goitre and hypothyroidism from birth. [5]

Guidelines and the regional picture

The ATA 2016 hyperthyroidism guideline (Ross et al.) sets the standard for Graves, toxic MNG or adenoma, the destructive thyroiditides, amiodarone-induced thyrotoxicosis and thyroid storm, formalising RAIU as the discriminator and the ordered storm bundle. The ATA 2017 pregnancy and postpartum guideline (Alexander et al.) addresses postpartum thyroiditis — anti-TPO screening, monitoring, and the recognition that a substantial minority become permanently hypothyroid. The ATA 2015 nodule guideline (Haugen et al.) codifies the ultrasound TI-RADS score and the size-based FNA thresholds. [2][6][8]

The Lancet and Lancet Diabetes and Endocrinology reviews by Taylor (hypothyroidism) and Wiersinga (hyperthyroidism) synthesise global epidemiology and pathogenesis — confirming Hashimoto as the dominant cause in iodine-sufficient regions and iodine deficiency as the dominant cause worldwide. The Riedel or IgG4 reviews consolidate the modern understanding of Riedel thyroiditis as an IgG4-related fibrosing disease, justifying glucocorticoid and tamoxifen therapy. [1][5][9]

Regional picture: in iodine-sufficient regions the burden of goitre and hypothyroidism is autoimmune (Hashimoto), whereas iodine deficiency remains the dominant cause across much of India and the developing world — addressed by universal salt iodisation. A paradox worth knowing: iodine repletion in a previously deficient population transiently increases the incidence of autoimmune thyroiditis and Jod-Basedow thyrotoxicosis, as the now-abundant iodine fuels autoimmune destruction and autonomous nodules. [1][5]

The memory devices

Cluster the thyroiditides by pain and you hold the fastest bedside discriminator. [1]

[1]

The cluster rule for the painful neck: painful thyroid plus high ESR plus low RAIU is subacute; painful thyroid plus a septic child and a left-lobe abscess is suppurative; a sudden painful nodule overnight is haemorrhage into a cyst. [1]

The mantra, once more: low uptake, beta-blocker; high uptake, antithyroid. [1]

Ward-round test

Stem 1 — the painful neck. A 40-year-old man has a painful tender thyroid radiating to his ear, fever and palpitations two weeks after a flu-like illness. TSH is suppressed, free T4 is high, ESR is 64 mm per hour. What is the diagnosis, the confirming test, and the first-line and escalation treatment? [1]

Reveal

This is subacute (de Quervain) thyroiditis — the painful thyroiditis, post-viral, with the pathognomonic high ESR. A low radioactive iodine uptake confirms the destructive (leak) mechanism versus Graves. First-line is NSAIDs (ibuprofen 400 to 600 mg three times daily, or naproxen 500 mg twice daily) plus a beta-blocker for the thyrotoxic phase. If pain is severe or NSAIDs fail, escalate to oral prednisolone 40 mg daily tapered over 2 to 4 weeks — the rapid response helps confirm the diagnosis. [1][10]

Stem 2 — the painless postpartum neck. A 29-year-old, four months postpartum, has palpitations and weight loss for two weeks, then fatigue and low mood. Her thyroid is painless and slightly firm, anti-TPO is positive, TSH is suppressed. What is the diagnosis, the confirming mechanism test, and the first drug? [6]

Reveal

This is postpartum thyroiditis — the painless, anti-TPO-positive, transient form within 12 months of delivery. A low radioactive iodine uptake confirms the destructive mechanism versus Graves. Reach for a beta-blocker at the lowest effective dose for the thyrotoxic phase — not antithyroid drugs — and monitor TSH for 6 to 12 months, as 20 to 30 percent become permanently hypothyroid. [6]

Stem 3 — amiodarone and a tremor. A 68-year-old man on amiodarone for atrial fibrillation presents with new tremor, weight loss and worsening heart failure. TSH is suppressed, free T4 is high. How do you tell type 1 from type 2, and why does it matter? [7]

Reveal

This is amiodarone-induced thyrotoxicosis. RAIU is low in both types (the iodine load suppresses uptake), so distinguish them by colour-flow Doppler (increased vascularity in type 1, decreased in type 2) and interleukin-6 (markedly raised in type 2). It matters because they are treated oppositely — type 1 needs carbimazole 40 to 60 mg daily plus potassium perchlorate 250 mg four times daily; type 2 needs prednisolone 40 to 60 mg daily tapered over weeks. Mislabelling them harms the patient. [7]

Stem 4 — the storm. A thyrotoxic patient arrives in the emergency department with a temperature of 40.5 degrees C, atrial fibrillation at 150, agitation and vomiting. What is the diagnosis, and give the drug bundle in order. [2]

Reveal

This is thyroid storm — a clinical diagnosis, Burch-Wartofsky likely 45 or above. Admit to ICU and give, in order: beta-blocker (propranolol 60 to 80 mg every 4 to 6 hours), then thionamide (PTU 500 to 1000 mg loading then 250 mg every 4 hours), wait at least 1 hour, then iodine (Lugol's 8 drops every 6 hours), then glucocorticoid (hydrocortisone 100 mg every 8 hours), with supportive cooling (avoid aspirin) and precipitant treatment throughout. [1][2]

References

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2. [2]Ross DS, Burch HB, Cooper DS, et al. 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism and Other Causes of Thyrotoxicosis Thyroid, 2016.PMID 27521067
3. [3]Ralli M, Angeletti D, Fiore M, et al. Hashimoto's thyroiditis: An update on pathogenic mechanisms, diagnostic protocols, therapeutic strategies, and potential malignant transformation Autoimmun Rev, 2020.PMID 32805423
4. [4]Liontiris MI, Mazokopakis EE. A concise review of Hashimoto thyroiditis (HT) and the importance of iodine, selenium, vitamin D and gluten on the autoimmunity and dietary management of HT patients.Points that need more investigation Hell J Nucl Med, 2017.PMID 28315909
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6. [6]Alexander EK, Pearce EN, Brent GA, et al. 2017 Guidelines of the American Thyroid Association for the Diagnosis and Management of Thyroid Disease During Pregnancy and the Postpartum Thyroid, 2017.PMID 28056690
7. [7]Macchia PE, Feingold KR. Amiodarone Induced Thyrotoxicosis 2000.PMID 25905259
8. [8]Haugen BR, Alexander EK, Bible KC, et al. 2015 American Thyroid Association Management Guidelines for Adult Patients with Thyroid Nodules and Differentiated Thyroid Cancer: The American Thyroid Association Guidelines Task Force on Thyroid Nodules and Differentiated Thyroid Cancer Thyroid, 2016.PMID 26462967
9. [9]Czarnywojtek A, Pietrończyk K, Thompson LDR, et al. IgG4-related sclerosing thyroiditis (Riedel-Struma): a review of clinicopathological features and management Virchows Arch, 2023.PMID 37204493
10. [10]Hennessey JV Subacute Thyroiditis 2000.PMID 25905310