De Quervain's thyroiditis is a self-limiting, subacute granulomatous inflammation of the thyroid gland, typically following a viral infection, presenting with painful thyroid swelling and transient thyrotoxicosis.

De Quervain's Thyroiditis

Parameter	Detail
Incidence	Generally uncommon ^[2]; accounts for approximately 5% of all thyroid disorders
Sex	Female predominance (F:M ≈ 4–5:1), consistent with most thyroid conditions
Age	Peak incidence 30–50 years old (working-age adults)
Seasonal variation	Often peaks in summer/autumn, paralleling enteroviral and adenoviral seasons
Geographic	No strong geographic predilection; occurs worldwide, but less common in areas with severe iodine deficiency (where thyroid autoimmune disease is rarer)
HK context	Hong Kong has borderline iodine intake (no mandatory salt iodination) → relatively low incidence of autoimmune thyroid disease ^[3]^[4], but viral-triggered subacute thyroiditis still occurs; awareness important in differential of painful neck swelling
Genetic	Associated with HLA-B35 (up to 70% of patients carry this allele) — suggests a genetic susceptibility to virus-triggered thyroid inflammation
Temporal association	Often follows an upper respiratory tract infection by 2–8 weeks

Risk Factor	Explanation
Recent viral URTI	The most consistently reported risk factor; preceding viral illness triggers the autoimmune/inflammatory cascade
HLA-B35 positivity	Genetic predisposition; this MHC class I allele may facilitate aberrant viral antigen presentation on thyrocytes
Female sex	As with most thyroid diseases, oestrogen may modulate immune responses making women more susceptible
Post-COVID-19	Increasing case reports since 2020 of de Quervain's thyroiditis following SARS-CoV-2 infection — relevant in the 2025–2026 post-pandemic era

4. Anatomy and Function (Relevant Review)

Hypothalamus → TRH → Anterior Pituitary → TSH → Thyroid → T4/T3
                                                      ↑
                                              Negative feedback

In de Quervain's, the flood of released T4/T3 suppresses TSH via negative feedback. This is why:
- TSH is low during the thyrotoxic phase
- Radioactive iodine uptake (RAIU) is low — the suppressed TSH means no stimulation of iodine trapping, AND the damaged follicles cannot trap iodine even if stimulated

5. Etiology and Pathophysiology

De Quervain's thyroiditis usually occurs after viral infection ^[2].

Viral Agents Implicated	Evidence
Coxsackievirus (A and B)	Coxsackie ^[2] — most commonly cited
Mumps virus	Mumps ^[2]
Adenoviruses	Adenoviruses ^[2]
Measles, influenza	Case reports
SARS-CoV-2	Emerging post-COVID association (2020 onwards)
Echovirus, EBV, CMV	Less commonly reported

The classification within the goitre schema is: Thyroiditis — viral (subacute) ^[5].

Not Directly Viral

It is debated whether the virus directly infects thyrocytes or whether the viral infection triggers an aberrant immune response against the thyroid in genetically susceptible individuals (HLA-B35). The granulomatous histology and the temporal lag (2–8 weeks post-URTI) favour an immune-mediated mechanism rather than direct cytopathic viral effect. Think of it as: virus → immune trigger → collateral thyroid destruction.

5.2 Pathophysiology — The Triphasic Course

This is the single most important concept in de Quervain's. The clinical course follows three predictable phases, each with a clear mechanistic explanation:

Understanding the histology explains the alternative names:

Feature	Description
Granulomatous inflammation	Aggregates of macrophages, lymphocytes, and plasma cells around damaged follicles — hence "granulomatous thyroiditis"
Multinucleated giant cells	Formed by fusion of macrophages engulfing leaked colloid — hence "giant cell thyroiditis"
Follicular disruption	Destroyed follicular epithelium with leakage of colloid into the interstitium
Fibrosis	In later stages, fibrosis replaces the inflammatory infiltrate as healing progresses
Microabscess formation	Neutrophilic infiltration in early acute phase, then replaced by granulomatous response

The presence of granulomas with giant cells surrounding colloid material is pathognomonic and distinguishes de Quervain's from other forms of thyroiditis (Hashimoto's has lymphocytic infiltration with Hürthle cells, not granulomas).

6. Classification

De Quervain's thyroiditis sits within a broader framework of thyroid inflammatory conditions:

Type	Onset	Pain	Mechanism	Example
Acute	Days	Severe	Bacterial infection	Acute suppurative (bacterial) thyroiditis ^[5]
Subacute	Weeks	Painful (de Quervain's) or Painless (lymphocytic)	Viral/immune	Viral (subacute) thyroiditis ^[5] = De Quervain's; Subacute lymphocytic thyroiditis; Postpartum thyroiditis
Chronic	Months–years	Usually painless	Autoimmune, fibrous	Lymphocytic/Hashimoto/autoimmune (chronic) thyroiditis ^[5]; Riedel's thyroiditis

De Quervain's falls under thyrotoxicosis without hyperthyroidism ^[1]:

Category	Causes
Primary hyperthyroidism	Graves' disease, toxic MNG, toxic adenoma
Secondary hyperthyroidism	TSH-secreting pituitary adenoma, gestational thyrotoxicosis
Thyrotoxicosis without hyperthyroidism	Subacute (De Quervain's) thyroiditis, silent thyroiditis, destructive thyroiditis (amiodarone/irradiation), levothyroxine overdose ^[1]

De Quervain's also appears under transient hypothyroidism ^[1]:

Category	Causes
Permanent primary	Autoimmune (Hashimoto's, atrophic), iatrogenic (RAI, surgery), infiltrative
Secondary	Pituitary/hypothalamic disease
Transient	Subacute (De Quervain's) thyroiditis, silent thyroiditis, post-partum thyroiditis, withdrawal of T4, post-RAI, post-thyroidectomy ^[1]

De Quervain's/subacute thyroiditis falls under the diffuse goitre category of thyroiditis ^[6]:

Goitre Type	Examples
Thyroiditis	Bacterial (acute suppurative), viral (subacute), lymphocytic/Hashimoto/autoimmune (chronic) ^[5]
Simple goitre	Endemic (iodine deficiency), sporadic — diffuse or nodular
Toxic goitre	Graves' (diffuse toxic), toxic MNG (Plummer's), toxic adenoma
Neoplastic	Benign, malignant

7. Clinical Features

Symptom	Pathophysiological Basis
Neck pain — the hallmark symptom	Inflammatory destruction of thyroid follicles → oedema, distension of the thyroid capsule, and stimulation of pain fibres in the pretracheal fascia. The thyroid capsule is richly innervated by cervical sensory nerves.
Pain radiating to the angle of jaw and ears ^[2]	Referred pain via shared sensory innervation — the thyroid receives sensory fibres from the cervical plexus (C2–C4) which also innervate the mandibular angle and external ear (great auricular nerve, C2–C3).
Pain increased by swallowing, coughing, movement of neck ^[2]	Swallowing elevates the thyroid (it is attached to the pretracheal fascia), stretching the inflamed capsule. Coughing increases intrathoracic pressure transmitted to the neck. Head turning stretches cervical structures against the swollen gland.
Preceding URTI symptoms (sore throat, malaise, myalgia)	The viral prodrome 2–8 weeks before thyroid symptoms; may be mistaken for ongoing pharyngitis
Sore throat / odynophagia	Can mimic pharyngitis/tonsillitis — the anterior neck pain may be mislocalized to the throat. A common diagnostic pitfall.
Fever ^[2]	Systemic inflammatory response — release of IL-1, IL-6, TNF-α from activated macrophages and lymphocytes during granulomatous inflammation
Thyrotoxic symptoms (Phase 1): palpitations, tremor, heat intolerance, anxiety, weight loss, diarrhoea, irritability	Due to damage to follicles → release of stored T4 ^[2]. Excess circulating T4/T3 increases basal metabolic rate, enhances catecholamine sensitivity (↑β-adrenergic receptor expression), and drives all the classic hypermetabolic symptoms
Hypothyroid symptoms (Phase 2): fatigue, weight gain, cold intolerance, constipation, dry skin, depressed mood	Damage to follicular cells → ↓synthesis of thyroid hormones ^[2]. Insufficient T3/T4 decreases BMR, reduces thermogenesis, and slows GI motility
Malaise and fatigue	Non-specific systemic inflammation; elevated cytokines cause constitutional symptoms similar to any viral illness

Diagnostic Pitfall — Misdiagnosed as Pharyngitis

De Quervain's thyroiditis is frequently misdiagnosed initially as pharyngitis/tonsillitis because patients complain of "sore throat" and have fever. The KEY distinguishing feature: the pain is in the anterior lower neck (thyroid region), NOT the posterior pharynx. Always palpate the thyroid in any patient with anterior neck pain and constitutional symptoms!

Sign	Pathophysiological Basis
Palpable goitre ± tenderness ^[2]	Thyroid swelling from oedema and inflammatory infiltration of the gland. Tenderness is due to capsular distension and inflammatory mediators stimulating nociceptors.
Firm, diffusely enlarged thyroid	Inflammatory cell infiltration and oedema; initially the entire gland is involved (may start unilaterally then migrate — "creeping thyroiditis")
Unilateral → bilateral progression ("migratory" tenderness)	Inflammation may begin in one lobe and "creep" to the other over days to weeks — this migratory pattern is characteristic and rarely seen in other thyroid conditions
Low-grade to moderate fever	Systemic inflammation (pyrogenic cytokines — IL-1β, IL-6, PGE2 acting on the hypothalamic thermoregulatory centre)
Tachycardia, tremor, warm moist skin (Phase 1)	Thyrotoxicosis → T3/T4 upregulate β1-adrenergic receptors in the heart (tachycardia), increase CNS catecholamine sensitivity (tremor), and increase peripheral vasodilation and sweating (warm, moist skin)
Bradycardia, dry skin, delayed relaxation of reflexes, periorbital oedema (Phase 2)	Hypothyroidism → ↓BMR, ↓β-receptor expression, accumulation of glycosaminoglycans in tissues (myxoedema)
↑ESR (often markedly elevated, > 50 mm/hr) ^[2]	Hepatic acute-phase response — IL-6 stimulates hepatic production of fibrinogen, which increases rouleaux formation of RBCs → elevated ESR. ESR > 50 is typical; values > 100 are not uncommon
↑WBC ^[2]	Leukocytosis from systemic inflammatory response (margination and release of neutrophils from bone marrow stores)
Absence of Graves' ophthalmopathy	Important negative sign — no proptosis, lid lag, or chemosis because there are no TSH-receptor antibodies (TRAb). Helps distinguish from Graves' thyrotoxicosis
Absence of thyroid bruit	No increased blood flow from glandular hyperactivity (unlike Graves' where the hypervascular gland produces an audible bruit/thrill)

These are crucial for differential diagnosis:

Absent Feature	Why It's Absent
No exophthalmos/ophthalmopathy	No TRAb → no orbital inflammation
No pretibial myxoedema	No TRAb
No thyroid acropachy	No TRAb
No thyroid bruit	Not hypervascular — the gland is inflamed, not hyperactive
No lymphadenopathy	Not a malignant or bacterial process

The differential for a diffuse thyroid swelling includes ^[6]:

Graves' disease — diffuse toxic goitre (but painless, with ophthalmopathy and positive TRAb)
Hashimoto's thyroiditis — chronic lymphocytic (usually painless, firm, "rubbery" goitre)
De Quervain's / subacute thyroiditis — painful, with the triphasic course
Physiological — pregnancy, puberty (painless)

For a painful thyroid specifically:

De Quervain's (most common cause of painful thyroid)
Acute suppurative thyroiditis (bacterial — extremely rare, with abscess formation, severe systemic toxicity)
Haemorrhage into thyroid cyst or nodule (sudden onset, localised)
Rapidly expanding anaplastic thyroid carcinoma (hard, fixed, elderly patient)

High Yield Summary

De Quervain's (Subacute Granulomatous) Thyroiditis — Key Points:

Definition: Self-limiting, viral-triggered granulomatous thyroiditis causing painful thyroid swelling with a triphasic course (thyrotoxicosis → hypothyroidism → recovery).
Etiology: Follows viral URTI (Coxsackie, mumps, adenovirus); associated with HLA-B35.
Key distinction: Thyrotoxicosis WITHOUT hyperthyroidism — hormone release from follicular destruction, NOT overproduction. Therefore: low RAIU, no role for anti-thyroid drugs.
Triphasic course:
- Phase 1 (4–6 weeks): Thyrotoxic — stored T4 released from destroyed follicles
- Phase 2 (4–6 months): Hypothyroid — depleted stores, damaged cells can't synthesise
- Phase 3: Recovery (>90% return to euthyroid)
Cardinal features: Neck pain (radiating to jaw/ear, worse with swallowing), tender goitre, fever, markedly ↑ESR, ↑WBC.
Low-titre thyroid autoantibodies (transient); high titres suggest autoimmune overlap → ↑risk of permanent hypothyroidism.
Management: Self-limiting → NO anti-thyroid drugs. NSAIDs/steroids for pain, β-blockers for thyrotoxic symptoms, temporary T4 for hypothyroid phase if symptomatic.
Permanent hypothyroidism in 5–15% of cases.

Active Recall - De Quervain's Thyroiditis

Differential Diagnosis of De Quervain's Thyroiditis

The differential diagnosis of de Quervain's thyroiditis is best approached by considering the presenting problem the patient walks in with. A patient with de Quervain's can present at different phases with different chief complaints, so the DDx changes depending on the clinical context. Let's break this down systematically.

This is the most specific DDx for de Quervain's. A painful thyroid is relatively uncommon — most thyroid pathology is painless. The conditions that cause pain in the thyroid region are few:

Differential	Key Distinguishing Features	Why It Can Mimic De Quervain's
De Quervain's (subacute granulomatous) thyroiditis	Preceding URTI, tender goitre ^[2], markedly ↑ESR, triphasic course, low RAIU	— (the index condition)
Acute suppurative thyroiditis	Bacterial (acute suppurative) ^[5] — extremely rare; severe toxicity, high fever, fluctuant swelling, often in immunocompromised or children with pyriform sinus fistula. Leukocytosis with left shift. Abscess on USG. Culture positive	Both cause a painful, tender thyroid with fever. However, suppurative thyroiditis is far more toxic, has purulent features, and ESR alone does not distinguish — you need imaging and aspiration
Haemorrhage into a thyroid cyst/nodule	Pain: bleeding into cyst/necrotic nodule ^[7]^[8]. Sudden onset of pain and rapid enlargement, history of pre-existing nodule or MNG. USG shows cystic lesion with internal debris	Both cause acute neck pain. However, haemorrhagic cyst has sudden onset (not gradual), no systemic inflammation (ESR normal), and euthyroid status. USG is diagnostic
Anaplastic thyroid carcinoma	Sudden ↑size: anaplastic carcinoma ^[7]^[8]. Elderly patient (> 60y), rock-hard fixed mass, rapidly progressive over weeks, compressive symptoms (dysphagia, stridor, RLN palsy), painless initially then painful as it invades	Both can cause a painful neck mass. Anaplastic CA is hard and fixed (not diffusely tender). No preceding URTI. No triphasic thyroid course. FNA/biopsy is diagnostic
Hashimoto's thyroiditis (painful variant)	Lymphocytic/Hashimoto/autoimmune (chronic) ^[5]. Occasionally Hashimoto's can be painful ("painful Hashimoto's"), but this is rare. Usually a firm, rubbery, painless, diffuse goitre with high-titre anti-TPO (90–100%) and anti-Tg (80–90%) ^[1]. Hypothyroid biochemistry	Hashimoto's is almost always painless. If painful, the ESR is typically only mildly elevated (not > 50 as in de Quervain's). High-titre antibodies distinguish it
Riedel's thyroiditis	Extremely rare fibrosing thyroiditis. Rock-hard "woody" thyroid, fixed to surrounding structures, can mimic carcinoma. Associated with IgG4-related disease	May cause discomfort, but not the acute pain/tenderness of de Quervain's. Open biopsy needed to distinguish from malignancy
Radiation thyroiditis	Occurs after radioactive iodine treatment or external beam radiation. History of recent RAI or neck irradiation is the key	Temporal association with treatment is diagnostic
Referred pain from pharyngitis/URTI	The most common misdiagnosis! Patient has sore throat, but the pain is pharyngeal, not in the anterior lower neck. Thyroid is non-tender on examination	Always palpate the thyroid — if it is tender, it's not just pharyngitis

Exam Trap — Painful Thyroid DDx

Students often forget that most thyroid conditions are PAINLESS. The painful thyroid DDx is short. If an exam question mentions a tender thyroid + elevated ESR + preceding URTI, the answer is de Quervain's until proven otherwise.

B. DDx of Thyrotoxicosis (When Patient Presents in Phase 1)

If the patient is caught in the thyrotoxic phase, you need to differentiate de Quervain's from other causes of thyrotoxicosis. The critical distinction is between thyrotoxicosis with hyperthyroidism (the gland is overactive) versus thyrotoxicosis without hyperthyroidism (the gland is being destroyed and leaking hormone) ^[1].

Category	Causes	RAIU	Key Features
Primary hyperthyroidism	Graves' disease (76%) ^[9]	↑↑ (diffuse)	Painless diffuse goitre with bruit, ophthalmopathy, pretibial myxoedema, positive TRAb
	Toxic multinodular goitre (14%) ^[9]	↑ (heterogeneous)	Older patient, multiple palpable nodules, no ophthalmopathy
	Toxic adenoma (5%) ^[9]	Focal ↑ with suppression elsewhere	Single "hot" nodule on scintigraphy
	Metastatic thyroid cancer, TSH receptor mutations	Varies	Rare
Secondary hyperthyroidism	TSH-secreting pituitary adenoma	↑	TSH elevated or inappropriately normal with high T4 — very rare (0.2%) ^[9]
	Gestational thyrotoxicosis / molar hyperthyroidism	↑	hCG mimics TSH structure → stimulates thyroid ^[9]
Thyrotoxicosis without hyperthyroidism	Subacute (De Quervain's) thyroiditis	↓↓	Painful tender goitre, ↑ESR, preceding URTI
	Silent (lymphocytic) thyroiditis	↓↓	Painless, normal ESR, high-titre anti-TPO
	Postpartum thyroiditis	↓↓	< 12 months post-partum, painless
	Destructive thyroiditis (amiodarone/irradiation)	↓↓	Drug history or recent radiation
	Levothyroxine (T4) overdose / factitious thyrotoxicosis	↓↓	Medication history, ↑T4:T3 ratio > 70:1 and ↓serum thyroglobulin ^[7]^[9]

The most important clinical and investigation-based distinguishing points:

Feature	De Quervain's	Graves' Disease	Silent Thyroiditis	Toxic MNG
Pain	Present ^[2]	Absent	Absent	Absent
Goitre	Tender, diffuse	Painless, diffuse, ± bruit	Small, painless	Multiple nodules
Ophthalmopathy	Absent	Present (Graves'-specific)	Absent	Absent
Pretibial myxoedema	Absent	May be present	Absent	Absent
ESR	Markedly ↑ (often > 50) ^[2]	Normal	Normal	Normal
TRAb	Negative	Positive (sens 97%, spec 99%) ^[7]^[9]	Negative	Negative
Anti-TPO	Low titre ^[2] (transient)	50–80% ^[1]	High titre	Low
RAIU	↓ (diffuse ↓uptake) ^[2]^[7]^[9]	↑ (diffuse ↑uptake) ^[7]^[9]	↓	Heterogeneous ↑uptake ^[7]^[9]
Serum thyroglobulin	↑ (released from damaged cells)	↑	↑	Variable
Preceding URTI	Yes (2–8 weeks prior)	No	No	No
Post-partum	No	Possible	Possible (< 12 months)	No

The RAIU 'Traffic Light' for Thyrotoxicosis DDx

Think of RAIU as a traffic light:

Green (↑ uptake) = the thyroid is actively making hormone → true hyperthyroidism (Graves', toxic MNG, toxic adenoma)
Red (↓ uptake) = the thyroid is NOT making hormone — it's leaking pre-formed hormone → destructive thyrotoxicosis (de Quervain's, silent thyroiditis, postpartum, factitious)

This single investigation separates the two categories definitively.

Thyroid scintigraphy findings ^[7]^[9]: Diffuse ↓uptake → destructive thyroiditis vs factitious thyrotoxicosis. Factitious thyrotoxicosis can be confirmed by ↑T4:T3 ratio and ↓serum thyroglobulin

Once you have established the thyrotoxicosis is "destructive" (low RAIU), you need to determine which specific destructive thyroiditis:

Feature	De Quervain's	Silent (Lymphocytic)	Postpartum	Drug-Induced	Factitious
Pain	YES — the key differentiator	No	No	No	No
ESR	Markedly ↑	Normal	Normal	Variable	Normal
Context	Post-viral URTI	Any time	< 12m post-partum ^[4]	Amiodarone, lithium, checkpoint inhibitors	Medication access; healthcare worker
Anti-TPO	Low titre (transient)	High titre	Often high titre	Variable	Negative
Thyroglobulin	↑	↑	↑	↑	↓ (exogenous T4 suppresses it) ^[7]^[9]
T4:T3 ratio	Normal (~30:1)	Normal	Normal	Variable	↑ (> 70:1) ^[7]^[9]

If the patient is caught in the hypothyroid phase, the DDx becomes the causes of hypothyroidism. The key clinical question is: Is this transient or permanent? ^[3]^[4]

Category	Causes	Distinguishing from De Quervain's
Permanent primary	Hashimoto's thyroiditis — most common autoimmune cause; firm, rubbery, painless goitre; anti-TPO (90–100%); irreversible ^[7]	No preceding neck pain, no preceding thyrotoxic phase, high-titre antibodies, usually older female
	Atrophic thyroiditis — end-stage autoimmune; no goitre, TSHr-blocking Ab	No goitre (gland atrophied)
	Iatrogenic: RAI, thyroidectomy	Clear history of prior treatment
	Drug-induced: amiodarone, lithium	Drug history
	Iodine deficiency or excess	Dietary/exposure history
Transient	De Quervain's thyroiditis	Preceding neck pain + thyrotoxic phase
	Silent/postpartum thyroiditis	Painless; post-partum context
	Post-RAI or post-thyroidectomy (< 6 months) ^[3]^[4]	Recent treatment history
	Drug-related (lithium, amiodarone) ^[3]^[4]	Drug history
Secondary	Pituitary/hypothalamic disease	Low TSH (not elevated) + low fT4 = "secondary" pattern; other pituitary hormone deficiencies

The approach to hypothyroidism is mainly directed to differentiate those who require life-long T4 replacement (autoimmune thyroiditis, thyroid ablation) from those who may only have transient hypothyroidism ^[3]^[4]. Clues to transient hypothyroidism: neck pain, < 12 months post-partum, recent symptoms of thyrotoxicosis, < 6 months since ¹³¹I or thyroidectomy, on lithium or amiodarone ^[3]^[4].

If the patient presents primarily with a neck lump that happens to be thyroid in origin, you should also consider the broader DDx of diffuse goitre ^[6]^[8]^[9]:

Pattern	DDx
Diffuse goitre ^[6]	Graves' disease, physiological (pregnancy, puberty), Hashimoto's thyroiditis, De Quervain's/subacute thyroiditis ^[6]
Solitary nodule ^[6]	Dominant nodule in MNG, cyst (true simple cyst, colloid nodule), neoplastic (adenoma, toxic adenoma, carcinoma) ^[6]
Multiple nodules ^[6]	MNG, multiple cysts, multiple adenoma ^[6]

And the goitre classification from the lecture ^[5]:

Category	Examples
Neoplastic goitre	Benign, malignant ^[5]
Thyroiditis	Bacterial (acute suppurative), viral (subacute), lymphocytic/Hashimoto/autoimmune (chronic) ^[5]
Simple goitre (endemic or sporadic)	Diffuse, nodular ^[5]
Toxic goitre	Diffuse toxic (Graves'), toxic nodular (Plummer's), toxic/functioning adenoma ^[5]

Thyroid nodule pathology ^[5]:

Nodular goitre: colloid / haemorrhagic cystic / complex / hyperplastic / adenomatous nodule (70%)
Benign follicular adenoma: mainly non-toxic (15%)
Well-differentiated thyroid carcinoma (10%)
Miscellaneous: other thyroid malignancies, thyroiditis (5%)

The Three Pillars of DDx in De Quervain's

When differentiating de Quervain's from other thyroid conditions, remember three pillars:

Pain + tenderness → separates de Quervain's from virtually all other thyroiditides (silent, postpartum, Hashimoto's are all painless)
↑ESR (markedly elevated) → separates de Quervain's from silent/postpartum thyroiditis (where ESR is normal)
Low RAIU → separates destructive thyrotoxicosis (de Quervain's, silent, postpartum) from true hyperthyroidism (Graves', toxic MNG, toxic adenoma)

If all three are present: Pain + ↑ESR + Low RAIU = De Quervain's

High Yield Summary

DDx of De Quervain's Thyroiditis:

As a painful thyroid: DDx includes acute suppurative thyroiditis (bacterial), haemorrhage into cyst/nodule, anaplastic carcinoma, painful Hashimoto's (rare), Riedel's thyroiditis, radiation thyroiditis
As thyrotoxicosis: The key distinction is hyperthyroidism (high RAIU: Graves', toxic MNG, toxic adenoma) vs destructive thyrotoxicosis (low RAIU: de Quervain's, silent, postpartum, drug-induced, factitious). Pain + ↑ESR distinguishes de Quervain's from other destructive causes
As hypothyroidism: Distinguish transient (de Quervain's — preceding pain and thyrotoxic phase) from permanent (Hashimoto's, iatrogenic)
Key investigations for DDx: TFT (TSH + fT4), ESR/CRP, TRAb, anti-TPO/Tg Ab, thyroid scintigraphy (RAIU), USG thyroid
The three pillars: Pain + Markedly ↑ESR + Low RAIU = De Quervain's

Active Recall - DDx of De Quervain's Thyroiditis

References

^[1] Senior notes: felixlai.md (Causes of thyrotoxicosis / thyroid antibody tables) ^[2] Senior notes: Ryan Ho Endocrine.pdf (Section 1.5.1 Subacute Thyroiditis, p.31) ^[3] Senior notes: Adrian Lui Pediatrics.pdf (Hypothyroidism section, p.274) ^[4] Senior notes: Ryan Ho Fundamentals.pdf (Section 3.8.1.2 Hypothyroidism, p.423) ^[5] Lecture slides: GC 177. A thyroid nodule benign thyroid nodules; thyroid cancer.pdf (p.4–5, Goitre Classification and Thyroid nodule pathology) ^[6] Senior notes: maxim.md (Approach to thyroid nodules — Differential diagnosis table) ^[7] Senior notes: Ryan Ho Endocrine.pdf (Aetiological Ix / thyroid scintigraphy findings, p.13; Hx of thyroid nodules, p.18) ^[8] Senior notes: Ryan Ho Fundamentals.pdf (Hx of goitre/thyroid nodules, p.425–427) ^[9] Senior notes: Ryan Ho Fundamentals.pdf (Thyrotoxicosis — causes, Dx, aetiological Ix, p.421–422)

Diagnostic Criteria, Algorithm and Investigations for De Quervain's Thyroiditis

1. Diagnostic Criteria

De Quervain's thyroiditis does not have a single, universally codified set of diagnostic criteria like, say, the Jones criteria for rheumatic fever. Instead, the diagnosis is made by a constellation of clinical, biochemical, and imaging findings. Think of it as a clinical diagnosis supported by investigations. Here is the practical diagnostic framework:

#	Feature	Rationale
1	Painful, tender thyroid gland	The hallmark — pain is present in de Quervain's but not in lymphocytic/postpartum thyroiditis ^[2]. Inflammatory destruction of follicles → capsular distension → nociceptor stimulation
2	Elevated ESR (typically > 50 mm/hr, often > 80)	Systemic symptoms: fever, ↑WBC, ↑ESR ^[2]. Acute-phase response: IL-6 drives hepatic fibrinogen synthesis → rouleaux formation → ↑ESR. This is the single most useful blood test to confirm the diagnosis
3	Suppressed TSH (in thyrotoxic phase) or elevated TSH (in hypothyroid phase)	Reflects the phase of illness. In Phase 1: flood of pre-formed T4/T3 suppresses TSH via negative feedback. In Phase 2: depleted stores and damaged follicles → low T4 → TSH rises
4	Low radioactive iodine uptake (RAIU)	↓Iodine uptake (↓TSH, follicular damage) ^[2]. The damaged gland cannot trap iodine AND the suppressed TSH provides no stimulus. This separates destructive thyrotoxicosis from true hyperthyroidism

Feature	Detail
Preceding viral URTI (2–8 weeks prior)	The classic temporal association — usually occur after viral infection (Coxsackie, mumps, adenoviruses) ^[2]
Low titres of thyroid autoantibodies ^[2]	Transient low-titre anti-TPO/anti-Tg may appear (released antigens trigger a weak immune response), but not the persistently high titres of Hashimoto's (anti-TPO 90–100%) or Graves' (TRAb 80–90%) ^[1]
Negative TRAb	Excludes Graves' disease — TRAb sens 97%, spec 99% with newer assays ^[7]^[9]
Characteristic USG findings	Diffuse hypoechoic areas, reduced vascularity (unlike the hypervascular pattern of Graves')
Triphasic clinical course	Thyrotoxicosis → hypothyroidism → recovery; pathognomonic if observed over time
Self-limiting course	Spontaneous resolution within 6–12 months without anti-thyroid drugs

There Is No 'Gold Standard' Single Test

Students often look for a single confirmatory test. For de Quervain's, there is none. The diagnosis rests on the clinical triad of painful tender thyroid + markedly elevated ESR + low RAIU in the context of preceding viral illness. If you have all three, the diagnosis is virtually certain. Biopsy showing granulomatous inflammation with giant cells is pathognomonic but is almost never needed clinically.

2. Diagnostic Algorithm

The diagnostic approach follows a logical stepwise process. You start with the presenting complaint, confirm thyroid dysfunction biochemically, then determine the aetiology of the thyroid dysfunction.

3. Investigation Modalities — Detailed Interpretation

3.1 Blood Tests

Blood tests: TSH + free T4 ^[5] — the first-line investigation for any thyroid disorder.

Phase of De Quervain's	TSH	fT4	fT3	Interpretation
Thyrotoxic phase (Phase 1)	↓↓ (often undetectable)	↑↑	↑	↓TSH ↑T3 ↑fT4: diagnostic of thyrotoxicosis (TSH usually undetectable) ^[3]. Pre-formed T4/T3 released from destroyed follicles. The TSH is suppressed by negative feedback
Hypothyroid phase (Phase 2)	↑	↓	↓	Stored hormones depleted, follicular cells still regenerating → cannot synthesise new hormone → TSH rises due to loss of negative feedback
Recovery phase (Phase 3)	Normal	Normal	Normal	Follicular regeneration complete → normal HPT axis
Early/prodromal	May be normal or borderline ↓	May be normal or borderline ↑	—	Very early inflammation may not yet have released enough hormone to alter TFT significantly; repeat in 2–4 weeks

The Moving Target

The TFT in de Quervain's is a snapshot of a moving target. A single TFT tells you which PHASE the patient is in — it does not confirm the diagnosis. You need the clinical picture (pain, ESR) AND the TFT together. Serial TFTs over weeks to months demonstrating the triphasic pattern are confirmatory.

Test	Expected Finding in De Quervain's	Why
ESR	Markedly elevated (often > 50, sometimes > 100 mm/hr) ^[2]	Hepatic acute-phase response: IL-6 from inflamed thyroid → ↑fibrinogen → ↑rouleaux → ↑ESR. This is the most useful blood test for confirming de Quervain's
CRP	Elevated	Same acute-phase response. CRP rises faster than ESR (within 6–12 hours) and falls faster. May be useful for monitoring treatment response
WBC	↑WBC ^[2]	Leukocytosis from systemic inflammatory response; usually mild (10–15 × 10⁹/L), predominantly neutrophilic

The ESR is by far the most discriminating simple blood test. In silent thyroiditis and postpartum thyroiditis (the main DDx), the ESR is normal. A markedly elevated ESR in the context of a tender thyroid essentially clinches the diagnosis.

Thyroid antibodies ^[1]^[7]^[9]:

Antibody	Finding in De Quervain's	Comparison	Clinical Significance
TRAb (anti-TSH receptor)	Negative	Graves': 80–90% positive ^[1]; sens 97%, spec 99% ^[3]^[7]	A negative TRAb in the presence of thyrotoxicosis effectively excludes Graves' disease and should prompt scintigraphy
Anti-TPO	Low titre ^[2] (transient, present in ~10–20%)	Hashimoto's: 90–100% ^[1]^[7]; Normal population: 10–15% ^[1]	Low-titre transient positivity reflects release of TPO antigen from destroyed follicles → weak secondary immune response
Anti-Tg	Low titre (transient)	Hashimoto's: 80–90% ^[1]^[7]; Normal population: 10–20% ^[1]	Same mechanism as anti-TPO

High titres suggest underlying autoimmune pathology → ↑risk of recurrence + ultimate progression to hypothyroidism ^[2]. If a patient with de Quervain's has unexpectedly HIGH-titre anti-TPO, suspect co-existing Hashimoto's and monitor more closely for permanent hypothyroidism.

Test	Role	Expected Finding
Serum thyroglobulin (Tg)	Differentiates thyroid destruction from factitious thyrotoxicosis	Elevated in de Quervain's (released from destroyed follicles). Factitious thyrotoxicosis confirmed by ↓serum thyroglobulin ^[7]^[9] — because exogenous T4 suppresses the gland, no Tg is released
T4:T3 ratio	Differentiates from factitious thyrotoxicosis	Normal (~30:1) in de Quervain's. In exogenous thyroxine intake, ratio can rise to > 70:1 ^[3]^[7] because T3 comes only from peripheral conversion
CBC	General workup	Mild leukocytosis ^[2]
ESR, antithyroid Ab (ATA) for thyroiditis ^[7]^[8]	Directed workup when thyroiditis suspected	As above
Calcitonin ^[7]^[8]	NOT indicated in de Quervain's	Only if Hx or clinical suspicion of familial medullary carcinoma or MEN2 ^[7]^[8]

3.2 Imaging

Ultrasound ^[5] — routine for ALL goitre/nodules ^[7]^[8].

Indication: Should be performed in all patients presenting with a thyroid swelling, including de Quervain's, primarily to:

Exclude a nodular process (dominant nodule, cyst with haemorrhage, malignancy)
Characterise the pattern of thyroid inflammation
Guide potential FNAC if a suspicious nodule is co-incidentally found

Findings in De Quervain's thyroiditis:

USG Feature	Description	Pathophysiological Basis
Diffuse or focal hypoechoic areas	Ill-defined, irregularly shaped hypoechoic regions corresponding to areas of inflammation	Inflammatory cell infiltration and oedema reduce echogenicity compared to normal thyroid parenchyma
Reduced or absent vascularity (on colour Doppler)	Decreased blood flow within the inflamed regions	Destruction of follicular architecture and surrounding microvascular damage; contrasts with Graves' (which shows "thyroid inferno" — diffusely increased vascularity)
Thyroid enlargement (diffuse or asymmetric)	The gland appears enlarged, often asymmetrically (one lobe more affected)	Inflammatory swelling; may start unilateral then become bilateral ("creeping thyroiditis")
Absence of nodules (typically)	No discrete solid or complex nodules; instead diffuse parenchymal change	De Quervain's is a diffuse inflammatory condition, not a neoplastic/nodular one
No suspicious lymphadenopathy	Cervical LNs are reactive at most	Not a malignant or granulomatous systemic process

Contrast with other conditions on USG:

Condition	USG Pattern
Graves' disease	Diffusely enlarged, ↑blood flow ^[3]^[7] ("thyroid inferno" on Doppler)
Hashimoto's	Diffusely heterogeneous, hypoechoic, coarse echotexture ("Swiss cheese" pattern), reduced vascularity
De Quervain's	Focal or diffuse hypoechoic areas, ↓vascularity, may be asymmetric
Toxic adenoma	Single well-defined hypervascular nodule
Thyroid malignancy	Hypoechoic, solid, microcalcifications, irregular margins, taller-than-wide, absent halo ^[1]^[7]^[8]

USG of thyroid: 7.5 or 10 mHz probes, B mode ^[7]^[8]:

Pros/cons: readily available, non-invasive, ↑Sens but ↓Spec ^[7]^[8]
Indication: for all patients with goitre/palpable nodules ^[7]^[8]
Use: as an extension of P/E to guide (not confirm) dx ^[7]^[8]

This is the key aetiological investigation that separates de Quervain's from other causes of thyrotoxicosis.

Radio-isotope scintigraphy (I¹²³ or Tc⁹⁹ᵐ) ^[5]^[10]:

Principle ^[10]^[11]:

Radioactive iodine handled in the same manner as normal iodine ^[10]
Level of uptake (and hence metabolic activity) reflected by localization of radioactive iodine ^[10]
99mTc pertechnetate has a similar ionic size as iodide ion, allowing it to be taken up by NIS ^[10] (NIS = sodium-iodide symporter on the basolateral membrane of thyrocytes)
Radiopharmaceuticals used: 99mTc pertechnetate (iodine trapping only), 123I or 131I (trapping + organification) ^[10]
Main use: assess metabolic function of thyroid gland ^[10]

Indications for scintigraphy ^[3]^[7]^[9]:

When suspecting destructive thyroiditis ^[3]^[7]
Diffuse toxic goitre with -ve TRAb ^[3]^[7]
S/S suggestive of destructive thyroiditis, e.g. painful goitre ^[3]^[7]
In event of ↓TSH with thyroid nodule(s) ^[3]^[7] — to differentiate toxic adenoma, toxic MNG, Graves' with co-existing nodule

Findings and interpretation in the context of thyrotoxicosis ^[3]^[7]^[9]:

Scintigraphy Pattern	Diagnosis	Why
Diffuse ↓uptake	Destructive thyroiditis (de Quervain's, silent, postpartum) vs factitious thyrotoxicosis ^[3]^[7]^[9]	In de Quervain's: follicular damage means thyrocytes cannot trap iodine + TSH is suppressed so no NIS stimulation. In factitious: exogenous T4 suppresses TSH → gland shuts down
Diffuse ↑uptake	Graves' disease vs 2° hyperthyroidism ^[3]^[7]^[9]	TRAb stimulates TSH receptors → NIS upregulated → avid iodine trapping throughout the gland
Heterogeneous ↑uptake	Toxic MNG ^[3]^[7]^[9]	Multiple autonomously functioning nodules with varying degrees of iodine trapping; suppressed surrounding tissue
Focal ↑uptake with ↓uptake elsewhere	Toxic adenoma ^[3]^[7]^[9]	Single autonomous nodule traps iodine avidly; the rest of the gland is suppressed by negative feedback

Distinguishing de Quervain's from factitious thyrotoxicosis (both show diffuse ↓ uptake):

Factitious thyrotoxicosis can be confirmed by ↑T4:T3 ratio (> 70:1) and ↓serum thyroglobulin ^[3]^[7]^[9]
In de Quervain's: T4:T3 ratio is normal (~30:1) and thyroglobulin is elevated (from follicular destruction)

Diagnosis of malignancy by scintigraphy: low sensitivity and specificity ^[5]. Functional assessment in thyrotoxic patients ^[5] — this is its main strength. Scintigraphy is NOT a cancer screening tool; it is an aetiological tool for thyrotoxicosis.

When NOT to Order Scintigraphy

Radionuclide scintigraphy should NOT be used if TSH is normal, because most cold nodules are benign and this would lead to unnecessary biopsy ^[8]^[9]. In de Quervain's, scintigraphy is indicated specifically because the TSH IS suppressed (thyrotoxic phase) and you need to confirm the destructive aetiology.

Modality	Role in De Quervain's
CXR	Not routinely needed; only if retrosternal extension suspected (rare in de Quervain's)
CT/MRI	CT/MRI for retrosternal extension and staging (NOT routine) ^[7]^[8]; not indicated in de Quervain's unless atypical features suggest malignancy
PET scan	No diagnostic role ^[6]; however, incidental FDG uptake in the thyroid on PET done for other reasons may sometimes lead to incidental detection of thyroiditis

Investigation	Category	Indication	Key Finding
TSH + fT4 ^[5]	Routine — 1st line	All patients	↓TSH + ↑fT4 (Phase 1) or ↑TSH + ↓fT4 (Phase 2)
ESR, CRP	Routine — 1st line	All patients	Markedly ↑ESR ^[2]; ↑CRP
WBC	Routine	All patients	↑WBC ^[2] (mild leukocytosis)
TRAb	Aetiological — 2nd line	To exclude Graves'	Negative in de Quervain's
Anti-TPO, anti-Tg	Aetiological — 2nd line	Antibody profile	Low titre (transient) ^[2]
USG thyroid ^[5]	Routine	All thyroid swellings	Diffuse hypoechoic areas, ↓vascularity, no nodules
Thyroid scintigraphy ^[5]	Aetiological — 2nd line	When aetiology of thyrotoxicosis unclear	Diffuse ↓uptake ^[3]^[7]^[9]
Serum thyroglobulin	Selective	To r/o factitious thyrotoxicosis	↑ in de Quervain's; ↓ in factitious ^[3]^[7]^[9]
T4:T3 ratio	Selective	To r/o factitious thyrotoxicosis	Normal (~30:1); > 70:1 in factitious ^[3]^[7]^[9]
FNAC ^[5]	Selective	Diagnostic uncertainty or suspicious nodule	Granulomatous inflammation, giant cells, colloid debris

Routine for all patients: TFT, thyroid USG ^[6]. Selective: thyroid scan (only in toxic + nodules), ESR and antithyroid antibodies for thyroiditis ^[6]^[7]^[8].

Exam Tip — The Minimum You Need

In clinical practice (and exams), the diagnosis of de Quervain's can often be made confidently with just three things:

Tender thyroid on examination
Markedly elevated ESR (> 50 mm/hr)
Low TSH + high fT4 (if in thyrotoxic phase)

Scintigraphy adds certainty but is not always needed if the clinical picture is classic. However, if asked in an exam about the key investigation to differentiate de Quervain's from Graves', the answer is thyroid scintigraphy (RAIU) — low uptake confirms destructive thyrotoxicosis.

High Yield Summary

Diagnostic Approach to De Quervain's Thyroiditis:

No formal diagnostic criteria — clinical diagnosis based on constellation: painful tender thyroid + ↑ESR + low RAIU + preceding URTI
First-line investigations: TFT (TSH + fT4), ESR/CRP, WBC, thyroid USG
Second-line aetiological investigations: TRAb (to exclude Graves'), thyroid scintigraphy (diffuse ↓ uptake confirms destructive thyrotoxicosis)
Key TFT pattern: Phase 1 = ↓TSH + ↑fT4; Phase 2 = ↑TSH + ↓fT4; Phase 3 = normal
ESR is the most discriminating simple blood test — markedly elevated (> 50) in de Quervain's, normal in silent/postpartum thyroiditis
Thyroid antibodies: TRAb negative; anti-TPO/anti-Tg low titre (transient)
Scintigraphy interpretation: Diffuse ↓ uptake = destructive (de Quervain's/silent/factitious); Diffuse ↑ = Graves'; Focal ↑ = toxic adenoma; Heterogeneous ↑ = toxic MNG
Factitious thyrotoxicosis also shows ↓ uptake but distinguished by ↓thyroglobulin + ↑T4:T3 ratio (> 70:1)
FNAC is NOT routinely needed; reserve for diagnostic uncertainty or co-incidental suspicious nodule
Always measure fT4, not total T4 — protein-binding factors can confound total T4

Active Recall - Diagnosis of De Quervain's Thyroiditis

References

^[1] Senior notes: felixlai.md (Causes of thyrotoxicosis, thyroid antibody tables, TFT evaluation flowchart, fT4 rationale) ^[2] Senior notes: Ryan Ho Endocrine.pdf (Section 1.5.1 Subacute Thyroiditis, p.31) ^[3] Senior notes: Adrian Lui Pediatrics.pdf (Thyrotoxicosis aetiological Ix, scintigraphy table, p.271–272) ^[5] Lecture slides: GC 177. A thyroid nodule benign thyroid nodules; thyroid cancer.pdf (p.4 Goitre Classification, p.7 Investigations, p.13 Other investigations — scintigraphy) ^[6] Senior notes: maxim.md (Approach to thyroid nodules — Investigations table) ^[7] Senior notes: Ryan Ho Endocrine.pdf (Aetiological Ix and scintigraphy findings, p.13; Ix for goitre, p.19; Hashimoto's Ix, p.30) ^[8] Senior notes: Ryan Ho Fundamentals.pdf (Ix for goitre/thyroid nodules, p.425–429; USG features, p.427; FNAC, p.428; Scintigraphy, p.429) ^[9] Senior notes: Ryan Ho Fundamentals.pdf (Thyrotoxicosis — aetiological Ix and scintigraphy, p.422) ^[10] Senior notes: Ryan Ho Diagnostic Radiology.pdf (Thyroid scintigraphy — principles, radiopharmaceuticals, p.59)

Management of De Quervain's Thyroiditis

Before diving into specifics, understand the foundational logic that governs every management decision in de Quervain's thyroiditis:

Mx: self-limiting → do NOT give antithyroid medications ^[2]

This single line from the notes captures the entire philosophy. Let me explain why from first principles:

Self-limiting: The granulomatous inflammation is a finite process triggered by a viral/post-viral immune response. Once the immune stimulus resolves and the follicular cells regenerate, the gland returns to normal function. Over 90% of patients recover completely within 6–12 months. Therefore, the management is supportive, not curative — you are managing symptoms while the disease runs its course.
No antithyroid drugs: This is the single most important management point and the most commonly tested concept. Do NOT give antithyroid medications ^[2]. Why?
- Antithyroid drugs (carbimazole, methimazole, propylthiouracil) work by inhibiting thyroid peroxidase (TPO), which catalyses the iodination and coupling reactions needed to synthesise new T3/T4
- In de Quervain's, the thyrotoxicosis is caused by release of pre-formed hormone from destroyed follicles — there is no excess synthesis to block
- Giving carbimazole to a patient with de Quervain's is like putting a fire extinguisher on a building that has already burned down and collapsed — the damage is done, the "fire" (hormone synthesis) is not the problem
- Furthermore, the follicular cells are damaged and are NOT actively synthesising — there is nothing for TPO inhibitors to act on
Phase-specific management: The treatment changes depending on which phase the patient is in (thyrotoxic vs hypothyroid vs recovery), because the pathophysiology and symptoms are fundamentally different in each phase.

The Cardinal Rule

Do NOT give antithyroid medications ^[2] (carbimazole, methimazole, PTU) in de Quervain's thyroiditis. This is the most commonly tested pitfall. The thyrotoxicosis is from hormone RELEASE, not hormone SYNTHESIS. Anti-thyroid drugs block synthesis — they have no role here.

3. Treatment Modalities — Detailed Breakdown

3.1 Pain and Inflammation Management

Pain is the dominant symptom in de Quervain's and often the reason the patient presents. It is caused by inflammatory destruction of thyroid follicles with capsular distension and release of inflammatory mediators (prostaglandins, IL-1, IL-6, TNF-α). Management follows a stepwise approach:

NSAIDs/corticosteroids for severe cases → manage systemic upset + pain ^[2]

Aspect	Detail
Drug examples	Naproxen 500 mg BD, ibuprofen 400–600 mg TDS, aspirin 600 mg QDS
Mechanism	NSAIDs inhibit cyclooxygenase (COX-1/COX-2) → ↓prostaglandin synthesis (PGE2, PGI2) → ↓pain, ↓fever, ↓inflammation. Prostaglandins sensitise nociceptors and cause vasodilation/oedema in the inflamed thyroid
Indication	First-line for all patients with pain and systemic symptoms. Most patients with mild-to-moderate de Quervain's respond adequately to NSAIDs alone
Duration	Typically 2–6 weeks, tapered as symptoms improve
Response rate	~70–80% of patients achieve adequate pain relief with NSAIDs
Contraindications	Active peptic ulcer disease, severe renal impairment, aspirin-sensitive asthma, third trimester pregnancy, anticoagulant use (↑ bleeding risk). Use with caution in elderly, CVD, heart failure
Monitoring	Assess response at 48–72 hours. If inadequate → escalate to corticosteroids

Why NSAIDs work: The pain in de Quervain's is fundamentally an inflammatory pain — prostaglandins produced at the site of thyroid follicular destruction sensitise nociceptors and lower the pain threshold. By blocking prostaglandin synthesis, NSAIDs address the root cause of the pain signal. They also reduce fever by blocking PGE2-mediated resetting of the hypothalamic thermostat.

Aspect	Detail
Drug	Prednisolone 30–40 mg/day PO initially
Mechanism	Corticosteroids have broad anti-inflammatory effects: (1) inhibit phospholipase A2 (via lipocortin) → ↓arachidonic acid release → ↓ALL downstream eicosanoids (prostaglandins AND leukotrienes); (2) ↓NF-κB transcription → ↓pro-inflammatory cytokine production (IL-1, IL-6, TNF-α); (3) ↓leukocyte migration and macrophage phagocytosis; (4) ↓capillary permeability → ↓oedema
Indication	Corticosteroids for severe cases ^[2] — specifically: (1) inadequate response to NSAIDs after 48–72 hours; (2) severe systemic symptoms (high fever, incapacitating pain); (3) recurrence of symptoms on NSAID taper
Tapering regimen	Start at 30–40 mg/day, then taper gradually over 4–8 weeks (e.g., reduce by 5 mg every 5–7 days). Rapid tapering risks symptom rebound
Response	Dramatic — most patients experience significant pain relief within 24–48 hours of starting corticosteroids. This rapid response is actually supportive of the diagnosis (if the pain does NOT respond to steroids, reconsider the diagnosis)
Relapse on tapering	20–30% of patients relapse when steroids are tapered too quickly. If this occurs, increase the dose back to the last effective dose and taper more slowly
Side effects	Short course: insomnia, hyperglycaemia, mood disturbance, dyspepsia. With longer courses: adrenal suppression, osteoporosis, immunosuppression, cushingoid features. Given the self-limiting nature, aim for shortest effective course
Contraindications	Uncontrolled diabetes (relative — can still use with close glucose monitoring), active infection (relative), psychosis

Why steroids are so effective: Corticosteroids act at a higher level in the inflammatory cascade than NSAIDs — they suppress the entire inflammatory response, not just the prostaglandin pathway. In a granulomatous condition like de Quervain's, where macrophages and giant cells are the primary effectors, steroids are particularly effective because they directly suppress macrophage function and cytokine production. Think of NSAIDs as blocking one tributary; steroids block the entire river.

The Steroid Response as a Diagnostic Clue

A dramatic response to corticosteroids within 24–48 hours supports the diagnosis of de Quervain's thyroiditis. If the patient does NOT respond to adequate steroid doses, you should reconsider the diagnosis — think about acute suppurative thyroiditis (needs antibiotics/drainage), anaplastic carcinoma, or other causes of neck pain.

β-blocker for hyperthyroid phase (usually mild) → for symptomatic control only ^[2]

3.2.1 Beta-Blockers (Symptomatic Control of Thyrotoxicosis)

Aspect	Detail
Drug of choice	Propranolol 20–40 mg TDS (three times daily); alternatives: atenolol 25–50 mg OD, nadolol 40–80 mg OD
Mechanism	Beta-blockers antagonise β-adrenergic receptors. In thyrotoxicosis, excess T3/T4 upregulates β1-adrenergic receptor expression in the heart and peripheral tissues, amplifying the effects of circulating catecholamines. Beta-blockers directly counteract this: (1) β1 blockade → ↓heart rate, ↓contractility, ↓myocardial oxygen demand → alleviates palpitations and tachycardia; (2) β2 blockade → ↓tremor (skeletal muscle), ↓glycogenolysis. Propranolol additionally inhibits peripheral T4 → T3 conversion (type 1 deiodinase) at higher doses — a minor but useful bonus
Why propranolol specifically	It is non-selective (blocks both β1 and β2) AND crosses the blood-brain barrier → addresses both peripheral symptoms (tachycardia, tremor) and central symptoms (anxiety, agitation). It also has the T4→T3 conversion-blocking effect
Indication	Symptomatic thyrotoxicosis in Phase 1: palpitations, tremor, anxiety, heat intolerance. Usually mild ^[2] — the thyrotoxicosis of de Quervain's is generally less severe than Graves' because the hormone release is finite (stores are depleted within 4–6 weeks)
Duration	Only for the duration of the thyrotoxic phase (4–6 weeks). Taper and discontinue as TFT normalises
Contraindications	Asthma/severe COPD (β2 blockade → bronchospasm), decompensated heart failure, severe bradycardia, second/third-degree AV block, Raynaud's disease (peripheral vasoconstriction). In asthma: use a cardioselective β1-blocker (atenolol, metoprolol) with caution, or consider a rate-limiting calcium channel blocker (verapamil, diltiazem)
Monitoring	Heart rate, blood pressure, symptom resolution. Aim for resting HR < 90 bpm

Why NOT antithyroid drugs — revisited with pharmacology:

Carbimazole (prodrug → converted to methimazole in vivo) and propylthiouracil (PTU): Both inhibit thyroid peroxidase (TPO), the enzyme that catalyses:
- Iodination of tyrosine residues on thyroglobulin (organification)
- Coupling of monoiodotyrosine (MIT) and diiodotyrosine (DIT) to form T3 and T4
PTU additionally blocks peripheral T4 → T3 conversion (type 1 deiodinase)
In de Quervain's, follicular cells are destroyed and are NOT synthesising new hormone. TPO is not active. There is no substrate for these drugs to work on. Giving them achieves nothing except exposing the patient to side effects (agranulocytosis, hepatotoxicity, rash) for zero benefit.

Temporary T4 replacement for hypothyroid phase if pronounced or symptomatic ^[2]

3.3.1 Levothyroxine (Temporary T4 Replacement)

Aspect	Detail
Drug	Levothyroxine (L-T4) 25–100 mcg/day PO
Mechanism	Exogenous synthetic T4 that is converted peripherally to T3 (the active hormone) by type 1 and type 2 deiodinases. Replaces the deficient endogenous thyroid hormone production during the period when follicular cells are regenerating
Indication	Temporary T4 replacement for hypothyroid phase if pronounced or symptomatic ^[2]. Specifically: (1) symptomatic hypothyroidism (fatigue, weight gain, cold intolerance, constipation, depression); (2) TSH > 10 mIU/L (significant biochemical hypothyroidism); (3) planning pregnancy (even mild hypothyroidism is detrimental to fetal neurodevelopment)
When NOT to treat	If the hypothyroid phase is mild and asymptomatic (borderline ↑TSH with normal fT4), observation with serial TFT monitoring every 4–6 weeks is appropriate. Many patients transit through the hypothyroid phase with minimal symptoms
Duration	Temporary — typically 6–12 months. After this period, attempt withdrawal by reducing the dose gradually and rechecking TFT 6–8 weeks after discontinuation
Starting dose	Start low (25–50 mcg) in elderly or those with cardiovascular disease (sudden increase in metabolic rate can provoke angina or arrhythmia in susceptible patients). Younger, otherwise healthy patients can start at 50–100 mcg
Monitoring	TFT (TSH + fT4) every 6–8 weeks after initiation or dose adjustment. Target: normalisation of TSH
Key point	This is temporary replacement — do NOT commit the patient to lifelong T4. Reassess at 6–12 months. Only ~5–15% will develop permanent hypothyroidism requiring lifelong replacement

Why only "temporary"? The hypothyroid phase is caused by follicular cell damage depleting hormone stores and preventing new synthesis. As follicular cells regenerate (typically over 4–6 months), normal hormone production resumes. The T4 replacement is a bridge to tide the patient over this regeneration period.

When Temporary Becomes Permanent

If the patient remains hypothyroid after 12 months AND has high-titre anti-TPO antibodies, suspect co-existing autoimmune thyroiditis (Hashimoto's). High titres suggest underlying autoimmune pathology → ↑risk of recurrence + ultimate progression to hypothyroidism ^[2]. These patients may need lifelong T4 replacement.

No Mx: spontaneous resolution! ^[2]

Aspect	Detail
Treatment	None needed — the patient is euthyroid
Monitoring	Check TFT at 6 and 12 months to confirm sustained euthyroidism and exclude late development of permanent hypothyroidism
Discharge	If TFT is normal at 12 months and the patient is asymptomatic, they can be discharged from follow-up
Counselling	Inform the patient that recurrence is possible (but rare, ~2%) and to return if neck pain recurs. Also inform that ~5–15% may develop permanent hypothyroidism requiring lifelong T4 — hence the importance of follow-up TFT

Phase	Duration	Pathophysiology	Treatment	Key Drugs	What NOT to Do
Phase 1: Thyrotoxic	4–6 weeks	Follicular destruction → release of stored T4/T3	NSAIDs ± corticosteroids for pain ^[2]; β-blocker for thyrotoxic symptoms ^[2]	Naproxen, prednisolone, propranolol	Do NOT give antithyroid drugs ^[2] (carbimazole, PTU) — no excess synthesis to block
Phase 2: Hypothyroid	4–6 months	Depleted stores + damaged follicles → ↓T4 synthesis	Temporary T4 replacement if symptomatic ^[2]	Levothyroxine 25–100 mcg	Do NOT commit to lifelong T4 without reassessment
Phase 3: Recovery	Resolution	Follicular regeneration → normal function	No Mx: spontaneous resolution ^[2]	None	Do NOT stop follow-up prematurely (5–15% → permanent hypothyroidism)

5. Special Scenarios

Time Point	Action	Purpose
At diagnosis	TFT, ESR, CRP, TRAb, anti-TPO/Tg, USG thyroid	Confirm diagnosis, establish baseline, exclude DDx
Every 2–4 weeks during active disease	TFT, ESR	Monitor phase transition (thyrotoxic → hypothyroid), assess treatment response, guide medication adjustments
At 6 weeks	Reassess TFT	Expected transition from thyrotoxic to hypothyroid or euthyroid. Discontinue β-blocker if TSH normalising. Consider T4 if hypothyroid
At 3–6 months	TFT	Assess hypothyroid phase. Titrate T4 if on replacement
At 6–12 months	TFT, attempt T4 withdrawal	Assess recovery. Reduce T4 dose → check TFT 6–8 weeks later. If TSH normal off T4 → recovery confirmed
At 12 months	Final TFT	Confirm sustained euthyroidism. If still hypothyroid → likely permanent → lifelong T4

High Yield Summary

Management of De Quervain's Thyroiditis — Key Points:

Self-limiting — the disease resolves spontaneously in > 90% of patients within 6–12 months
Do NOT give antithyroid medications ^[2] — the thyrotoxicosis is from hormone RELEASE, not synthesis; TPO inhibitors have no target
Pain management: NSAIDs first-line → corticosteroids (prednisolone 30–40 mg, taper over 4–8 weeks) if refractory or severe
Thyrotoxic symptoms: β-blocker (propranolol) for symptomatic control only ^[2] — usually mild and self-limited (4–6 weeks)
Hypothyroid phase: Temporary T4 replacement if pronounced or symptomatic ^[2] — reassess at 6–12 months; attempt withdrawal
Recovery: Spontaneous resolution ^[2] — monitor TFT at 6 and 12 months; 5–15% develop permanent hypothyroidism
High-titre autoantibodies suggest underlying autoimmune pathology → ↑risk of permanent hypothyroidism ^[2]
Dramatic response to steroids is diagnostically supportive; lack of response should prompt re-evaluation

Active Recall - Management of De Quervain's Thyroiditis

References

^[2] Senior notes: Ryan Ho Endocrine.pdf (Section 1.5.1 Subacute Thyroiditis — Management, p.31)

Complications of De Quervain's Thyroiditis

De Quervain's thyroiditis is fundamentally a self-limiting condition, and this is the single most reassuring fact. Over 90% of patients make a complete, uncomplicated recovery within 6–12 months. However, complications do occur, and understanding them requires understanding the underlying pathophysiology of each phase. Let me walk through them systematically, from the most common to the rare.

Aspect	Detail
Incidence	5–15% of patients — this is the most clinically significant long-term complication
Timing	Becomes apparent when the patient fails to recover from the hypothyroid phase (Phase 2) beyond 12 months
Mechanism	The granulomatous inflammatory destruction is usually reversible — follicular cells regenerate. However, in a minority of patients, the destruction is sufficiently severe or extensive that a critical mass of follicular cells is permanently lost. Additionally, high titres of thyroid autoantibodies suggest underlying autoimmune pathology → ↑risk of recurrence + ultimate progression to hypothyroidism ^[2]. This implies that some patients with de Quervain's have co-existing subclinical autoimmune thyroiditis (Hashimoto's) that was unmasked or accelerated by the inflammatory insult. The viral-triggered damage may expose thyroid autoantigens, triggering a persistent autoimmune response in genetically predisposed individuals (HLA-DR3/DR5)
Risk factors	High-titre anti-TPO antibodies at diagnosis, recurrent episodes, severe initial disease, older age
Clinical features	Persistent fatigue, weight gain, cold intolerance, constipation, dry skin, bradycardia, periorbital oedema — the standard features of hypothyroidism ^[4]^[8]. If untreated: hyperlipidaemia (both TG and cholesterol), menstrual irregularities, cognitive slowing
Diagnosis	Persistently elevated TSH with low fT4 at 12 months after onset, despite attempted levothyroxine withdrawal. Confirm with repeat TFT 6–8 weeks after T4 cessation
Management	Lifelong levothyroxine (T4) replacement. Thyroxine replacement: usually begin by gradually ↑dose ^[8]. Monitor TFT every 6–8 weeks until stable, then annually. Should not overtreat to ↓TSH → a/w ↑risk of osteoporosis and AF ^[8]

The 5–15% Rule

Although de Quervain's is self-limiting in the vast majority, always warn patients about the ~5–15% risk of permanent hypothyroidism and the need for follow-up TFT at 6 and 12 months. This is the reason you cannot simply discharge the patient after the acute phase resolves.

Why does permanent hypothyroidism happen from first principles?

The thyroid gland has a remarkable regenerative capacity — follicular cells can divide and reform functional follicles after injury. However, regeneration depends on:

The extent of destruction — if the inflammatory process destroys a majority of follicular cells beyond the regenerative threshold, the remaining cells cannot produce sufficient hormone
Co-existing autoimmunity — the release of thyroid autoantigens (thyroglobulin, TPO) during follicular destruction can trigger a persistent autoimmune response in genetically susceptible individuals, leading to ongoing lymphocytic destruction (essentially transitioning into Hashimoto's)
Fibrosis — in the healing phase, some areas of the gland may undergo fibrosis rather than functional regeneration, reducing the effective thyroid mass

2. Complications of the Thyrotoxic Phase

The thyrotoxic phase is usually mild and self-limited (4–6 weeks), and severe complications are uncommon. However, they can occur, especially in patients with pre-existing cardiovascular disease.

Complication	Mechanism	Clinical Significance
Tachycardia / palpitations	Excess T3/T4 upregulates β1-adrenergic receptors on cardiomyocytes → enhanced sensitivity to catecholamines → ↑heart rate, ↑contractility, ↑cardiac output	Usually mild and self-limiting in de Quervain's. Managed with β-blockers ^[2]
Atrial fibrillation (AF)	T3/T4 directly affects cardiac ion channels (↑INa, ↑IKs) → shortened atrial refractory period → re-entrant circuits → AF. Also ↑sympathetic tone predisposes to arrhythmia. CVS: ↑HR, ↑SBP ± AF ^[8]^[9]	Rare in de Quervain's (more common in Graves' due to prolonged thyrotoxicosis). Higher risk in elderly with pre-existing cardiac disease
Deterioration of CVS disease by thyrotoxicosis ^[1]	↑Workload of heart and worsens ischaemic symptoms → angina / arrhythmias / cardiac failure ^[1]. Excess thyroid hormone increases myocardial oxygen demand (↑HR × ↑contractility) while also potentially causing coronary vasoconstriction	Particularly dangerous in elderly patients with underlying IHD. The thyrotoxic phase, even if mild, can unmask previously compensated coronary artery disease
High-output heart failure	Thyroid hormone causes peripheral vasodilation (↓SVR) → compensatory ↑cardiac output → if the heart cannot keep up (pre-existing cardiomyopathy), decompensation occurs. High output HF: dyspnoea, effort tolerance ^[8]	Very rare in de Quervain's but possible in elderly with pre-existing LV dysfunction

Aspect	Detail
Incidence	Exceedingly rare in de Quervain's — more of a theoretical than practical complication
Mechanism	Thyroid storm develops in patients with longstanding untreated hyperthyroidism which is precipitated by acute event such as surgery, trauma or infection ^[1]. In de Quervain's, the hormone release is finite and self-limited, so the sustained high T4/T3 levels needed to precipitate storm are unusual. However, in a patient with severe initial follicular destruction releasing a massive bolus of hormone, or in a patient with concurrent intercurrent illness, storm is theoretically possible
Clinical features	Exaggeration of usual hyperthyroid symptoms to a life-threatening extent ^[9]: CVS: tachycardia > 140/min, AF, high output failure; Hyperpyrexia: may reach > 40°C; CNS disturbance: agitation, anxiety, delirium, psychosis, stupor, coma ^[9]
Management	Resuscitation (paracetamol + physical cooling, IV fluid) + Beta-blocker + high-dose dexamethasone (↓peripheral conversion) ^[9]. Note: thionamides and iodine (Lugol's solution), which are standard in Graves' thyroid storm, are of limited value in de Quervain's storm because the problem is hormone release, not synthesis. However, dexamethasone is doubly useful here — it blocks T4→T3 conversion AND treats the underlying thyroidal inflammation

Thyroid Storm in De Quervain's — A Nuance

While thyroid storm is taught as a complication of thyrotoxicosis, it is almost never seen in de Quervain's in clinical practice. The reason is physiological: the thyroid stores a finite amount of hormone, and the release in de Quervain's is gradual (over 4–6 weeks as follicles are progressively destroyed), not a sudden catastrophic dump. In contrast, Graves' disease involves continuous overproduction by a hyperactive gland, leading to sustained high T4 that can spiral into storm when provoked. If an exam question asks about thyroid storm, think Graves' first, not de Quervain's.

Aspect	Detail
Incidence	~2–4% of patients experience recurrence
Timing	Can occur months to years after the initial episode
Mechanism	Likely re-exposure to a different viral trigger in a genetically susceptible individual (HLA-B35). Some recurrences may represent relapse of the same episode if corticosteroids were tapered too rapidly (pseudo-recurrence vs true recurrence)
Risk factors	HLA-B35 positivity, high-titre anti-TPO (suggesting autoimmune predisposition), inadequate initial treatment duration
Management	Same as initial episode: NSAIDs → corticosteroids if needed → β-blocker for thyrotoxic symptoms → T4 for hypothyroid phase. Monitor more closely for permanent hypothyroidism, as recurrent episodes increase cumulative follicular damage
Significance	Each episode of follicular destruction reduces the functional thyroid reserve → cumulative risk of permanent hypothyroidism increases with each recurrence

Since many patients with de Quervain's require corticosteroids (prednisolone) for pain control, the complications of steroid therapy must be considered:

Complication	Mechanism	Relevance to De Quervain's
Steroid rebound on tapering	Premature reduction of steroids before the inflammation has fully resolved → recurrence of thyroid pain and systemic symptoms. Not a true "complication" but a common clinical problem (20–30% of patients)	The most common steroid-related issue. Managed by slower taper and increasing the dose back to the last effective level
Hyperglycaemia	Steroids promote gluconeogenesis, increase insulin resistance, and decrease glucose uptake by peripheral tissues	Monitor blood glucose, especially in patients with pre-existing diabetes or impaired glucose tolerance
Insomnia, mood disturbance	Corticosteroids affect the HPA axis and directly modulate neurotransmitter systems (serotonin, dopamine)	Usually mild with short courses; advise taking steroids in the morning
Gastric irritation	Steroids reduce mucosal PGE2 production → reduced gastric mucosal protection	Co-prescribe PPI if also on NSAIDs (double anti-inflammatory → ↑ GI risk)
Adrenal suppression	Exogenous steroids suppress endogenous ACTH → adrenal atrophy if used > 3 weeks	Relevant if steroid course extends beyond 3–4 weeks — must taper, not stop abruptly
Osteoporosis, immunosuppression	Chronic steroid effects	Usually not relevant in de Quervain's as courses are short (4–8 weeks)

If the hypothyroid phase is prolonged or unrecognised, the standard complications of hypothyroidism may develop:

Complication	Mechanism	Clinical Feature
Hyperlipidaemia	Hypothyroidism reduces LDL receptor expression on hepatocytes → ↓LDL clearance → ↑serum LDL cholesterol. Also ↓lipoprotein lipase activity → ↑TG. Hyperlipidaemia – both TG and cholesterol ^[4]^[8]	Accelerated atherogenesis if prolonged and untreated
Cardiovascular risk	Combination of hyperlipidaemia + ↑SVR (hypothyroid vasoconstriction) + diastolic hypertension → ↑cardiovascular risk	Note that hypothyroidism can lead to hyperlipidaemia → coronary atherosclerosis ^[8]
Menstrual irregularities / infertility	Hypothyroidism → ↑TRH → ↑prolactin (TRH stimulates lactotrophs as well as thyrotrophs) → hyperprolactinaemia → suppression of GnRH pulsatility → oligo/amenorrhoea, anovulation	Relevant in young women of reproductive age
Depression / cognitive impairment	T3 is essential for normal neurotransmitter function (serotonin, norepinephrine synthesis). Hypothyroidism reduces CNS metabolic activity	Usually reversible with T4 replacement
Myxoedema	Accumulation of glycosaminoglycans (hyaluronic acid, chondroitin sulphate) in the dermis and subcutaneous tissue → water retention → non-pitting oedema. Dry skin, hoarseness, periorbital oedema and myxoedema ^[4]^[8]	Seen only in prolonged, untreated hypothyroidism
Myxoedema coma	Very rare, medical emergency ^[8]. Extreme hypothyroidism → progressive hypothermia, respiratory failure, hypoxia, CNS depression → coma. Usually precipitated by infection, cold exposure, sedatives. Confusion, coma, ↓↓body temperature, convulsion, respiratory failure, hypoxia ^[8]	Virtually never seen in de Quervain's because the hypothyroid phase is typically mild and self-limited. However, worth knowing as an extreme of untreated hypothyroidism

Myxoedema Coma from De Quervain's?

This is essentially a theoretical complication. Myxoedema coma requires prolonged, severe, untreated hypothyroidism — the kind seen in end-stage Hashimoto's or post-thyroidectomy patients who stop taking levothyroxine. The hypothyroid phase of de Quervain's is mild and transient (4–6 months, self-resolving). Unless the patient has additional risk factors (e.g., co-existing Hashimoto's, elderly, intercurrent illness), myxoedema coma should not occur. If it appears in an exam as a complication of de Quervain's, it's likely a distractor.

Complication	Detail
Prolonged debilitating neck pain	Some patients experience severe pain lasting weeks to months, significantly impacting quality of life, ability to work, sleep, and eat (pain worsened by swallowing). This is a functional rather than structural complication
Dysphagia	The swollen, inflamed thyroid pressing on the oesophagus combined with pain exacerbated by swallowing can cause significant odynophagia and dysphagia, leading to reduced oral intake and weight loss
Misdiagnosis and delayed treatment	De Quervain's is frequently misdiagnosed as pharyngitis, dental infection, or cervical lymphadenitis. The delay in diagnosis means delayed symptom relief (NSAIDs/steroids). While not a complication of the disease per se, it is a complication of the clinical pathway

Complication	Frequency	Phase	Mechanism	Reversibility
Permanent hypothyroidism	5–15%	Post-recovery	Irreversible follicular destruction ± autoimmune co-pathology	Irreversible; requires lifelong T4
Cardiovascular (tachycardia, AF)	Uncommon	Phase 1 (thyrotoxic)	β-receptor upregulation + ion channel effects of T3/T4	Reversible with phase resolution + β-blocker
Thyroid storm	Exceedingly rare	Phase 1	Massive hormone release (theoretical)	Reversible with emergency treatment
Recurrence	2–4%	Any	Re-exposure to viral trigger in HLA-B35+ individual	Manageable; ↑ cumulative risk of permanent hypothyroidism
Steroid rebound	20–30% of steroid-treated	During treatment	Premature steroid taper	Reversible with slower taper
Hyperlipidaemia	Common if Phase 2 prolonged	Phase 2 (hypothyroid)	↓LDL receptor expression	Reversible with T4 replacement
Myxoedema coma	Virtually never	Phase 2 (extreme)	Extreme untreated hypothyroidism	Reversible with emergency T4/T3 + supportive care

High Yield Summary

Complications of De Quervain's Thyroiditis:

Permanent hypothyroidism (5–15%) — the most important complication; higher risk with high-titre anti-TPO antibodies suggesting co-existing autoimmune thyroiditis. Requires lifelong levothyroxine replacement.
Cardiovascular complications of thyrotoxic phase — tachycardia, AF (rare), exacerbation of pre-existing IHD. Managed with β-blockers. Thyroid storm is exceedingly rare.
Recurrence (~2–4%) — re-exposure to viral trigger in genetically susceptible individuals. Each episode increases cumulative risk of permanent hypothyroidism.
Steroid-related complications — rebound on tapering (20–30%), hyperglycaemia, GI irritation. Managed with slow taper and monitoring.
Hypothyroid phase complications — hyperlipidaemia, menstrual irregularities, depression — all reversible with T4 replacement if needed.
Myxoedema coma — virtually never occurs from de Quervain's alone; a theoretical extreme.
Overall prognosis is excellent — > 90% make a full recovery with no long-term sequelae.

Active Recall - Complications of De Quervain's Thyroiditis

References

^[1] Senior notes: felixlai.md (Complications of thyrotoxicosis — cardiovascular deterioration; thyroid storm; causes of hypothyroidism) ^[2] Senior notes: Ryan Ho Endocrine.pdf (Section 1.5.1 Subacute Thyroiditis, p.31 — including footnote 48 on high-titre antibodies) ^[4] Senior notes: Ryan Ho Fundamentals.pdf (Section 3.8.1.2 Hypothyroidism — clinical presentation, p.423) ^[8] Senior notes: Ryan Ho Fundamentals.pdf (Hypothyroidism Mx, p.424; Goitre Hx — complications, p.426) ^[9] Senior notes: Ryan Ho Fundamentals.pdf (Thyrotoxic crisis, p.422; S/S of thyrotoxicosis, p.421)

De Quervain's Thyroiditis

1. Definition

2. Epidemiology

3. Risk Factors

4. Anatomy and Function (Relevant Review)

4.1 Thyroid Gland Anatomy

4.2 Thyroid Follicle — The Functional Unit

4.3 The Hypothalamic-Pituitary-Thyroid (HPT) Axis

5. Etiology and Pathophysiology

5.1 Etiology

5.2 Pathophysiology — The Triphasic Course

Phase 1: Thyrotoxic Phase (4–6 weeks) [2]

Phase 2: Hypothyroid Phase (4–6 months) [2]

Phase 3: Recovery / Euthyroid Phase

5.3 Histopathology

6. Classification

6.1 Classification of Thyroiditis

6.2 Within the Subacute Category

6.3 Classification Within Causes of Thyrotoxicosis

6.4 Classification Within Causes of Hypothyroidism

6.5 Classification Within Goitre

7. Clinical Features

7.1 Symptoms

7.2 Signs

7.3 Important Negative Signs (What You Do NOT See)

7.4 Systemic Features Summary

8. Approach to Hypothyroidism in the Context of De Quervain's

9. Differential Diagnosis Context (from History/Examination Alone)

Active Recall - De Quervain's Thyroiditis

References

Framework: Three Clinical Presentations, Three DDx Lists

A. DDx of a Painful Thyroid Swelling

B. DDx of Thyrotoxicosis (When Patient Presents in Phase 1)

B1. Causes of Thyrotoxicosis — Systematic Classification [1]

B2. Key Differentiating Features in the Thyrotoxic Phase

B3. Distinguishing De Quervain's from Other Causes of Destructive Thyrotoxicosis

C. DDx of Hypothyroidism (When Patient Presents in Phase 2)

D. DDx of Anterior Neck Swelling (the "Lump" DDx)

E. DDx Summary — Decision Algorithm

Active Recall - DDx of De Quervain's Thyroiditis

1. Diagnostic Criteria

1.1 Core Diagnostic Features (All Should Be Present)

1.2 Supportive Features (Strengthen the Diagnosis)

2. Diagnostic Algorithm

2.1 Master Diagnostic Algorithm

2.2 The Evaluation of Thyrotoxicosis Algorithm (From Lecture) [1]

2.3 Why Free T4 (fT4) Instead of Total T4?

2.4 Why TSH Is the Most Sensitive Indicator

3. Investigation Modalities — Detailed Interpretation

3.1 Blood Tests

3.1.1 Thyroid Function Tests (TFT)

3.1.2 Inflammatory Markers

3.1.3 Thyroid Antibodies

3.1.4 Other Blood Tests

3.2 Imaging

3.2.1 Thyroid Ultrasound (USG)

3.2.2 Thyroid Scintigraphy (Radionuclide Scan)

3.2.3 Other Imaging (Usually NOT Needed)

3.3 Fine Needle Aspiration Cytology (FNAC)

3.4 Summary: Investigation Checklist for De Quervain's Thyroiditis

4. Diagnostic Algorithm — Practical Stepwise Summary

Active Recall - Diagnosis of De Quervain's Thyroiditis

1. Overarching Principles

2. Management Algorithm

3. Treatment Modalities — Detailed Breakdown

3.1 Pain and Inflammation Management

3.1.1 NSAIDs (First-Line for Pain)

3.1.2 Corticosteroids (Second-Line — For Severe/Refractory Pain)

3.1.3 Aspirin (Alternative)

3.2 Thyrotoxic Phase Management

3.3 Hypothyroid Phase Management

3.4 Recovery Phase Management

4. Summary: Phase-Specific Management Table

5. Special Scenarios

5.1 Recurrent De Quervain's Thyroiditis

5.2 Pregnancy

5.3 Elderly / Cardiovascular Disease

5.4 When to Consider Referral

6. Monitoring and Follow-Up Protocol

Active Recall - Management of De Quervain's Thyroiditis