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Summary Table

Category	Details
Risk Factors	Women aged 30-50, recent upper respiratory tract infection (typically 2-8 weeks prior), HLA-B35 association
Etiology	Post-viral inflammatory destruction of thyroid follicles (commonly following Coxsackievirus, mumps, measles, adenovirus, influenza)
Patient Presentation	Anterior neck pain radiating to the jaw or ear, often preceded by a prodrome of fever, malaise, and myalgias. Symptoms follow a triphasic pattern: thyrotoxicosis, hypothyroidism, then recovery
Classic Physical Exam	Exquisitely tender, firm, enlarged thyroid gland. Pain often lateralizes or migrates from one lobe to the other. Low-grade fever may be present
Key Diagnostic Results	Markedly elevated ESR (often >50 mm/hr), low radioactive iodine uptake (RAIU) during the thyrotoxic phase, elevated free T4 with suppressed TSH early on
Management	NSAIDs for mild cases, glucocorticoids (prednisone) for moderate-to-severe pain, beta-blockers for symptomatic thyrotoxicosis. No antithyroid drugs
Keywords	"Painful thyroid," "tender neck after URI," "jaw/ear pain with thyroid enlargement," "low radioactive iodine uptake," "elevated ESR"

1. Pathophysiology

Subacute thyroiditis is a self-limiting inflammatory disorder of the thyroid gland triggered by a preceding viral infection. The virus induces a cytotoxic immune response against thyroid follicular cells, leading to follicular disruption and unregulated release of preformed thyroid hormone (T3 and T4) into the bloodstream. This is not new hormone synthesis; it is a spillage phenomenon from damaged storage.

This mechanism directly explains the triphasic clinical course. In the first phase (thyrotoxic phase, lasting 3-6 weeks), destruction of follicles dumps stored hormone into circulation, producing symptoms of thyrotoxicosis: tremor, palpitations, anxiety, heat intolerance, and weight loss. Because the gland is being destroyed rather than stimulated, TSH is suppressed and RAIU is very low. This is the single most important concept separating destructive thyrotoxicosis from Graves disease.

In the second phase (hypothyroid phase, lasting weeks to months), the gland's hormone reserves are depleted and the damaged follicular cells cannot synthesize new hormone. TSH rises, and the patient may develop fatigue, weight gain, cold intolerance, and constipation.

In the third phase (recovery/euthyroid phase), follicular cells regenerate, hormone production normalizes, and the patient returns to a euthyroid state. Approximately 90-95% of patients recover full thyroid function, though a small subset develops permanent hypothyroidism.

The intense inflammatory infiltrate in the gland also explains the hallmark physical finding: a markedly tender thyroid. Granulomatous inflammation with multinucleated giant cells is the characteristic histologic pattern, which is why this condition is also called subacute granulomatous thyroiditis.

2. Classification and Clinical Manifestation

Based on Phase

Phase	Timeline	Thyroid Status	TSH	fT4	RAIU	Clinical Features
Phase 1: Thyrotoxic	Weeks 1-6	Thyrotoxicosis	Low	High	Very low (<5%)	Neck pain, fever, tremor, palpitations, weight loss, anxiety
Phase 2: Hypothyroid	Weeks 6-12+	Hypothyroidism	High	Low	Low to normal	Fatigue, weight gain, constipation, cold intolerance, dry skin
Phase 3: Recovery	Months 3-6+	Euthyroid	Normal	Normal	Normal	Resolution of all symptoms

It is worth noting that not every patient passes through all three phases. Some patients present only in the thyrotoxic phase and recover directly without a clinically evident hypothyroid phase. The vignette will typically test phase 1 because this is where the diagnostic challenge lies.

Based on Type

Type	Pain	Etiology	RAIU	Key Feature
Subacute (De Quervain)	Yes, prominent	Post-viral	Very low	Tender thyroid, elevated ESR
Painless (Silent)	No	Autoimmune	Very low	Often postpartum, anti-TPO antibodies
Acute (Suppurative)	Yes	Bacterial infection	Variable	Abscess formation, very ill patient
Hashimoto	Usually no	Autoimmune (chronic)	Variable	Anti-TPO/anti-thyroglobulin, gradual hypothyroidism

3. Diagnostic Workup

Test	Role	Expected Finding
ESR / CRP	Best initial test (supports clinical suspicion)	ESR markedly elevated, often >50 mm/hr
TSH, Free T4, Free T3	Assess thyroid functional status	Phase 1: low TSH, high T4/T3. Phase 2: high TSH, low T4
Radioactive Iodine Uptake (RAIU)	Most important confirmatory test	Diffusely low uptake (<5%) in thyrotoxic phase
Thyroid ultrasound	Adjunctive imaging	Hypoechoic, heterogeneous gland; may show focal or diffuse changes
Fine-needle aspiration (FNA)	Rarely needed	Granulomatous inflammation with multinucleated giant cells
Anti-TPO antibodies	Rule out autoimmune thyroiditis	Typically negative or low titer

The clinical scenario of a patient with anterior neck pain, tenderness on palpation, and a recent viral illness combined with elevated ESR is often enough to raise strong suspicion. The thyroid function tests then confirm the phase.

The key diagnostic step that test-writers focus on is the RAIU. In Graves disease, the thyroid is overactive and avidly traps iodine, resulting in high RAIU. In subacute thyroiditis, the gland is being destroyed and is not trapping iodine at all, resulting in very low RAIU. Both conditions present with thyrotoxicosis (low TSH, high T4), but RAIU cleanly separates them. This is the most commonly tested distinction.

Thyroid ultrasound is supportive but not definitive. It typically shows poorly defined hypoechoic regions corresponding to areas of inflammation. FNA is almost never required unless there is diagnostic uncertainty or concern for malignancy (e.g., a dominant nodule in the setting of pain).

Anti-TPO antibodies help distinguish subacute thyroiditis from painless (silent) thyroiditis. In painless thyroiditis, anti-TPO antibodies are usually positive because the underlying mechanism is autoimmune. In subacute thyroiditis, they are typically absent or present at very low titers.

4. Management and Treatment

Severity	Treatment	Details
Mild pain	NSAIDs	Ibuprofen 400-600 mg every 6-8 hours or naproxen 500 mg twice daily
Moderate to severe pain or NSAID failure	Glucocorticoids	Prednisone 40 mg/day, taper over 4-6 weeks
Thyrotoxic symptoms	Beta-blockers	Propranolol 20-40 mg every 6-8 hours or atenolol 25-50 mg daily
Hypothyroid phase (symptomatic)	Levothyroxine	Low-dose replacement (25-50 mcg/day), temporary, reassess in 6-8 weeks
Recurrence on steroid taper	Extend glucocorticoid course	Slower taper over 8-12 weeks

Acute management centers on symptom control. The neck pain is the primary complaint, and NSAIDs are the first-line treatment for mild disease. If pain does not respond within 1-2 days or if the patient presents with severe symptoms (high fever, inability to swallow, debilitating pain), prednisone is the next best step. The response to glucocorticoids is typically dramatic and rapid, often within 24-48 hours. This brisk response is itself considered supportive of the diagnosis.

A common pitfall is the temptation to prescribe antithyroid drugs (methimazole, propylthiouracil). These drugs block new hormone synthesis, but in subacute thyroiditis, the thyrotoxicosis results from release of preformed hormone from damaged follicles, not from increased synthesis. Therefore, antithyroid drugs have no role in this condition. Beta-blockers alone are used to control adrenergic symptoms such as tachycardia, tremor, and anxiety.

During the hypothyroid phase, most patients are either asymptomatic or mildly symptomatic and do not require treatment. If symptoms are bothersome, a short course of low-dose levothyroxine can be given with the plan to discontinue after 6-8 weeks and recheck thyroid function. Permanent hypothyroidism occurs in roughly 5-10% of cases and requires lifelong levothyroxine.

Patients should be counseled that recurrence during glucocorticoid tapering is common (occurring in up to 20% of cases). This does not represent treatment failure; it simply requires extending the taper duration.

5. Differential Diagnosis and Distractors

Differential Diagnosis	Why It Looks Similar	Key Discriminator
Graves disease	Both present with thyrotoxicosis (low TSH, elevated T4, tachycardia, tremor)	Graves has high RAIU, diffuse goiter is typically nontender, and thyroid-stimulating immunoglobulin (TSI) is positive. Subacute thyroiditis has low RAIU and a painful gland
Painless (silent) thyroiditis	Both have low RAIU and thyrotoxicosis from glandular destruction	Painless thyroiditis is nontender. Often occurs postpartum. Anti-TPO antibodies are positive
Acute suppurative thyroiditis	Both cause a painful, tender thyroid with fever	Suppurative thyroiditis presents with a severely ill patient, unilateral fluctuant swelling, leukocytosis with left shift, and abscess on imaging. It is bacterial, not viral
Hashimoto thyroiditis	Both can cause a firm, enlarged thyroid and hypothyroidism	Hashimoto is painless, has strongly positive anti-TPO/anti-thyroglobulin antibodies, and presents with chronic progressive hypothyroidism rather than a triphasic course
Thyroid lymphoma or anaplastic carcinoma	Both can cause a rapidly enlarging, firm thyroid mass	Malignancy causes a rock-hard, fixed mass with compressive symptoms (dysphagia, hoarseness, stridor). ESR elevation is nondiagnostic. FNA or core biopsy is needed
Pharyngitis / peritonsillar abscess	Anterior neck pain with fever after a viral illness	Pharyngitis pain localizes to the oropharynx, not the anterior neck/thyroid. No thyroid tenderness, no thyrotoxicosis, no elevated ESR to the degree seen in subacute thyroiditis

6. Traps and High-Yield Pearls

The most common way students lose points on subacute thyroiditis questions is by selecting antithyroid drugs for the thyrotoxic phase. The vignette will show a patient with classic thyrotoxicosis (low TSH, high T4, tremor, tachycardia), and methimazole will appear as an answer choice. The critical reasoning step is recognizing that destructive thyrotoxicosis from hormone spillage does not respond to drugs that inhibit hormone synthesis. The treatment is supportive: beta-blockers for symptoms and NSAIDs or glucocorticoids for pain.

The second major trap involves confusing subacute thyroiditis with Graves disease. Both produce thyrotoxicosis, but the discriminating features are pain and RAIU. A tender thyroid with low RAIU points to subacute thyroiditis. A nontender thyroid with high RAIU and possibly exophthalmos points to Graves disease. If the vignette describes a patient with thyrotoxicosis and does not mention pain, do not select subacute thyroiditis.

A subtler trap involves the hypothyroid phase. A vignette may describe a patient who had neck pain and thyrotoxicosis weeks ago and now presents with fatigue, weight gain, and elevated TSH. The test is checking whether you recognize this as the natural progression of subacute thyroiditis rather than new-onset Hashimoto disease. The history of a preceding painful thyrotoxic episode is the giveaway.

Finally, remember that the dramatic response to glucocorticoids is both a therapeutic and a diagnostic clue. If a patient with a painful thyroid and elevated ESR improves rapidly on prednisone, this strongly supports the diagnosis of subacute thyroiditis.

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