Subacute Thyroiditis Clinical Overview
I. The "On-Call" Snapshot
Clinical Significance in Malaysia: This is a frequent cause of a painful goitre and transient thyrotoxicosis. You will see this in primary care, A&E, and the medical clinic. The key is to differentiate it from Graves' disease or a thyroid abscess to avoid incorrect treatment.
High-Yield Definition: Subacute thyroiditis is a self-limited inflammatory thyroid disease, likely of viral origin, characterised by a triphasic clinical course of hyperthyroidism, hypothyroidism, and eventual return to euthyroid function. (UpToDate, 2024).
Clinical One-Liner: Think of it as a post-viral, painful neck swelling with thyrotoxic features and a sky-high ESR.
II. Etiology & Risk Factors
Etiology: The exact cause is unknown, but it is strongly associated with a preceding viral upper respiratory tract infection. Common triggers include Coxsackievirus, adenovirus, influenza, mumps, and SARS-CoV-2.
Risk Factors:
Recent viral illness (typically 2-8 weeks prior).
Female sex (3-5:1 female-to-male ratio).
Age: 30-50 years.
Genetic predisposition: Association with HLA-B35.
III. Quick Pathophysiology
This is a destructive thyroiditis.
Viral Trigger & Inflammation: A virus or a post-viral inflammatory response causes granulomatous inflammation within the thyroid gland.
Follicular Destruction: This inflammation destroys thyroid follicles.
Hormone Dump: Preformed T4 and T3 are dumped into the circulation, causing a transient thyrotoxicosis. This is release, not overproduction.
Depletion & Hypothyroidism: As hormone stores are depleted and follicles are damaged, the patient transitions into a hypothyroid phase.
Recovery: The follicles regenerate over several weeks to months, and the patient usually returns to a euthyroid state.
IV. Classification
There is no formal staging system. The disease is defined by its clinical phases, which drive management decisions:
Thyrotoxic Phase (initial): Lasts 3-8 weeks. Patient has symptoms of hyperthyroidism.
Hypothyroid Phase (transient): Lasts 2-8 weeks. Patient may be asymptomatic or have mild hypothyroid symptoms.
Euthyroid Phase (recovery): Most patients recover fully over months.
V. Clinical Assessment
🚩 Red Flags & Immediate Actions
Severe dysphagia or stridor: Suggests significant tracheal compression. Action: Keep patient nil by mouth, get urgent ENT review for potential airway compromise.
High-grade fever with fluctuance on palpation: This is not subacute. This is a thyroid abscess until proven otherwise. Action: Admit, start empiric IV antibiotics, and request an urgent ultrasound for drainage assessment.
History
Key Diagnostic Clues (Classic Presentation): Prodrome of fever, myalgia, and malaise followed by the acute onset of severe anterior neck pain. The pain often radiates to the jaw, ears, or throat and is aggravated by swallowing or turning the head.
Symptom Breakdown:
Common (>50%): Neck pain, fever, fatigue, palpitations, heat intolerance, anxiety, weight loss.
Less Common (10-50%): Hoarseness, dysphagia, lethargy and weight gain (in the later hypothyroid phase).
Pertinent Negatives:
Absence of eye signs (proptosis, lid lag, ophthalmoplegia) makes Graves' disease less likely.
Absence of a history of neck irradiation or significant family history of thyroid cancer.
Physical Examination (OSCE Approach)
General Inspection: Patient often appears unwell, anxious, and in pain.
Vitals: Low-grade fever (38-39°C), sinus tachycardia.
Disease-Specific Examination (Neck):
Inspection: May see a visible, diffuse, or asymmetrical swelling over the thyroid gland.
Palpation: The key finding is an exquisitely tender, firm, and diffusely enlarged goitre. It can be unilateral initially before migrating to the other lobe ("creeping thyroiditis"). No discrete nodules or fluctuance.
Pertinent Negatives: No significant cervical lymphadenopathy. No signs of Graves' orbitopathy.
Examination for Differentials: Check for tremor and brisk reflexes (thyrotoxicosis). Assess for fluctuance to rule out an abscess.
Clinical Pearl
Thyrotoxicosis with a very painful thyroid and a markedly elevated ESR is subacute thyroiditis until proven otherwise. Do not start Carbimazole.
VI. Diagnostic Workflow
Differential Diagnosis
Infectious (Suppurative) Thyroiditis:
Points For: Fever, severe neck pain, elevated inflammatory markers.
Points Against: Usually more systemically unwell, higher fever, marked leukocytosis, often immunocompromised. Goitre is typically fluctuant.
How to Differentiate: Ultrasound will show a collection/abscess. Fine-needle aspiration will yield pus.
Graves' Disease:
Points For: Thyrotoxicosis, goitre.
Points Against: Painless goitre, often has orbitopathy and pretibial myxedema. ESR is typically normal.
How to Differentiate: Positive TRAb antibodies. A radioactive iodine uptake scan shows high uptake.
Haemorrhage into a Thyroid Nodule:
Points For: Acute onset of neck pain and swelling.
Points Against: No preceding viral illness, no fever, no systemic thyrotoxic symptoms.
How to Differentiate: Ultrasound will show a complex cyst or nodule.
Investigations Plan
Bedside / Initial (First 15 Mins):
ECG: To check for sinus tachycardia or arrhythmias.
First-Line Labs & Imaging:
Thyroid Function Test (TFT): Suppressed TSH, elevated free T4 and/or T3. This pattern will evolve over time.
Inflammatory Markers: Markedly elevated ESR (often >50 mm/hr, classically >100 mm/hr) and CRP. This is a hallmark feature.
Full Blood Count (FBC): May show a mild normocytic anaemia and neutrophilia.
Ultrasound Neck: Not for diagnosis, but essential to rule out a thyroid abscess. Typically shows ill-defined, hypoechoic regions with decreased vascularity on Doppler.
Confirmatory / Gold Standard:
Radioactive Iodine Uptake (RAIU) Scan: Shows near-absent, low uptake (<5%) during the thyrotoxic phase. This confirms hormone release from damaged follicles, not hyper-synthesis as seen in Graves' disease (which has high uptake). This is usually reserved for diagnostically challenging cases.
VII. Staging & Severity Assessment
Severity is judged clinically based on:
The intensity of pain.
The degree of thyrotoxic symptoms (heart rate, tremor, anxiety).
The magnitude of inflammatory marker elevation.
This assessment guides the choice between NSAIDs and corticosteroids.
VIII. Management Plan
A. Principle of Management
Control inflammation and pain.
Provide symptomatic relief for thyrotoxicosis.
Monitor for and manage the transient hypothyroid phase.
B. Immediate Stabilisation (The ABCDE Plan)
Immediate stabilisation is not relevant here as this is an ambulatory/ward-based condition, not typically a medical emergency. Thyroid storm is exceedingly rare.
C. Definitive Treatment (The Ward Round Plan)
1. Anti-inflammatory Therapy:
First-Line (Mild-to-Moderate Pain): High-dose NSAIDs.
Drug: Mefenamic Acid 500mg TDS PO or Naproxen 500mg BD PO.
Duration: Continue until pain and fever resolve, then taper over 2-4 weeks.
Second-Line (Severe Pain or NSAID Failure): Corticosteroids.
Drug: Prednisolone 20-40mg OD PO.
Response: Expect dramatic improvement in pain within 24-48 hours. If there's no response, question the diagnosis.
Duration: Maintain the initial dose for 1-2 weeks, then taper SLOWLY over 4-6 weeks based on symptoms and ESR levels. Tapering too quickly risks relapse.
2. Symptomatic Control (Thyrotoxic Phase):
Drug: Beta-blockers, e.g., Propranolol 20-40mg TDS/QDS PO.
Purpose: To control palpitations, tremor, and anxiety.
NOTE: Anti-thyroid drugs (Carbimazole, PTU) have NO ROLE. The thyroid is not overproducing hormones; it is leaking them. These drugs are ineffective and inappropriate.
3. Management of Hypothyroid Phase:
Most patients are asymptomatic and do not require treatment.
If symptomatic or TSH >10 mIU/L, consider a short course of levothyroxine (e.g., 25-50 mcg OD) for 2-3 months, then attempt to wean off.
D. Long-Term & Discharge Plan
Follow-up: Monitor TFTs every 4-6 weeks to track the evolution through the phases.
Patient Education: Explain the triphasic nature of the illness and the expected timeline for recovery. Reassure them that it is self-limiting and rarely recurs.
IX. Complications
Short-Term: Recurrence (5-10%), especially if steroids are tapered too rapidly.
Long-Term: Permanent hypothyroidism (5-15% of patients). This is the most important long-term sequela to monitor for.
X. Prognosis
Excellent. The vast majority of patients achieve complete recovery and return to a permanent euthyroid state within 12-18 months.
XI. How to Present to Your Senior
Use the SBAR format.
(Situation): "Dr, reviewing Mdm A, a 40-year-old lady admitted from A&E for a painful neck swelling."
(Background): "She had a flu-like illness 3 weeks ago. For the past week, she developed fever, anterior neck pain radiating to her ears, and palpitations. On exam, she is febrile at 38.2°C, tachycardic at 115 bpm, with a diffusely enlarged and exquisitely tender thyroid."
(Assessment): "Her bloods show a suppressed TSH, high fT4, and a very high ESR of 110. My working diagnosis is subacute thyroiditis. I have ruled out a thyroid abscess clinically and with a bedside ultrasound."
(Recommendation): "I have started her on Propranolol for tachycardia. Given the severity of her pain, I plan to start Prednisolone 30mg OD. I will monitor her TFTs and ESR weekly as an inpatient."
XII. Summary & Further Reading
Top 3 Takeaways:
Suspect in any patient with a post-viral syndrome, painful goitre, and thyrotoxic features.
The diagnostic triad is neck pain, suppressed TSH, and a markedly elevated ESR.
Management is supportive: NSAIDs or steroids for inflammation and beta-blockers for symptoms. Avoid anti-thyroid drugs.
Key Resources:
UpToDate: "Subacute thyroiditis"
Amboss: "Subacute thyroiditis"
There is no specific Malaysian CPG for this condition. Management is guided by international consensus and resources like UpToDate.
