Thyroid Eye Disease

👁️ Thyroid Eye Disease (TED), also known as Graves' orbitopathy or Graves' ophthalmopathy, is an autoimmune condition linked to Graves' disease (hyperthyroidism). It causes inflammation and swelling of orbital tissues (muscles, fat, connective tissue) → symptoms include proptosis (bulging eyes) 🤯, diplopia (double vision) 👀, lid retraction ⬆️, and in severe cases, vision loss ⚠️. Primarily affects adults, but can occur at any age.

🔬 Pathophysiology

• Autoimmune attack: TRAbs (thyrotropin receptor antibodies) activate orbital fibroblasts → cytokine release → inflammation + glycosaminoglycan deposition.
• ⬆️ Volume of muscles + fat → proptosis, restricted eye movements, and compressive neuropathy.
• Key processes:
  • 🔥 Muscle inflammation → diplopia.
  • 🤯 Proptosis → bulging, exposure risk.
  • ⬆️ Lid retraction → “staring” appearance.
  • 💧 Corneal exposure → dryness/ulceration.
  • 🧠 Optic neuropathy → vision loss if untreated.

⚡ Risk Factors

• 🧬 Graves' disease (25–50% develop TED).
• 🚬 Smoking: strongest modifiable risk factor; worsens severity + treatment response.
• ♀️ Female gender: more common, but men often more severe.
• 🔄 Thyroid dysfunction: TED can occur in hyper-, hypo-, or euthyroid states.
• ☢️ Radioactive iodine therapy: may trigger/worsen TED unless covered with steroids.

🩺 Clinical Presentation

TED ranges from mild irritation to vision-threatening disease. Early recognition is key 🚨.

• 👀 Early: Grittiness, watering, photophobia, periorbital swelling, conjunctival redness, mild proptosis, lid retraction.
• ⚠️ Moderate–Severe: Marked proptosis (asymmetrical), diplopia, severe lid retraction, exposure keratopathy, corneal ulceration, compressive optic neuropathy → ↓ acuity/colour vision/field defects.

🔎 Diagnosis

Diagnosis = clinical, supported by imaging + thyroid tests.

• 👓 Eye exam: Visual acuity, colour vision, RAPD check, exophthalmometry, ocular motility.
• 🖼️ Imaging: CT/MRI → muscle belly enlargement (sparing tendinous insertions) + optic nerve compression.
• 🧪 Bloods: TFTs, TRAbs, ± TPO antibodies.
• 🖥️ Visual fields: Detect early optic neuropathy.

💊 Management

• Multidisciplinary: Endocrinology + Ophthalmology + sometimes Surgery.
• 🌡️ Control thyroid function: Achieve euthyroidism (ATDs, RAI ± steroids, or thyroidectomy).
• 🚭 Smoking cessation = essential (biggest modifiable factor).
• 💊 Corticosteroids: IV methylprednisolone (preferred) for active, moderate–severe TED.
• ☢️ Orbital radiotherapy: Consider in steroid-responsive disease.
• 💉 Teprotumumab / Rituximab: Biologics in resistant cases (expensive, specialist use).

🩺 Phases of Management

• 🔥 Active (Inflammatory): Steroids, immunosuppression, treat thyroid, stop smoking, artificial tears for corneal protection.
• 😴 Quiescent: Manage residual diplopia/proptosis (e.g., prism glasses, strabismus/orbital decompression surgery).
• 🔧 Rehabilitative: Lid surgery, strabismus correction, cosmetic repair after disease stabilises.

🧠 Key Clinical Pearls

• 🧾 Optic neuropathy = red flag → urgent steroids ± decompression.
• 💧 Always protect the cornea (lubricants, taping, moisture chambers).
• ☢️ RAI should be given with steroid cover if TED risk factors present.
• 👓 Exophthalmometry: >21 mm = abnormal;>24 mm = usually TED.

📌 Conclusion

TED is a complex autoimmune orbitopathy requiring early recognition + MDT care. 🔑 Priorities = control thyroid, stop smoking, reduce inflammation, protect vision. Timely treatment → prevents blindness and improves quality of life. 🌟