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Thyroid eye disease
Thyroid eye disease is an autoimmune inflammation of the orbital tissues — muscles and fat — occurring mainly in Graves disease; it passes through an active inflammatory phase and then an inactive "burnt-out" phase, and treatment depends on activity and severity: drugs in the active phase, rehabilitative surgery in the quiet phase.
Why it matters in the exam
The commonest sign is upper lid retraction with a "startled stare", together with lid lag on downgaze, proptosis, swelling and redness of the lids and conjunctiva, double vision from muscle restriction — usually the inferior rectus, hence difficulty elevating the eye — and corneal exposure. On CT the muscles are thickened in the belly with sparing of the tendons. Smoking is the most important modifiable risk factor, and radioactive iodine may worsen active disease — patients at risk receive prophylactic steroids.
Activity is measured by the Clinical Activity Score (CAS): 3 points out of 7 or more — active disease. Severity: mild, moderate-to-severe, and sight-threatening — compressive optic neuropathy at the orbital apex (dysthyroid optic neuropathy) or corneal breakdown. In mild disease: thyroid control, smoking cessation, lubrication and selenium 100 µg twice daily for 6 months. In active moderate-to-severe disease: intravenous methylprednisolone in weekly pulses — a usual cumulative dose of 4.5 g over 12 weeks — combined with mycophenolate, or teprotumumab (an IGF-1R inhibitor, with side effects of hearing loss and hyperglycaemia).
Optic neuropathy — reduced acuity and colour vision and an RAPD — is an emergency: methylprednisolone 500–1000 mg intravenously for 3 days, and if there is no improvement within 1–2 weeks — urgent orbital decompression. When the disease has been quiet for at least several months, surgery follows a fixed order: orbital decompression, then strabismus surgery, and finally eyelid surgery — because each step changes the next. The cumulative dose of intravenous steroids should not exceed 8 g because of liver toxicity.
Key points
- Autoimmune inflammation of orbital muscles and fat, mainly in Graves disease.
- Commonest sign: lid retraction.
- Smoking and radioactive iodine make it worse.
- Active moderate-to-severe → intravenous methylprednisolone or teprotumumab.
- Optic neuropathy → steroids at once and decompression.
Summary table
| Stage | Finding | Treatment |
|---|---|---|
| Mild | Lid retraction, mild proptosis, dryness | Thyroid control, stop smoking, lubrication, selenium |
| Active moderate-to-severe | CAS of 3 or more, diplopia, proptosis | Methylprednisolone 4.5 g over 12 weeks with mycophenolate, or teprotumumab |
| Optic neuropathy | Reduced acuity and colour, RAPD | Methylprednisolone 500–1000 mg for 3 days; decompression |
| Corneal exposure | Ulcer, incomplete lid closure | Intensive lubrication, urgent treatment |
| Inactive phase | Fixed proptosis and strabismus | Decompression, strabismus, lids — in that order |
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Sources
- European Group on Graves' Orbitopathy (EUGOGO) Clinical Practice Guidelines, 2021 — Assessment and management of Graves' orbitopathy
- ATA/ETA Consensus Statement on the Management of Thyroid Eye Disease, 2022 — Medical and surgical treatment
- AAO Basic and Clinical Science Course, Section 7: Oculofacial Plastic and Orbital Surgery, 2024-2025 — Thyroid eye disease
Sources are given for further reading; the text is written afresh and not copied from them.
Reviewed by the Examqo AI Professor · 2026-11-06. The text may contain errors; when in doubt, check the source.