OP2.3 | Thyroid Eye Disease — Summary & Reflection

KEY TAKEAWAYS

Thyroid eye disease is a systemic autoimmune condition caused by TRAb stimulating orbital fibroblasts, leading to glycosaminoglycan accumulation, EOM muscle belly enlargement (with tendon sparing — distinguishing it from myositis on imaging), orbital fat expansion, and proptosis. The hallmark clinical signs are proptosis, upper lid retraction (Dalrymple's sign), lid lag (von Graefe's sign), restricted EOM, and chemosis. Disease is classified by activity (CAS ≥3/7 = active) and severity (EUGOGO: mild, moderate-severe, sight-threatening). Management is: selenium for mild active; IV methylprednisolone for moderate-severe active; high-dose IVMP plus urgent orbital decompression for sight-threatening CON; rehabilitative surgery (orbital decompression → squint → lids) for inactive disease. Smoking cessation is mandatory. RAI therapy can worsen TED and requires steroid cover in at-risk patients.

REFLECT

Thyroid eye disease links ophthalmology, endocrinology, and oncology (orbital tumour differential). Reflect on how you would explain to a patient with newly diagnosed Graves' disease that they must monitor their eyes even if they feel their thyroid is under control — what would you say specifically about smoking? How would you decide, at a joint thyroid-eye clinic, whether a patient's change in vision is from thyroid-related optic nerve compression versus a co-existing refractive change? What is the role of the general physician in identifying the earliest warning signs of TED?