Thyroid Eye Disease (Graves Ophthalmopathy)

A syndrome of clinical and orbital imaging abnormalities caused by deposition of mucopolysaccharides and infiltration with chronic inflammatory cells of the orbital tissues, particularly the extraocular muscles

Usually occurs in association with autoimmune hyperthyroidism

Radioiodine therapy, possibly indirectly due to induction of hypothyroidism, and cigarette smoking increase its severity

Ethanol injection of thyroid nodules has been reported to be followed by severe disease

Ocular myasthenia and thyroid eye disease are associated and may coexist; presence of ptosis rather than eyelid retraction is characteristic of the former

Primary clinical features

• Proptosis

• Lid retraction and lid lag

• Conjunctival chemosis and episcleral inflammation

• Extraocular muscle dysfunction

Resulting symptoms

• Cosmetic abnormalities

• Surface irritation, which usually responds to artificial tears

• Diplopia

Important complications are corneal exposure and optic nerve compression, both of which may lead to marked visual loss

The primary imaging features are enlargement of the extraocular muscles, usually affecting both orbits

Clinical or laboratory evidence of thyroid dysfunction and thyroid autoantibodies may not be detectable at presentation or even on long-term follow-up

Clinical and imaging abnormalities of thyroid eye disease may be mimicked by dural carotico-cavernous fistula

Euthyroidism should be established and maintained in all cases

Mild disease: Oral selenium seems to be beneficial

Moderately severe disease: Treatment options when there is no visual loss is controversial

• Peribulbar corticosteroid injections have been advocated

• Surgical decompression may be justified in patients with marked proptosis

• Lateral tarsorrhaphy may be used for moderately severe corneal exposure

Severe disease: Treatment options for optic nerve compression or severe corneal exposure include

• Intravenous pulse methylprednisolone therapy (eg, 1 g daily for 3 days, repeated weekly or monthly for up to 3 months)

• Oral prednisolone 80–100 mg/day

• Radiotherapy

• Surgery (usually consisting of extensive removal of bone from the medial, inferior, and lateral walls of the orbit)

Other procedures are particularly useful for correcting lid retraction but should not be undertaken until the orbital disease is quiescent and orbital decompression or extraocular muscle surgery has been undertaken

Diplopia should be treated conservatively (eg, with prisms) in the active stages of the disease and only by surgery when the disease has been static for at least 6 months