In sight-threatening thyroid eye disease, compressive dysthyroid optic neuropathy (DON) poses an immediate risk to vision. When urgent intravenous glucocorticoid (IVGC) therapy does not achieve adequate visual recovery within 2 weeks, a defined next-line protocol applies.
The patient has sight-threatening thyroid eye disease with dysthyroid optic neuropathy caused by compression of the optic nerve by enlarged extraocular muscles at the orbital apex. DON may result from compression of the optic nerve by enlarged extraocular muscles at the apex of the orbit, or infrequently from stretch of the nerve due to proptosis.
The previous step was urgent intravenous glucocorticoid (IVGC) therapy with high-dose intravenous methylprednisolone, aimed at achieving visual recovery and improvement in visual acuity. This protocol applies when visual acuity has not improved — or visual function has deteriorated — at 2 weeks of monitoring under IVGC therapy.
doi: 10.1089/thy.2022.0251
Patients with DON and/or corneal breakdown and/or globe subluxation.
DON may result from compression of the optic nerve by enlarged EOM at the apex of the orbit, or infrequently (<5%), due to stretch of the nerve because of proptosis.
In patients with compressive DON, orbital decompression of the deep medial wall and orbital floor should be considered to restore vision by reducing apical compression on the optic nerve.
RT may be considered for preventing or as an adjunct to treating DON.
Visual improvement may be noted within days of the procedure, and even severe or longstanding visual loss may have partial or full visual recovery.
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