The classic signs and symptoms of thyroid-related ophthalmopathy (TRO) are proptosis, diplopia, lid retraction, and restriction of extraocular movements. While it is classically associated with Graves disease, only eighty percent of patients with TRO are hyperthyroid. 10% are hypothyroid, while another 10% are euthyroid.

TRO appears to be an autoimmune process. Early in the disease, the extraocular muscles are infiltrated by inflammatory cells which in turn attract fibroblasts. The fibroblasts produce mucopolysaccharides resulting in orbital swelling. The inferior and medial rectus muscles are typically most severely affected.

The indications for orbital imaging in a patient with unilateral proptosis include suspicion of optic nerve compression, evaluation for orbital decompression surgery, or an unclear diagnosis. Orbital CT is the study of choice. Rectus muscle belly enlargement with sparing of the tendinous insertion is the classic finding in TRO.

While thyroid eye disease is the most common cause for unilateral as well as bilateral proptosis, other causes of unilateral proptosis include pseudotumor, orbital cellulitis, tumors (benign or malignant), carotid-cavernous fistula, and trauma(retrobulbar hemorrhage). While orbital pseudotumor, like TRO, causes extraocular muscle enlargement, it typically does not spare the tendinous insertion.

Treatment is initiated by referral to an endocrinologist for management of any systemic thyroid disease. Exposure keratopathy is treated with artificial tears or lubricating ointment. Optic nerve compression is the most urgent ocular complication. Medical therapy involves systemic steroids to decrease acute inflammation. Orbital radiation decreases inflammation on a more long-term basis. Orbital nerve compression and corneal exposure are indications for surgery. Orbital decompression (removal of bone or fat to allow the eye to settle back into the orbit), eye muscle surgery, and eyelid surgery can be performed, usually in that order.