Orbital decompression is a surgery to help with prominent eyes (proptosis). Frequently, bone of the orbit (eye socket) is removed to allow more room for tissues within the orbit to expand and thus for the eye to recess some into the orbit. There are various approaches to orbital decompression depending which bones of the orbit are to be addressed. Most commonly, this procedure is performed for patients suffering from thyroid eye disease.

In this specific case, this patient underwent a bilateral medial orbital wall decompression. In this before and after coronal (oriented like the patient is looking at us) CT scan, the medial walls of both of the orbits (bone shows up as bright white on CT) has been removed. In the 'before' scan, we can appreciate that the optic nerve (indicated by the yellow arrow) is within a tight space due to extraocular muscle enlargement associated with thyroid eye disease. This patient had vision loss on both sides due to optic nerve compression. Note the purple arrow that indicates the medial rectus muscle (the muscle that moves the eye inward toward the nose). After the medial orbital wall has been removed and the periorbita (layer of tissue around the orbit) has been opened, the medial rectus muscle is now able to occupy space in the ethmoid sinus and there is more space around the optic nerve.

This was a combined case with ENT surgeon Nathan Calloway, MD

Thyroid eye disease (TED) is an autoimmune orbital inflammatory condition most commonly associated with hyperthyroidism. TED can also be seen in other forms of thyroid dysfunction including primary hypothyroidism and Hashimoto's thyroiditis. Interestingly, TED can present in the setting of normal thyroid function. Classic clinical findings in TED include eyelid retraction (the eyelids opening more than they should), proptosis (bulging of the eye or eyes) and strabismus (ocular misalignment). 

During the active phase of the disease, these findings and associated symptoms fluctuate. Consequently, rehabilitative surgery to improve appearance and comfort is delayed until the disease enters the stable (chronic) phase. This approach yields more predictable results from surgery. When needed, rehabilitative surgery is typically done in a specific order (orbital decompression for proptosis followed by strabismus surgery for ocular misalignment which is then followed by eyelid retraction repair). Surgery is done in these three stages with a period of months in between because one stage can affect the next. Some patients may need all three stages, while others may benefit from one or two of the stages.

Rarely, surgery may be indicated more urgently in the small percentage of patients who experience sight-threatening disease. Patients who may need urgent surgery include those who have optic nerve compression resistant to medical therapy and those who have corneal exposure from eyelid retraction that does not respond well to ocular lubrication. 

Modifiable risk factors for TED progression include smoking as well as thyroid levels. Dr. Mettu communicates his findings routinely with the involved endocrinologist or primary care provider. 

Oral supplementation with selenium 100 micrograms twice a day may be beneficial in some patients with mild TED.

An FDA approved medication for TED called Tepezza is now available. Tepezza is given as a series of infusions, and in certain patients, it can result in improvement of signs and symptoms of TED (eye bulging, double vision, swelling, eye redness, eye pain). Click here to learn more about how Tepezza can help. Click here to read about the safety and side effects of Tepezza.

After careful evaluation, Dr. Mettu helps develop a customized treatment plan for each patient.

To learn more about TED, click to read informational from the North American Neuro-Ophthalmology Society. 

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