Graves Ophthalmopathy/Orbitopathy, Thyroid-Associated Orbitopathy, or Autoimmune Orbitopathy Frequently Asssociated with Dysthyroidism
Your body has an immune system that combats infection and cancer. Sometimes the immune system makes mistakes and “attack”the patient’s own body i.e. an autoimmune disease.
The orbit and ocular adnexae are the tissues that surround the eye. Graves orbitopathy or G.O. (more accurately Thyroid-Associated Orbitopathy or Autoimmune Orbitopathy Frequently Associated with Dysthyroidism) is an autoimmune disease that affects the orbital tissues, the thyroid gland and sometimes the skin of the shins. The thyroid gland in and of itself does NOT cause the eye problem. Rather both are “innocent targets” of the body’s autoimmune attack.
Most patients with G.O. have an overactive thyroid gland (hyperthyroidism). Some have normal thyroid function (euthyroidism), and still others have an underactive thyroid gland (hypothyroidism). Thus the most accurate term for this disease is Autoimmune Orbitopathy Frequently Associated with Dysthyroidism (AOFAD), but it is a mouthful.
Even if the thyroid gland function is normalized, the double vision and lid scarring usually persists! Even if the thyroid gland function is normalized, the eyes may continue to worsen! Even if the thyroid gland function is normalized, the eyes may not recover!
In many respects the orbital tissues and thyroid gland fight their own separate battle. G.O. may precede, coincide or follow the thyroid gland dysfunction. Some feel that radioactive iodine used to ablate the thyroid gland can adversely affect the eyes. See the subpage.
SYMPTOMS & SIGNS OF G.O.
The initial phase of G.O. is charac-terized by swelling and inflammation that lasts up to a year or more. This is usually followed by a phase of scarring. G.O. can sometimes appear so asymmetric that the disease seems to affect only one eye. G.O. commonly causes the upper eyelid of one or both eyes to become lifted higher. Patients may perceive that they look angry, that they have a staring appearance, or that they eyes appear bulgy. Because more of the ocular surface is exposed, corneal drying or ocular irritation may occur.The inflammation of G.O. may cause puffiness of the eyelids which is often worse in the morning. Inflammation and later scarring of the extraocular muscles that move the eyeball may cause restricted eye movements or double vision. Inflammation of the orbital fat and eye muscles may cause the eye to protrude forwards, causing proptosis or exophthalmos. This also may result in corneal drying. Occasionally the optic nerve may be compressed, which may result in vision loss.
TREATMENT: Most patients with G.O. do NOT require surgery. During the active phase of the inflammation, you may have to be checked every 1 to 3 months. Patients are encouraged to keep a dated monthly photo album of their eyes, and to bring it with them during clinic visits. Ocular lubrication (artificial tears 4-6 X during the day and Lacrilube ointment at night) are usually comforting. IF your diet is deficient in selenium, Selenium (100 micrograms 2x/day) for 6 months has been suggested for mild G.O.. The safety of over the counter selenium is unproven, and should not be used if your serum selenium level is above 122 micrograms per litre. Likewise Quercetin is unproven.
If you smoke, STOP SMOKING. Smokers get the worst G.O.. If you smoke, STOP SMOKING. Second hand smoke is also bad. If you smoke, STOP SMOKING. Smokers get the worst G.O.. Resources to help you stop smoking are available at: https://smokershelpline.ca/
Work with your endocrinologist to normalize your thyroid function tests.
If there is marked swelling of the eyelid tissues, sleeping with the head of the bed elevated may help decrease morning tissue congestion.
If there is double vision, patching or occasionally prism glasses will help.
If it is essential that you use radioactive iodine (RAI) for hyperthyroidism, your endocrinologist or ophthalmologist may suggest you use oral steroids (prednisone) before and after the iodine treatment. The need for prednisone with RAI is remains contro-versial.
If there is significant visual loss from optic nerve compression, urgent removal of the orbital bones (orbital decompression) or orbital fat, intravenous and oral steroids, radiation or a combination of all three may be required. The routine use of rituximab, tocilizumab , mycophenolate, methotrexate, teprotumumab and K1-70 requires much further research.
Teprotumumab is the leading contender in the treatment of active G.O., but is not commercially available for humans as of 2019. In the phase 3 trial, “adverse events more common with teprotumumab than placebo included muscle spasms (31.7% vs 9.5%), alopecia (19.5% vs 11.9%), hyperglycemia (4.9% vs 0%), potential infusion-related reaction (14.6% vs 9.5%), and hearing impairment. (9.8% vs 0%). Most were mild to moderate and resolved by study end.”
Only about 5% of patients require surgery for G.O. In the absence of vision-threatening G.O., elective surgery is performed AFTER theinflammatory phase of the disease has settled. If a bulgy eye is particularly disturbing to the patient, orbital decompression (fat or bone) may be considered. If feasible, it may be safer to do “camouflage” surgery on the upper eyelid, to decrease the appearance of the protruberant eye. If there is persistent double vision that cannot be fixed with glasses, then STRABISMUS SURGERY (eye muscle surgery) can be performed. If the eyelids remain retracted, eyelid lengthening can be done. If there is significant puffiness of the eyelids, then blepharoplasty can be performed.
For more detailed medical information see
Dr. Ing’s 2019 YouTube update https://www.youtube.com/watch?v=n2_8q1Uwx6w
or Dr. Ing’s chapter on Graves Ophthalmopathy on emedicine.com https://emedicine.medscape.com/article/1218444-overview