Thyroid-associated ophthalmopathy (TAO) is eye damage caused by a variety of thyroid disorders, 97% of which are caused by Graves’ disease, which is generally referred to as diffuse goiter with hyperthyroidism. Studies have shown that thyrotropin receptor antibodies (TRAb) play an important role in Graves’ ophthalmopathy (GO). The order of occurrence of hyperthyroidism and GO is 43% of the time; 44% of the time, hyperthyroidism occurs before GO; and 5% of the time, there is only significant proptosis without hyperthyroidism. In a few cases, GO can be seen in Hashimoto’s thyroiditis. The diagnosis of GO should be made by retro-orbital CT or MRI to exclude retrobulbar occupying lesions. The disease may spontaneously resolve in 66% of cases after onset, with no change in signs in 20% and continued deterioration in 14% of cases. In most cases, the disease activity lasts for 6 to 12 months, and then the inflammatory symptoms gradually resolve and enter a stable phase. Some cases can recur. Factors that contribute to the aggravation of proptosis are: 1. hyperthyroidism is controlled too quickly and thyroid tablets are not combined. 2. Hypothyroidism has occurred. 3. Increased antigen release related to surgery or nuclear therapy. After remission of the disease, some degree of eyelid constriction and protrusion of the eyeball is usually still left. There are two types of proptosis based on pathogenesis: non-infiltrative eye disease, which is mainly due to sympathetic excitation of the extraocular muscles and epicanthalmos; and infiltrative eye disease, which is characterized by increased volume of intraorbital and retrobulbar tissue, lymphocytic infiltration, edema, and proptosis. Patients complain of intraocular foreign body sensation, distension, photophobia, lacrimation, diplopia, strabismus, and decreased visual acuity; examination reveals proptosis (eyeball projection exceeding the upper limit of normal by 4 mm), eyelid swelling conjunctival congestion and edema, eye movement restriction in severe cases with eye fixation, incomplete eyelid closure, corneal ulceration due to corneal exposure, total uveitis, or even blindness, and swollen and thickened extraocular muscles on orbital CT. According to the 1977 American Thyroid Association (ATA) classification of ocular signs of Graves’ disease, a grade III or higher is required for the diagnosis of the disease. Clinical grading: Grade I: no symptoms, signs limited to upper lid recession with or without delayed upper lid descent. Grade II: Orbital soft tissue involvement, including symptoms and signs. Grade III: protrusion of the eyeball (>18 mm). Grade IV: extraocular muscle involvement. Grade V: corneal involvement. Grade VI: optic nerve involvement and loss of vision. Criteria for assessing severity of disease: Grade: Mild 19-20 intermittent occurrence of optic nerve evoked potentials or other detection abnormalities with visual acuity > 9/10. Moderate 21-23 non-persistent presence of visual acuity 8/10, C5/10. Severe >23 persistent presence of visual acuity <5/10. Treatment of GO begins with differentiation of the degree of disease. According to the EUGOGO report, mild GO accounts for 40%, moderate GO for 33%, and severe GO for 27%. The course of mild GO is generally self-limiting and does not require intensive treatment. Local treatment and control of hyperthyroidism is the main focus, such as wearing tinted glasses to reduce photophobia and shame; using artificial tears and covering the cornea at night to eliminate corneal foreign body sensation and protect the cornea; elevating the head of the bed to reduce periorbital edema; wearing prismatic lenses to correct mild diplopia. Control of hyperthyroidism is the basic treatment, because hyperthyroidism or hypothyroidism can promote GO progression; patients should be advised to quit smoking. Mild GO is stable and usually does not progress to moderate and severe GO. Moderate and severe GO are intensively treated on the basis of the above treatment. The effectiveness of treatment depends on the degree of disease activity. Treatment can be effective in cases that are in an active phase, such as the acute phase of the disease or newly developed inflammation or extraocular muscle disorders. In contrast, treatment is not effective in cases with a long history of disease, chronic proptosis, and stable diplopia. Ophthalmic rehabilitation surgery is often required for correction. Optic nerve involvement is the most serious manifestation of the disease, which can lead to blindness and requires emergency treatment with intravenous glucocorticoid drips and orbital decompression surgery. To select a reasonable treatment plan, an assessment of the severity and activity of GO needs to be performed simultaneously. The active phase means that the inflammatory response is active and immunosuppressive therapy is effective; the quiescent phase is considered for rehabilitative surgical treatment. 1. Corticosteroids: Prednisone 40-80mg/day orally in divided doses for 2-4 weeks. After that, the dose should be reduced by 2.5-10mg/day every 2-4 weeks. Glucocorticoid therapy needs to be continued for 3-12 months. The therapeutic effect of intravenous route is better than oral administration (80%-90% for the former; 60%-5% for the latter). There are various methods of intravenous administration, and the commonly used method is methylprednisolone 50-10Omg added to saline intravenous drip shock therapy, once every other day for three times. Regarding the treatment of glucocorticoids, the more severe the degree of GO and the higher the titer of thyroid hormone receptor antibodies in the blood of GO patients, the better the efficacy. However, systemic application of glucocorticoids can lead to various complications such as water and sodium retention, headache, gastritis, hypertension, stress ulcers, etc., thus making it difficult for patients to tolerate and terminate the treatment. 2.Radiation therapy: The indications are basically the same as glucocorticoid therapy. The effectiveness rate is 60%, and it is better for recent soft tissue inflammation and recent occurrence of ocular muscle dysfunction. People with diabetes and hypertensive retinopathy are contraindications to orbital radiation therapy. This therapy can be applied alone or in combination with glucocorticoids, and the combination can increase the efficacy. The combination of the two reduces the incidence of temporary exacerbations with radiation therapy alone and the recurrence rate with discontinuation of glucocorticoid therapy alone. The combination of glucocorticoid therapy can reduce the orbital and conjunctival edema caused by radiation therapy, which can cause increased inflammation in the orbit within 1 week. The method used nowadays is unilateral irradiation using a linear gas pedal releasing 4-6 MV of energy. The irradiation field includes the entire orbit and orbital apex, avoiding the crystalline lens anteriorly and the pituitary region posteriorly. Radiation therapy is very effective in relieving the patient's inflammatory symptoms, which tend to subside within 2-4 wk after radiation therapy. The relief of other signs is incomplete and sometimes uncertain. We know that cases with poor efficacy of hormonal therapy are often insensitive to radiation therapy as well. 3. Decompression surgery: The aim is to remove the orbital wall and/or retrobulbar fibrofatty tissue and increase the orbital volume. Indications include optic neuropathy that may cause loss of vision; recurrent subluxation of the eye resulting in pulling the optic nerve may cause loss of vision; severe protrusion of the eye causing corneal damage. Complications are that the surgery may cause diplopia or aggravate diplopia, especially in those with extended surgical resection. 4. Control of hyperthyroidism: Three recent clinical studies have confirmed that radical treatment of hyperthyroidism can improve the therapeutic effect of GO. In addition, 131 iodine treatment of the thyroid gland under glucocorticoid protection is now allowed. However, hypothyroidism can aggravate GO, so regardless of the method used, controlling hyperthyroidism and maintaining normal thyroid function is beneficial for GO. 5. Smoking can aggravate the disease and smoking should be stopped. We should actively treat active GO and choose the appropriate regimen by taking different modes and routes of administration according to the severity.