Thyroid-associated ophthalmopathy, also known as GraveS ophthalmopathy, infiltrative proptosis, and thyroid-associated immuno-orbital disease, is the most common cause of ocular protrusion in adults in one and both eyes. Clinically, thyroid-related ophthalmopathy can be divided into two types: type I is mostly seen in females, with symmetric proptosis and eyelid regression, mild inflammation of orbital and extraocular muscles, and moderate muscle hypertrophy; type II has obvious inflammation of extraocular muscles and orbits, often with bulbar conjunctival edema, obvious and asymmetric hypertrophy of extraocular muscles, and is often accompanied by compressive optic neuropathy and diplopia. I. Etiology of thyroid-related ophthalmopathy The exact pathogenesis is unclear, and most scholars believe that it is a cell-mediated autoimmune disease, and that the thyroid gland and the orbit may be the same tissue organs that are secondary reactions to the immune system lesions. Clinically, thyroid function tends to be hyperactive, but can also be hypo- or normal, post-disease. The pathological changes of thyroid-related ophthalmopathy are mainly extraocular muscle edema, lymphocyte infiltration, muscle degeneration and necrosis and fibrosis, active fibroblasts in the orbital retrobulbar fat and connective tissue, mucopolysaccharide deposition and edema. Symptoms of thyroid-related ophthalmopathy The lesions of thyroid-related ophthalmopathy mainly damage the levator ani muscle and extraocular muscle, and the following are common: ① eyelid regression, especially the most common eyelid regression, which is characterized by the widening of the eyelid fissure, exposure of the upper edge of the cornea and the upper sclera. When the eyeball looks down, the upper eyelid does not move down with the eyeball, called eyelid lag. (ii) eyeball protrusion, diplopia and limited eye movement, mainly due to extraocular myopathy, early hypertrophy and edema, cellular infiltration, often accompanied by bulbar conjunctival congestion, late degeneration and fibrosis, limiting eye movement. The first involved is often the lower rectus muscle, followed by the inner rectus muscle, and then the upper rectus muscle, and the outer rectus muscle is the least common. ③ Optic neuropathy, excessive hypertrophy of extraocular muscles in the orbital tip can compress the optic nerve, resulting in visual function damage or even loss. ④ Exposure keratitis and corneal ulcer, eyeball protrusion and eyelid regression and lagging can cause difficulty in lid closure, leading to exposure keratitis and corneal ulcer, which also seriously threaten vision. Third, the examination of thyroid-related ophthalmopathy 1, laboratory tests The state of thyroid function is closely related to TAO, so it is important to understand the status of thyroid function for the diagnosis of TAO.There are a variety of laboratory tests for TAO, such as basal metabolic rate (BMR), serum thyroid-stimulating hormone (TSH) measurement, serum total T3, total T4 (TT3, TT4) and free T3, Free T4, Free T4 Index (FT3, FT4, FT4I), Radioactive Iodine Uptake (RAIU) test, T3 suppression or Werner suppression test, Thyrotropin-releasing hormone (TRH excitotoxicity) test, and Antibody Tests for TAO (Thyroid Stimulating Antibodies, Anti-Thyroid Microparticulate Antibodies, Thyroid-Stimulating Hormone Receptor Antibodies), each test from a side It is necessary to understand the advantages and disadvantages and clinical significance of these tests, so as to select the necessary tests according to the specific conditions of the patients and improve the diagnosis rate. 2.Orbital CT examination CT scanning examination Modern CT scanning has high resolution, which can clearly show the soft tissues and orbital bones in the orbit, and it plays a significant role in the diagnosis of TAO, and it is a kind of routine examination for TAO, and the commonly used examination methods are horizontal scanning, coronal scanning and sagittal scanning. The most prominent CT feature of TAO is bilateral hypertrophy of multiple extraocular muscles, and it is generally believed that the inferior rectus muscle is the most susceptible to involvement, followed by the medial rectus, superior rectus and lateral rectus muscles. All involved extraocular muscle bellies were hypertrophied and the tendons were unaffected so that the anterior end of the muscle tapered. Generally the hypertrophied extraocular muscles had clear borders and the lesions were mainly concentrated within the muscle. However, in acute infiltrative TAO, inflammatory cells can go beyond the extraocular muscle to the orbital fat, or excessive hyaluronic acid deposition between the muscle fiber bundles causing muscle edema, so the hypertrophied extraocular muscle edges are not clear, the density is uneven, and some of them are nodular changes. 3, ultrasonography ultrasonography is an effective method to diagnose TAO, can show and measure the hypertrophy of extraocular muscle, and more accurate, is an objective method of examination. type B ultrasonography shows that the thickened extraocular muscle is hypoechoic strip lesion, the border may not be clear. type A ultrasonography can measure the thickness of extraocular muscle. A-mode ultrasound can measure the thickness of extraocular muscle, the disadvantage is that ultrasound can not show the lesions in the posterior orbital region and orbital bone, and CT scan can show the intraorbital lesions and their relationship with the surrounding structures better than ultrasound examination. 4, magnetic resonance imaging and CT examination, MRI examination also take horizontal, coronal, sagittal scan. Magnetic resonance imaging can not only show extraocular muscle hypertrophy, but also provide objective evidence for assessing the active or quiescent phase of TAO, which is helpful for planning TAO immunosuppressive therapy.When TAO has no clinical symptoms, MRI can also show some changes in extraocular muscle. 5, eye pull test This test plays an important role in identifying TAO restrictive extraocular myopathy and other causes of abnormal eye muscle function. The test is done under general anesthesia in children, and adults can be examined on an outpatient basis under local surface anesthesia. 6. Intraocular pressure examination The rotation of the eyeball in the direction opposite to that of the affected muscle may cause an increase in intraocular pressure. In some patients with hyperthyroidism without eyeball protrusion, the intraocular pressure is higher than normal when the eyeball is in its original position. Examination method: when the eyeball looks downward, the inferior rectus muscle does not contract and compress the eyeball, measure the intraocular pressure; when the eyeball is in its original position or when the eyeball is turned upward by 10°～15°, measure the intraocular pressure again, if the difference between the two intraocular pressures is more than 4mmHg, it is positive, indicating that there is restrictive extraocular myopathy. Diagnosis of thyroid-related ophthalmopathy Thyroid-related ophthalmopathy can be diagnosed according to the typical clinical ocular manifestations, and CT examination confirms hypertrophy of extraocular muscles without tendon involvement, which can help to confirm the diagnosis. Treatment of thyroid-related eye disease The treatment of thyroid-related eye disease includes protective eye treatment, anti-inflammatory treatment, radiotherapy and surgery. Eye drops or ointment are used to protect the cornea and relieve exposure keratitis. In acute inflammation of the orbit, systemic application of glucocorticoids or immunosuppressants can control the damage to the extraocular muscles and reduce edema as well as the compression of the optic nerve. Eye deviation that has been stabilized for six months or more can be improved by local injection of botulinum toxin A into the extraocular muscles or by extraocular muscle surgery to improve diplopia. Thyroid-related ophthalmopathy can also be treated with radiation therapy or orbital decompression surgery for severely protruding eyes or eyes with compressive optic neuropathy, or when drug therapy is ineffective. Prevention of thyroid-related ophthalmopathy Actively adjust the level of thyroid hormone to maintain it in the normal range, and avoid sudden reduction or increase in the dosage of drugs. Avoid spicy and stimulating food, quit smoking, prevent eye fatigue, wear sunglasses when encountering strong light, avoid emotional excitement. Avoid emotional stress. Sleep with the head in a high position, and apply ophthalmic ointment or wet room to protect those with incomplete lid closure.