Diagnosis and treatment of thyroid-related ophthalmopathy (hyperthyroidism and proptosis)

   What is thyroid-associated ophthalmopathy?  Thyroid-associated ophthalmopathy (TAO), also known as Graves’ ophthalmopathy, is an atopic autoimmune disease that involves both the thyroid gland and the orbit, and is the most common orbital disease, accounting for 20% of adult orbital disease.  TAO is closely associated with thyroid disease. Approximately 25-50% of patients with Graves’ hyperthyroidism have a combination of ocular symptoms, and this percentage can be as high as 90% if an MRI or CT examination of the eye is performed. In addition, it can also be seen in patients with Hashimoto’s thyroiditis and hypothyroidism.   What are the clinical manifestations of thyroid-related ophthalmopathy?  Patients often have complaints of foreign body sensation in the eye, distension, photophobia, tearing, diplopia, strabismus, and even loss of vision. Typical signs include eyelid recession, late upper lid drop, eyelid swelling, conjunctival congestion and edema, protrusion of the eye, limited eye movement, or in severe cases, fixation of the eye, incomplete eyelid closure, corneal ulceration due to corneal exposure, total uveitis, and even blindness.  What tests are needed to diagnose thyroid-related ophthalmopathy?  Thyroid function tests, including TT3, TT4, TSH, and thyrotropin receptor antibodies (TRAb).  Imaging examinations, there are orbital MRI and CT examinations. MRI can image in three sections and has better resolution than CT for soft tissues such as orbital contents and optic nerve without radiological damage. MRI can also help determine the activity of the disease and guide treatment.   What are the diagnostic criteria for thyroid-related ophthalmopathy?  If there are symptoms of receding eyelids, combined with abnormal thyroid function or protruding eyes with protrusion greater than or equal to 18 mm, or optic nerve dysfunction, including decreased visual acuity and abnormal visual fields, or extraocular muscle involvement with limited eye movement and hypertrophy of the extraocular muscles on imaging.  If there are no symptoms of eyelid regression, thyroid function abnormalities are required and combined with ocular protrusion, or extraocular muscle involvement, or optic nerve function involvement.  What is the active stage of thyroid-related ophthalmopathy and what does it mean?  The active stage of TAO is closely related to the choice of treatment plan and the outcome of treatment. The active stage has obvious effect of medical treatment, while the stable stage has poor effect of medical treatment, and surgical treatment is preferred. However, the active stage varies widely among individuals, generally ranging from 6 months to 24 months, and is not characterized by specific signs and symptoms. Clinically, there are no satisfactory tests with high specificity to help determine activity, except for orbital histopathological biopsy. Because pathological biopsy is dangerous and not easily accepted by patients, how to objectively and accurately stage the activity of TAO is currently a hot spot and a difficult area of research in thyroid-related eye disease.  Prevention of thyroid-related ophthalmopathy The prevention of TAO is determined based on a combination of the degree of the patient’s disease and the stage of disease activity. In mild TAO, local treatment and normalization of thyroid function is the main focus. This includes wearing tinted glasses to reduce photophobia and blindness, using artificial tears and covering the cornea at night to eliminate foreign body sensation and protect the cornea, elevating the head of the bed to reduce periorbital edema, and wearing glasses to correct mild diplopia. Restoring normal thyroid function is fundamental. Smoking patients should quit smoking.  For moderate to severe TAO, intensify treatment on top of the above basic treatment. Patients in the active phase, the main treatment methods are: 1. Glucocorticoids: can be given by oral or intravenous route, the latter effect is better than the former (the latter efficiency is 80-90%, the former is 60-65%), but can lead to significant side effects and adverse reactions, including hypokalemia, Cushing’s syndrome, steroidal diabetes or aggravation of pre-existing diabetes, gastric ulcer, osteoporosis increased intraocular pressure, and decreased immunity. Methylprednisolone shock therapy can cause severe toxic liver damage.  2, linear gas pedal therapy: indications and glucocorticoid therapy is basically the same. The efficiency is 60-80%, better for recent soft tissue inflammation and recently occurred eye muscle dysfunction. 20Gy fractionated irradiation, small side effects, easy to tolerate by patients. Diabetes and hypertensive retinopathy are contraindications. This therapy can be applied alone or in combination with glucocorticoids, and the combination can increase the efficacy.  Patients in the stable stage or patients with severe proptosis causing exposure keratitis may opt for surgical treatment, including eyelid suturing, eyelid orthopedic surgery, and orbital decompression.