The pathological basis of thyroid-related ophthalmopathy is an autoimmune process that can cause soft tissue edema within the orbit, resulting in impaired venous return to the cavernous sinus and, in turn, back to the facial circulation. The positive feedback loop process leads to an increase in orbital pressure and the typical signs of ophthalmopathy. Any procedure aimed at reducing orbital pressure by enlarging the bony orbital cavity and/or reducing orbital fat is orbital decompression surgery. Orbital decompression surgery has been used for a century as a treatment for thyroid-related ophthalmology. Initially, it was used only to treat vision-threatening thyroid-related eye disease, such as optic neuropathy that is difficult to control medically, or exposure keratitis where topical treatment and/or simple eyelid surgery has not been effective. In recent years, the indications for orbital decompression surgery have gradually expanded to include disfiguring ocular proptosis and related signs. Acute optic neuropathy and exposure keratopathy with possible etiology of ocular subluxation, postural blurring of vision in resting congestive thyroid-related ophthalmopathy, and choroidal folds due to compression of the eye by enlarged extraocular muscles are functional indications for orbital decompression surgery that have only been recognized in recent years. Protruding eyes, widened lid fissures, altered blink frequency, receding eyelids, incomplete eyelid closure, impaired upturning and lack of Bell’s phenomenon in patients with thyroid-related ophthalmopathy can all contribute to dry eye. In the active phase, reduced tear production due to autoimmune lacrimal gland damage is closely associated with ocular surface damage. Additional studies have shown that for a short period of time, lacrimal gland secretion is normal in patients with thyroid-related ophthalmopathy, and that proptosis, lid retraction, and incomplete lid closure are not associated with ocular surface damage, which is mainly associated with lid widening. Widening of the lid fissure can cause excessive evaporation from the ocular surface, resulting in increased tear film permeability and pathological changes similar to those seen in dry keratoconjunctivitis. Orbital decompression surgery, which reduces the lid fissure width, improves the abnormal upper and lower lid position in approximately 50% of patients undergoing orbital decompression surgery. The role of orbital decompression surgery in the treatment of severe corneal damage is inconclusive. Although most studies confirm that orbital decompression surgery can improve the symptoms of exposure keratitis, there are also severe corneal ulcers that are refractory to orbital decompression surgery. Ocular subluxation is a rare complication (0.1%) of thyroid-related eye disease that can cause severe visual impairment and requires early management by a specialized orbital surgeon. Ocular subluxation occurs in thyroid-related eye disease type I (fatty type) and not in type II (muscle thickening type). Ocular subluxation causes stretching of the extraocular muscles and orbital bone wall decompression or/and orbital fat decompression should be effective for vision threat. In resting congestive thyroid-related ophthalmopathy, there is critical optic nerve perfusion: blood flow is just able to maintain optic nerve function. The critical perfusion pressure causes patients to be prone to transient postural hypotension with recurrent episodes of blurred vision. Diabetic patients are more prone to postural hypotension. Orbital decompression surgery can effectively address the optic nerve vascular distress caused by high orbital pressure, while aborting postural blurred vision. Serious complications of thyroid-related ophthalmopathy are rare, while signs of varying degrees of venous congestion, strabismus, eyelid edema and regression, protrusion of the eyeball, periorbital pain, and foreign body sensation are relatively common. Orbital decompression surgery is the mainstay of treatment for disfiguring changes and signs that are stable in the resting phase. Orbital decompression surgery is not mandatory and is only necessary when the protrusion of the eye is beyond the normal reference range. Even a normal degree of ocular prominence can cause serious cosmetic problems if a patient with thyroid-related ophthalmopathy has a flat forehead combined with rare brow bone elevation or zygomatic elevation, or if the patient has deep sunken eye sockets themselves. Therefore, it is critical to assess the patient’s pre-onset cosmetic picture to ensure that the patient can regain as normal an appearance as possible before the onset of the disease. Most patients with thyroid-related ophthalmopathy with orbital decompression have significant relief of periocular pressure. As early as the 1990s, it was demonstrated that orbital decompression surgery significantly improved orbital discomfort in thyroid-related eye disease using the McGill Pain Questionnaire and the Visual Acuity Questionnaire. In summary, indications for orbital decompression surgery include: 1) vision-threatening thyroid-related ophthalmopathy, such as optic neuropathy that is difficult to control medically or exposed keratitis where local treatment and/or simple eyelid surgery is ineffective; 2) disfiguring eye protrusion and related signs; 3) functional indications, such as subluxation, postural blurring of vision in resting congestive thyroid-related ophthalmopathy, enlarged extraocular muscles choroidal folds caused by extrusion of the eye.