Ocular atrophy is a degenerative disease of the eye tissue secondary to various serious eye diseases, characterized by softening and shrinking of the eye and loss of visual function. Severe ocular trauma, intraocular inflammation, tumors, massive vitreous hemorrhage, retinal detachment and glaucoma can cause ocular atrophy. Clinical manifestations: early eye softening, lowering of intraocular pressure, refractive interstitial clouding, and further diminution of visual function until complete loss. In the late stage, the volume of the eye shrinks, the cornea is smaller than normal and is cloudy with banding degeneration, and there may be calcification on it. In post-traumatic eye atrophy, the cornea or sclera is often deformed due to scar contraction. If the cornea is still transparent, the anterior chamber depth is abnormal or disappears, the iris is atrophied, pre-machine adhesions or with neovascularization, the pupil is small and irregular, often with posterior adhesions or membrane formation, the lens is cloudy and the fundus cannot be seen. Imaging: In early atrophy, the shape of the eye does not change much. Due to low intraocular pressure, B-mode ultrasonography compresses the eye, revealing a shortening of the eye axis, thickening of the eye wall, and sometimes visible vitreous clouding mechanization and old retinal detachment. In advanced stage of atrophy, ultrasound shows wrinkled eye and disorganized internal structure; in case of choroidal calcification and ossification, irregularly shaped band-like echoes followed by acoustic shadow are visible. CT shows smaller and deformed eye volume, increased density and thinning of optic nerve. Treatment: Most of the visual functions of the atrophic eye have been lost or nearly lost, and it is impossible to restore its visual function. The main purpose of treatment is to relieve pain and discomfort, prevent sympathetic ophthalmia and improve the appearance. For patients who have no value in preserving the eye and have frequent congestion and pain, eye removal is feasible; for patients who wish to restore the aesthetic appearance of the eye, eye removal combined with mobile eye seat implantation and then wearing a suitable prosthetic eye is the most ideal treatment option at present. Eye Seat I Implantation: For patients who have had their eyeballs removed or eye contents removed for various reasons, but is contraindicated for intraocular tumors or intraocular infectious diseases. After removal of the eye, a sterile steel ball is placed in the muscle cone to estimate the size of the orbital cavity and the absence of orbital contents in order to select the appropriate size of the eye seat; the eye seat is then drilled and prefabricated with sutures, implanted in the muscle cone and fixed to the rectus muscle, and the incision is finally closed in layers. The eye content is removed and the eye seat is implanted in stage I. The cornea is removed circumferentially along the corneoscleral margin, then the intraocular uvea is removed, the optic nerve is cut, and windows are made in the sclera next to the ends of the four rectus muscles, and the corresponding size eye seat is implanted in the scleral cavity, and then the incision is closed in layers. All postoperative procedures require placement of a thin prosthetic eye in the conjunctival sac, application of antibiotic eye ointment, and pressure bandaging for 1 week. Eye seat stage II implantation: For patients whose eyes have been removed without eye seat implantation and who still have a sunken supraorbital area after wearing a prosthetic eye; for patients whose previously implanted eye seats are exposed and need surgical replacement; for patients whose implanted eye seats are not the right size. The procedure is contraindicated in patients with active orbital infections, or in patients with recurrent intraorbital malignancies. In stage II eye seat implantation, because the patient has already undergone prior removal of the eye, the four external rectus muscles have lost their attachment to the eye and have retreated deeper into the orbit, thus making it more difficult to find the muscles. The key to ocular seat stage II implantation is to find the four rectus muscles, which not only ensures that the seat is implanted in the correct anatomical position, but also maximizes its mobility and the shape of the prosthetic eye. Scleral-less eye seat stage II implantation: The conjunctiva and Tenon’s capsule are incised in layers, the extraocular muscles are searched for and pre-set sutures are made, then the appropriate size eye seat is selected, the eye seat is drilled and threaded and implanted into the muscle cone, the extraocular muscles are fixed and the wound is closed in layers. If the conjunctival sac is normal in size, a thin prosthetic eye should be placed immediately after stage II implantation, with antibiotic eye ointment and pressure bandage for 1 week. If the conjunctival capsule is narrow, reconstructive conjunctival capsuloplasty should be performed 3-6 months after surgery.