Corneal changes: Fuchs endothelial dystrophy has a typical shattered silvery appearance of the central posterior cornea, often called corneaguttata. The incidence increases significantly with age. Many patients with dropsy corneas have otherwise normal corneal performance and do not affect their vision. In a small number of patients, corneal stromal and epithelial edema occurs, which can cause significant vision loss. What are the easily confused symptoms? 1, ICE syndrome In Fuchs endothelial dystrophy is bilateral and does not have the atrial angle and iris changes of ICE syndrome. 2, PPMD In Fuchs endothelial dystrophy is rarely seen with bridge-like iris corneal adhesions, iris changes and posterior corneal irregularities characteristic of PPMD. Fuchs endothelial dystrophy has a typical silvery appearance of the central posterior cornea, often called “corneaguttata”. The clinical course is usually 10 to 20 years and can be divided into 3 stages. In the first stage, the patient is asymptomatic, with irregularly distributed punctate redundancies and dusty pigment dots in the posterior central cornea. Subsequently, the posterior elastic layer may be gray and thickened. In stage 2, corneal stroma and epithelium become edematous and the patient has blurred vision and a dazzling sensation. The stromal edema initially appears in front of the posterior elastic layer and immediately in front of the anterior elastic layer, after which the entire stroma gradually becomes hairy and fluid-laden fissures appear in the swelling, causing folds to form in the posterior elastic layer. The epithelial edema initially gives the corneal surface a pigskin-like appearance or appears to be sprinkled with small drops of water, and then gradually forms large ovoid or curved subepithelial vesicles that cause episodic pain when ruptured. As a result of stromal blurring and irregular astigmatism, vision decreases dramatically. Visual acuity is particularly poor upon awakening, as the decrease in tear volatilization during sleep reduces its permeability, resulting in increased corneal edema. In stage 3, subepithelial connective tissue appears and epithelial edema decreases, and visual acuity is more comfortable than before, although it is extremely poor and reduced to only manual discernment. Complications such as epithelial detachment, microbial ulcers, peripheral neovascularization, and increased intraocular pressure may occur during this stage. Slit-lamp examination of the cornea begins centrally and gradually expands peripherally. From the posterior to the anterior aspect of the cornea, the following changes may occur: punctate corneal degeneration with thickening and wrinkling of the posterior elastic layer; endothelial pigmentation; stromal edema with subepithelial connective tissue and superficial neovascularization in the periphery; epithelial edema and large vesicles. The prominent change is a silver foil-like (beatensilver) appearance of posterior central corneal degeneration, with changes similar to those seen in ICE syndrome, but rougher. The most striking pathologic histologic change is located posterior to the posterior elastic lamina, where endothelial cells produce new collagenous tissue, which clinically manifests as a thickening of the posterior elastic lamina. The posterior elastic lamina forms a multilamellar structure with the new collagen tissue, which appears as a thick and light layer on PAS staining and produces the gray disc-like pattern seen clinically. Fuchs endothelial epithelial dystrophy can be associated with two types of glaucoma: open-angle glaucoma and closed-angle glaucoma, with an estimated incidence of 10% to 15%. The mechanism of their open-angle glaucoma occurrence may be related to trabecular endothelial network involvement. Acute angle-closure glaucoma occurs when the corneal parenchyma gradually thickens in shallow anterior chamber and Fuchs’ dystrophy, resulting in complete closure of the iridocorneal angle. In many cases, closure of the atrial angle occurs before the onset of corneal edema. The mechanism of glaucoma in these cases is related to hyperopia and shallow anterior chamber, and may also have some association with Fuchs’ dystrophy. Fuchs dystrophy differs from ICE syndrome in terms of the mechanism of glaucoma development.