Diabetes mellitus is a disorder of glucose metabolism that affects all organs and tissues and blood vessels of the body, of which diabetic retinopathy (referred to as glycosuria) is the most serious ocular microvascular complication of diabetes mellitus and has become one of the major blindness-causing eye diseases worldwide. Its incidence is related to the duration of diabetes, age of onset, genetic factors and glycemic control. The longer the duration of the disease, the higher the incidence. In patients diagnosed with diabetes before the age of 30, the incidence of glucose network is about 50% after 10 years and up to 90% after 30 years. About 10% of diabetic patients develop fundopathy about 5 to 9 years after the onset of the disease. Blood glucose control also affects how early or late the onset of glucose reticulum occurs. Obesity, smoking, hyperlipidemia, pregnancy, hypertension, and kidney disease can aggravate the condition of the glycoplasmic reticulum. With the dramatic increase in the number of diabetic patients worldwide in recent years, the number of blindness due to diabetic retinopathy is also on the rise. In the early stages of the disease, there are usually no obvious ocular symptoms. As the disease progresses, it can cause varying degrees of visual impairment, visual distortion, floating black shadows in front of the eyes and visual field defects, which can eventually progress to blindness. Since most of the symptoms are painless and progressive, they are often overlooked and many patients are already in advanced stages when they are seen. In 1984, the National Conference on Fundus Disease divided it into two types. One of them, the simple type, has microaneurysms, intraretinal microhemorrhages, hard or soft exudates, and retinal edema as the main manifestations on examination of the glycosuria. As the disease worsens, neovascularization grows on the retinal surface in and around the fundus optic disc or along the fundus vascular arch, marking the progression of the glycogenic retinal changes to the proliferative type. This neovascularization not only causes bleeding in the front of the retina or vitreous, but more seriously, it also grows into the vitreous and shrinks together with its surrounding fibrous proliferative membrane, causing traction retinal detachment, which can lead to blindness. The first thing to emphasize in the prevention and treatment of glucose retinal is the control of blood glucose. On this basis, regular eye examinations are required, especially regular dilated fundus examinations and, if necessary, fundus fluorescence imaging to detect early lesions. In terms of treatment, for early simple lesions, fundus laser retinal photocoagulation can be used, i.e., focusing the laser beam on the retinal lesion tissue to destroy the non-perfused peripheral retinal tissue to reduce oxygen consumption on the one hand, and destroy the neovascularization and close the leaking vessels to improve the supply of normal retinal blood flow on the other. For a small amount of fundus hemorrhage, oral or injectable drugs can be given to promote clot absorption, and then laser coagulation treatment can be given when the hemorrhage subsides and the fundus can be seen clearly. For patients with extensive hemorrhage that cannot be absorbed within a month, vitrectomy is required to not only remove the hemorrhagic cloudy vitreous to restore the clear refractive media, but also to debulk the fundus neovascular membrane to reduce rebleeding and prevent tractional retinal detachment. However, vitrectomy should be given as soon as possible to calm the retina in patients with hemorrhage with retinal detachment. Whenever surgery is performed, a combined intraoperative and postoperative total retinal laser coagulation is required. With good glycemic control, regular fundus examination, and early and adequate laser coagulation, most patients with glucose retinal detachment have a good prognosis and can preserve useful central vision in the long term. The key is early intervention and long-term follow-up.