Diabetic retinopathy is the most important manifestation of diabetic microangiopathy, a fundus lesion with specific changes, and is one of the serious complications of diabetes mellitus. Clinically, diabetic retinopathy without retinal neovascularization is called nonproliferative diabetic retinopathy (or simple or background type) according to whether retinal neovascularization is present as a marker, while diabetic retinopathy with retinal neovascularization is called proliferative diabetic retinopathy. I. Epidemiology The occurrence of diabetic retinopathy is closely related to the duration and degree of control of diabetes mellitus, but not much related to the age of onset, gender and type of diabetes mellitus. The longer the duration of diabetes, or the poorer the glycemic control, the higher the incidence of diabetic retinopathy. In general, about 25% of diabetic patients have diabetic retinopathy and about 5% have proliferative lesions. Its incidence is 7% in the group with diabetic disease duration <10 years, 26% in the group with 10-14 years, 63% in the group with more than 15 years, and up to 95% in the group with 30 years. About 25% have proliferative lesions, and 2% to 7% are blinded by retinopathy. Diabetic retinopathy is one of the serious eye complications of diabetes and is the leading cause of blindness in adults of working age, with 1 in 3 legally blind adults going blind due to diabetic retinopathy, and the risk of blindness is 25 times higher in diabetics than in normal people. According to the American Diabetes Association (ADA) in 2003, 21% of first-time patients with type 2 diabetes have retinopathy, and 70% of type 2 diabetes will eventually develop proliferative retinopathy, which has a very high rate of blindness. Therefore, epidemiological investigation, early screening, prevention and intervention of diabetic retinopathy are important aspects to improve the quality of life of diabetic patients. II. Etiology Diabetic patients mainly suffer from abnormal insulin and cellular metabolism, causing changes in the nerve and vascular microcirculation of ocular tissues resulting in damage to the nutrition and visual function of the eye. The blood-retinal barrier is damaged due to the abnormal function of vascular endothelial cells caused by the change of blood composition in diabetic patients. The connections between retinal capillary endothelial cells and pigment epithelial cells are disrupted, resulting in leakage of small vessels. The pathogenesis of diabetic retinopathy is still not fully understood. Diabetic retinopathy has five basic pathological processes: 1) formation of retinal capillary microaneurysms; 2) increased vascular permeability; 3) vascular occlusion; 4) proliferation of neovascular and fibrous tissue; and 5) contraction of the fibrovascular membrane. The clinical signs of a specific patient with diabetic retinopathy depend on the relative manifestations of these 5 processes. Clinical manifestations In the early stage of retinopathy, there are usually no ocular conscious symptoms. As the disease progresses, it can have different manifestations. Retinal edema can cause light scattering and make patients have a sense of flash in front of the eyes; macular edema, ischemia or exudation involving the central recess can cause different degrees of vision loss with large vision, small vision, colored vision, visual distortion, etc.; small retinal artery rupture, a small amount of bleeding into the vitreous can make patients feel a black shadow floating in front of the eyes; neovascularization, vitreous hemorrhage or proliferative vitreoretinopathy and traction Retinal detachment can lead to severe loss of vision. The basic clinical fundus manifestations of diabetic retinopathy are retinal capillary microangioma formation, vascular dilatation, wall leakage causing retinal edema, exudation, hemorrhage and then capillary and small artery occlusion, retinal ischemia, and retinal neovascularization. The neovascularization causes massive hemorrhage in the retina and vitreous. With the proliferation of fibrous tissues, proliferative vitreoretinal lesions are formed and tractional retinal detachment occurs. V. Diagnosis 1. Medical history: Detailed medical history is essential. In addition to the presence of typical diabetic manifestations such as polyphagia, polyphagia, polyuria and wasting, attention should be paid to the duration of diabetes. The longer the duration of the disease, the higher the incidence and more severe the degree of diabetic retinopathy. In particular, the time of discovery of diabetes in some diabetic patients does not represent the true duration of the disease, because the systemic symptoms are not obvious and the actual duration of the disease is often long when diabetes is discovered. Blood glucose and urine glucose tests are an important basis for understanding the degree of control of diabetes. 2. Fundus examination: Fundus examination is the main means to diagnose diabetic retinopathy. Microaneurysms and small hemorrhagic spots are always the earliest and more definite signs of retinopathy. Waxy, hard, yellowish-white exudative spots indicate abnormal function of the vascular system, increased permeability, and escape of blood components. In contrast, white soft exudate indicates severe microcirculatory disturbances and vascular destruction. There is no neovascularization at this stage, so it is called simple lesion. As the disease progresses, multiple focal or extensive retinal nonperfusion complicating this stage is indicative of neovascularization soon. From the onset of neovascularization, the proliferative phase is entered, indicating that the retinal circulation is no longer compensatory for tissue hypoxia. Diabetic retinopathy has certain subclinical changes such as abnormal fluorescence pattern, retinal electrophysiology and visual contrast sensitivity before the appearance of lesions in the fundus, which are of reference value for its early diagnosis. During the progression of the lesion, various special manifestations of fundus fluorescence angiography are of great significance for the diagnosis and staging of the disease.