The incidence of diabetes is now increasing, and many people are treating their diabetes while neglecting the examination and timely treatment of their eyes, especially the fundus retina, leading to irreversible fundus disease and even blindness. In fact, if the fundus lesions are detected early and the necessary treatments, such as drugs or fundus laser, are taken decisively in the early or just proliferating period, the progression of the disease can be effectively stopped and surgery or even blindness can be avoided. Etiology In diabetic patients, abnormalities in insulin hormone and cellular metabolism cause changes in ocular tissue, nerve and vascular microcirculation, resulting in damage to the nutrition and visual function of the eye. Microvasculature refers to the tiny blood vessels and capillary network between tiny arteries and tiny veins with lumen less than 100-150 μm, which is the place where tissues and blood exchange substances. 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 association between pigment epithelial cells of the retinal capillary endothelium is disrupted, causing leakage from small vessels. Microangiopathy in diabetic patients mainly occurs in the retina and kidney, and is the main cause of blindness, renal failure and death. Clinical manifestations Retinal capillary lesions manifest as microaneurysms, hemorrhagic spots, hard exudates, absorbent cotton spots, vein beading, intraretinal microtunnel abnormalities (IRMA), and macular edema. Extensive ischemia causes neovascularization of the retina or optic disc, preretinal hemorrhage, volumetric blood, and retinal detachment by traction. Patients have severe visual impairment. Diabetes can cause two types of retinopathy, proliferative and non-proliferative retinopathy. Diabetic retinopathy is one of the major blinding eye diseases. In proliferative retinopathy, retinal damage stimulates the growth of new blood vessels. Neovascular growth is detrimental to the retina and can cause fibroplasia and sometimes retinal detachment. Neovascularization can also grow into the vitreous or cause vitreous hemorrhage. Compared with non-proliferative retinopathy, proliferative retinopathy is more harmful to vision and can lead to severe vision loss or even complete blindness. Examination 1. Blood glucose examination: Regular measurement of blood glucose level to monitor the development of diabetes. 2, kidney function test: timely detection of diabetic nephropathy complications. 3.Cholesterol and lipid examination: to detect cholesterol and lipid level. 4.Fundus fluorescence angiography: If diabetic retinopathy has not been detected under fundoscopy, fundus fluorescence angiography can show abnormal fluorescence pattern. Microangiomas are found earlier and much more often under fundus fluorescence angiography than what is seen under fundoscopy. Others, such as capillary dilation, increased permeability, non-perfused areas, arteriovenous abnormalities, exudation and hemorrhage, and neovascularization, have special manifestations on fundus fluorescence angiography. 5. Electroretinogram oscillatory potentials (OPs): OPs is a subcomponent of electroretinogram (ERG), which can objectively and sensitively reflect the state of blood circulation in the inner retinal layer. In eyes without fundus lesions, it reflects the abnormal amplitude of OPs, and in patients with diabetic retinopathy, it further shows the progression and improvement of the disease process. 6.Other examinations: such as visual contrast sensitivity examination, it can be seen that the average contrast sensitivity of medium and high spatial frequency is significantly reduced in early patients; the application of color Doppler flow imaging technology can reveal the hemodynamic changes of the posterior bulb artery of patients, which shows low flow rate, low flow rate and high resistance type changes; blood viscosity test can show an increase in viscosity; serum SOD vitality test can show a decrease in vitality, etc. Treatment 1, drug treatment (1) long-term control of diabetic retinopathy is the fundamental treatment of diabetes. In principle, blood glucose should be controlled to normal or near normal level first and often. (2) Reduce blood lipids For diabetic patients with high blood lipids and ring-shaped hard exudates in and around the retinal macula, a low-fat diet should be consumed and lipid-lowering drugs should be applied: such as heparin and clobetine. Heparin lowers lipids by activating lipoprotein esterase, and it also lowers lipid storage in the retina, and clofibrate has a similar effect. (3) Control blood pressure Elevated blood pressure can aggravate diabetic retinopathy. When hypertension is controlled, fluorescence leakage is significantly reduced, so blood pressure should be controlled in patients with diabetes combined with hypertension. Captopril, an oral angiotensin-converting enzyme inhibitor, has a mitigating effect on diabetic retinopathy, which may be related to its anti-hypertensive effect. (4) Guoxin (calcium 2,5-dihydroxybenzenesulfonate) is said to have a significant inhibitory and reversal effect on the “three high” factors that cause diabetic retinopathy: high capillary permeability, high blood viscosity and high platelet activity. (5) Aspirin can inhibit the production of thromboxane and prostaglandin metabolites, inhibit platelet agglutination, and have a certain preventive effect on microthrombosis, but it has been reported that aspirin does not slow down the progression of retinopathy in clinical practice. 2, photocoagulation therapy Laser therapy is considered to be an effective method for treating diabetic retinopathy. Clinical trials have demonstrated that photocoagulation therapy has beneficial effects on the pathogenesis of the disease in 2 ways: first, by causing degeneration of neovascularization and preventing their regeneration; and second, by reducing macular edema. Complete and clear fundus photography and fundus fluorescence angiography should be available before photocoagulation to understand the condition and the location of the lesion in detail. After photocoagulation, regular follow-up and review should be made to understand the efficacy, and if new lesions appear, additional photocoagulation treatment can be considered. 3.Condensation therapy Condensation is mainly used for patients who are not suitable for photocoagulation therapy or as a complementary therapy to photocoagulation therapy, such as patients with refractive interstitial opacities or retinal peripheral lesions that cannot be treated by photocoagulation. The method is circumferential condensation of the conjunctival or scleral surface between the serrated edge and the vascular arch. 4, vitrectomy For diabetic retinopathy, the basic indications for vitrectomy are vitreous hemorrhage and severe proliferative lesions. It is generally believed that vitrectomy is required for those with extensive vitreous hemorrhage that cannot be spontaneously absorbed for more than 3 months.