Treatment of diabetic retinal disease by
1.Drug treatment
(1) Long-term control of diabetes mellitus
The fundamental treatment of diabetic retinopathy is the treatment of diabetes mellitus. In principle, blood glucose should be controlled to normal or near normal level first and often.
(2) Lowering blood lipids
For diabetic patients with high blood lipids and cyclic hard exudates in and around the retinal macula, they should consume a low-fat diet and apply lipid-lowering drugs: e.g. heparin and clobetasol. Heparin lowers lipids by activating lipoprotein esterase, and it also lowers lipid storage in the retina, and clofibrate has a similar effect. It has been reported that taking clofibrate 4 times/day can reduce retinal exudation and improve visual acuity.
(3) Blood pressure control
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 hypertensive disease. Oral administration of angiotensin-converting enzyme inhibitor captopril twice/day has a mitigating effect on diabetic retinopathy, which may be related to its anti-hypertensive effect.
(4) Conductin
It has been said that the “three high” factors that cause diabetic retinopathy, namely high capillary permeability, high blood viscosity and high platelet activity, are significantly inhibited and reversed by conoximin (calcium 2,5-dihydroxybenzenesulfonate).
(5) Aspirin
It can inhibit the production of thromboxane and prostaglandin metabolites, inhibit platelet agglutination, and have a certain preventive effect on microthrombosis. 1 time/day, orally, to prevent the occurrence of retinopathy. However, 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. A complete and clear fundus photograph and fundus fluorescence angiogram are required before photocoagulation treatment to understand the condition and 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 treatment
Condensation is mainly used for patients who are not suitable for photocoagulation or as a complementary therapy to photocoagulation, such as patients with refractive interstitial opacities or retinal peripheral lesions that cannot be treated by photocoagulation. The method is circumferential condensation on 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.
5.Pituitary gland removal
Based on the theory that growth hormone is associated with diabetic retinopathy, a variety of pituitary suppression methods have been used over the years, ranging from external radiation to transfrontal pituitary removal. Currently, pituitary removal is becoming a thing of the past as photocoagulation has become increasingly effective. The significance of pituitary removal for the treatment of diabetic retinopathy may only be in contributing to our further understanding of the pathogenesis of the disease.