Proceedings PaperLaser photocoagulation stops diabetic retinopathy by controlling lactic acid formation
|Format||Member Price||Non-Member Price|
|GOOD NEWS! Your organization subscribes to the SPIE Digital Library. You may be able to download this paper for free.||Check Access|
Many different types of proliferative retinopathy induced by various types of initial disorders have a common pathology in their mid and terminal stages. Thus, proper therapy is devoted toward elimination of the initial cause as well as alleviation of the proliferative processes. Vasodilatation, which is an initial symptom of diabetes, is itself destructive to the retinal capillary bed and appears to be a constant feature in all stages of diabetic retinopathy. In the mid and late stages, the vasodilatation seems very dependent upon capillary dropout, whereas the initial vasodilatation may derive from quite different causes. The efficacy of photocoagulation as a therapy for all stages seems to derive from decreasing the metabolism in the photoreceptor layer sufficiently to result in vasoconstriction of the retinal vessels. A model is proposed to show how diabetes, by altering the metabolism in the photoreceptor layer to produce excess lactic acid, causes the initial vasodilatation. The lactic acid also induces free radical (superoxide) formation; both act together to destroy the retinal capillary bed followed by vasoproliferation. Photocoagulation, thus, is even more appropriate for this particular syndrome than previously had been thought, as it not only reduces potentially destructive vasodilatation but also removes the metabolic cause of the free radical induced destruction of the capillary endothelium which is the initial step in capillary drop-out. A review of the present data indicates that the best type of pan- retinal photocoagulation is a very light type affecting the photoreceptors only with a minimal amount of damage to other parts of retina and the vessels in the choroid. The possible use of photochemical types of destruction of the photoreceptor as a therapeutic modality is attractive, but it is certainly too speculative to use until more detailed investigations have been completed. However, the basic therapeutic approach of choice may be to prevent the initial vascular involvement by preventing lactic acid buildup (or keeping the tissue pH normal) or by blocking the generation of superoxide with Allopurinol or similar medication.