Virtual Health Library

Diabetic retinopathy is a leading cause of blindness through out the world. Vision loss occurs because of diabetic macular oedema, ischaemic maculopathy and proliferative retinopathy. Although we understand some of the mechanisms involved, the biochemical basis of proliferative retinopathy is still obscure. Kinoshita and his co-workers have led advances in research on the polyol pathway and the role of aldose reductase in this disease. Cogan and Kuwabara showed that one of the earliest manifestations of diabetic retinopathy is selective loss of pericyte from the retinal capillary wall. In addition, to a lesser extent, there is loss of capillary endothelial cells. Pericytes have been shown to stain with immuno-histochemical stains for aldose reductase. They are thought to be concerned with the regulation of the vascular calibre. Their loss results in vasular dilation and microaneurysm formation. Endothelial cell loss causes increased vascular permeability and capillary drop-out. The resulting retinal ischaemia is a stimulus for neovascularization. This may be due to a direct effect of angiotensim II or to stimulating the elaboration of growth factors such as insulin-like growth factor I. The optic nerve head has a rich blood supply in health, from the retinal, choroidal and pial circulation. Involvement of these vessels in microvascular disease results in the development ofischaemic opti neuropathy which can result in significant visual loss. Visual fields show loss ranging from arcuate scotomas to microvascular infarcts of the III, IV and cranial nerves. The pupil is usually spared in III nerve lesion. Patients present with diplopia and extra-ocular motility disturbance. The rule is spontaneous recovery without aberrant regeneration, usually within 12 weeks. Diabetics are at increase risk developing primary open angle glaucoma. This results in a slowly progressive optic neuropathy with cupping of the optic nerve, characteristic visual field loss and eventual blindness. Diabetics frequently develop cataracts. Cataract treatment, although very successful is still a major cause for visual loss in the world, and weights heavily on the resources of the developing world. A rare but serious life - threatening complication of diabetes, occurring particularly in ketoacidosis, is mucormycosis. Patients present with orbital and sinus infection with mucor. The manifestations include external ophthalmoplegia, lid oedema, proptosis, fever, necrosis of skin, nasal mucosa or palate, and symptoms related to involvement of the central nervous system. The severity of the ocular complications of diabetes mellitus is related to the duration of diabetes, genetic patterns and diabetic control. The Diabetes Control and Complication Trial recently showed that tight control of blood sugars resulted in the lowering of the complications of nephropathy, neuropathy and ocular disease in insulin-dependent diabetics. With the advent of laser photo-coagulation, medication for management of glaucoma and the development of instrumentation and techniques for advanced vitreo-retinal surgery, we have at our disposal the ability to prevent and to treat diabetic blindness. Most important, however, is the need for the patient and health team education in influencing referral patterns and the timing when patients first present to the ophthalmologist. The onus is on the public health officials to ensure that appropriate programmes of screening and education are in place. The funding of research into the mechanism of the pathogenesis of the ocular complications of diabetes should help us to intervene in weays which will reduce morbidity and possibly truly eliminate preventable blindness from diabetes mellitus (AU)