الفهرس | Only 14 pages are availabe for public view |
Abstract SUM MAR Y Retinal neovascularization is a serious compli~ation which occurs in a varity of disease entities such as diabetes mellitus, retinal vein occlusion, sickle cell disease, retinopathy of prematurity, Eales’ disease, sarcojdosis and others. The exact mechanism by which these diseases can induce retinal neovascularization is unknpwn. It seems that the retinal ischaemia, localized or generalized, produced by these disease plays a fundamental role in the pathogenesis of neovascularization. In diabetes, retinal ischaemia is produced by the pathology in the vessels’ wall .1n retinal vein occlusion, stagnation produces retinal ischaemia. In sickle cell disease, retinal ischaemia is produced by microemboli or by viscosity induced thrombosis. In retrolental fi~roplasia, retinal ishcaemia is produced by arteriolar occlusions due to oxygen toxicity. In Eales’ disease and sarcoidosis, inflammation of the vascular walls cause narrowing and may be occlusion of retinal vessels with resultant retinal ischaemia. Regardless how retinal ischaemia is produced, it is speculated that such hypoxic retinal areas elaborate a vasoformative substance that stimulates the growth of new vessels. Most of these neovascularization occur in the areas of retinal ischaemia or at the interface between ischaemic and perfused areas with the neovascular tufts growing into the ischaemic zones. This has made some investigators suspect that the neovascular tissue is growing in response to a stimulus generated by the hypoxic retinal tissue. The site of the neovascular tufts either in the retinal periphery or on the disc,which is considered more serious as it is more vulnerable to cause vitreous haemorrhage and retinal detachment than peripheral retinal neovascularization. Significant progress has been achieved in photocoagulation therapy techaniques and vitrectomy surgery by which major benefit in control of retinal neovascularization is ful£illed • However many cases seem to be away from control and will not be controllable until we have a firm grasp of the mechanism of neovascularization. |