Retinal Vascular Disease
Ischaemic retinal vascular diseases ultimately lead to glaucoma and are found in the globes that are enucleated to relieve intractable pain in a blind eye. The clinical diagnosis is usually “neovascular glaucoma” with the addition of “central retinal vein
- PDF / 6,399,233 Bytes
- 32 Pages / 595.28 x 790.87 pts Page_size
- 61 Downloads / 160 Views
Retinal Vascular Disease
Introduction
Pathogenesis of Retinal Ischaemia
With regard to the spectrum of inner retinal ischaemia and infarction, the range extends from total (white) infarction of the inner retina (after occlusion of the central retinal artery (CRAO)) to total red (haemorrhagic) infarction (after thrombosis of the central retinal vein (CRVO)). Between these two ends of the spectrum, a variety of disease processes (which occlude individual branch arterioles or venules) can produce areas or sectors of focal ischaemia. The end-stage effects of focal retinal ischaemia are shown diagrammatically in Fig. 4.2 and are characterised by: 1. Localised areas of breakdown in the retinal vasculature with leakage of plasma and red cells 2. Intra- and preretinal neovascularisation 3. The formation of microaneurysms on the capillaries 4. Secondary angle closure with bullous keratopathy and ulceration 5. Cataract The changes produced in ocular tissues as a result of inadequate metabolic exchange and hypoxia have a limited range of morphological expression, although the pattern is variable.
The consequences of retinal ischaemia in terms of the end result, neovascular glaucoma, have already been discussed (see Chap. 3). While the retina has a dual blood supply, it is disease in the branches and tributaries of the central retinal artery and vein that are of greater importance in vasoproliferative disorders and these in turn lead to retinal detachment and blindness. The arterioles and venules radiate from the disc and on the temporal side bend around to form a spokelike pattern around the macula (Fig. 4.1). The capillary bed connecting the arterioles and venules loops down to supply the inner layers of the retina. The outer layers (outer nuclear and photoreceptor) of the retina are maintained by the posterior ciliary arteries via the choriocapillaris, and the ischaemic responses in this vascular territory are far less well defined. An important consequence of the dual blood supply is that there is a watershed zone in the outer plexiform layer and the effects of ischaemic capillary endothelial damage are seen here as leakage of plasma.
Fig. 4.1 Congested retinal blood vessels in a glaucomatous eye with a deeply cupped disc: The column of blood in the venules is thicker than that in the arterioles. Note the pattern of supply to the macula (arrowhead)
This chapter describes the ischaemic retinal vascular diseases that ultimately lead to glaucoma and are found in the globes that are enucleated to relieve pain in a blind eye. The clinical diagnosis is usually “neovascular glaucoma” (NVG) with the addition of “central retinal vein occlusion” (CRVO) or “diabetes,” but occasionally, rarer entities such as retinopathy of prematurity (ROP) or Coats’ disease will be seen at this end stage. Although choroidal neovascularisation (disciform degeneration) does not per se lead to anterior segment neovascularisation, this is the end stage of age-related macular degeneration, so that inclusion of this topic in the present chapter is a
Data Loading...
