Retinal hemorrhages are a common feature of diabetic retinopathy and vary in their appearance based on their location within the retina. The superficial capillary bed is located in the nerve fiber layer and hemorrhages from superficial capillaries have a flame-shaped appearance as the blood spreads between nerve fibers that run parallel to the retinal surface. Hemorrhages occurring from the deep capillary beds, where the arrangement of cells is perpendicular and more compact, tend to be circular and called dot (small) or blot (larger) hemorrhages depending on their size (see Fig. 1). Loss of pericytes results in microaneursyms, small outpouchings of vessel walls that leak plasma into the surrounding retina, causing retinal edema. When the edema spreads into the macula, the center portion of the retina that is responsible for our best vision, it is referred to as macular edema. Macular edema is the most prevalent cause of visual loss in diabetics. As edema fluid diffuses away from the major sources of leakage, it is resorbed by more normal areas of the capillary bed. Poorly soluble serum lipoproteins frequently precipitate near sites of resorption, resulting in hard exudates (see Fig. 2).
Pericyte loss is initially followed by endothelial cell proliferation, which, along with leukostasis, may result in occlusion of capillaries. When capillary occlusion becomes widespread, there is retinal ischemia, which is often recognized clinically by its effects on adjacent larger vessels, including venous dilation, beading, reduplication, and loop formation (see Fig. 3). IRMAs (Figs. 3 and 4) probably represent new vessel formation that is within the retina; it is only when new vessels penetrate the internal limiting membrane and grow along the surface of the retina into the vitreous cavity that they are recognized as neovascularization (see Figs. 3 and 4). A cotton-wool spot (or soft exudate) is thought to develop as a result of obstruction of a retinal arteriole. The resultant focal hypoxia leads to blockage of axoplasmic flow in the nerve fiber layer that is clinically recognizable as a cotton-wool spot (see Fig. 4).
Neovascularization occurs at the border of the perfused and nonperfused retina. Some outflow of fluid from the eye occurs at the optic nerve, and when retinal ischemia becomes severe enough, vasoproliferative factors may become concentrated at the optic nerve, resulting in neovascularization at the disk (NVD) (see Fig. 5). Neovascularization that occurs elsewhere in the retina is called neovascularization elsewhere or NVE (see Figs. 3 and 4). Because NVD tends to be associated with more severe retinal ischemia than comparable sized areas of NVE, NVD is associated with a greater risk of visual loss. When retinal ischemia is extremely severe, vasoproliferative factors may become concentrated at the anterior outflow channels of the eye, resulting in neovascularization on the trabecular meshwork and the iris that make up the anterior chamber angle. This is referred to as neovascularization of the iris (NVI) or rubeosis. Blockage of outflow through the trabecular meshwork by new vessels results in neovascular glaucoma.
Vitreous hemorrhages seen in PDR arise secondary to NVD and/or NVE and occur anterior to the retina, in the vitreous cavity. They can be either diffuse, as a result of bleeding into the vitreous humor, or bow shaped, an appearance that arises from the accumulation of blood in the potential space between the retina and vitreous (see Fig. 6).
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