The retinopathies are a group of retinal diseases that cause vascular and neurological changes in the retina of the eye. They are reflective of such ongoing systemic diseases as diabetes, arteriosclerosis, hypertension, and sickle cell anemia.
The retina is an outward extension of the central nervous system that lines the inside of the eye. It has 10 layers and is comprised of the photoreceptor rods and cones and such support cells as Mueller cells. The retinal pigment epithelium (RPE) is a single cell layer located behind the retina, which services the photoreceptors. Bruch's membrane is a basement membrane found between the RPE and the choriod, a highly vascular layer that includes the choriocapillaris, which supplies nutrients to the RPE and to the photoreceptors. The central retinal artery and its branches supply blood to the rest of the retina. The cilio-retinal artery that emerges from the optic nerve supplies the macula. The macula is located temporal to the optic nerve and is the part of the retina that contains the highest concentration of photoreceptors, especially cones. The part of the macula with the highest concentration of cones is the fovea. The vitreous humor is a gelatinous body that is located between the retina and the lens of the eye. The optic nerve is a large nerve in the posterior part of the eye through which the central artery and vein pass. It is actually formed from the axons of cells in the retina. It is through the optic nerve that visual stimuli leave the eye for the occipital lobe of the brain, where vision is processed. Hemoglobin is a molecule in red blood cells responsible for the transport of oxygen.
The presentation and pathogenesis of each of these retinal diseases are unique; and the signs can be seen by an ophthalmologist or an optometrist upon dilation of the eye. All of these retinopathies can lead to blindness.
Diabetic retinopathy is the leading cause of blindness in the United States for people between 20 and 74 years of age. Risk factors for diabetic retinopathy include hypertension, elevated HgA1C (a hemoglobin test), a history of smoking, and number of years as a diabetic. Within 10 years of diagnosis, over 70% of type I diabetics will have some retinopathy, and within 16 years diagnosis, 60% of type II diabetics will have retinopathy. A diabetic may have normal vision, yet still have severe retinopathy.
The underlying pathogenesis of diabetic retinopathy is hypoxia, a decreased oxygen supply that is caused by elevated blood sugar or hyperglycemia. Glucose is needed in the cells of the body for energy, and oxygen and insulin are required for entry of the glucose molecules. The diabetic, because of insufficient insulin or because of cellular resistance to insulin, cannot absorb glucose into the cell effectively. The pathologic response of the retina to a decreased oxygen supply is first a thickening of, and then a breakdown of the retinal capillary basement membrane. Pericytes, cells that surround the capillaries and produce an inhibitor for angiogenesis, also degenerate. In the absence of this inhibitor, retinal neovascularization, or new vessel formation, is stimulated by vascular endothelial growth factor (VEGF). The new vessels that form are very fragile and can easily rupture, causing bleeding in the vitreous and subsequently leading to vitreous traction. Degeneration of retinal neural cells precedes the vascular changes of diabetic retinopathy.
Diabetic retinopathy is a condition that initially affects only the posterior pole of the retina. The peripheral retina is affected only in the extreme cases. Diabetic retinopathy is divided into two phases: nonproliferative and proliferative. In the nonproliferative phase the retina has microaneurysms, dot and blot hemorrhages, hard lipid exudates, a beading pattern of some of the venules, areas of local ischemia where there is little or no oxygen perfusion (called cotton-wool spots), or macular edema. The macular edema is called clinically significant macula (CSME) when there are hard exudates and macular thickening or edema, close to the fovea. In the proliferative phase of diabetic retinopathy, neovascularization of the retina and of the optic nerve can be observed. A fibrous substance that materializes when the new retinal vessels form adheres to the vitreous, causing retinal traction and retinal detachments. The newly formed blood vessels can invade the anterior part of the eye, causing neovascular glaucoma. Vitreous hemorrhaging occurs when the blood vessels attach to the vitreous. Venous and arterial occlusions are also seen in diabetic retinopathy.
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Author Info: Martha S. Reilly OD, The Gale Group Inc., Gale, Detroit, Gale Encyclopedia of Nursing and Allied Health, 2002 |