Figure 5-2C shows an eye that suffers from proliferative retinopathy. If untreated, this condition results in partial or complete loss of vision. Just as in many other parts of the body, when the blood supply in the eye is reduced, new vessels form to carry more blood to the retina. When this happens, the patient is entering the stage of proliferative retinopathy. The blood vessels grow into the vitreous body where they can hemorrhage and block vision. A hemorrhage forms a clot, which contracts, pulling up the retina to produce retinal detachment. The lens can no longer focus the light on the macula, resulting in complete loss of vision.
Many studies have aimed to develop drugs that may block proliferative retinopathy, but none has been successful so far. However, laser surgery may be used to reduce the damage caused by retinopathy and prevent blindness. Laser surgery causes burns in the retina that result in scars that prevent the retina from being pulled away by a hemorrhage in the vitreous body. Only 5 percent of diabetics with proliferative retinopathy who undergo laser treatment develop severe vision loss. However, there's some minor loss of vision at the sites where the retina is burned, and there's a decrease in night vision and the visual field (the area the eye can see at one time). Laser treatment can be used to treat macular edema that affects vision as well.
If a person with T1DM has already experienced retinal detachment, an operation called a vitrectomy is necessary. Under general anesthesia, the vitreous body is replaced with a sterile solution. Attachments to the retina are cut, and the retina falls back into place. Vitrectomy restores vision 80 to 90 percent of the time.
The exact cause of microvascular complications isn't certain, but a number of different mechanisms have been proposed (persistent high blood glucose is the basis for all the mechanisms as shown by the DCCT study discussed in the earlier sidebar "The Diabetes Control and Complications Trial"):
I When glucose is elevated, some of it gets converted to another compound called sorbitol. Sorbitol accumulates in the lens of the eye, where it causes swelling and damage to the lens; the result is a cataract, an opaque area that you can't see through. Sorbitol also accumulates in the retina of the eye, the glomeruli in the kidneys, and the Schwann cells that provide insulation for nerve tissue. In each area, excess sorbitol causes damage.
I Protein kinase C consists of a group of chemicals in the body that help to control movement of substances in and out of cells and enlargement of blood vessels to improve flow. Persistent high blood glucose leads to increase in protein kinase C, especially in the retina and the glomeruli as well as in nerve tissue. At these high doses, the protein kinase C leads to reduced blood flow by promoting atherosclerosis in small vessels and therefore diminished oxygen to these tissues. The tissues then may die or fail to function normally.
I Elevated glucose causes advanced glycation end products (AGEs) to form in tissues. AGEs cause increased flow of damaging substances into cells and increased production of new cells, which block the tiny spaces needed for proper function in the kidneys and proper vision in the eyes.
I Vasoproliferative factors are compounds that cause increased production of small blood vessels in the retina of the eye that are very fragile and can bleed and block vision. In nerve tissue, new vessels may carry blood away from the nerves that need it.
Was this article helpful?