Ординатура / Офтальмология / Английские материалы / The Eye Book A Complete Guide to Eye Disorders and Health_Cassel, Billig, Randall_2001

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prone to developing cataracts and glaucoma. But within the eye, diabetes has its worst effect on the retina.

What diabetes does to the retina—and this encompasses a broad spectrum of mutations, ranging from pinpoint blood clots to retinal detachments, which may result in blindness—is known as diabetic retinopathy. Fortunately, most people with diabetes do not wind up blind from diabetic retinopathy; only about 3 percent of all people with diabetes eventually develop severe vision loss. But most people with diabetes do, at some point, experience some eye complications.

Before we discuss these, let’s take a minute to review diabetes itself, which is in fact two diseases: Type I, or in- sulin-dependent diabetes, and Type II, or non-insulin-de- pendent diabetes. Only about 10 percent of all people with diabetes have Type I, which is usually diagnosed in childhood or adolescence. Because these people have the disease throughout their lives—as opposed to those with Type II, who tend to develop it later on—the disease has plenty of time to cause trouble. Diabetic retinopathy is especially prevalent in this group. (In one study of people with Type I diabetes, 25 percent had some retinal changes after three or four years; but after fifteen years of having diabetes, a staggering 80 percent showed signs of diabetic retinopathy.)

The vast majority of people with diabetes have the Type II variety. Because the classic symptoms of this dis- ease—increased thirst, frequent urination, weight loss, and lack of energy—are often ignored, not recognized as warning signs, or confused with other ailments, it may

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be years before the condition is discovered. And because of this delay, in many people retinopathy is found soon after the diabetes is diagnosed. (Fortunately, it doesn’t seem to be as severe as the retinopathy found in Type I disease.)

What Diabetes Can Do to the Retina

Diabetes attacks the small blood vessels of the body— the essential pathways that help supply blood and nutrients to the brain, peripheral nerves, kidneys, and eyes.

Briefly, diabetes targets the small blood vessels’ basement membrane—which, as its name suggests, is their foundation, or cement. On top of this basement membrane, lining the inside of the blood vessels, are endothelial cells. Other tiny yet important cells are pericytes, whose job seems to be to help the basement membrane support the retinal blood vessels. In the eye, diabetes causes the basement membrane to thicken and the number of pericytes to dwindle, particularly in the retina. This in turn makes the blood vessel cells more porous and less able to carry oxygen and nutrients to the retinal tissues—which over time become malnourished and sickly. And this, basically, is diabetic retinopathy.

The damages here can be classified into two general types: nonproliferative diabetic retinopathy (tiny blood bulges, or microaneurysms, pinpoint hemorrhages, cot- ton-wool spots, changes to the wall of blood vessels, macular edema, and shunts), and proliferative diabetic retinopathy (an unwanted surge in the growth of blood vessels, or retinal neovascularization).

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Nonproliferative Diabetic Retinopathy

The retinal changes of nonproliferative diabetic retinopathy, described below, can be ranked according to their severity. They may be mild to moderate, moderate to severe, or very severe. These ratings are particularly important when determining when someone should undergo laser treatment.

Microaneurysms, tiny blood vessel outpouchings that look like small red dots in the retina (particularly in the macula), can go away all by themselves. But they also have a tendency to leak fluid into the retina, contributing to a far more serious condition called macular edema (see below).

Dot hemorrhages are pinpoint areas of bleeding in the retina. Blot hemorrhages are larger, irregular, and roundish. Both of these types of bleeding also may be absorbed by the retina without causing any long-term damage.

Cotton-wool spots, or soft exudates, are localized areas of retinal infarction (loss of blood flow to an area of tissue). These happen when tiny capillaries clamp themselves shut, halting the blood supply to nerves in the retina. The nerve tissue then swells (under the microscope, this looks like wisps of cotton on the retina).

Venous beading can cause the normally smooth walls of retinal blood vessels to look bumpy. Other results of retinal blood vessel changes are abnormal blood flow patterns and shunts (small, tubular areas of mutated capillaries that look like spaghetti). These are called IRMA, or intraretinal microvascular abnormalities. (Both of these

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are common in advanced forms of nonproliferative diabetic retinopathy.)

Macular edema is the most common cause of visual impairment in people with diabetic retinopathy. Nearly all of the retina’s surface area is devoted to peripheral, or side, vision. A surprisingly small area—about 10 per- cent—is responsible for our fine central, or reading, vision. This is the macula (see figure 1.1B). And the heart of this minute but critical region, the fovea, is a tiny area (less than 2 millimeters wide) of nerve cells—yet this is the epicenter of vision, the site of our most important sensory vision cells.

Macular edema doesn’t just erupt overnight. As diabetic retinopathy takes its slow toll on the retinal blood vessels, they get progressively weaker and form tiny mi- croaneurysms—particularly in the macula. These micro- aneurysms—which actually are abnormal areas of the blood vessel walls—leak; they ooze a nasty, fatty fluid into the retina. The swelling this causes is called macular edema. Imagine trying to watch a TV screen behind a fish tank: the water would blur the picture. Well, the same thing happens in macular edema: The fluid obscures central vision. Reading is blurry. Looking straight ahead is blurry. And frustratingly, eyeglasses can’t do anything to help. No matter how sharply light rays are focused onto this swollen retina, the retina’s machinery simply can’t function any better because the leaking fluid is in the way.

Although sometimes this fluid buildup gets reabsorbed on its own, mostly it doesn’t. And over time this

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Image not available.

Fig. 18.3. Microscopic section showing macular edema

edema can cause irreversible damage to the retinal sensory cells, resulting in permanent vision problems. Fortunately, with early and appropriate treatment (see below) to slow the leakage and reduce the fluid, macular edema rarely causes blindness anymore. Remember, all of these changes to the retina may be either mild or very severe, or something in between.

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Proliferative Diabetic Retinopathy

Sometimes the problem isn’t bleeding from existing blood vessels, it’s bleeding from a “baby boom” of new blood vessels that have formed in the retina. These proliferative changes, primarily retinal neovascularization, also cause vision problems. To complicate matters, a person can have diabetic macular edema, proliferative or nonproliferative diabetic retinopathy, or any combination of these.

Nobody knows exactly why these new blood vessels spontaneously begin to grow in the retina. We do know that the new vessels usually stem from old ones, and that this happens after someone has had diabetes for many years. One theory is that as the retinopathy progresses— to the point of extensive capillary closure, poor blood flow, and severe nonproliferative complications including venous beading and IRMA—new blood vessels begin to sprout up, as if to reroute blood flow and offer the retina a fresh source of oxygen and nutrients. These offshoots grow either in the peripheral retina or on the optic disc. They develop particularly quickly in patients who have other health problems—breathing problems such as emphysema, for example, or the extra burden of pregnancy. (Pregnancy may also spark new blood vessel growth because of surges in hormones, changes in the body’s blood flow, or changes in the blood’s oxygen levels.) Interestingly, some eye conditions, such as advanced glaucoma, actually seem to protect the retina from these problems. Carotid disease, which can affect the blood

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Image not available.

Fig. 18.4. View of the retina with proliferative diabetic retinopathy

flow to the eye, may also increase or decrease someone’s risk of proliferative retinopathy.

In general, this neovascularization is believed to occur in response to blood vessel changes caused by a lack of oxygen. Many investigators believe that the oxygenstarved retina releases a chemical cry for help—a substance that’s been termed the angiogenic or vasoproliferative factor—to the ailing retinal blood vessels. In response, they grow, spewing tiny new blood vessels into the retina.

If you think about it, this process is pretty similar to what the body does elsewhere to repair injuries: we cut ourselves, and then the body efficiently heals the cut, lay-

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ing a foundation of new blood vessels, connective tissue, and skin cells over the wound. The big problem in the eye is that these newly formed blood vessels are not normal.

They’re tiny, spindly, flimsy blood vessels—not at all like the mature vessels found in a healthy retina. Also, they grow in a haphazard pattern, with an unfortunate tendency to poke through the retina into the vitreous gel. In short, they’re puny imitations of the original blood vessels, with a bad habit of breaking and bleeding into the retina and vitreous.

It is this awful bleeding of the new crop of blood vessels that leads to proliferative diabetic retinopathy’s most devastating complications. These new vessels appear to rupture at the drop of a hat—in response to sudden jerks of the head, for instance, or even to eye movements like those in normal REM (rapid eye movement), or “dream,” sleep. Coughing, throwing up, sneezing, not to mention anything really traumatic, such as having a baby—you name it, and it will cause these blood vessels to break. Then they bleed, either directly into the retina or between the retina and vitreous jelly, resulting in intraretinal or preretinal hemorrhages. Blood can also gush out into the vitreous, producing a hemorrhage there— vitreous hemorrhage.

Whatever the cause for this bleeding, or wherever the hemorrhage, the change in vision is usually immediate. Patients may have a localized loss—a “hole” in part of their visual field—or they may see “spots” and “cobwebs,” which gradually worsen to a dense haze or, in the case of a vitreous hemorrhage, a total loss of vision.

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Given enough time, the body can usually remove this blood from the retina or vitreous. However it may not necessarily accomplish this quickly enough—or, even worse, the body’s “cure” may be as bad as or worse than the initial problem. As cells inside the eye begin the cleanup process, they may also produce scar tissue in the retina and vitreous. (Scar tissue is the body’s basic way of protecting itself against almost any injury.) Sometimes this scar tissue gets carried away, attaching itself to various areas of the retina, optic disc, and vitreous gel.

As scar tissue heals, it tends to contract. In the eye this contraction can tug on the retina, leading to a retinal detachment (see chapter 15). This kind of tractional retinal detachment is particularly devastating when it occurs in the macula. At its worst, it may result in permanent and severe vision loss.

Who’s at Risk?

Although most people with diabetes eventually develop some degree of diabetic retinopathy, some have relatively minor trouble while others may wind up with severe impairment (but again, most never go blind from it).

By far the most significant risk factor is how long someone has had diabetes: the longer the diabetes has a chance to cause trouble—and here, people with Type I are at a major disadvantage—the greater the odds of developing some form of retinopathy.

Can severe damage be prevented? Actually, there is much you can do to lower your risk of eye complications from diabetes. One huge favor you can do for yourself