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

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weeks afterward; when this happens, most doctors believe, it’s because of relief from the swollen retinal tissue, not from a return of blood flow to already dead tissue.

Because, as mentioned above, this blockage might indicate other serious health problems that need prompt medical attention, patients with retinal artery blockages need a careful physical exam—perhaps including an evaluation of the carotid arteries and heart— beginning with a thorough and complete medical history. So, although this problem may begin in the eye, your family physician, internist, or cardiologist definitely needs to see you as soon as possible.

Retinal Vein Blockages

As you can see from figure 15.1, the retinal veins form almost a mirror image of the retinal arteries, only the flow is reversed. Instead of bearing oxygen-rich blood into the eye, the veins take oxygen-poor blood out of it. So instead of depriving retinal tissue of blood, a blockage in the veins causes blood to back up and pool there, like a clogged drain in a sink with the water still running. This can happen either acutely (a total block, causing sudden symptoms of vision loss) or gradually (a partial block, progressively slowing the outflow over months to years).

Again, there are two types of blockages: central and branch.

Central Retinal Vein Blockages

The main vessel, or “trunk,” of the retinal vein lies at the optic nerve head. As with the central artery line, an

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obstruction here can cause major trouble: a huge backup of blood into the retina, usually resulting in a sudden loss of vision (see figure 15.2). When the blockage is more gradual, symptoms are less severe but may still end in vision loss.

The two big complications associated with central retinal vein blockages are damage to the macular region in the retina, causing swelling and permanent vision loss, and neovascular glaucoma, a rare but devastating form of glaucoma that can happen days to months after the fact (especially within the first ninety days). Fortunately, most people with a central retinal vein occlusion do not develop neovascular glaucoma. This extremely serious condition can be excruciating. Even worse, it can cause patients to develop uncontrollable elevated eye pressure and chronic discomfort. Neovascular glaucoma may require laser, cryotherapy, or surgical treatment to alleviate pain and preserve the eye, even when there is no hope of recovering vision. Because of this, although there’s practically no way to treat a central retinal vein block- age—laser treatment for the macular damage has not been proven effective—patients need careful monitoring afterward, in case neovascular glaucoma develops.

Again, as with artery blockages in the retina, problems in the veins may indicate larger health problems, particularly hypertension, cardiovascular disease, and diabetes. Thus, patients also need a general medical workup to avert any further trouble, either in the other eye or elsewhere in the body.

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Branch Retinal Vein Blockages

The central retinal vein splits into two main branches, which serve the superior and inferior halves of the retina. Blockage in either of these veins causes trouble in the corresponding half of the retina. These major branches are fed by the temporal and nasal retinal venules (smaller veins), and by their own tributaries. A blockage in any of these branches causes swelling and a backup of blood and fluid—but smaller, more focused areas of damage.

As in central retinal vein blockages, macular swelling, or edema, is a common complication that may lead to vision loss. (The threat of neovascular glaucoma is much less common in these smaller blockages.) Note: Branch blockages here usually don’t mean both eyes are at risk; in fact, if you’ve had one in one eye, your risk of having a similar blockage in the other eye is only about 10 percent. Branch retinal vein blockages tend to occur mostly in people with hypertension or cardiovascular disease.

Within the first six months after the branch retinal vein blockage, there is often so much pooled blood that it’s difficult to determine the extent of injury to the retina. As this hemorrhage gradually clears, your eye doctor will probably want to use fluorescein angiography to assess the damage, and to see whether macular edema is present.

As the excess blood and swelling recede, some people spontaneously regain their vision; others may need laser treatment to treat the macular edema. Because some people do get better on their own, most doctors hesitate

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to attempt laser treatment for the first six months or so, to give the retina a chance to heal itself.

Macular Cysts and Holes

It’s rare, but sometimes—for reasons that aren’t clear, despite much speculation—people develop a small cyst or hole in the center of the macula. (The macula, remember, is the most important part of the retina, the part that’s responsible for our central vision.) Some people experience absolutely no change in vision; others may suffer a total loss of central vision.

What’s happening here? Could the vitreous gel be pulling at this area, causing these changes? Are they early forms of degeneration of the retinal pigment epithelium, part of the more severe changes seen in age-related macular degeneration? Again, nobody knows.

Often people first notice the problem—manifested as a subtle distortion—when they’re reading. The lines of the crossword puzzle, for instance, start to bend. Letters of words in a book may seem distorted or appear to be missing. If you’re experiencing any changes like these, see your eye doctor for a complete eye examination, including a dilated retinal evaluation.

To date, the treatment for macular holes and cysts has met with limited success. Both laser and surgical treatments have been attempted. Some doctors have even tried to seal these holes by injecting growth factors that promote healing into the back of the eye—with debatable results. These treatments, because of potential com-

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plications, are usually reserved for people with poor visual acuity due to the hole or cyst. For many people the only help we can offer is to monitor the condition and provide education, support, and counseling for low-vi- sion problems, if this becomes necessary.

Fortunately, macular cysts progress slowly, if at all, and macular holes essentially never lead to a retinal detachment.

Macular Wrinkling

There are many names for this phenomenon, including macular pucker, epiretinal membrane formation, surface wrinkling retinopathy, and cellophane maculopathy. The basic problem is the growth, over the surface of the macula, of a membrane—think of a cellophane wrap over a plate of cookies—that causes it to contract and wrinkle. Usually these membranes are harmless. But occasionally they can progress, leading to marked distortion of the retina, and sometimes impeding vision.

Abnormal membranes can be found after vitreous hemorrhages or eye trauma, or after eye surgery (to repair a retinal detachment, or remove a cataract, for instance); they may also be associated with certain retinal diseases, especially those that cause inflammation. They can show up, for no apparent reason, in healthy eyes— one or both—as well.

For most people these membranes remain stable for years, causing no deterioration in vision (85 percent of

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people retain a visual acuity of 20/70 or better, and 67 percent have 20/30 or better; fewer than 5 percent ever progress to 20/200 or worse). However, if epiretinal membranes do grow to a point where they begin to distort the retina and cause vision problems, symptoms usually begin with mild distortion or blurred vision.

There is a treatment—surgical stripping of epiretinal membranes from the retina—for certain patients. However, most retinal surgeons will attempt this procedure only if it’s clear that the vision problems are definitely being caused by the membrane, and, depending on the membrane’s location and growth, that removing it will actually improve someone’s vision. Microsurgical vitrectomy techniques have come a long way in recent years and have also proved very effective in removing advanced epiretinal membranes. However, as with all procedures, there are risks involved—including infection—and you and your doctor will need to discuss them thoroughly before deciding whether this procedure is for you.

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The Optic Nerve

Here we are, in the eye’s nerve center—a massive cable that links the eye to the brain, allowing us to make sense out of what we see. Like a mighty river fed by countless streams, the optic nerve cable, made up of more than a million tiny fibers, starts small—in the ganglion cells of the sensory retina. These fibers connect to the retina’s interior, where they form the nerve fiber layer, and then amass in a giant bundle at the back of the eye to form the optic nerve. The next stop, via the sclera at the eye’s “back door,” is the brain.

As you can see from figure 1.1A, the optic nerve is the only game in town: every single visual impulse that travels from point A, the eye, to point B, the brain, must take this route. Thus, even the slightest disruption—from inflammation, poor blood flow, infection, trauma, or a tumor—can have devastating consequences for someone’s vision. Two important optic nerve problems that

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warrant special mention here are optic neuritis (inflammation of the optic nerve) and ischemic optic neuropathy (a tiny stroke in the optic nerve).

Optic Neuritis

Optic neuritis is an inflammation of the optic nerve. It can be caused by infection and immune-related illnesses, or its cause can be idiopathic (a medical term that means, essentially, “We don’t know why this has happened”).

When the optic nerve becomes inflamed, the impact on vision is prompt: a marked decrease in central or fine visual acuity, or loss of visual field. Usually only one eye is affected at a time. Other symptoms almost always include pain or tenderness of the eyeball, with discomfort as the eye muscles pull or rub on the optic nerve sheath surrounding the optic nerve. In optic neuritis, it may be difficult to see straight ahead, colors may appear washed out, and lights may seem dim; trouble with depth perception is also common. Exercise, a hot shower, or any other activity that raises body temperature may make the vision problems worse.

In a typical episode of optic neuritis, the decline in vision tends to level off within a few days; eyesight improves gradually over the next four to six weeks. At least 85 percent of people with an episode of optic neuritis regain useful vision, and any loss of central, peripheral, or color vision is often mild, detectable only on testing. Also, the majority of patients with optic neuritis never

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suffer another episode. Only in very rare cases, when involvement has been particularly severe, does it happen that vision fails to recover from the initial decline.

Although, as mentioned above, most cases of optic neuritis are idiopathic, many ailments can also take their toll on the optic nerve, including viral illnesses (such as mumps, rubella, and cytomegalovirus), bacterial infections (such as cat-scratch fever and TB), sinus infections, and inflammations elsewhere in the body or eye. Also, because the optic nerve is, in effect, an extension of the brain, it seems to be susceptible to some of the brain’s own disorders, particularly multiple sclerosis.

Multiple sclerosis is what’s called a demyelinating condition: it erodes myelin, the protective sheath of insulation around the nerve fibers, leaving the bare “wire” exposed. No one understands why it happens, but for some reason spots of myelin just melt away, disrupting the conduction of electrical impulses, causing delayed transmission, and leading to such classic symptoms as numbness and tingling in the arms and legs, difficulty walking, and double vision (due to an effect on the nerves that control the eye muscles). Note: One episode of optic neuritis certainly doesn’t mean that you have, or that you are going to develop, multiple sclerosis. However, up to 95 percent of people who do develop multiple sclerosis will have an episode of optic neuritis at least once in their lives. (It’s also worth noting that multiple sclerosis has many degrees of severity. Many people live completely normal lives with very mild forms of the disease. In fact, scientists believe, some cases of multiple sclerosis are

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never even diagnosed because the symptoms are so minor!)

Treatment: Treatment begins with an exhaustive medical history and a physical examination—and that’s the easy part, because there is no one widely accepted treatment for optic neuritis. Sometimes you can see the inflamed optic nerve in an eye exam. Rarely does treating an underlying disease or condition alter the course of optic neuritis; only time can tell whether vision will return after the inflamed optic nerve gets better on its own.

For years controversy surrounded the use of steroids (medications known to decrease swelling in the body) in various dosages and regimens against optic neuritis. In a search for better, more definitive answers, the National Eye Institute sponsored the national Optic Neuritis Treatment Trial (ONTT), a large, multicentered clinical trial designed to study the effects of steroids on optic neuritis. The study’s striking results have completely changed the way we treat people with optic neuritis. Scientists found, to their surprise, that steroids did not significantly improve vision after the episode, nor did they lower the odds of recurrence. But in people with optic neuritis and brain scan evidence suggesting multiple sclerosis, they found that steroids helped slow the course of multiple sclerosis.

Today, as a result of these findings, all patients newly diagnosed with optic neuritis are advised to have an MRI (magnetic resonance imaging) of the brain (a painless, noninvasive test) as soon as possible. If the scan suggests the possibility of multiple sclerosis, then high-dose in-