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

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travenous steroid therapy should begin soon—within eight days of the onset of optic neuritis symptoms. Even though this probably won’t help the optic neuritis, it appears to help protect brain cells against further demyelination. The results of the ONTT are still being evaluated, and data from four-year and five-year follow-ups suggest that the protective effect of steroids, unfortunately, may begin to wane after three years: the people taking steroids begin to catch up with those not taking steroids in the incidence of clinically definitive multiple sclerosis. This is an evolving field, though, where much research is being done all the time. The ONTT at least established that the use of high-dose IV steroids seems to delay the onset of MS in the short term.

Ischemic Optic Neuropathy (Poor Blood Flow to the Optic Nerve)

When the supply of blood—and the vital oxygen it carries—is shut off, the result is called ischemia. This can happen, in mild or severe form, anywhere in the body. In the heart, major ischemia can cause a heart attack; fleeting ischemia can cause the intense chest pain of angina. In the brain, severe ischemia causes a stroke; temporary ischemia can lead to TIAs (transient ischemic attacks), or “mini-strokes.” In the eye, episodes of temporary is- chemia—usually from atherosclerotic narrowing of the carotid artery, hindering blood flow to the retina—can cause “gray-outs” (also called amaurosis fugax; see chapter 18). And severe ischemia—a shutoff of blood flow

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thought to result from artery disease within the optic nerve—can lead to the eye’s version of a stroke: nerve cell damage and a sudden, dramatic, and usually permanent loss of vision in one eye. This is called ischemic optic neuropathy.

There are two distinct varieties of ischemic optic neuropathy. The first is nonarteritic ischemic optic neuropathy (nonarteritic ION). It’s a long name, but the word idiopathic (meaning “we don’t know”) ought to be in there somewhere, because although we know what happens to the optic nerve, we don’t know why, or what causes it. Equally serious but with systemic implications is arteritic ischemic optic neuropathy (arteritic ION). We do know what’s causing this: an inflammatory condition of the blood vessels supplying the optic nerve and of other blood vessels throughout the body.

Nonarteritic Ischemic Optic Neuropathy

People with nonarteritic ION experience a scary, painless sudden loss of vision, sometimes the upper or lower half of their visual field. There are no early warning signs. The problem seems to be age-related: it tends to strike people in their sixties. Many of these people also have hypertension or diabetes. It is assumed that these diseases play a role in causing nonarteritic ION, although we don’t know exactly how. (Some experts speculate that the problem is caused by atherosclerosis, or “hardening” of the eye’s blood vessels.) Unfortunately, most of the vision loss is immediate and permanent; recovery of the lost vision is rare. Plus, in about 10 percent of people,

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nonarteritic ION strikes the second eye as well—and sadly, we have no means of preventing this loss.

Arteritic Ischemic Optic Neuropathy

Arteritic ION happens when the blood vessels that feed the optic nerve become inflamed. The inflammation chokes, or sometimes blocks completely, blood flow to the optic nerve. It is not an isolated problem: this same inflammation also occurs in blood vessels elsewhere in the body, causing symptoms that may include headache, scalp tenderness, jaw discomfort when chewing or talking, fever, malaise, weight loss, and muscle weakness in the arms and legs. This generalized inflammation of the blood vessels—also known as temporal arteritis or giant cell arteritis—is usually confirmed by a blood test called a sedimentation rate.

Temporal, or giant cell, arteritis is characterized by a classic headache along the artery at the temples; when samples of the affected artery are examined under the microscope, we can see telltale enlarged (or giant) cells in the blood vessel walls. A biopsy of the temporal artery is usually needed to confirm this diagnosis. Your doctor may need samples of both temporal arteries (called a bilateral biopsy) to be certain. Fortunately, unilateral and bilateral biopsies don’t interfere with blood flow to the head or face. Giant cell arteritis is thought in some patients to be related to a larger disorder known as polymyalgia rheumatica, characterized by pain and discomfort in the large muscles of the shoulders, neck, and thighs.

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Both conditions tend to occur in older people, often in their seventies, most commonly in women.

In arteritic ION the vision loss is usually more severe than in the nonarteritic form. Some people experience transient visual disturbances, or fluctuations in vision, before the acute loss of vision with ION—probably caused by intermittent blockages of blood flow.

Treatment: There is no proven treatment for arteritic ION, although many patients experience a modest improvement in vision over time. The big thing to worry about here, as in nonarteritic ION, is the second eye. In 70 percent of people with arteritic ION, the second eye becomes involved within days to weeks after the first eye.

Therefore, when arteritic ION is suspected, high-dose oral steroid therapy should begin immediately in order to protect the other eye. This prophylactic, or preventive, steroid therapy is often needed for months or years to keep the giant cell arteritis under control. Unfortunately, however, prolonged use of steroids can cause problems of its own. Be sure to discuss these with your doctor, who will almost certainly want to monitor you closely, to check for the development of any steroid-related side effects.

P A R T V

Other Things

You Need to Know

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•Gradual loss of vision over days or weeks

•Recent onset of light flashes and floaters

•Red eye without loss of vision or severe pain

•Recent onset of sensitivity to light

In this chapter we’ll take a close look at some of these emergency and urgent situations. Other situations (like flashes and floaters) are covered in other chapters (check them out in the Index).

Chemical Burns

It hurts like crazy; it may also cause permanent damage. When chemicals get splashed or sprayed in the eye, you need emergency attention—fast. How bad is the injury? Can the eye recover? This depends not only on which chemical has injured your eye and on how severe the injury is, but also on how quickly you get medical help.

There are two main categories of chemical burns in the eye: those caused by alkalis, such as lime, lye, and ammonia, and those caused by acids, such as battery acid.

Alkali burns generally do the most damage. These chemicals react rapidly with fats in the cell membranes, the protective barrier covering the eye’s outer surface. Weakening this natural shield allows the chemical to penetrate even deeper, into the cornea—often causing serious corneal swelling, inflammation, and even cataracts. Sometimes the cornea becomes so severely scarred that it can’t even be fixed by a corneal transplant; the result is permanent vision loss.

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Acid burns, surprisingly enough—even those caused by such harsh chemicals as battery acid—are usually tolerated better than alkali burns by the cornea. Because they tend not to damage the cell membranes, they usually don’t penetrate deep into the cornea. Therefore, the risk of major corneal scarring, as described above, is much lower.

Detergents are other chemicals that often find their way into the eyes. More often than you might think, people inadvertently mistake liquid dishwashing soap for a contact lens cleaning solution, causing painful inflammation. Despite the irritation and swelling they may produce, detergents in the eye, as chemicals go, are usually pretty harmless. Even when, as sometimes happens, they injure the cornea’s epithelium (its outermost layer of cells), the eye almost always recovers completely.

Treatment: No matter what caused the injury, your immediate response should be copious irrigation. In other words:

Step 1: Wash it out! The long-term health of your eye depends on how quickly you can begin rinsing it. You can use tap water, contact lens wetting solution, or saline. Tap water is usually the fluid most readily available in large quantities; it’s best to splash water into the eye with your hand, rather than stare up into the gushing faucet.

Step 2: Don’t stop. Keep irrigating vigorously for about thirty minutes.

Step 3: Go to the eye doctor or emergency room. An eye exam at this point will reveal the extent of the damage and the need for further treatment. (This may include