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

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gled mirrors to observe the anterior chamber angle. In people with a narrowed anterior chamber angle, the iris appears to crowd this area, limiting aqueous access to the trabecular meshwork.

Farsighted people, who have smaller eyeballs to begin with, are more prone to developing closed-angle glaucoma; as you might imagine, in a smaller eye it’s easier for the iris to block the anterior chamber angle.

Also, some people were just born with narrow anterior chamber angles; although most of them have normal eye pressures, their risk of acute closed-angle glaucoma is higher. And for these people, even normal activities can bring on an attack—watching a movie in a darkened theater, for example, which causes the pupil to dilate mildly, displacing the iris into the narrow anterior chamber angle. Or trouble can be incited by certain dilating eye drops or oral medications such as antihistamines, which can affect the position of the iris and lead to a precarious further narrowing of this angle. If this narrowing becomes extreme enough to block or close a significant portion of the anterior chamber angle, the eye pressure will rise. This will develop into a harmful cycle of increased angle blockage and higher eye pressure. Eventually, when the eye pressure rises to very high levels, the person will have a painful, red eye. Most people also experience nausea, vomiting, and a severe headache during an attack of acute closed-angle glaucoma. Again, the consequences of an acute angle-closure attack can be devastating. This is a medical emergency and must be treated immediately and aggressively to preserve vision.

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anatomical problem causing the drainage block, as in closed-angle glaucoma. Instead, many conditions can lead to open-angle glaucoma; but in each of these the trabecular meshwork is clogged or obstructed.

What are some of the things that can go wrong and lead to open-angle glaucoma? For one, inflammation in the anterior portion of the eye, such as iritis, can temporarily clog the trabecular meshwork with inflammatory cells. Also, bleeding, or hyphema, a separate problem in the anterior chamber, can lead to elevated eye pressure through a similar mechanism. In hyphema, red blood cells collect in and on the trabecular meshwork, impeding the outflow of aqueous fluid.

In pigment dispersion syndrome, another form of open-angle glaucoma, pigment granules from the iris spill into the aqueous-filled anterior chamber, especially during exercise or other exertion. These pigment cells are jiggled loose from the surface of the iris and flow with the aqueous to the trabecular meshwork filter in the anterior chamber angle. The trabecular meshwork can eventually become clogged with these cells; this impedes further aqueous drainage and leads to temporary elevations in eye pressure. People with this condition may experience dull pain in their eyes and see halos around lights after exercise or vigorous exertion. Pigmentary glaucoma is more common in men between the ages of thirty-four and forty-six who are mildly to moderately nearsighted.

Pseudoexfoliative glaucoma, yet another form of openangle glaucoma, happens when the trabecular meshwork

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becomes clogged with cells that flake off, like dandruff, in the anterior chamber of the eye.

The most common form of open-angle glaucoma is primary open-angle glaucoma. In this case the use of the word primary means that doctors are not certain what’s causing the blockage at the trabecular meshwork. They know it’s not, however, due to a narrowed anterior chamber angle (thus, by default, it’s a form of open-angle glaucoma). Nor is it caused by a recognizable cell or substance clogging the trabecular meshwork, as in the forms of open-angle glaucoma mentioned above. Some researchers believe that the pressure elevation in primary open-angle glaucoma may be due to a change in the structural integrity of the trabecular meshwork that just happens with age. Others have suggested that a problem exists with the drainage through Schlemm’s canal.

Whatever the exact mechanism, the changes in the trabecular meshwork seen in this form of glaucoma have also been observed in older people who do not have glaucoma. Therefore, these may simply be normal aging changes which for some reason are accelerated or further advanced in people with glaucoma. This is why many ophthalmologists, in moments of frustration when trying to control difficult cases of glaucoma, have declared that this disorder is an aging process that is often as tough to treat as wrinkling skin. This is not true! We have many successful ways of controlling glaucoma, as we will soon discuss.

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Normotensive (Low-Tension) Glaucoma

Normal eye pressure is usually considered to be 21 millimeters of mercury (mm Hg) or less. Some people have normal pressures within the eye but nevertheless have progressive optic disc and visual field changes similar to those observed in people with primary open-angle glaucoma (which, as noted above, is due to elevated eye pressures). When someone develops glaucoma despite having normal eye pressures, that person is said to have normotensive glaucoma or low-tension glaucoma. This diagnosis is made only after other ocular or systemic problems that can damage the optic nerve and cause visual field loss are ruled out. These include a period of elevated eye pressure (in this case, even though the ocular pressure has returned to normal, there is residual optic nerve damage); daily fluctuations of eye pressures in and out of the “normal” range; and a past episode of very low blood pressure as the result of severe blood loss or myocardial infarction.

It is believed that many people have undiagnosed normotensive glaucoma. Eye doctors often miss diagnosing this disorder because the person has normal intraocular pressure during an eye examination. This is why the doctor must carefully evaluate the eye for other signs of glaucoma, such as significant optic disc changes and visual field loss. Many glaucoma screening programs at health fairs and senior centers also rely heavily on the intraocular pressure readings to screen large numbers of

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people for glaucoma, so (obviously!) they often miss picking up normotensive glaucoma.

What’s causing optic nerve damage in people with normotensive glaucoma despite eye pressures in the normal range? Unfortunately, we don’t yet know the answer to this question. Perhaps normal eye pressure is a relative term, since some people can tolerate intraocular pressures of 24 mm Hg for years without developing optic nerve damage. For other people an intraocular pressure of even 16 mm Hg may be too high, causing damage to their optic nerve and visual field loss. It has also long been speculated that this increased susceptibility may be related to a poor blood supply to the optic nerve. Or there may be a defect in the support tissues of the optic nerve that makes the nerve more likely to be damaged at lower eye pressures.

The treatment of normotensive glaucoma, as in other forms of glaucoma, is directed at lowering the eye pressure as much as possible, first medically and later surgically, if necessary. Patients are also thoroughly evaluated medically to make sure they do not have an underlying anemia or other condition that can directly or indirectly affect the optic nerve. A brain scan is sometimes part of this workup to evaluate the health of the optic nerve behind the eyeball.

We still know little about what makes one person’s optic nerve susceptible and another person’s resistant to changes in eye pressure. Normotensive glaucoma underscores this problem as well as the complex nature of glaucoma.

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Diagnosing Glaucoma

Measuring Pressure within the Eye

Although today we recognize that glaucoma can occur in eyes with “normal” eye pressure, the relationship between elevated eye pressure and visual field loss was recognized centuries ago, though at that time physicians were unable to measure eye pressure accurately. For many years the accepted method of estimating the pressure in the eyeball was simply to feel, or “ballot,” the eye with one’s fingers. Eye doctors of the eighteenth and early nineteenth centuries prided themselves on their ability to judge eye pressure simply “by feel.” So confident were they, in fact, that they scoffed at the development of more objective methods to measure pressure.

But eventually eye doctors were won over by the sensitivity of measurements made through tonometry, a noninvasive way to measure pressure within the eye. Over the years many tonometry techniques have been developed, all of them measuring how much force is required to indent or flatten the cornea. This measurement, in turn, allows the ophthalmologist to estimate the pressure in the eye.

Many tonometers use weights or specially designed contact tips, which are placed on the eye or cornea. The

Goldmann contact tonometer, or “blue light” test—many people are familiar with this from eye examinations—is the most accurate method of measuring eye pressure. This is an applanation tonometry system, in which a circular tip is placed on an anesthetized cornea. A scale

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measures the amount of pressure in millimeters of mercury required to cause a specific degree of corneal flattening. Fluorescein (orange) dye and a cobalt blue filtered light are used to help illuminate the tip as it comes in contact with the eye. Many patients are fearful of tonometry, or the “glaucoma test.” Most are squeamish about having someone touching their eyes (in applanation tonometry, it’s often necessary for the examiner to hold open the patient’s eyelids). Others are afraid because they remember some negative past experiences with tonometry techniques, particularly the frightening and sudden loud click associated with some “air-puff ” tonometers.

Although it’s difficult to define normal eye pressure— since what’s “normal” varies from person to person—it is generally accepted that the “average” intraocular pressure of individuals without glaucoma is around 16 millimeters of mercury. In the general population, however, there appear to be more people with pressure readings above 16 than would be expected on a purely statistical basis. Therefore, it is only when someone’s pressures reach above 20 or 21 millimeters of mercury that ophthalmologists may consider additional tests to diagnose or rule out a diagnosis of glaucoma.

Anyone with intraocular pressures above 21 millimeters of mercury is considered to have elevated intraocular pressure (or simply “elevated IOP”). Many people with elevated IOP never go on to develop glaucoma, but they must be carefully monitored for early signs of it. Some people have eye pressures of 24 for their entire lives

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and do not develop any signs of glaucoma, while other people with this pressure develop severe glaucoma. Even more perplexing are those patients with low eye pressure (see above) who develop glaucoma, which suggests, again, that glaucoma is caused by other factors besides elevated eye pressure. And although IOP does appear to be the most important factor, intraocular pressure readings by themselves are inadequate predictors of glaucoma.

To make things still more complicated, although intraocular pressures are usually highest in the early morning, they can fluctuate day to day and even hour to hour. They can be affected by such variables as age, gender, race, the presence of myopia, a family history of glaucoma, medications (for example, steroids and antihistamines), and certain systemic disorders (such as eye disease related to a thyroid disorder). Hypertension, or high blood pressure, has been associated with elevated eye pressure but not with the development of glaucoma.

The Effects of Elevated Eye Pressure in Glaucoma

Let’s take a moment to review the machinery of the eye. First, of course, light rays enter the eye. They strike the retina, where they induce chemical reactions in specialized cells called rods and cones. (For more on the eye’s anatomy, see chapter 1.) These cells then send impulses to the brain via nerve fibers—tiny telegraph lines, if you will, conveying essential information. The mass of all of these nerve fibers—approximately one million in all!— forms the optic nerve, way at the back of the eye. The