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© Robert Ritch, MD
Professor and Chief, Glaucoma Service
The New York Eye and Ear Infirmary
310 East 14th Street, New York, NY 10003

This is the first posting of this FAQ sheet. It is still under development and extensive additions will appear over the next few months.

Permission to copy all or part of this work is granted provided that the copies are not made or distributed for resale, and provided that the AUTHOR, COPYRIGHT and NO WARRANTY sections are retained verbatim and displayed as is.











It is important to note that glaucoma is NOT a DISEASE. A disease has a specific etiology, mode of onset, pathophysiology, and course, or natural history. Intervention can potentially occur at a number of different stages, from prevention, to intervention to limit progression, to cure, and to reversal of damage caused by the disease.

Over the last 50 years, what we could call the CENTRAL DOGMA has held sway. This dogma goes as follows: Glaucoma is a disease caused by elevated intraocular pressure (IOP). The elevated IOP damages and destroys the axons of the optic nerve, leading to progressive blindness. Glaucoma can be divided into two broad types - OPEN-ANGLE and ANGLE-CLOSURE. Each of these, in turn, can be divided into primary and secondary forms.

This dogma has played a major role in retarding thinking and inhibiting new approaches to understanding and therapy, and should be discarded.

Glaucoma is an end stage, analogous to congestive heart failure or liver failure. Glaucoma is an optic neuropathy characterized by a specific pattern of optic nerve head and visual field damage, which represents a final common pathway resulting from a number of different conditions which can affect the eye. While elevated IOP is the most important risk factor for the development or progression of glaucomatous damage, it is still only a risk factor and not the disease itself.

Some of the entities which lead to glaucoma are becoming well characterized, although most related conditions remain to be discovered or fully elucidated.

There are other risk factors which can lead to glaucomatous damage in the face of normal IOP. The hot research topic at the present time is that of blood supply to the eye and its regulation. An insufficient blood supply is believed to be a major risk factor for glaucomatous damage. Other possible risk factors, most of which have been as yet little explored, include autonomic insufficiency, low blood pressure, inherited or acquired abnormalities of the connective tissue of the lamina cribrosa, abnormally low intracranial pressure, autoimmune phenomena, primary ganglion cell degeneration, excitotoxins (aspartate, glutamate), and other as yet unconsidered possibilities.

Terminology is another source of confusion. The way the term "glaucoma" is used creates confusion in the minds of physicians and patients alike. For instance, we use the term primary open-angle glaucoma to refer to a patient with elevated IOP and visual damage, while reserving the term "ocular hypertension" for persons with elevated IOP but no detectable disc or visual field damage. We can also use the term "glaucoma suspect," which then includes ocular hypertensives and persons with large cup/disc ratios who may have normal-tension glaucoma but still have normal visual fields. A patient presenting with acute angle-closure, a markedly elevated IOP, but with a normal disc and field is considered to have "glaucoma," while a patient with appositional closure and peripheral anterior synechiae, but with normal IOP, discs and fields, has "chronic angle-closure glaucoma." In some instances we use the term to describe the disc and field damage, in others the angle damage, and in still others the pressure alone.

Within the category of angle-closure, the terminology is inconsistently used. Some use "angle-closure," others "closed-angle," and still others "narrow angle." The latter is particularly misleading, since it can describe a patient with primary open-angle glaucoma and narrow angles or one with actual angle-closure.

Open-angle glaucoma and angle-closure glaucoma will be described below. As a general rule, in the open-angle glaucomas, the eye is anatomically normal, but blockage or malfunction of the drain of the eye (the trabecular meshwork) leads to elevated IOP. In low-tension glaucoma, the abnormality is not in the meshwork but at the level of the optic disc. In the angle-closure glaucomas (yes, there are more than one), the trabecular meshwork is normal, but the iris is pushed against the meshwork, blocking the flow of fluid (aqueous humor) from the eye.

The analogy to a sink is a useful one. In a normal eye, the faucet is always on and the drain is always open. In open-angle glaucoma, the drain gets clogged. When this happens, aqueous can not leave the eye as fast as it produced, causing the fluid to back up. But since the eye is a closed compartment, the "sink" doesn't overflow; instead the backed up fluid causes increased pressure to build up within the eye. We need to use chemical drain-cleaner (eyedrops) to open the drain or turn down the faucet. If this is insufficient, we can snake the train (laser trabeculoplasty), and if that doesn't work, we need to put in new plumbing (surgery).

In angle-closure glaucoma, the drain is normal, but it's covered by a stopper. We need to remove the stopper (laser iridotomy or laser iridoplasty) rather than treat with medications. Open-angle and angle-closure glaucomas are about as alike as a heart attack and a bullet wound to the heart. The disease mechanisms, the basic approach to treatment, and the prognosis all differ. And that is why the terminology is confusing.


The eye captures information about shape, color, and movement and relays it in the form of nerve impulses to the brain. The brain processes this information into the "pictures" we see.

The outer, white layer of the eyeball is the sclera, a tough, leathery protective shell. The front, transparent portion of the shell is the cornea, through which light enters the eye. The cornea is much like the lens of a camera, providing the eye with much of its focusing power.

The colored portion of the eye is the iris, which functions like the diaphragm of a camera. The iris contains muscles which control the size of the pupil, regulating the amount of light entering the eye. The pupil constricts in bright light and dilates in dim light, adjusting the amount of light which passes through the pupil to the retina, which is analogous to the camera's film.

The lens behind the iris is also transparent, and adjusts its shape and thickness to fine focus the image onto the retina. When we read, the eye accommodates to refocus a near image. The lens enlarges throughout life and, after age 40, the accommodative mechanism decreases to the point at which reading glasses become necessary. When the lens opacifies, a cataract results.

After passing through the lens, the light enters the vitreous, a gel-like substance which serves as the shock absorber for the eye, and then reaches the retina. The retina then delivers the image to the brain via nerve signals which are sent through the optic nerve to the brain, which processes these signals into a "picture", or visual image.

The anterior chamber, or front compartment of the eye, is bounded by the cornea, iris, pupil, and lens. It is filled with a watery fluid called the aqueous humor. This fluid nourishes the cornea and the lens, providing them with oxygen and vital nutrients. The aqueous humor also provides the necessary pressure (IOP) to maintain the shape of the eye. The aqueous is produced by a tiny gland (the ciliary body) which runs circumferentially behind the iris, is secreted into the posterior chamber (the fluid compartment behind the iris), passes between the iris and the lens into the anterior chamber, and then flows out through the trabecular meshwork, a tiny sponge-like tissue which runs circumferentially at the corneal periphery just anterior to the iris. After passing through the trabecular meshwork, the aqueous humor enters a tiny circumferential capillary called Schlemm's canal.

In order to comprehend how increased IOP affects the eye, think of your eye as a balloon. When too much air is blown into the balloon, the pressure builds, causing it to pop. But the eye is too strong to pop. Instead, it gives at the weakest point, which is the site in the sclera at which the optic nerve leaves the eye. The optic nerve, which carries visual information to the brain, is made up of over one million nerve cells, and while each cell is several inches long, it is extremely thin-about one twenty-thousandth of an inch in diameter. When the pressure in the eye builds, the nerve cell become compressed, causing them to become damaged and, eventually, die. The death of these cells results in permanent visual loss. Early diagnosis and treatment of glaucoma can help prevent this from happening.


This is the most common glaucoma affecting Caucasians and persons of African ancestry. Its incidence increases with age. POAG has no symptoms - IOP slowly rises and the disease often goes undetected - for which reason it has been termed the "sneak thief of sight". It is painless and the patient often does not realize that he or she is slowly losing vision until the later stages of the disease. However, by the time the vision is impaired, the damage is irreversible.

In POAG, there is no visible abnormality of the trabecular meshwork. It is believed that something is wrong with the ability of the cells in the trabecular meshwork to carry out their normal function, or there may be fewer cells present, as a natural result of aging. Some believe it is due to a structural defect of the eye's drainage system. Others believe it is caused by an enzymatic problem.

Glaucoma is really about the problems which occur as a result of increased IOP. The average IOP ranges between 14 and 20 millimeters of mercury (mmHg). A pressure of 22 is considered to be suspicious and possibly abnormal. However, not all patients with elevated IOP develop glaucoma-related eye damage.

Once a sufficient number of nerve cells are destroyed, "blind spots", or scotomas, begin to form in the field of vision. These scotomas usually develop first in the peripheral field. Later, the central vision, which we experience as "seeing", is affected. Once visual loss occurs, it is irreversible because once the nerve cells are dead, nothing can restore them at the present time.

POAG is a chronic disease which is presently uncurable. However, it can be slowed or arrested by treatment. Since there are no symptoms, many patients find it difficult to understand why lifelong treatment with expensive drugs is necessary, especially when these drugs are often bothersome to take and have a variety of side effects.

When POAG occurs under the age of 35 years, it is by convention called Juvenile POAG. This is often familial. The gene is presently being actively sought. At this time, it has been localized in several large families to the short arm of chromosome 1.

Pigment dispersion syndrome is inherited as an autosomal dominant. It is expressed more commonly in myopes (nearsighted persons). The greater the myopia, the earlier the glaucoma develops. Open-angle glaucoma develops more frequently in men than in women. It most often begins in the twenties and thirties, which makes it particularly dangerous to a lifetime of normal vision. Pigmentary glaucoma is the most common glaucoma in persons under age 40, and it is far more common than previously suspected.

The anatomy of the eye plays a key role in the development of pigmentary glaucoma. Myopic eyes tend to have a concave-shaped iris which creates an unusually wide angle. In pigment dispersion syndrome, the iris seems to be extra large, so that it becomes even more concave. This causes the pigment layer of the iris to rub against the zonules, which are like wires holding the lens in place. This rubbing action causes disruption of the posterior pigmented epithelial cells of the iris, releasing pigment particles into the aqueous humor. The pigment is deposited throughout the anterior segment, including the trabecular meshwork, which becomes densely clogged with pigment, visible on examination.

Miotic therapy is the treatment of choice, but these drugs in drop form can cause disabling visual blurring in younger patients. Fortunately, a slow-release form, pilocarpine Ocuserts, are well tolerated by younger individuals. Laser iridotomy is presently being investigated in the treatment of this disorder.

This is the most common identifiable cause of glaucoma worldwide. Like pigmentary glaucoma, it has been often underdiagnosed. It is found everywhere in the world, but is most common among people of European descent. In about 10% of the population over age 50, a whitish material, which looks on slit-lamp examination somewhat like tiny flakes of dandruff, builds up on the lens of the eye. This exfoliation material is rubbed off the lens by movement of the iris and at the same time, pigment is rubbed off the iris. Both pigment and exfoliation material clog the trabecular meshwork, leading to IOP elevation, sometimes to very high levels.

Exfoliation syndrome can lead to both open-angle glaucoma and angle-closure glaucoma, often producing both kinds of glaucoma in the same individual. Not all persons with exfoliation syndrome develop glaucoma. However, if you have exfoliation syndrome, your chances of developing glaucoma are about six times as high as if you don't. It often appears in one eye long before the other, for unknown reasons. If you have glaucoma in one eye only, this is the most likely cause. It can be detected before the glaucoma develops, so that you can be more carefully observed and minimize your chances of vision loss.

Low-tension glaucoma or, as ophthalmologists now call it, normal-tension glaucoma, has been classically defined as open-angle glaucoma developing in a person in whom the IOP never goes above 22 mmHg. For a long time, this was thought to be a rare disease. It is now being realized that the number of persons with low-tension glaucoma has been vastly underestimated. In Japan, for instance, twice as many people have low-tension glaucoma as high-tension glaucoma. It is this disease (or really, group of diseases waiting to be elucidated) in which risk factors other than IOP account for damage.

The terms high-tension and low-tension glaucoma are misleading. Glaucomatous damage can be thought of as consisting of two basic forms - mechanical and nonmechanical (vascular and other). The higher the pressure, the greater the component of mechanical damage. The lower the pressure at which damage occurs or progresses, the greater the nonmechanical component. If you have a pressure of 25 mmHg and no other risk factors, it is likely that you won't develop damage. However, if you have a pressure of 25 mmHg AND other risk factors, the chance of developing damage is greater the more in number or more severe these other factors are. In the coming decade, these factors

will hopefully become much more understood. In the meantime, there is no magic number cutting off one disease from another. It is merely a statistician's reference point.


Angle-closure glaucoma affects nearly half a million people in the United States. In China and surrounding countries, it is more common than open-angle glaucoma. There is a tendency for this disease to be inherited. It is more common in hyperopes (far-sighted people).

In people with a tendency to angle-closure glaucoma, the anterior chamber is smaller than average. As mentioned earlier, the trabecular meshwork is situated in the angle formed where the cornea and the iris meet. In most people, this angle is about 45 degrees. The narrower the angle, the closer the iris is to the trabecular meshwork. As we age, the lens routinely grows larger. The ability of aqueous humor to pass between the iris and lens on its way to the anterior chamber becomes decreased, causing fluid pressure to build up behind the iris, further narrowing the angle. If the pressure becomes sufficiently high, the iris is forced against the trabecular meshwork, blocking drainage, similar to putting a stopper over the drain of a sink. When this space becomes completely blocked, an angle-closure glaucoma attack (acute glaucoma) results.

Unlike POAG, in which IOP increases slowly, in acute angle-closure, it increases suddenly. This sudden rise in pressure can occur within a matter of hours and become very painful. If the pressure rises high enough, the pain may become so intense that it can cause nausea and vomiting. The eye becomes red, the cornea swells and clouds, and the patient may see haloes around lights and experience blurred vision.

If the attack goes untreated, scarring of the trabecular meshwork may occur and result in permanent glaucoma, which is much more difficult to control. Cataracts may also develop. Damage to the optic nerve may occur quickly and cause permanently impaired vision.

Many of these sudden "attacks" occur in darkened rooms, such as movie theaters, which cause the pupil to dilate. Acute stress is another predisposing condition. When the pupil dilates, the contact between the lens and the iris is maximized. This further narrows the angle and may trigger an attack. A variety of drugs can also cause dilation of the pupil and lead to an attack of glaucoma. These include anti-depressants, cold medications, antihistamines, and some medications to treat nausea.

Acute glaucoma attacks are not always full blown. Sometimes a patient may have a series of minor attacks. A slight blurring of vision and haloes (rainbow-colored rings around lights) may be experienced, but without pain or redness. These attacks may end when the patient enters a well lit room or goes to sleep-two situations which naturally cause the pupil to constrict, thereby allowing the angle to open spontaneously.

An acute attack is an emergency condition. If the pressure is not relieved within a few hours, vision can be permanently lost. An acute attack may be stopped with a combination of drops which constrict the pupil, and drugs that help reduce aqueous production. When IOP has dropped to a safe level, laser iridotomy is the treatment of choice. This is an outpatient procedure in which a laser beam is used to make a small opening in the iris, allowing aqueous to pass directly from the posterior chamber to the anterior chamber. Since it is common for the other eye also to have a narrow angle, laser iridotomy on the unaffected eye is done as a preventative measure.

Routine examination using a technique called gonioscopy can predict one's chances of developing angle-closure. A special lens which contains a mirror is placed lightly on the front of the eye and the width of the angle examined visually. Patients with narrow angles can be warned of early symptoms, so that they can seek immediate treatment.

Not all people with angle-closure experience an acute attack. Many develop what is called chronic angle-closure glaucoma. In this case, the iris gradually closes over the drain, causing no overt symptoms. When this occurs, scars slowly form between the iris and the drain and the IOP will not rise until there is a significant amount of scar tissue formed-enough to cover the drainage area. If the patient is treated with medication, such as pilocarpine, an acute attack may be prevented, but the chronic form of the disease may still develop.


Since glaucoma is produced by many different disorders, it occurs at all ages and in all races. However, some people are at greater risk than others.

A. People over age 45. While glaucoma can develop in younger patients, it occurs more frequently with age.

B. People with a family history of glaucoma. This applies particularly to people with pigmentary glaucoma, which is strongly inherited. Juvenile POAG is also commonly inherited. A number of rare types are genetic. Adult onset POAG and exfoliation syndrome may have some hereditary tendency, but data is tenuous.

C. Myopes are more prone to develop open-angle glaucoma. Hyperopes are more prone to develop angle-closure glaucoma.

D. There is no glaucoma exclusive to any race or ethnic group. However, there are some rough epidemiologic rules. Persons of African descent are more prone to develop POAG, by a ratio to about 4:1 compared to Caucasians. Pigmentary glaucoma occurs almost exclusively in Caucasians. Angle-closure is more common than open-angle glaucoma in Asians. Everyone can develop exfoliation syndrome, but it appears to be most common in those of European descent.


A variety of diagnostic tools aid in determining the presence, absence, or predisposition to glaucoma.

The tonometer measures IOP pressure. In applanation tonometry, the eye is anesthetized with drops and, at the slit lamp, a plastic prism is lightly placed on the cornea. A strain gauge determines IOP. In air tonometry, which is less accurate, a puff of air is sent onto the cornea to take the measurement. Since this instrument does not come in direct contact with the cornea, no anesthetic eye drops are required.

Testing the visual field is the most definitive proof of glaucomatous optic nerve damage. At the present time, almost all visual field testing is done using computerized automated perimetry. The patient sits facing a computerized screen and asked to press a button whenever a flash of light appears. If the flash of light fallsinto a scotoma, it is not seen, and this registers on the printout as a blind spot. Sequential visual fields in a glaucoma patient can be used to determine whether the disease is stable or progressing

The optic nerve can be seen directly by the examiner using an instrument called an ophthalmoscope. The color and appearance of the disc can indicate whether or not damage from glaucoma is present and how extensive it is.

In this test, a mirrored lens is placed on the cornea, allowing the examiner to view the angle directly. Narrow angles and angle-closure can be detected. This test should be performed routinely on any initial complete eye examination and patients with narrow angles should be gonioscoped at routine intervals to inspect for further narrowing or capability of closure.


Glaucoma can be treated with eyedrops, pills, laser surgery, eye operations, or a combination of methods. The whole purpose of treatment is to prevent further loss of vision. LOSS OF VISION IN GLAUCOMA IS IRREVERSIBLE. Bringing the pressure under control will not restore lost vision, but only prevent further vision from being lost. Keeping the IOP under control is the key to preventing loss of vision from glaucoma. New approaches are being developed for the treatment of low-tension glaucoma [section under development].

In order to prevent further visual loss from glaucoma, the IOP must be constantly controlled. This requires taking medications chronically. If a drop is given four times a day, it is because the effect of the drop only lasts about 6 hours. Drops given twice a day have a "duration of action" of about 12 hours. Proper taking of drops and use of punctal occlusion will result in more of the drop getting into the eye and less into the blood stream, resulting in more effective treatment. Punctal occlusion and proper drop instillation are very important.

One of the most difficult problems faced by glaucoma patients is that of having to take medications which may have both ocular and systemic side effects to control a disease which is usually painless and has no symptoms. Understanding the necessity for the medication often helps to reduce the severity of a side effect, since it is often magnified by anxiety.

A side effect is any action produced by a drug beyond the intended one of lowering IOP. Some patients have no side effects whatsoever, while others find them too severe to tolerate. Why a drug causes side effects in some persons and not others or why the same side effect of the same drug is severe in one person and mild in another are poorly understood.

Quality of life is important. We sometimes have to make the decision to perform laser or surgery, even if the pressure can be controlled, if the side effects of the medications necessary for control are intolerable. It is up to the patient to participate in and ultimately make the decision in such a situation. What one should not do is skip taking the medications and lose vision because of side effects. One should also not be afraid to mention any side effects one might have or attribute to the drugs, since it is not one's fault that the drugs cause them.

All drops may cause some burning or stinging when instilled. Often, this effect is due not to the drug but to the antibacterial preservatives in the solution. It is rarely intolerable and can be used to advantage, since it lets the patient know that the drop got into the eye. Many patients don't think a drop is really medicine if it doesn't cause a little irritation.

MIOTICS are drops which help to open the drain and increase the rate of fluid flow out of the eye. The most common is PILOCARPINE. We often use CARBACHOL, which is somewhat stronger. ECHOTHIOPHATE (PHOSPHOLINE IODIDE) is even stronger but has a tendency to cause cataracts and is only used in patients who have already had cataracts removed.

EPINEPHRINE also lowers intraocular pressure by increasing the rate of fluid flow out of the eye. DIPIVEFRIN is converted to epinephrine once inside the eye.

BETA-BLOCKERS decrease the rate at which fluid flows into the eye. TIMOLOL and LEVOBUNOLOL appear to have a slightly greater pressure-lowering effect than BETAXOLOL, but the latter is safer in patients with pulmonary disease, such as asthma or emphysema, and may have less of an effect on blood pressure. Oral beta-blockers are commonly used for hypertension and angina and in these situations, also lower intraocular pressure. The latter group includes PROPRANOLOL, TIMOLOL, ATENOLOL, AND NADOLOL.

CARBONIC ANHYDRASE INHIBITORS reduce fluid flow into the eye. Formerly, pills were the only method of administration, and these had significant side effects. DORZOLAMIDE (Trusopt) is a topical carbonic anhydrase inhibitor recently approved for marketing. The most commonly used pills are ACETAZOLAMIDE (Diamox). Others are METHAZOLAMIDE (Neptazane) and DARANIDE.


It is important not to become neurotic when reading a list of possible side effects of a drug. Most patients do not get any side effects, or side effects may only be a minor bother. Serious side effects are rare. If they weren't, we wouldn't use the drugs in the first place. Sometimes, the only way to prove a side effect is due to the medication is to stop using it, wait for the reaction to go away, and try it again. This is known as retesting. If you think you have an unusual reaction to a drug, mention it. Remember that all drops may cause burning and stinging and that any drug may produce a rash. If you have an allergic reaction to a drug, you should stop using it.

MIOTICS may cause periorbital pain, browache, and pain inside the eye. This often disappears after a few days of taking the drop. Blurred vision and extreme nearsightedness are most common in younger patients, who often cannot tolerate these drops. Because miotics reduce the size of the pupil and prevent it from dilating normally in the dark, many patients complain of dim vision, particularly at night or when going into a dark room.

Systemic side effects are rare with pilocarpine, more common with carbachol, and not unusual with echothiophate. These include stuffy nose, sweating, increased salivation, and occasional gastrointestinal problems.

Rare side effects include retinal detachment, mostly on circumstantial evidence. Patients with high myopia and pigment dispersion are more prone to both retinal detachment and glaucoma.

PILOCARPINE GEL is applied at bedtime and may be substituted for drops in many patients. In addition to the convenience of not having to use drops four times a day, the effect on the pupil is often less.

OCUSERTS are pilocarpine membranes worn under the lids and changed every 5 days. These cause less blurring of vision and are especially useful in younger patients.

EPINEPHRINE COMPOUNDS frequently cause burning on instillation. A red eye is common and is an effect not of the drop initially, which whitens the eye by constricting blood vessels, but of the rebound effect when it wears off. The most common problem is development of an allergic reaction, which may occur after years of use. Epinephrine may cause palpitations, elevated blood pressure, tremor, headache, and anxiety. Dipivefrin has a much lower rate of systemic side effects.

BETA-BLOCKERS cause few ocular side effects. A few patients have complained of blurring of vision. This is more common when beta-blockers and epinephrine are used together, because this combination dilates the pupil. The most common systemic side effects include exacerbation of pulmonary disease, difficulty breathing, slowing of the pulse, and decreased blood pressure. More recently, central nervous system side effects have been reported. these include dizziness, fatigue, weakness, decreased exercise tolerance, hallucinations, insomnia, and impotence.

CARBONIC ANHYDRASE INHIBITORS commonly cause side effects. The most common are urinary frequency and tingling in the fingers and toes. These are often transient and disappear after a few days. Kidney stones may occur, but are also common without their use. A rare but serious side effect is aplastic anemia. Rashes are not uncommon. Potassium loss may occur when these drugs are taken simultaneously with digitalis, steroids, or chlorothiazide diuretics. Depression, fatigue, and lethargy are common side effects and are often not realized by the patient or by close family. These side effects may not appear immediately but develop gradually. Since many patients with glaucoma are elderly, these side effects are attributed to getting older. Patients and their families should be on the alert for these side effects and, when suspected, the drug can be stopped for a short time for verification.

Other common side effects are gastrointestinal upset, metallic taste to carbonated beverages, impotence, and weight loss. A teaspoon of sodium bicarbonate with water once or twice a day may lessen symptoms in some cases, as may taking the pills with milk before meals. These side effects have been much reduced but not eliminated with the advent of topical carbonic anhydrase inhibitor treatment.

OPEN-ANGLE GLAUCOMA. Argon laser trabeculoplasty (ALT) has become increasingly popular. It was first used as an intermediate step between drugs and surgery, but is now being used earlier in the disease process. This procedure takes between ten and twenty minutes, is painless, and is performed on an outpatient basis. The laser beam is focused on the trabecular meshwork and 50 to 100 burns over 180° to 360° placed on the meshwork. Contrary to what most people think, the laser does not burn a hole through the eye. Instead, its intense heat causes some areas of the eye's drain to shrink, resulting in adjacent areas stretching open and permitting the fluid to drain more easily. It is also possible that the laser stimulates regrowth of trabecular cells.

ALT is successful in POAG and exfoliation syndrome. Its success increases with the age of the patient and the amount of pigment on the trabecular meshwork. It is also successful in younger patients with pigmentary glaucoma. It produces borderline or poor results in most other open-angle glaucomas. Aside from pigmentary glaucoma, it should not be performed in patients under age 40.

ANGLE-CLOSURE GLAUCOMA. Laser iridotomy is the definitive procedure. Drops are not used for maintenance unless IOP remains elevated. In somewhat under 10% of patients, unusual mechanisms leading to angle-closure require an additional type of laser treatment - PERIPHERAL IRIDOPLASTY.

The most common operation is called a trabeculectomy. In this procedure, the surgeon removes a small section of the trabecular meshwork. This allows the aqueous humor to drain more easily, reducing the pressure in the eye. This procedure is usually done under local anesthesia either as an outpatient or with a brief hospital stay.

Although this is relatively safe, about one-third of patients develop cataracts within five years of surgery. After surgery, most patients are able to discontinue all medications. Perhaps ten to fifteen percent of patients require additional surgery.

Trabeculectomy has become much more successful with greatly reduced complications in the past few years with the increasing use of anti-scarring agents (5-fluorouracil and mitomycin C) and postoperative manipulations (laser suture lysis and bleb needling). [section under development]

Other procedures include implantation of plastic drains and procedures designed to reduce aqueous inflow by destroying the ciliary body. [section under development]

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