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In This Report

•	Highlights
•	Introduction
•	Causes
•	Symptoms
•	Outlook
•	Risk Factors
•	Diagnosis
•	Treatment
•	Medications
•	Surgery
•	Lifestyle Changes
•	Resources
•	References

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Glaucoma

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Glaucoma

Highlights

Risk Factors

Family history is a significant risk factor for developing glaucoma. A 2005 study indicated that siblings of patients with open-angle glaucoma have a 20% chance of developing glaucoma by the time they are 70 years old.

Treatment Research

• Dorzolamide (Trusopt) may work well in reducing eye pressure in young children with glaucoma. Promising results from a trial involving children younger than 6 years old were published in the Archives of Ophthalmology.
• The trabectome is a new type of surgical instrument that is used to perform a less invasive type of glaucoma surgery. Researchers reported at the 2005 meeting of the American Academy of Ophthalmology that surgery using this new instrument successfully reduced eye pressure in 90% of patients with open-angle glaucoma.
• Treating glaucoma in its early stages can significantly reduce economic costs for patients. According to a 2006 study in the Archives of Ophthalmology, early-stage glaucoma treatment costs patients around $600 per year, while late-stage glaucoma treatment costs more than $2500 per year.

Take Your Eye Drops

Consistently taking glaucoma medication is the best way to prevent blindness, but recent research suggests that nearly half of patients do not follow their doctor's orders. If you are skipping your medication, or have problems taking it, be sure to talk with your doctor. Here are some tips for taking eye drops:

• Tilt your head back.
• With one hand, pull the lower eyelid down to form a pocket.
• With your other hand, hold the bottle near your eye.
• After the drop, press your index finger against the corner of the eye near your nose. Gently move the lower lid upward until the eye is closed.
• Keep your eye closed for at least 1 minute.
• Wait at least 5 minutes before applying another drop.

Introduction

Glaucoma is defined as a disease of the optic nerve, in which the nerve cells in the front of the optic nerve (the ganglion cells) die. The process is irreversible. Previously, it was believed that glaucoma was almost always due to increased intraocular pressure. However, glaucoma has been observed in many patients with normal and even low eye pressure, so the definition now rests on the damage to the optic nerve.

The Aqueous Humor. For some understanding of glaucoma, it is important to first consider aqueous humor, the clear, watery fluid that circulates continuously through the anterior chamber of the healthy eye and is a primary focus of glaucoma research. (This fluid is not related to tears, nor is it the dense jelly-like substance called vitreous humor that is contained in the rear chamber.) It serves two important functions in the eye:

• It nourishes the area around the colored iris and behind the cornea.
• It exerts pressure to help maintain the eye’s shape.

Draining the Fluid and Intraocular Pressure. The aqueous fluid is continuously produced within the front of the eye, causing pressure known as intraocular pressure (IOP). To offset the in-flowing fluid and to maintain normal IOP, the fluid drains out between the iris and cornea (an area known as the drainage angle). It does so through two channels within this angle:

• The trabecular meshwork, a sponge-like, porous network, and its connecting passageways are referred to as the "conventional" outflow pathway. Most of the eye fluid outflow occurs in this region and flows from the trabecular meshwork to a group of vessels encircling the anterior chamber, called Schlemm's canal. From here, the fluid enters collection chambers and then flows out into the general blood circulatory system of the body.
• The uveoscleral pathway is located behind the trabecular meshwork and is called the "unconventional" pathway. Up to 30% of the fluid flows out through this channel.

Intraocular Eye Pressure. Previously, it was believed that glaucoma was almost always due to an abnormal rise in intraocular pressure.

Glaucoma is a condition of increased fluid pressure inside the eye. The increased pressure causes compression of the retina and the optic nerve which can eventually lead to nerve damage. Glaucoma can cause partial vision loss, with blindness as a possible eventual outcome.

Increased IOP is, indeed, present in most cases of glaucoma, but some patients have normal IOP, which is usually maintained at measurements of 10 to 20 mm Hg. Measurements above this, however, do not necessarily predict glaucoma. For example, only about 10% of people with IOP levels between 21 and 30 mm Hg will actually develop glaucoma. This still puts such individuals at considerable risk for glaucoma, however.

Primary Open-Angle Glaucoma

Most people with glaucoma have the form called primary-open-angle glaucoma (also called chronic open-angle glaucoma). Open-angle glaucoma is essentially a plumbing problem.

The disease process may occur as follows:

• The drainage angle remains open, but tiny drainage channels in the trabecular meshwork pathway become clogged. This pathway is responsible for most aqueous humor fluid outflow. An imbalance then occurs as fluid continues to be produced but does not drain out efficiently. Experts have still not definitely determined the precise area in the pathway where the blockage is most likely to occur. (In rare instances the pressure is high because the eye produces too much aqueous humor.)
• The fluid in the eye’s anterior chamber builds up and increases pressure within the eye. This is called intraocular pressure (IOP).
• The intraocular pressure exerts force on the optic nerve at the back of the eye.
• Over time, the persistent pressure or other factors irreversibly damages the delicate long fibers of the optic nerve, called axons, which convey images to the brain.
• As these axons die, the small cup-like head of the optic nerve may eventually collapse into an enlarged irregular shape.

Optic nerve damage is the basic glaucoma condition. If it is untreated, eventually the nerve deteriorates until a person loses sight, first in the peripheral vision (the vision in the "corner of the eyes"). If it becomes severe, the person loses central vision (in the middle of the eyes), and may eventually become blind. (Blindness is fortunately nearly always preventable with early treatment.)

Primary open-angle glaucoma tends to start in one eye but eventually involves both. In about half of patients the damage in the eye is diffuse, that is the nerve damage is generalized. In the other half the disease is localized, causing wedge-shaped abnormalities in the nerve fiber layers of the retina.

Normal Tension Glaucoma

Intraocular eye pressure is normal (between 12 and 22 mmHg) in about 25 - 30% of U.S. glaucoma cases, a condition known as normal tension glaucoma. (In Japan, the rates may be as high as 70%.) Other factors are present then that cause optic nerve damage but do not affect IOP.

Closed-Angle Glaucoma

Closed-angle glaucoma (also called angle-closure glaucoma) is responsible for 15% of all cases. It is less common than open-angle glaucoma in the U.S., but it constitutes about half of the world's glaucoma cases because of its higher prevalence in Asians. The iris is pushed against the lens, sometimes sticking to it, closing off the drainage angle. This can occur very suddenly, resulting in an immediate rise in pressure. It often occurs in genetically susceptible people when the pupil shrinks suddenly. Closed-angle glaucoma can also be chronic and gradual, a less common condition.

Congenital Glaucoma

Congenital glaucoma, in which the eye's drainage canals fail to develop correctly, is present from birth. It is very rare, occurring in about 1 in every 10,000 newborns. This may be an inherited condition and often can be corrected with microsurgery.

Causes

No single factor has been identified as a cause of primary open-angle glaucoma. A number of conditions, alone or in combination, are needed to trigger the processes leading to pressure in the first place and then to the nerve damage that destroys sight. The damage done to the optic nerve in glaucoma is triggered in most cases by the excessive pressure on the optic nerve that, over time, causes damage. Because optic nerve damage occurs in patients with normal as well as high intraocular pressure, however, researchers are investigating a number of other abnormal events that occur and can damage the optic nerve.

Genetic Factors

A number of genes have now been identified as possible factors in many cases of glaucoma. A gene called MYOC is of particular interest. Defects in this gene occur in between 3 - 6% of patients with adult-onset and juvenile open-angle glaucoma. They appear to overproduce a sticky protein called myocilin, which clogs the trabecular meshwork. The genes WDR36 and OPTN may cause primary open-angle glaucoma. Researchers hope that identification of genes will help improve screening of high-risk patients.

Syndromes Associated with Increased Optic Pressure and Glaucoma

Specific syndromes have been identified with glaucoma. Many have an inherited component, although in most cases, other factors must be present to activate the disease process.

Pseudoexfoliation Syndrome. Pseudoexfoliation (PEX) syndrome (also known as exfoliation syndrome) is the most common identifiable condition associated with glaucoma. In one study, 9% of patients with open-angle glaucoma had the syndrome. PEX occurs when dandruff-like matter flakes off the outer layer of the lens and collects in the drainage angle. The substance is composed of proteins produced by the lens, iris, and other parts of the eye. People can have this condition and not develop glaucoma, but they are at high risk. In one Australian study, 14% of the people with this condition had glaucoma compared to 2% of those without exfoliation. PEX has a strong genetic component but other factors (possibly sunlight, an autoimmune response, or slow virus) may be needed to trigger the disease.

Pigment Glaucoma. Pigment glaucoma starts with a condition called pigment dispersion syndrome, an inherited condition in which granules of pigment (the substance that colors the iris) flakes off into the intraocular fluid. In about 30% of cases, these fragments clog the trabecular meshwork and pressure builds up, causing glaucoma. In one study, 2% of patients had this form of glaucoma.

Irido Corneal Endothelia Syndrome. In irido corneal endothelial syndrome (ICE), cells on the back surface of the cornea spread to the drainage angle, sometimes forming scars that connect the iris to the cornea.

Neovascular Glaucoma. Neovascular glaucoma is always associated with other disorders, usually diabetes, that result in abnormal formation of new blood vessels on the iris and in the drainage system.

Aniridia. Aniridia is a rare inherited disorder (in which the iris is abnormal and increases the risk for glaucoma) that is difficult to treat. (A surgical approach called goniosurgery may help prevent glaucoma in young people with aniridia.)

Congenital Glaucoma. When an infant is born with glaucoma (congenital glaucoma), it is usually caused by an inherited abnormality in the drainage canal. Researchers have identified the gene responsible for 85% of these cases.

Causes of Closed-Angle Glaucoma

People with acute closed-angle glaucoma often have a structural defect that causes a narrow angle between the iris and cornea where the aqueous humor circulates. Conditions that suddenly dilate the pupils may cause this shallow angle to close and precipitate attacks of acute glaucoma in susceptible people. Such conditions may include the following:

• Certain drugs such as antihistamines, tricyclic antidepressants, some asthma medications  (nebulized ipratropium), some anti-seizure drugs (topiramate)
• Darkness
• Emotional stress

Causes of Secondary Glaucoma

When intraocular pressure leading to glaucoma is caused by other diseases or conditions, it is known as secondary glaucoma. Secondary glaucoma may be chronic or acute, mild or severe.

Medical Conditions. A number of diseases can contribute to the development of intraocular pressure leading to glaucoma:

• Diseases that affect blood flow to the optic nerve (diabetes, high blood pressure, migraine)
• Hypothyroidism
• Sleep apnea
• Physical injury in the eye
• Extreme nearsightedness (myopia)
• Previous eye surgery
• Other disorders, including leukemia, sickle cell anemia, and some forms of arthritis

Corticosteroids. Corticosteroids, commonly called steroids, have multiple effects on the trabecular meshwork and may even cause genetic changes. In fact, studying the effects of steroids on the eye is helping researchers understand the glaucoma disease process. Steroids pose a higher or lower risk depending on the form:

• Taking topical steroid treatments in the eye poses the highest risk. It must be monitored carefully since, in some cases, damage may be permanent.
• Taking oral corticosteroids, particularly in high doses or for long periods, increases the chance of glaucoma. In such cases, the eye disorder typically develops almost immediately and reverses within 2 weeks after the drug has been withdrawn.
• Inhaled steroids were not thought to cause glaucoma, but there is some risk in people with a family history of glaucoma and other risk factors.

Symptoms

Chronic glaucoma is insidious; if the pressure increases slowly, it will not produce any symptoms until it has done irreversible damage. In such cases, people may notice visual problems at first only when light is dim. Patients are often sensitive to glare. Eventually they may lose contrast sensitivity; that is, they might have trouble differentiating between varying shades and brightness.

Symptoms of Closed-Angle Glaucoma

In acute closed-angle glaucoma, the pressure inside the eye increases quickly, and the symptoms are dramatic. Intense pain in the eyebrow area and blurred vision develop usually in one eye and the patient often feels like the eye will burst (although it won't). The eye usually reddens. A person may see rainbow-like halos around lights. Sometimes nausea and vomiting occur. These symptoms may occur on and off and not appear as a full-attack. In either case, they indicate a medical emergency. In chronic closed-angle glaucoma the process is gradual and painless.

Symptoms of Congenital Glaucoma

Although congenital glaucoma is usually present at birth, symptoms generally don’t develop in the infant for a few months. If parents notice that an infant’s eyes are enlarging, becoming cloudy, often watering, or tending to close in the presence of light, they should have an ophthalmologist examine the child’s eyes. Port-wine stains on an infant’s face could indicate the Sturge-Weber syndrome, a disorder that occasionally causes glaucoma.

Outlook

Worldwide, glaucoma ranks as one of the leading causes of blindness. Even if people with glaucoma do not become blind, vision can be impaired. In developed countries, most people get treatment in time to preserve their vision. Even so, glaucoma causes between 3 - 6% of blindness cases in Caucasian Americans, and even more cases in African Americans. In a 20-year study of Caucasian American patients with glaucoma, blindness in at least one eye occurred in 27% of patients and blindness in both eyes occurred in 9% of patients. The blindness rates in African Americans are most likely higher. In fact, glaucoma is the leading cause of blindness in African Americans. Despite this higher prevalence, this ethnic group receives surgical treatment at half the rate of Caucasian Americans.

Outlook for Primary Open-Angle Glaucoma

The Process Leading to Vision Loss. Chronic glaucoma is often called “the silent thief of sight," because the afflicted person has no warning sign, no hint that anything is wrong. Untreated, the destruction develops slowly over time:

• Over years or decades, the increased pressure compresses nerves at the back of the eyes.
• Glaucoma gradually destroys first the outer fibers of the optic nerve, which reduces peripheral vision (the top, sides, and bottom areas of vision), but not central vision.
• By the time a person notices that peripheral vision has been lost, permanent damage has already occurred.
• If the eye pressure remains high, the destruction can progress until tunnel vision develops, and the person is only able to see objects that are straight ahead.
• The last nerve fibers destroyed are those responsible for central vision; if this occurs, the glaucoma victim becomes totally blind.

Although there is no cure for open-angle glaucoma, a number of treatments are available that lower intraocular pressure and slow progression of vision loss.

Risk Factors for Vision Loss. Estimates of progression rates in vision deterioration range from 9 - 30% over a 2 to 7 year period.

According to a study on patients with elevated IOP, for every 1-mm Hg increase in IOP, there is a 10% higher risk of disease progression. A very elevated IOP (above 30 mm Hg) is certainly hazardous. An elevated IOP that is below 30 mm Hg, however, is not necessarily the most important factor in determining the risk for disease progression. Some evidence suggests that frequent and large daily fluctuations in intraocular pressure, not simply high IOP, are associated with the greatest risk for loss of vision. Having normal-tension glaucoma with optic nerve damage also carries a high risk for progression, even if eye pressure is reduced.

In any case, factors other than IOP play a role in increasing the chances for progression and vision loss in patients with slightly elevated IOP and normal tension glaucoma:

• Both eyes affected
• Pseudoexfoliation (PEX) syndrome. PEX occurs when proteins produced in the eye flake off the outer layer of the lens and collects in the drainage angle.
• Bleeding in a specific region called the peripapillary nerve fiber layer
• Thin corneas. (People who have thick corneas and elevated IOP may only need to be monitored if they have no other risk factor for vision loss.)
• Larger cup-to-optic disc ratio. (The cup of the optic disc is the center portion, which enlarges as nerve damage progresses.)

Non-eye related factors associated with disease progression include being elderly, African American, female, or having a history of migraines.

Severity of Acute Closed-Angle Glaucoma

Acute closed-angle glaucoma is a medical emergency; if the high pressure is not reduced within hours, it may permanently damage vision. Anyone who experiences its symptoms should immediately contact an ophthalmologist or go to a hospital emergency room.

Risk Factors

An estimated 2 million Americans have open-angle glaucoma, but an exact count is unclear. Half of people with glaucoma are unaware of this problem because the condition causes no symptoms. Elevated intraocular pressure in the eye occurs in 5 to 10 million Americans but only about 10% of such people develop glaucoma because of this pressure. And, in 15% of actual glaucoma cases, IOP is normal. Major studies are helping to clarify the people who are at highest risk for glaucoma and optic nerve damage, including those with normal tension glaucoma.

Elderly. The prevalence of chronic glaucoma increases with age. In a major study, 0.6% of people aged 60 to 64 had primary open-angle glaucoma. Among people who were ten years older, the prevalence had more than doubled to 1.3%, and among those who were aged 80 to 84, it had more than doubled again to 3%.

People of African Descent. Across all age groups, according to a 2000 report, the prevalence of glaucoma in African Americans is about 3.5% compared to about 1% in Caucasian Americans. In addition, US studies suggest that glaucoma develops earlier in African population groups (starting at age 45 instead of 60 in Caucasians). And, their risk for blindness once they have glaucoma is 14 to 17 times that of Caucasians with glaucoma. African American men are at higher risk than women are. African American children who are extremely near-sighted and have relatives with glaucoma should begin regular eye examinations for glaucoma as early as possible.

In a major glaucoma study in Barbados, where most people are of African descent, over 10% of those 50 and older had open angle glaucoma, and over 15% were afflicted after 70. About half of the cases had normal or lower eye pressure. There was an interesting 2001 study in which African Americans tended to have significantly thinner central corneas than Caucasians. This could lead to misleadingly lower pressure scores in African American patients who actually may have high IOPs.

Family History. Glaucoma tends to run in families.  Brothers and sisters of patients with open angle glaucoma are 5 times more likely to develop glaucoma by the time they are 70 years old than people whose siblings do not have the disease.Previous studies have also found that people with family histories of glaucoma are more likely to already have some vision loss when they are  first diagnosed with glaucoma.

Effects of Blood Pressure. The association between a person's blood pressure and intraocular pressure in the eye is not entirely clear. A number of studies have found a higher risk for glaucoma in people with high blood pressure. A 2002 study suggests, however, that people with blood pressure that is low relative to their intraocular pressure may be at higher risk for glaucoma. The same study found no higher risk for glaucoma in people with hypertension, and in fact, high blood pressure was associated with a lower risk.

Having Certain Medical Disorders. Individuals with certain medical or physical conditions, including diabetes, migraine, nearsightedness, and sleep apnea, appear to have a higher risk. Conditions that require the use of any oral or inhaled steroid, particularly high doses for prolonged periods of time, can cause glaucoma. Previous eye surgery also puts people at risk.

Risk Factors for Other Forms of Glaucoma

Risk Factors for Closed-Angle Glaucoma. Chronic closed-angle glaucoma tends to be more common in people of Asian and African descent. Those who have this condition are often extremely farsighted. Acute closed-angle glaucoma occurs much more frequently in women than in men.

Risk Factors for Normal Tension Glaucoma. Risk factors for normal tension glaucoma include Japanese ancestry and a family history of the disease. It is more common in women than in men. A family history of cardiovascular disease also increases the risk.

Risk Factors for Pigmentary Glaucoma. Pigmentary glaucoma occurs three times more often in men then in women and at a younger age.

Risk Factors for Irido Corneal Endothelial Syndrome. This condition occurs more often in light-skinned women.

Diagnosis

A diagnosis of glaucoma no longer simply relies on the presence of pressure within the eye. It requires that there be optic nerve damage or a strong suggestion of damage, which can be clearly seen during a dilated eye examination of the optic nerve. In general, the hallmark sign of this condition is a loss of peripheral vision. With peripheral vision loss a person can see in front of him- or herself but has lost the vision to the side.

The optic nerve carries the information of vision from the eye to the brain.

Because chronic glaucoma has no warning symptoms, half of its victims are unaware that they have the condition. Early diagnosis, however, is the key to successful treatment of glaucoma. One study reported that the more years since the last visit to an eye professional, the greater the risk for having visual loss.

Tonometry and Pressure Tests

Doctors determine the intraocular pressure (IOP) of the aqueous humor inside the eye using tonometry, which measures the force necessary to make an indentation in the eye. There are several methods:

• In the Schiotz method, the doctor first anesthetizes the eye with drops, then presses very lightly against it with tonometer, a tiny smooth instrument that is used to measure the pressure.
• In the applanation method, the doctor touches a strip of orange-dyed paper to the side of the eye. The stain helps with the examination and rinses out with tearing. The doctor uses a slit-lamp, which is moved forward toward the patient's face until the tonometer touches the eye.
• The noncontact approach applies a puff of air and measures the force needed to indent the eye.

Attempting to close the eyelids during the test can increase eye pressure and produce errors in the results.

In general, normal IOP is usually maintained at measurements of 10 to 20 mm Hg. Glaucoma pressure over 21 mmHg indicates a potential problem. The test is not completely accurate, however. Only about 10% of people with IOP levels between 21 and 30 mm Hg will actually develop glaucoma and optic nerve damage. On the other hand, many people with glaucoma have normal pressure, at least part of the time.

Measurement of Cornea Thickness

The cornea thickness may be an important indicator of disease progression in patients with elevated IOP. According to some research, patients with thinner corneas have a significant risk for developing damage from glaucoma, while those with thicker corneas have a low risk.

Tests for Optic Nerve Damage

In order to determine early damage in the optic nerve, a number of diagnostic instruments have been developed to assess the nerve fiber layers at the back of the eye (the fundus) and to check for optic disk cupping. (The cup of the optic disc is the center portion, which enlarges as nerve damage progresses.) The two most common procedures for identifying nerve damage are ophthalmoscopy and fundus photography. Other instruments have been developed, including those that use laser technology and computers, but none have proved to be infallible. No test has proven to be completely accurate, however, and none is routinely performed by all eye professionals.

In order to be accurate, the tests require a skilled professional and there are certain common factors:

• The pupils must also be widely dilated using eye drops before the procedure.
• Even mild cataracts and a slightly less-than-optimally dilated pupil can degrade the results. Such conditions are common in elderly people, who are the most likely to develop glaucoma.
• If the back of the eye is lightly pigmented (colored), the area under observation is less distinct.
• If the glaucoma is diffuse and there is a generalized loss of nerve fiber (which occurs in half of patients), it is more difficult to detect than if the glaucoma is more localized.

If IOP is low or normal and tests report optic nerve damage and peripheral visual loss, doctors should also check for other conditions before starting any treatment for glaucoma. Such problems include steroid use, anemia, and previous hemorrhage or severe low blood pressure.

Ophthalmoscopy. The eye professional (or even a primary care doctor) uses an ophthalmoscope to peer through the pupil directly at the optic nerve. The examiner can then check the shape and color of the nerve fibers to evaluate whether they have been damaged by the high pressure of glaucoma. Damaged nerve fibers may be indicated by the following:

• An asymmetrical or elongated cupped optic nerve.
• The optic nerve color may be pale or an unhealthy-pink.

If results show no optic nerve damage in patients who have mild elevations in pressure, the ophthalmologist may want to retest frequently but delay drug treatment, unless the patient has significant risk factors.

Fundus Photography. Fundus photography may be used to take pictures of the optic nerve and can reveal changes years in advance of vision loss. It is an unpleasant procedure requiring drops and a bright flash. This procedure has the same limitations as ophthalmoscopy.

Laser Polarimetry. Polarimetry uses laser technology to scan the eye and does not require any response from the patient. It is reported to be able to measure nerve fiber thickness in the eye and so be able to reveal early signs of deterioration. Preliminary studies have indicated that it has a diagnostic accuracy of over 90% for both confirming and ruling out glaucoma. A recent study, however, reported that laser polarimetry was sensitive enough to detect glaucoma in only up to 57% of patients with early glaucoma, 71% of those with moderate disease, and 81% of those with severe glaucoma. More work is needed.

Other Devices. Computer-assisted devices, such as the confocal scanning laser ophthalmoscope, are now available that may be useful for evaluating the retinal nerve layer. Another instrument, the optical coherence tomograph, measures the echo time delay of light that is scattered back from different layers in the retina. The value of these tests has not yet been determined.

Perimetry and Other Tests of the Visual Fields

If there is indication of optic nerve damage, the eye professional will conduct tests of the visual fields (the areas that the patient can see). In most people with glaucoma, the first areas to become noticeably impaired are the peripheral visual fields (areas of sight that are not directly in front of a person but more to the sides).

Click the icon to see an image of the visual field test.

Standard Perimetry Tests. Perimetry tests are used to check peripheral vision. One variation of this test is as follows:

• A person sits closely facing a large computer-like monitor.
• Small bright white lights flicker on and off hundreds of times, at different places on the screen, while the patient clicks a button whenever one of the lights is seen.
• The machine prints out a report that maps any blanked-out areas in the person’s vision.

The test is complex and lengthy; elderly people and those with short attention spans may be inappropriate candidates. Other perimetry tests, some requiring less time to administer and some using "virtual reality" techniques, are currently being developed.

Other Tests. Other visual field tests are being developed that can detect abnormalities years before they can be detected by standard perimetry. Experts recommend some of these tests in selected patients with suspected glaucoma.

For example, a screening test called frequency doubling technology (FDT) checks for changes in particular cells in the retina that are indications of early glaucoma. It takes less than a minute to perform.

Another test called short wave automated perimetry (SWAP) uses colors (blue-on-yellow) and also detects very early abnormalities in the visual field. Testing time is longer than with FDT, however, and the presence of certain types of cataracts can interfere with its accuracy.

Markers

ELAM-1. Endothelial leukocyte cell adhesion molecule 1 (ELAM-1) is a molecule that has been found in glaucoma but not in healthy eyes. This molecule may prove to be a "marker" and its presence may be helpful in diagnosing glaucoma.

Test for Acute Closed-Angle Glaucoma

A simple test using a penlight helps determine the risk for acute closed-angle glaucoma. A beam of light is directed from the side of the face toward the patient's iris. If no shadow appears on the nose, then most likely the angle is wide enough to dilate. Using an instrument called a gonioscope, ophthalmologists can also inspect the front of the eyes and assess the drainage angle between the cornea and the iris and the channels in the trabecular meshwork. This test can differentiate between closed and open angle glaucoma.

Treatment

Most treatments for glaucoma are aimed at reducing ocular pressure and its fluctuations. Early treatment with medications, surgery, or both can nearly always maintain safe pressure of the aqueous humor, thus preventing optic nerve damage and blindness. The choice between surgery and medications and when to start treatment is not always straightforward. For example, with the introduction of beta blockers and newer glaucoma drugs, there has been a decline in surgeries. It is not clear, however, which drugs are more effective than others and if, over time, any will actually prevent surgery. The patient should discuss all issues with both the regular doctor and ophthalmologist.

Decision to Start Treatment

Many people have high IOP but no sign of nerve damage, and over 20 years, only between 10 - 30% of these people will actually develop glaucoma. Nevertheless, once glaucoma has destroyed optic nerve fibers, no known treatment can reverse the damage.

Indeed, studies are suggesting that in people with glaucoma, even very small differences in pressure may mean the difference between disease progression and stability. An important trial reported that, on average, treating patients when their glaucoma was first detected reduced IOP by 25%. In addition, treatment reduced the risk for progression by 17%. This well-conducted trial confirmed previous findings supporting early treatment for glaucoma. Another study found that treatment with eye drops halved the risk of developing open-angle glaucoma in African Americans who had elevated intraocular pressure. Some evidence suggests that early treatment to lower IOP may be beneficial even in patients with normal tension glaucoma.

However, not all individuals with early signs of glaucoma (elevated IOP or normal tension glaucoma) develop optic nerve damage and serious vision problems. Nor does treatment prevent progression in a large minority of patients. Medications used for glaucoma also can carry significant side effects and risks, including for serious cataracts.

Some experts suggest, then, that treatment is warranted only in people with early signs of glaucoma who have risk factors for progressive disease and vision loss (e.g., thinner corneas, larger cup to optic disc ration, older age, and elevated pressure).

Considerations for Drug Treatments

A number of effective drugs are now available for treating glaucoma. The drugs reduce pressure in the eye but all have a number of side effects that affect other parts of the body. Some of these side effects can be quite severe. Many of the drugs used for glaucoma also interact with common medications for other conditions. To compound the difficulties, many patients require multiple drugs. As a result, only about half of patients comply with their treatments. (About a quarter can be cajoled into resuming treatment, but the rest refuse their medications.)

Experts generally recommend topical drugs first (those that can be used as eye drops or ointments rather than taken orally).

• Topical beta blockers are the standard first-line drugs, most commonly timolol (Timoptic). Newer beta blockers include betaxolol (Betoptic), levobunolol (Betagan), carteolol (Ocupress), and metipranolol (OptiPranolol). Timolol has been used for years, and these drugs are well tolerated.
• Topical prostaglandins are alternatives if beta blockers fail. They include latanoprost (Xalatan) and unoprostone (Rescula). Of the standard drugs used for glaucoma, these drugs have the greatest effect on lowering IOPs. They also have fewer widespread effects than the beta blockers.
• Topical carbonic anhydrase inhibitors (CAIs) are less effective than standard beta blockers or prostaglandins but have fewer widespread effects than the beta blockers. They may be helpful in certain cases. Topical forms are dorzolamide (Trusopt) and brinzolamide (Azopt). (Oral CAIs are available and more effective, but they have severe side effects and are rarely used for the long term.)
• Alpha2-adrenergics, also called selective alpha adrenergics, are effective but may not be as well tolerated as timolol. They include brimonidine (Alphagan).
• Miotics, which include pilocarpine and others, were the standard drugs before the introduction of topical beta blockers. They have now been largely replaced by timolol and others, although they are sometimes used in combinations.
• Beta blockers and newer drugs (prostaglandins, topical CAIs, and selective alpha adrenergics) are now preferred over the older drugs, which include miotics, oral CAIs, and nonselective alpha adrenergics.

Combinations. Combinations of these drugs can be very effective, because they tend to have different actions. Single medications that contain two drugs are becoming available. For example, Cosopt combines timolol and dorzolamide; Timpilo is a combination of timolol and pilocarpine. Studies of these and other combinations compared to each other to single drugs are ongoing. To date, results on any superior combinations have been mixed. It should be noted that the side effects of each drug apply to any combination.

Treating the Pregnant Patient. Considerations for a pregnant woman with glaucoma can be complicated. All of the drugs used for glaucoma are absorbed by the body, cross the placenta, and are excreted in breast milk. Many have effects that can interfere or adversely affect the pregnancy itself.

Women should discuss going off medication, particularly during the first trimester, and be monitored during that time for an increasing pressure. IOP tends to drop during pregnancy, although usually not to a significant degree. If women need medications, they should try to achieve the lowest dose possible. Some drugs may have fewer effects than others. Animal studies, for example, suggest that brimonidine may be safer than other glaucoma drugs during pregnancy.

They must also be very scrupulous about administering eye drops to allow as little medication as possible to enter the body's system. Even this approach, however, does not guarantee safety. Women with glaucoma who are planning to become pregnant might want to consider surgery before they conceive.

Considerations for Surgery

The object of standard glaucoma surgery is to reduce pressure in the eye by increasing the outflow of the aqueous fluid. Two methods are now available:

• Filtration surgery (trabeculectomy). This employs standard surgical instruments to open a passage in the eye for draining fluid.
• Laser trabeculoplasty. This procedure uses a laser to burn 80 to 100 tiny holes in the drainage area.

Both are effective, but certain patient groups may respond to one more than the other. For example, in general, African Americans may do better with laser surgery while trabeculectomy may be a better choice for Caucasians with no serious medical problems.

In general, surgery is a last resort. Doctors may, however, recommend surgery before drug therapies for patients unlikely to comply with difficult drug regimens or for patients who may have severe reactions from the glaucoma drugs. Women who plan on becoming pregnant should also discuss surgery with their doctor.

Some studies are indicating that laser treatment performed as the initial treatment for glaucoma is as effective as medications in some cases. Findings in 2003 from a major comparison study suggested that 4 years after surgery there was little difference in visual field loss between trabeculectomy and medical treatment. There was, however, a higher risk for cataracts and loss of vision sharpness with surgery. On the other hand, side effects from medications may be ongoing and troublesome. It is important to note, however, that even surgery does not cure glaucoma, and over half of patients will require medication within 2 years. Experts who are against early surgeries also argue that studies on their success often omitted serious postoperative problems, such as late-onset infection, and quality of life assessments.

Medications

Nearly all glaucoma medications are are prescribed for reducing eye pressure. Lowering IOP is even proving to be beneficial for about two-thirds of patients with normal pressure glaucoma.

Beta Blockers (Timolol and Others)

Topical beta adrenoceptor blockers (common called beta blockers) are the drugs most often prescribed to treat glaucoma. They lower the pressure inside the eye by inhibiting the production of aqueous humor.

Brands. These drugs are categorized as either nonselective or selective beta blockers:

• Nonselective adrenoceptor beta blockers. Timolol (Timoptic, Betimol) has been the standard beta blocker for years. Newer nonselective drugs are levobunolol (Betagan), carteolol (Ocupress), and metipranolol (OptiPranolol). A few studies suggest some are more beneficial than timolol with similar side effects.
• Selective beta1-adrenoceptor blockers. Betaxolol (Betoptic) and levobetaxolol (Betaxon) are selective beta blocker. These drugs appear to have fewer adverse effects on the heart than the nonselective beta blockers, although they still have widespread effects. Studies also suggest that they slow progression more than timolol does, although timolol is more effective at lowering IOP. Such findings indicate that these selective beta blockers may also have nerve-protecting properties.

All beta blockers are effective and generally well tolerated. Because they cause less eye irritation than many other glaucoma medications, they are often prescribed for patients who also have cataracts.

Side Effects and Complications. After the beta-blocker is administered, only a tiny amount of the drug is absorbed by the cornea. Most of it enters in the bloodstream. These drugs, therefore, can cause side effects in parts of the body other than the eyes, called systemic side effects:

• Common systemic side effects include reduced sexual drive, fatigue, depression, anxiety, severe nausea and vomiting, and breathing difficulties.
• Beta-blockers affect the heart. They lower heart rate and reduce blood pressure. (The newer selective beta-1 blockers may not have as adverse effects on the heart as the nonselective beta blockers.) They may also cause unhealthy cholesterol and triglyceride changes.
• All beta-blockers can worsen severe asthma or other lung diseases. Beta-blockers should only be used very cautiously or not at all by anyone with asthma, emphysema, bronchitis, or heart disease. Lung function was found to be reduced in 40% of elderly people who took timolol, even those without previous symptoms of lung problems. (Selective beta blockers may produce fewer of these adverse effects.)
• If the patient is switching to a beta blocker from other glaucoma medication, there may be a sudden rise in eye pressure. It is important, therefore, that the pressure be checked shortly after the other drug has been withdrawn.
• When beta blockers are used to treat one eye, the other (contralateral) eye also experiences a lesser, but still significant reduction in IOP.

Interactions with Other Medications. The effects of the eye medication may be additive to other oral medications, such as oral beta-blockers, calcium-channel blockers, or the antiarrhythmic drug quinidine. Diabetics on insulin or hypoglycemic medications should realize that timolol side effects may resemble and mask the symptoms of hypoglycemia.

Prostaglandins

Prostaglandins are hormone-like substances that help open blood vessels. Drugs that resemble prostaglandins increase outflow through the uveoscleral pathway (not the trabecular meshwork). Some experts believe that the uveoscleral pathway may be responsible for up to 50% of outflow in healthy eyes, which could explain the very large benefit produced by drugs acting on this channel.

Brands. Latanoprost (Xalatan) and unoprostone (Rescula) are the standard brands.Latanoprost is the first prostaglandin to be approved as first-line treatment for elevated eye pressure. Two newer prostaglandins, travoprost (Travatan) and bimatoprost (Lumigan), are showing great promise and may effective in some patients who do not respond to latanoprost. These drugs may also benefit patients with normal-tension glaucoma. Latanoprost, travoprost, and bimatoprost need to be taken only once daily. Unoprostone needs to be taken twice a day and is not as effective as others, but it still can reduce IOP significantly and is the least expensive of these drugs.

Latanoprost has been shown to reduce pressure by between 45 - 70%. Some, but not all studies, have suggested that newer prostaglandins travoprost (Travatan) and bimatoprost (Lumigan) are more effective than latanoprost, but the older drug appears to be better tolerated. All of these drugs may be more effective than timolol in lowering IOP. The newer prostaglandins may be especially superior to timolol in treating African American patients. In comparison studies, latanoprost achieved better IOP pressure reduction than brimonidine. Studies have suggested that bimatoprost is more effective in lowering eye pressure than a combination of timolol and dorzolamide (Cosopt). Studies have been mixed on whether latanoprost is superior to the combination.

Side Effects. These drugs do not slow the heart rate down and also appear to be safe for people with asthma. Side effects include itching, redness, and burning during administration. Muscle and joint pain may also occur. All of these drugs may permanently change eye color from blue or green to brown. To date, such color changes do not seem to be hazardous. (The only significant problem appears to be cosmetic in people who treat only one eye, since the color may differ from the other.) These drugs can increase blood flow in the eye and also make eyelashes become thicker and longer in some patients. (These latter effects are more common with bimatoprost and travoprost than with latanoprost.)

Carbonic Anhydrase Inhibitors

Carbonic anhydrase inhibitors (CAIs) decrease eye pressure by reducing the fluid in the chambers of the eye (aqueous humor). Research suggests that CAIs reduce aqueous humor fluid by as much as 40%. These drugs are used for glaucoma when other drugs do not work. They may be combined with other medications.

CAIs may also improve blood flow in the retina and optic nerve (beta blockers do not). Improving blood flow can keep the disease from getting worse

Brands and Side Effects. CAIs are available in the following forms:

• Eye drop CAIs include dorzolamide (Trusopt) and brinzolamide (Azopt). About 10% of patients report fatigue, stinging in the eye, and loss of appetite using dorzolamide. Taste changes can occur. Research suggests that dorzolamide can be helpful for children with glaucoma, including those younger than 6 years old. Brinzolamide is a newer medication that was chemically designed to be closer in pH to human tears and may cause less stinging than dorzolamide.
• Oral forms include acetazolamide (Diamox), methazolamide (Neptazane), and dichlorphenamide (Daranide). Although they are more effective than eye drops, they have significantly more side effects and are rarely used for long-term treatment. The oral forms have very unpleasant side effects that include frequent urination, depression, stomach problems, fatigue, weight loss, sexual dysfunction, and, in infants, failure to thrive. Long-term use of the oral forms, in rare cases, can cause serious anemia and kidney problems, including the risk for stones. They can also produce a toxic reaction when taken with large doses of aspirin.

Adrenergic Agonists

Adrenergic agonists activate muscles in the eye that dilate pupils and, therefore, increase outflow of aqueous fluid. Newer variations called alpha 2-adrenergic agonists reduce production of aqueous humor and also increase outflow through the uveoscleral pathway (the alternative channel to the trabecular meshwork). Older adrenergic agonists include epinephrine.

Alpha 2-Adrenergic Agonists. Apraclonidine (Iopidine) and brimonidine (Alphagan) are alpha 2-adrenergic agonists. These have generally been used before glaucoma surgery, but a number of studies are indicating that they may even be useful as primary therapy when used in combination with beta-blockers or other standard drugs.

Brimonidine is proving to be particularly effective for long-term therapy. (Apraclonidine is used for the short term.) It also may have nerve-protecting properties and may be safer than other drugs during pregnancy and for patients with asthma.Studies are finding that brimonidine was as effective and resulted in a better quality of life than the newer beta-blocker betaxolol. Comparison studies indicate that the combination of brimonidine and latanoprost is superior to timolol/dorzolamide (Cosopt) in lowering IOP.

The most common side effects of brimonidine and apraclonidine are dry mouth and altered taste. They also commonly trigger an allergic reaction that causes red and itching eyes and lids, a major drawback. Brimonidine causes less of an allergic response than apraclonidine. Unlike apraclonidine, however, it can cause lethargy and mild low blood pressure. It also appears to remain effective longer.

Miotics (Pilocarpine and Others)

Miotics, also called cholinergic agonists, narrow the iris muscles and constrict the pupil. This action pulls the iris away from the trabecular meshwork and allows the aqueous humor to flow out through the drainage channels, reducing the pressure inside the front of the eye.

Brands. Pilocarpine (Pilocar, Adsorbocarpine, Almocarpine, Isoptocarpine, Ocusert) and was the most widely used anti-glaucoma drug before timolol was introduced. It is the preferred miotic. Because pilocarpine is used up by the body fairly quickly, however, patients must take it several times a day; many people, therefore, fail to take their medication regularly. A combination of timolol or latanoprost with pilocarpine is more effective than either drug used alone. Carbachol is another miotic.

Demecarium (Humorsol), isoflurophate (Floropryl), and echothiophate (Phospholine) are a group of long-acting drugs known as anticholinesterase miotics. Because of their potential for serious side effects, however, some authorities even prefer surgery to their use.

Epinephrine and its derivatives are the older anticholinergics. Epinephrine is now rarely prescribed because of side effects. Dipivefrin (Dipivefrin), a newer form of epinephrine, remains inactive until it reacts with enzymes in the cornea. It is effective in low doses and causes few systemic side effects.

Side Effects. Side effects include the following:

• Teary eyes, brow-aches, eye pain, and allergic reactions.
• A miotic narrows the pupil and so can cause nearsightedness. Vision can also become dim and it may difficult to see in darkened rooms or at night, when driving could be hazardous. A gel form administered once a day or wafer placed under the lid once a week may help reduce these side effects. Small amounts of an adrenergic drug, such as epinephrine, may also help.
• The anticholinesterase miotics increase the risk of cataract development and are therefore used mostly in patients in whom cataracts have already been removed. Retinal detachment is an uncommon but dangerous side effect in susceptible individuals. Excessive use of these miotics may cause toxic reactions, including convulsions, muscular paralysis, and even death from respiratory failure.
• Epinephrine can produce burning in the eyes, enlarged pupils, and allergic reactions. Occasionally it can cause anxiety and headaches. Rare side effects include high blood pressure and disturbances in heart rhythm. It is rarely prescribed now. Although dipivefrin, the newer form of epinephrine, has fewer systemic side effects, it still causes problems in the eyes similar to those of epinephrine.

Experimental Therapies

Cannabinoids. Cannabinoids, compounds in marijuana (cannabis), are being studied for their effects on glaucoma. For example, oral or inhaled tetrahydrocannabinol (THC), the active ingredient in marijuana, has been shown to reduce IOP in 60 - 65% of patients. The effects of smoking marijuana on IOP last only 3 hours, however. THC also increases the release of glutamate--a nerve protecting chemical. Experts are hoping that topical use of THC or other cannabinoids may help prevent optic nerve damage without the widespread effects of oral or inhaled administration.

Drug Therapy for Acute Closed-Angle Glaucoma

In this emergency situation, ophthalmologists may administer a combination of two or more anti-glaucoma medications to reduce eye pressure quickly before it can damage the optic nerve and cause visual loss. Apraclonidine (Iopidine) is a powerful drug used before and after laser surgery to prevent an increase in fluid pressure and is more effective than other medications. In addition to standard drugs, doctors may also administer glycerin (Glyrol, Osmoglyn) by mouth or mannitol or acetazolamide intravenously. Surgery is almost always performed once the pressure is reduced.

Therapies for Less Common Glaucomas

Most rare forms of glaucoma respond to the same medications and surgery used for open angle glaucoma. Irido corneal endothelial syndrome (ICE) is difficult to treat and if surgery is required, filtering surgery is the best choice. Neovascular glaucoma is also very hard to treat; researchers are investigating drainage implants for this disorder.

Surgery

If medications do not control eye pressure or if they create intolerable side effects, surgery may be necessary in a small percentage of people with chronic glaucoma. It may be particularly beneficial for patients with pseudoexfoliation glaucoma.

The standard procedures are usually one of the following:

• Filtration surgery (trabeculectomy). This procedure opens the full thickness of the drainage area.
• Laser trabeculoplasty. This procedure partially opens the drainage area. It does not reduce pressure to the extent of trabeculectomy but it has fewer adverse effects.

African Americans may respond better to initial laser surgery than to conventional trabeculectomy while the opposite may be true in Caucasians. Some experts now recommend that, in most circumstances, African Americans should start with laser surgery and Caucasians who have no serious medical problems should have trabeculectomy first.

In addition, a number of experimental and less invasive procedures are under development.

Filtration Surgery (Trabeculectomy)

The Procedure. Filtration surgery has been used for more than 100 years with only minor modifications. It employs conventional surgical techniques known as full-thickness filtering surgery or guarded filtering surgery (trabeculectomy).

• The surgeon creates a sclerostomy, a passage in the sclera (the white part of the eye) for draining excess eye fluid.
• A flap is created that allows fluid to escape but which does not deflate the eyeball.
• The surgeon may also remove a tiny piece of the iris (called an iridectomy) so that fluid can flow backward into the eye.
• A small bubble called a bleb nearly always forms over the opening, which is a sign that fluid is draining out. Although surgeons aim for a thick bleb, which poses less risk than a thin one for later leakage, paradoxically the ideal operation would have no bleb at all.

The procedure has a high success rate. About 50% of patients no longer need medication after surgery. Thirty-five to 40% of those that still need medication have better control of their glaucoma. A new instrument called a trabectome has allowed for a less invasive type of trabulectomy surgery The trabectome procedure appears to be a safe and simple way to lower eye pressure. It can be performed before a traditional trabulectomy, if needed. . Results from a small study, presented at the 2005 meeting of the American Academy of Ophthalmology, showed that the new approach successfully reduced eye pressure in 90% of patients with open-angle glaucoma.

Side Effects. Many of the serious side effects or complications that occur with filtration surgery involve blebs.

• Bleb Leaks and Infections. Blebs, particularly thin ones, commonly leak. Leakage can occur early on or sometimes as late as months or years after surgery. Untreated, such leaks can be serious and even cause blindness. Late-onset leakage significantly increases the risk for infection as well as a number of other serious conditions, including bleeding, a flattening of the eye ball, and harmful inflammation. Surgical repair is the most effective way of managing leaking blebs, although drug therapies, pressure patching, and other nonsurgical techniques may be tried first. Due to the dangers of leaking blebs, experts recommend lifelong monitoring after surgery. Unfortunately, the incidence of late-onset leaking blebs is increasing due to the use of drugs used filtration surgery to prevent scarring, another complication.
• Scarring. In up to 20% of cases, scars form around the incision, closing up the drainage channels and causing pressure to rebuild. These scars are formed from fibroblasts, which are immature collagen cells that form at the surgical site. Scarring is a particular problem in young patients, African Americans, patients who have taken multiple drugs, have had an inflammatory disease, or have had cataract surgery. Releasing the surgical stitches used in the procedure may help prevent scarring and pressure build-up. A second procedure called bleb needling sometimes can open up the scarred area and restore drainage. With this technique, the tip of a very fine hypodermic needle is used carefully to cut loose the particles closing off the drainage area. A new technique that does not require sutures may prove to be effective and have fewer complications.
• Cataracts. The procedure is highly associated with the development of cataracts over time. Because cataracts are associated with glaucoma anyway, it is not entirely clear whether the cataracts are caused by the surgery or would develop in any case.

Click the icon to see an illustrated series detailing cataract surgery.

Supportive Medication for Preventing Scarring. Specific drugs, usually mitomycin C, are often used in conjunction with the procedure to prevent scarring and closure. A large meta-analysis on studies of mitomycin C supported its effectiveness in increasing surgical success in nearly all patients. Fluorouracil (5-FU) appears to be similar in effectiveness but has a high risk for complications and is not used as often as in the past.

Laser Trabeculoplasty

The Procedure. Laser trabeculoplasty involves the following steps:

• The procedure employs an instrument, usually a YAG laser, to burn 80 to 100 tiny holes in the drainage area.
• A tiny scar forms, which increases fluid outflow.
• The procedure takes 15 minutes, causes almost no discomfort, and has very few complications.

In a 2-year study, laser surgery of the trabecular meshwork reduced pressure by one third in 70 - 97% of patients. Patients still need to take anti-glaucoma eyedrop medications every day.

Laser surgery is not a cure. Within 2 to 5 years, about half of patients need either additional surgery or new medications.

Complications. In about 35% of patients, pressure increases after surgery. In most cases it is temporary, but rarely the increased pressure is permanent and vision loss can occur. Use of the drug apraclonidine (Iopidine) or pilocarpine can help prevent this elevated pressure. About a third of patients also develop adhesive-like substances called peripheral anterior synechiae that cause the iris to stick to part of the cornea.

Drainage Implants

Implants may be used to drain fluid in certain cases, such as if glaucoma is not responsive to any standard procedure or is caused by certain conditions.

Candidates. Success rates are highest (75% pressure control over 5 to 7 years) in appropriate patients. Drainage implants may be useful in the following conditions:

• Glaucoma caused by swelling in the iris
• Glaucoma caused by abnormal vessel formations
• Iridocorneal endothelial (ICE) syndrome

The Procedure. In general the procedure is as follows:

• An implant, most commonly a 1/2 inch silicone tube, is inserted into the eye's front chamber (anterior). The Molteno implant used with mitomycin C is currently the most effective approach, with reported success rates of 80%. Other implants, such as the Ahmed implant, may have fewer complications.
• The tube drains the fluid onto a tiny plate that is sewn to the side of the eye.
• Fluid collects on the plate and then is absorbed by the tissues in the eye.

Complications. Complications include the following:

• Hypotony (very low eye pressure) is a serious complication that has been reduced using better techniques and improved implants.
• Cataracts, detached retina, breakdown of the cornea, and bleeding are potentially significant complications.
• There is also a risk for eye movement disorders, such as strabismus (crossed eyes) or diplopia (double-vision).

The implant often becomes blocked and repeated operations are needed. Some investigators are studying the use of a drug called tissue plasminogen activator (tPA) to open up tubes that have been blocked by blood or blood factors. (This so-called clot-busting drug is normally used to break up blood clots during heart attacks.) In one 2002 study, tPA prevented such blocks in 89% of eyes. Unfortunately, significant complications rates were high (11%).

Nonpenetrating Surgical Techniques: Deep Sclerectomy and Viscocanalostomy

Deep sclerectomy and viscocanalostomy are less invasive techniques than filtering surgery that leave the anterior chamber (front of the eye) intact and avoid creation of blebs.

In deep sclerectomy, the surgeon removes a deep piece of the sclera (the white part of the eye), part of the trabecular meshwork, and the front of Schlemm's canal (the vessels that return fluid into the blood stream).

• In both deep sclerectomy and viscocanalostomy, the surgeon first creates a flap in the outer part of the sclera (the white part of the eye) and then removes a deep piece of the sclera underneath. This opens up Schlemm's canal (the vessels that return fluid into the blood stream) and exposes a layer above the anterior chamber called Descemet's membrane. A space has also been created between the inner and outer layers of the sclera.
• In deep sclerectomy, this space now serves as a tiny reservoir for aqueous fluid that flows now through the membrane and pools here. The fluid then flows out without the surgeon having to open the anterior chamber (as in standard filtering surgery).
• In viscocanalostomy, the surgeon typically injects gel-like materials into the ends of Schlemm's canal in order to enlarge the canal for fluid outflow and lower IOP. The tiny reservoir is sewn tightly up.

Many variations are under investigation. In general, the procedures have fewer complications afterward than standard filtering surgery, although they require excellent surgical skill. Nonpenetrating techniques do not lower IOPs as much as conventional surgery does, however. In time, however, these nonpenetrating techniques are expected to be as effective as filtration surgery.

Treatment for Patients with both Glaucoma and Cataracts

Cataracts and Glaucoma. For patients with both glaucoma and cataracts, experts recommend the following:

• In patients with cataracts and poorly controlled glaucoma, a two-step procedure for both eye conditions is needed. These are typically first trabeculectomy for glaucoma followed by cataract surgery. Fluid leakage and the presence of blood in the back chamber of the eye are potential complications of this combined procedure. Phacoemulsification has improved success rates and reduced high complication rates of the double procedure compared with extracapsular cataract extraction. New advances that replace trabeculectomy with nonpenetrating glaucoma surgery may prove to be beneficial.
• In patients who have cataracts plus either closed-angle glaucoma or open angle glaucoma that is stabilized with medication, the cataract may be able to be extracted and medication continued for the glaucoma.

A major 2002 analysis suggested that the combined approach generally offers better control over eye pressure for patients with both cataracts and glaucoma. The best surgical procedures, however, is still uncertain. [For descriptions of cataract surgery, see In-Depth Report #26: Cataracts.]

Laser Cyclophotocoagulation (or Cycloablation) for End-Stage Glaucoma

Diode laser transscleral cyclophotocoagulation (TSCPC), also called laser cycloablation, reduces aqueous production by destroying the muscles that control the lens for near and far vision (the ciliary body ). These is a chance of vision loss with this procedure, so it is reserved for people with end-stage glaucoma or those who fail to benefit from any other therapies. Nevertheless, researchers continue to explore the possibilities for this effective procedure, especially for people who may not have access to expensive medications. Studies have suggested it may even be suitable as first-line surgery for some patients.

Surgery for Acute Closed-Angle Glaucoma

For an acute closed-angle glaucoma attack, emergency microsurgery is usually necessary after reducing pressure with medications.

Iridotomy or Iridectomy. Either laser (iridotomy) or conventional (iridectomy) surgery may be used. With either procedure an ophthalmologist makes a tiny opening in the iris to let the aqueous humor flow out more freely. Because acute glaucoma commonly occurs later in the other eye, surgeons will often recommend surgery in the unaffected eye to prevent a second attack.

Laser iridotomy almost never requires hospitalization, and postsurgical treatment includes only aspirin and eyedrops. It has almost completely replaced conventional surgery, which requires anesthesia and hospitalization.

Vision will be blurred and recovery can take 4 to 8 weeks. Once surgery has been performed, such patients can usually use previously restricted anticholinergic medications, such as antihistamines and certain antidepressants, with safety.

Phacoemulsification and Intraocular Lens Implantation. Phacoemulsification and intraocular lens implantation, a procedure ordinarily used for cataracts, may prove to be beneficial for some patients with acute angle-closure glaucoma requiring surgery. [For descriptions of phacoemulsification and intraocular lens implantation, see In-Depth Report #26: Cataracts.]

Lifestyle Changes

Studies suggest that patients with glaucoma who exercise regularly (at least 3 times a week) can reduce their intraocular pressure by an average of 20%. If they stop exercising for more than 2 weeks, pressure increases again. In one study, those who walked briskly 4 times a week for 40 minutes were able to go off their medications. (Although not confirmed by any evidence, yoga or other exercises that involve head-down or inverted positions may be harmful for patients with glaucoma and should be discussed with the doctor.)

Exercise has no effect on closed angle glaucoma. It may, in fact, increase eye pressure in patients with pigmentary glaucoma. Vigorous high-impact exercise may cause more pigment to be released from the iris in these patients. Patients should talk to their doctor about an appropriate exercise program.

Diet

Antioxidants in Foods and Supplements. Diet most likely plays very little role in glaucoma. For example, a 2003 study found no association between important nutrients associated with protection against other eye disorders, including vitamins C, E, A, and carotenoids.

Caffeine. Some studies have shown that large amounts of caffeine drunk in a short period of time can elevate eye pressure for up to 3 hours. One study suggested that such changes in eye pressure could be significant in patients with both normal eye pressure and high IOP.

Fluids. Drinking large amounts (a quart or more) of any liquid within a short time, about half an hour, appears to increase pressure. Patients with glaucoma should have plenty of fluids, but they should drink them in small amounts over the course of a day.

Sunglasses

Glaucoma can cause the eyes to be very sensitive to light and glare. Medications can worsen this problem. Sunglasses solve this problem and are important for prevention of cataracts. Protective sunglasses do not have to be expensive. Sunglasses are classified into three categories based on protection against ultraviolet radiation (UV) A or B:

• Cosmetic-purpose sunglasses block at least 70% UVB and up to 60% UVA. People should avoid these glasses if they have any risk for cataracts or eye problems.
• General-purpose sunglasses block at least 95% UVB and a minimum of 60% UVA. At the very least, people should purchase general purpose sunglasses and they should be labeled "Meets ANSI Z80.3 General Purpose UV Requirements.” Labels should indicate that sunglasses block UV radiation up to 400 nm.
• Special-purpose sunglasses block at least 99% UVB and a minimum of 60% UVA rays. These are the optimal sunglasses for people at risk for eye disease. Special purpose glasses should wrap around the head and block light coming from above, below, and both sides of the glasses. They should also fit snugly on the nose.
• Lenses that are simply dark but not coated with UV-absorbing material may increase the risk of cataracts because the pupil widens to compensate for the shaded glass. This may allow more harmful ultraviolet waves to enter the Polarized glasses cut glare but have no effect on UV radiation. Mirror finishes without additional processing for UV blockage also are not fully protective. There is some controversy over whether blue light is harmful to the eyes. Some people, then, prefer amber lenses, which block out the blue spectrum.

Nontraditional Treatments

Meditation, biofeedback, and relaxation methods can help counteract stress, and there are some reports that they may help some people with open-angle glaucoma. A number of herbal and nontraditional remedies have been advertised as glaucoma remedies. Studies report that the herbal remedy ginkgo biloba may have properties that offer benefits to patients with glaucoma, including increasing blood flow in the eye without altering overall blood pressure, heart rate, or intraocular pressure. More research is needed.

Resources

• www.glaucoma.org -- Glaucoma Research Foundation
• www.nei.nih.gov -- National Eye Institute
• www.glaucomafoundation.org -- The Glaucoma Foundation
• www.aao.org -- American Academy of Ophthalmology
• www.glaucomaweb.org -- American Glaucoma Society
• www.lighthouse.org -- Lighthouse International

References

Joshi AB, Parrish RK 2nd, Feuer WF. 2002 survey of the American Glaucoma Society: practice preferences for glaucoma surgery and antifibrotic use. J Glaucoma. 2005;14(2):172-174.

Lee PP, Walt JG, Doyle JJ, Kotak SV, Evans SJ, Budenz DL, et al. A multicenter, retrospective pilot study of resource use and costs associated with severity of disease in glaucoma. Arch Ophthalmol. 2006;124(1):12-19.

Minckler DS, Baerveldt G, Alfaro MR, Francis BA. Clinical results with the Trabectome for treatment of open-angle glaucoma. Ophthalmology. 2005;112(6):962-967.

Monemi S, Spaeth G, DaSilva A, Popinchalk S, Ilitchev E, Liebmann J, et al. Identification of a novel adult-onset primary open-angle glaucoma (POAG) gene on 5q22.1. Hum Mol Genet. 2005;14(6):725-733.

Ott EZ, Mills MD, Arango S, Getson AJ, Assaid CA, Adamsons IA. A randomized trial assessing dorzolamide in patients with glaucoma who are younger than 6 years. Arch Ophthalmol. 2005;123(9):1177-1186.

Robin AL, Covert D. Does adjunctive glaucoma therapy affect adherence to the initial primary therapy? Ophthalmology. 2005;112(5):863-868.

Sung VC, Koppens JM, Vernon SA, Pawson P, Rubinstein M, King AJ, et al. Br J Ophthalmol. Longitudinal glaucoma screening for siblings of patients with primary open angle glaucoma: the Nottingham Family Glaucoma Screening Study. 2006;90(1):59-63.

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