The anatomy of the eye is complex. The main structures of the eye include:
Anatomy of eye:
Cornea: Clear tissue in the very front of the eye
Iris: Colored part of the eye surrounding the pupil
Pupil: A dark hole in the iris that regulates the amount of light going into the eye
Lens: Small clear disk inside the eye that focuses light rays onto the retina
Retina: A layer that lines the back of the eye, senses light, and creates electrical impulses that travel through the optic nerve to the brain
Macula: The small central area of the retina that allows us to see fine details clearly
Optic nerve: connects the eye to the brain and carries the electrical impulses formed by the retina to the visual cortex of the brain.
Aqueous: Clear, watery fluid that fills front part of the lens.
Vitreous: Clear, jelly-like substance that fills the middle of the eye.
Glaucoma: A Silent killer of Vision
A glaucoma is a group of eye diseases that develop due to elevated intraocular pressure (IOP) within the eye. The increased pressure affects the optic nerve and may cause vision loss. In the early phases of glaucoma, there are often no symptoms. By the time vision is affected, the damage is permanent. Progression of glaucoma can be slowed or halted with eye drops, laser treatments, or surgery so early diagnosis is key.
People with a family history of glaucoma, the elderly, and are at increased risk of the disease, refers to certain eye diseases that affect the optic nerve and cause vision loss. Most, but not all, of these diseases typically produce elevated pressure inside the eye, called intraocular pressure (IOP). Normal IOP is measured in millimeters of mercury and can range from 10-21 mm Hg. An elevated IOP is the most important risk factor for the development of glaucoma.
Elevated IOP is sometimes called ocular hypertension. If the doctor diagnoses ocular hypertension, it does not mean we have glaucoma, but it does mean we are at a higher risk of developing the condition, and we should see an ophthalmologist (a medical doctor who specializes in eye care and surgery) frequently.
Half of the people with glaucoma are usually unaware of it until a serious loss of vision has occurred.
The two main types of glaucoma are angle closure and open angle.
In angle-closure glaucoma, the normal drainage canals within the eye are physically blocked.
Angle-closure glaucoma can be acute (sudden) or chronic (long-lasting). In acute angle-closure glaucoma, a sudden increase in IOP occurs because of the buildup of fluid known as aqueous humor. Acute angle-closure glaucoma is considered an emergency because optic nerve damage and vision loss can occur within hours of the onset of the problem. Chronic angle-closure glaucoma may cause vision damage without symptoms.
Open-angle glaucoma, the most common form of glaucoma, accounting for at least 90% of all glaucoma cases:
- Is caused by the slow clogging of the drainage canals, resulting in increased eye pressure
- Has a wide and open angle between the iris and cornea
- Develops slowly and is a lifelong condition
- Has symptoms and damage that are not noticed.
“Open-angle‖” means that the angle where the iris meets the cornea is as wide and open as it should be. Open-angle glaucoma is also called primary or chronic glaucoma. Open-angle glaucoma also may cause vision damage without symptoms.
Angla closure glaucoma
Angle-closure glaucoma, a less common form of glaucoma:
- Is caused by blocked drainage canals, resulting in a sudden rise in intraocular pressure
- Has a closed or narrow-angle tween the iris and cornea
- Develops very quickly
- Has symptoms and damage that are usually very noticeable
- Demands immediate medical attention. It is also called acute glaucoma or narrow-angle glaucoma. Unlike open-angle glaucoma, angle-closure glaucoma is a result of the angle between the iris and cornea closing.
There are several other types of glaucoma:
Normal-Tension Glaucoma (NTG)
Also called low-tension or normal-pressure glaucoma. In normal-tension glaucoma, the optic nerve is damaged even though the eye pressure is not very high. We still don’t know why some people’s optic nerves are damaged even though they have almost normal pressure levels.
- Secondary glaucoma refers to any case in which another disease causes or contributes to increased eye pressure, resulting in optic nerve damage and vision loss.
- Secondary glaucoma can occur as the result of an eye injury, inflammation, tumor, or in advanced cases of cataract or diabetes. It can also be caused by certain drugs such as steroids. This form of glaucoma may be mild or severe. The type of treatment will depend on whether it is open-angle or angle-closure glaucoma.
- Pigmentary Glaucoma is a form of secondary open-angle glaucoma. It occurs when the pigment granules that are in the back of the iris (the colored part of the eye) break into the clear fluid produced inside the eye. These tiny pigment granules flow toward the drainage canals in the eye and slowly clog them. This causes eye pressure to rise. Treatment usually includes medications, laser surgery, or conventional surgery.
- This form of secondary open-angle glaucoma occurs when a flaky, dandruff-like material peels off the outer layer of the lens within the eye. The material collects in the angle between the cornea and iris and can clog the drainage system of the eye, causing eye pressure to rise. Pseudoexfoliative Glaucoma is common in those of Scandinavian descent. Treatment usually includes medications or surgery.
- Injury to the eye may cause secondary open-angle glaucoma. Traumatic glaucoma can occur immediately after the injury or years later. It can be caused by blunt injuries that bruise the eye (called blunt trauma) or by injuries that penetrate the eye.
- The abnormal formation of new blood vessels on the iris and over the eye’s drainage channels can cause a form of secondary open-angle glaucoma.
- Neovascular glaucoma is always associated with other abnormalities, most often diabetes. It never occurs on its own. The new blood vessels block the eye’s fluid from exiting through the trabecular meshwork (the eye’s drainage canals), causing an increase in eye pressure. This type of glaucoma is very difficult to treat.
Irido Corneal Endothelial Syndrome (ICE)
- This rare form of glaucoma usually appears in only one eye, rather than both. Cells on the back surface of the cornea spread over the eye’s drainage tissue and across the surface of the iris, increasing eye pressure and damaging the optic nerve. These corneal cells also form adhesions that bind the iris to the cornea, further blocking the drainage channels.
- Irido Corneal Endothelial Syndrome occurs more frequently in light-skinned females. Symptoms can include hazy vision upon awakening and the appearance of halos around lights. Treatment can include medications and filtering surgery. Laser therapy is not effective in these cases.
Congenital Glaucoma (Childhood Glaucoma)
- Childhood Glaucoma refers to the presence of glaucoma in a child and occurs in 1 out of every 10,000 births in the United States. Congenital glaucoma is the common term used for glaucoma diagnosed in infancy or early childhood.
- This glaucoma is caused by abnormal intraocular fluid drainage from the eye as a result of a blocked or defective trabecular meshwork (the mesh-like drainage canals in the eye). Congenital glaucoma may be due to a hereditary defect or abnormal development during pregnancy.
- In other cases, an abnormal drainage system may be the result of some other disease in the eye which results in secondary glaucoma. In these cases, glaucoma may be associated with recognizable iris (the colored part of the eye), corneal, or other eye problems. Signs of Childhood Glaucoma
Unusually large eyes
- Excessive tearing
- Cloudy eyes
- Light sensitivity
Glaucoma involves increased pressure within the eye. In the normal eye, a clear fluid called aqueous humor is produced in the rear chamber and flows through the pupil into the front chamber. Once in the front part of the eye, the fluid drains out of the eye through an area called the canal of Schlemm. Aqueous humor provides structural support, oxygen, and nutrition to tissues within the eye.
- Increased IOP results from either increased production or decreased drainage of aqueous humor. The resulting increase in pressure within the eye may eventually damage the optic nerve. This increase in IOP is by far the most common risk factor for vision loss due to glaucoma, but it is not the only factor involved.
- For many years, it was believed that high IOP was the primary cause of optic nerve damage in glaucoma. Now we know that even people with normal IOP can experience vision loss from glaucoma. On the other hand, some people with high IOP never develop the optic nerve damage of glaucoma. Therefore, other factors may affect the optic nerve even when IOP is within the normal range.
- Elevated IOP is still considered a major risk factor for glaucoma, though, because studies have shown that the higher the IOP is, the more likely the optic nerve will be damaged.
- Most people with glaucoma do not notice symptoms until they begin to have significant vision loss. As optic nerve fibers are damaged by glaucoma, small blind spots may begin to develop, usually in the peripheral or side vision. If the entire optic nerve is destroyed, blindness results.
- Other symptoms usually are related to sudden increases in IOP, particularly with acute angle-closure glaucoma, and may include blurred vision, halos around lights, severe eye pain, headache, abdominal pain, nausea, and vomiting.
Glaucoma Exams and Tests
Many different methods are used to measure pressure within the eye. Other tests determine whether you have glaucoma and how advanced your glaucoma may be. Most diagnostic tests need to be repeated on a regular basis to follow the presence or progression of glaucoma.
- Air puff test: The “air puff” test is the most common. This test is a way to measure the IOP without having to actually touch the eye. For this test, you sit in front of a machine with your chin resting on a brace. The eye doctor points a small jet directly at your eye. This jet then delivers a quick puff of air onto the surface of your eye. By measuring the response of the eye to the puff of air, the doctor can make a rough estimate of the intraocular pressure. This is a good screening test for elevated IOP, but it is not very accurate.
- Direct tonometry: Direct tonometry on the surface of the front part of the eye is a much more accurate measurement of IOP. It, however, requires greater skill and expertise to perform. A sensor is placed gently on the surface of an anesthetized eye, and a very accurate IOP is measured.
- Dilation: An examination to inspect the back of the eye through dilated (widened) pupils is required to diagnose glaucoma. To do this, drops are put into the eyes to enlarge, or dilate, the pupils. This allows the eye doctor to see more of the inside of the eye. An eye doctor can recognize a characteristic divot or depression in the optic nerve at the back of the eye caused by damage from the elevated eye pressure. This enlargement is called “cupping” of the optic nerve and means the condition may be relatively advanced.
- Perimetry: Another test, perimetry, is used to determine the presence of defects within the visual fields, particularly vision to the side (called your peripheral vision). Because people with glaucoma tend to lose their vision from the outer edges to the center, checking peripheral vision is very important. In perimetry, a machine is used to test your peripheral vision. You are asked to look at a series of blinking lights. By recording when you see the lights, an accurate map of your peripheral vision can be made. If you have glaucoma, you will have decreased peripheral vision. This test can be performed to follow the progress of your glaucoma or to determine the severity of the initial diameter.
Before leaving the hospital or your doctor’s office, you should make sure you have information concerning the following:
- Medications – When and how they should be taken
- Signs and symptoms – What symptoms to look for that suggest medication failure, side effects, or other problems
- Limitations – What activities you must refrain from and for how long
- Follow-up – When to set up an appointment with your doctor for follow-up examination and to repeat the visual field test
Beta-adrenergic blocking agents, alpha-adrenergic agonists, and prostaglandin analogues are some of the most commonly used medications.
- Beta-blockers, such as timolol (Timoptic), can reduce the amount of aqueous humor produced.
- Alpha-adrenergic agonists, such as brimonidine (Alphagan), decrease the production of aqueous humor and also improve the drainage of aqueous humor.
- Another group of drugs called prostaglandin analogs has recently been used. One that may be prescribed is latanoprost (Xalatan). They work near the drainage area within the eye to increase the secondary route of aqueous humor outflow in order to lower IOP.
- Aerie Pharmaceuticals announced the launch of Rhopressa (netarsudil ophthalmic solution) 0.02%, a novel eye drop indicated for lowering elevated intraocular pressure in patients with glaucoma and ocular hypertension.
In certain cases, surgery may be required.
- If you have angle-closure glaucoma, an operation called an iridotomy may need to be done. During an iridotomy, a drainage hole is created in the iris in order to relieve the increased pressure inside the eye. This technique can be performed using a laser; therefore, an incision in the eye is not needed. You may choose to have an iridotomy after an acute episode of angle-closure glaucoma or to prevent an attack of angle-closure glaucoma.
- Medication normally does not work well for congenital glaucoma, so surgery is usually required.
- Other types of surgery that are performed to help glaucoma include trabeculoplasty, cyclophotocoagulation, and filtering. All of these procedures try to ease the drainage of aqueous humor in the affected eye or eyes to decrease IOP. For more information on these procedures, consult your eye doctor.
Surgery involves either laser treatment or making a cut in the eye to reduce the intraocular pressure. The type of surgery your doctor recommends will depend on the type and severity of your glaucoma and the general health of your eye.
Surgery can help lower pressure when medication is not sufficient. However, it cannot reverse vision loss.
Doctors often recommend laser surgery before incisional surgery, unless the eye pressure is very high or the optic nerve is badly damaged. During laser surgery, a focused beam of light is used to treat the eye’s trabecular meshwork (the eye’s drainage system). This helps increase the flow of fluid out of the eye.
In contrast, incisional surgery (also called filtering surgery) involves creating a drainage hole with the use of a small surgical tool. This new opening allows the intraocular fluid to bypass the clogged drainage canals and flow out of this new, artificial drainage canal.
When laser surgery does not successfully lower eye pressure, or the pressure begins to rise again, the doctor may recommend incisional surgery. Occasionally, glaucoma surgery may have to be repeated especially if excessive scarring cannot be prevented or after long periods of time.
When medicines and laser surgeries do not lower eye pressure adequately, doctors may recommend a procedure called filtering surgery (also called incisional surgery).
In filtering surgery, a tiny drainage hole is made in the sclera (the white part of the eye) in a procedure called a trabeculectomy or a sclerotomy. The new drainage hole allows fluid to flow out of the eye and helps lower eye pressure. This prevents or reduces damage to the optic nerve.
In most cases, there is no pain involved. The surgery is usually done with a local anesthetic and relaxing medications. Often a limited type of anesthesia, called intravenous (I.V.) sedation, is used.
In addition, an injection is given around or behind the eye to prevent eye movement. This injection is not painful when I.V. sedation is used first. The patient will be relaxed and drowsy and will not experience any pain during surgery.
Most of the related studies document follow-up for a one year period. In those reports, it shows that in older patients, glaucoma filtering surgery is successful in about 70-90% of cases, for at least one year.
Occasionally, the surgically-created drainage hole begins to close and the pressure rises again. This happens because the body tries to heal the new opening in the eye as if the opening were an injury. This rapid healing occurs most often in younger people because they have a stronger healing system. Anti-wound healing drugs, such as mitomycin-C and 5-FU, help slow down the healing of the opening. If needed, glaucoma filtering surgery can be done a number of times in the same eye.
For at least one week after surgery, patients are advised to keep water out of the eye. Most daily activities can be done, however, it is important to avoid driving, reading, bending, and doing any heavy lifting. Each case is different, so check with your doctor for specific advice.
The appearance of the Eye after Surgery
The eye will be red and irritated shortly after surgery, and there may be increased eye tearing or watering. The inner eye fluid flows through the surgically-created hole and forms a small blister-like bump called a bleb. The bleb, usually located on the upper surface of the eye, is covered by the eyelid and is usually not visible.
Changes in Vision and Medication
There may be some vision changes, such as blurred vision, for about six weeks after the surgery. After that time, vision will usually return to the same level it was before surgery.
Vision can sometimes improve after surgery in patients who had been using pilocarpine. After stopping pilocarpine drops, the pupil returns to normal size, allowing more light to enter the eye.
In a few cases, the vision may be worse due to very low pressure. Cataracts or wrinkle in the macula area of the eye may develop.
After surgery, you may need to change your contact lenses or glasses. Gas permeable or soft contact lenses may be worn. However, the bleb may cause fitting problems, and special care will be needed to avoid infection of the bleb. Contact lens users should discuss these problems with their eye doctor following surgery.
MIGS has become a commonly used abbreviation in the glaucoma world. It stands for minimally invasive glaucoma surgery.
The goal of all glaucoma surgery is to lower eye pressure to prevent or reduce damage to the optic nerve. Standard glaucoma surgeries are very often effective at lowering eye pressure and preventing progression of glaucoma, they have a long list of potential complications.
The MIGS group of operations have been developed in recent years to reduce some of the complications of most standard glaucoma surgeries.
MIGS procedures work by using microscopic-sized equipment and tiny incisions. While they reduce the incidence of complications, some degree of effectiveness is also traded for the increased safety.
The MIGS group of operations are divided into several categories:
- Miniaturized versions of trabeculectomy
- Trabecular bypass operations
- Totally internal or suprachoroidal shunts
- Milder, gentler versions of laser photocoagulation
Using tiny, microscopic-sized tubes that can be inserted into the eye and drain fluid from inside the eye to underneath the outer membrane of the eye (conjunctiva), two new devices seem to make the trabeculectomy operation safer. These devices (the Xen Gel Stent and InnFocus Microshunt) have shown excellent pressure lowering with an improved safety over trabeculectomy in studies done outside the United States. If US study results are as good as those from overseas, FDA approval could follow within a year or two.
Most of the restriction to fluid drainage from the eye rests in the trabecular meshwork. Several operations have been devised using tiny equipment and devices to cut through the trabecular meshwork without damaging any other tissues in the ocular drainage pathway. Using a special contact lens on the eye, a tiny device is inserted into the eye through a tiny incision into the trabecular meshwork under high power microscopic control. The trabecular meshwork can either be destroyed (Trabectome or Trab360) or bypassed using a tiny snorkel-like device (the iStent). These procedures are FDA-approved but generally don’t get the eye pressure very low so are most useful in early to moderate stages of glaucoma.
Using tiny tubes with very small internal openings, the front of the eye is connected to the suprachoroidal space between the retina and the wall of the eye (Cypass or Glaukos shunts) to augment the drainage of fluid from the eye. This operation has relatively few serious complications and lowers pressures enough to be useful even in moderately severe glaucoma. The Cypass has had extensive study in Europe and has successfully completed its US trials; it is currently under consideration by the FDA for potential approval. It may be available by late 2016.
New Laser Procedures
Previously, laser cyclophotocoagulation was reserved for advanced glaucoma that could not be controlled despite trabeculectomy or tube shunts. The procedures were designed to reduce the fluid-forming capacity of the eye by targeting the delicate tissue (ciliary body) that makes the fluid. They sometimes produced severe inflammation that could reduce vision. Two recent additions to the laser treatment procedures have proven useful even before the glaucoma is far advanced. These are endocyclophotocoagulation and micropulse cyclophotocoagulation. These procedures may be discussed in a future article.
Surgery and his research interests include early methods in diagnosing glaucoma to prevent vision loss and evaluating new surgical procedures for glaucoma.
Identifying molecular biomarkers for glaucoma promises many possible benefits. A molecular biomarker might have predictive use that could help guide more specific therapy in some glaucoma patients.
For example, it might help a glaucoma specialist know when to intervene earlier. In addition, a good biomarker could be used to demonstrate the efficacy of drug activity, potentially accelerating federal approval for glaucoma drugs, particularly those that protect the retina and optic nerve.
In the early stages of the initiative, the team’s strategy has been to cast a wide net, investigating diverse candidate biomarkers, and during the first year, the team has shown considerable progress.
Retinal ganglion cells (RGCs), the cells that degenerate and are responsible for vision loss in glaucoma, have been divided into many subtypes and certain subtypes may get injured or die first in glaucoma. The CFC researchers completed a detailed and systematic analysis of RGC subtypes, and preliminary results show that one subtype changes its shape much earlier in the disease. They are developing techniques to identify whether these and other potential candidate biomarkers may signal early changes that lead to vision loss in glaucoma.
A Decade of Innovation
The first team of Catalyst for a Cure investigators — David Calkins, PhD (Vanderbilt Eye Institute), Philip Horner, PhD (University of Washington), Nicholas Marsh-Armstrong, PhD (Johns Hopkins), and Monica Vetter, PhD (University of Utah) — working collaboratively since 2002, made a significant impact on the field of glaucoma research. New ideas and research findings from the Catalyst for a Cure have fundamentally changed how the scientific and medical communities view vision loss in glaucoma.
The CFC researchers have obtained a detailed understanding of this complex disease, and have revealed novel approaches for slowing disease progression. Importantly, they characterized glaucoma as a progressive, neurodegenerative disease, and provided significant evidence that targeting early events has the greatest therapeutic potential. They showed that RGCs undergo functional decline and genetic deprogramming before they are permanently lost, and they defined a window of ―vulnerability‖ for RGCs during which there is the potential for rescue.
Collaborative Research to Find a Cure
At Glaucoma Research Foundation, we have made a serious long-term commitment to collaborative research. Projects are focused on clear goals and useful results. Annually, we are investing more than one million dollars in research grants to better understand this complex disease and speed the pace of finding a cure for glaucoma. We believe the innovative design of the Catalyst for a Cure and the talented scientists it has brought together are our best hope for finding a cure for this devastating disease.
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Author: Ranjini Chakraborty