Glaucoma Basics & FAQs

Glaucoma is an eye problem that can cause vision loss or blindness. It happens because a part of the eye called the optic nerve gets damaged.  But Glaucoma can be prevented with timely care.

Sometimes, glaucoma does not show any signs until it is in the advanced stages. Glaucoma cannot be cured, but it can be managed with a doctor’s help. You may need to take medicine and see your eye doctor regularly.

There are three important parts of the eye: the optic nerve, the ciliary body, and the angle of the front part of the eye. 

  1. The optic nerve is like a cable that sends pictures from your eye to your brain. 
  2. The ciliary body is where the eye makes a watery liquid that helps the front part of your eye stay healthy. 
  3. The angle of the front part of your eye is like a tiny space between the clear part of your eye and the colored part. When too much liquid builds up, it can make the pressure in your eye go up, and that can damage your eye.

Yes, there are different types of glaucoma: 

  1. It is the main problem (primary) or caused by something else (secondary). 
  2. How the front part of the eye is shaped: either open or closed. 
  3. Whether it lasts a long time (chronic) or happens suddenly (acute). 

Most people have the slow kind where the angle is open.

The majority of glaucoma cases in North America and Europe are associated with elevation of the intraocular pressure. Elevated intraocular pressure could result from either an excessive production of aqueous humor from the ciliary body or an obstruction of aqueous humor outflow through the chamber angle (trabecular meshwork). In fact, virtually all elevation of intraocular pressure arises from some form of blockade of aqueous humor outflow through the trabecular meshwork. Some patients exhibit the progressive optic nerve damage of glaucoma but seldom or never manifest increased intraocular pressure. Controversy exists about whether these individuals have exquisitely pressure-sensitive optic nerves or whether other damaging factors, such as compromised circulation, cause the optic neuropathy. Glaucomatous optic nerve damage without elevated intraocular pressure is sometimes referred to as "low tension glaucoma" or "normal pressure glaucoma."

The optic nerve is like a cable connecting the eye to the brain. When the optic nerve gets damaged, it can lead to permanent vision loss. The good news is that doctors can use a tool to look at the optic nerve and spot the early signs of glaucoma.

Glaucoma can also cause parts of the optic nerve to get thinner. This can lead to vision problems, too.

Early vision loss happens in the side part of your vision. It is slow, so you might not notice it at first.

Doctors can spot changes in your optic nerve early, even before you lose a lot of vision. They use special tests to check your side vision, called the "visual field."

Glaucoma damage starts from the blind spot in your eye, curves around the center, and stops suddenly on the inner side. So, doctors watch these changes closely to manage glaucoma and protect your vision.

The eye is like a basketball, and it needs to have the right amount of pressure inside to work properly. Doctors will measure your eye pressure with special tools. If your eye pressure is too high, it could mean you have glaucoma.

Your doctor will look at the angle in your eye, the optic nerve, and your vision to make sure everything is okay.

This kind of glaucoma is linked to diabetes and happens when new blood vessels grow and block the eye's fluid from draining, making the pressure go up. It is a complex condition that needs careful attention.

Some babies are born with glaucoma.

Babies with this type of glaucoma might be sensitive to light, have watery eyes, and blink a lot. Their eyes might look big and cloudy. It is important to get treatment from an eye doctor quickly to prevent permanent blindness.

The doctor’s goal is to bring down the pressure inside the eye. That can help slow down or stop the disease in most cases.

There are three main ways to lower eye pressure in glaucoma: using special eye drops, using laser therapy, or having surgery. The goal is to keep your vision stable and protect the optic nerve from further damage.

Your doctor may use laser therapy to help lower eye pressure. It is a simple office procedure. Some patients might need more laser treatment if the first one is successful.

Primary Open Angle Glaucoma:

The vast majority of glaucoma patients have primary open angle glaucoma. These patients manifest a chronic, idiopathic disease associated with progressive degeneration of the anterior optic nerve, known as glaucomatous optic neuropathy. Although elevated intraocular pressure is an important causative risk factor, only half of the 2 to 3 million North Americans with glaucoma will manifest elevated intraocular pressure at a single measurement. Therefore, measurement of intraocular pressure alone is a poor screening technique for glaucoma. Like most biologic parameters, eye pressure fluctuates throughout the day and varies with other influences, including hydration, sleep, blood pressure and body position. With multiple measurements at different testing sessions, most, but not all of these glaucoma subjects, will eventually exhibit elevated intraocular pressure at least part of the time.

The rise in intraocular pressure associated with primary open angle glaucoma derives not from a visible obstruction of the trabecular meshwork, but rather from cellular dysfunction of the trabecular meshwork tissue, which leads to increased aqueous humor outflow resistance. Risk factors for primary open angle glaucoma include family history, corticosteroid sensitivity, myopia, African-American race, systemic high blood pressure, high intraocular pressure, diabetes, and age. In addition to these risk factors, early age of onset of disease and poor compliance with a medical regimen and physician visits are associated with a worse prognosis. As mentioned above, some patients with progressive optic nerve damage characteristic of glaucoma never manifest intraocular pressures above the statistically normal range. These patients are commonly diagnosed with "low pressure glaucoma,” “low tension glaucoma,” “or normal pressure glaucoma.” While recognizing that non-pressure risk factors may play a stronger role in these than in than in their high-pressure counterparts, these patients are managed similarly to those with conventional primary open angle glaucoma.

Closed Angle Glaucoma:

All physicians need be cognizant of another form of glaucoma, closed angle or angle-closure glaucoma, which may present acutely or may be silent and chronic. This disorder, quite unrelated to open angle glaucoma, derives entirely from blockade of the trabecular meshwork by the peripheral iris, either by simple and reversible anatomical apposition, or pressing together, of the two tissues or by generally irreversible scarring and adhesion. These irreversible fibrotic adhesions may occur after unrecognized long-standing appositional angle closure (chronic angle closure glaucoma) or from other ocular conditions, such as uveitis or neovascularization (secondary angle closure glaucomas).

Classically, angle closure glaucoma is the well known, less common variety of glaucoma that presents acutely with severe eye pain, blurring of vision, colored halos around lights, nausea and vomiting. Angle closure usually occurs in the hyperopic (farsighted) eye, which is smaller than the average eye and thus crowds the iris, cornea, lens and anterior chamber angle into a smaller than average space. Eventually, usually in the fifth to sixth decade of life as the lens gradually increases in size with aging, the lens becomes more firmly applied to the pupillary opening through which aqueous humor from the ciliary body must pass. This obstruction of aqueous humor flow at the pupil, known as relative pupillary block, eventually becomes clinically significant and traps the aqueous behind the pupil, raising the pressure in the posterior chamber above that in the anterior chamber and driving the iris anteriorly to lie against and block the trabecular meshwork. This trabecular meshwork blockade, or angle closure, leads to a sudden and dramatic rise of the intraocular pressure from its baseline normal level in the 10-20 mm Hg range to 60 mm Hg or more. This sudden change in pressure leads to swelling of the cornea with blurring, haloes, and severe ocular pain from iris ischemia and corneal edema. The pupillary margin of the iris becomes most tightly applied to the lens surface when the pupil is in the mid-dilated position; hence, it is often dilation of the pupil by exposure to stress, darkness, or drugs that precipitates an acute attack.

The immediate treatment of acute angle closure is directed toward reversal of the pupillary block, usually by moving the pupil with constriction. Ultimately, however, the pupillary block can be reversed and prevented by creating a new aqueous channel with peripheral iridectomy. (see Treatment)

If you have glaucoma, you need to see your doctor regularly to check your eyes and make sure treatment is working.

Glaucoma may develop after ocular trauma. Penetrating injuries to the globe disrupt, or even destroy, intraocular contents and may lead to sustained elevation of intraocular pressure and glaucoma. (see Ocular Trauma) A more subtle, insidious glaucoma may arise from blunt ocular injury or ocular contusion, as occurs when the globe is struck with a fist, ball or other object. Blunt injury temporarily deforms the globe, causing shearing between its internal tissue layers. These shearing forces may tear the insertion of the iris (iridodialysis) or ciliary body (cyclodialysis) from its attachment to the sclera. Most commonly, the fibers of the ciliary muscle that both controls accommodation and modulates aqueous humor outflow become detached, leading to collapse of the trabecular meshwork (known as angle recession) and subsequent secondary glaucoma.

Acutely, the contused eye typically presents with intraocular bleeding (hyphema), and the intraocular pressure may be low, normal, or elevated. Angle recession glaucoma may not manifest for months or even years after the original injury. Treatment of glaucoma from blunt ocular trauma follows a similar protocol to more common open angle glaucomas, except that these eyes do not respond well to pupil-constricting drops such as pilocarpine because of the damage of the ciliary muscle. Because of the damage to the trabecular meshwork, laser trabeculoplasty is similarly ineffective. Thus, when regular glaucoma drops are ineffective, filtration surgery usually becomes necessary.

Pigmentary glaucoma is relatively common secondary glaucoma in the young adult and appears to be exclusively an ocular disorder. This disease is relevant because of the potentially severe consequences in young people. Pigmentary glaucoma occurs primarily in young myopic (nearsighted) adults and is more common in males, usually manifesting between the ages of 20 and 40 years. Melanin pigment granules from the iris circulate freely in the aqueous humor, become deposited or entrapped in the surrounding tissues of the cornea, iris, lens, and particularly within the trabecular meshwork. This leads to obstruction of the meshwork, elevation of intraocular pressure, and glaucoma. This condition may manifest with intermittent visual blurring or dull ocular pain, but like other glaucomas may go unnoticed until severe visual loss occurs. Vigorous physical activity or pupillary dilation may induce a shower of pigment granules to be released from the iris in these patients, resulting in a transient, acute rise in eye pressure, corneal edema, blurred vision and ocular pain. Treatment of pigmentary glaucoma is similar to that for primary open angle glaucoma.

During the early 1970's, attempts were made with a variety of lasers to enhance aqueous humor outflow through the trabecular meshwork in open angle glaucoma by puncturing the trabecular meshwork with the laser energy. Despite the failure of these procedures to create holes in the trabecular meshwork, a subsequent decrease in the intraocular pressure, several days to weeks following some of the procedures, was often observed. In 1979, Wise and Witter published a pilot study describing an argon laser procedure for the control of intraocular pressure. This technique, known as argon laser trabeculoplasty, has changed little since its original description. Many theories attempting to explain the effect of the trabeculoplasty laser burns have emerged. It is now thought that a cascade of biological events that involves renewal of trabecular meshwork cells and accelerated turnover of the extracellular matrix, or tissues between the trabecular cells, enhances outflow through the trabecular meshwork following laser treatment. Argon laser trabeculoplasty is a relatively uncomplicated office procedure and has gained wide acceptance in the treatment of open angle glaucoma. In approximately 80% of eyes treated with argon laser trabeculoplasty, a significant lowering of the intraocular pressure will be achieved. However, the intraocular pressure lowering effect will diminish over time and approximately 10% of initially successful treatments will fail with each year. In patients in whom the initial laser trabeculoplasty was successful, additional laser therapy may be warranted. A modification of this therapy, Selective Laser Trabeculoplasty, is also available to treat open angle glaucoma.

Trabeculectomy or Filtering Surgery

Trabeculectomy is the most common operation for the control of elevated intraocular pressure in adult glaucoma. Various filtering procedures have been developed to shunt the aqueous humor from the anterior chamber to a reservoir under the conjunctiva on the surface of the eye. These procedures provide an alternative low-resistance pathway for aqueous humor egress from the eye. It is believed that the aqueous humor either filters through the conjunctiva from the reservoir, mixing with the tears, or it is absorbed by the blood vessels on the surface of the eye. Postoperative management includes topical dilating drops and antibiotics for the first one to two weeks following surgery. Topical corticosteroids are also used to suppress inflammation. The corticosteroid therapy is thought to reduce scar formation and failure of the filtering bleb. Youth, skin pigmentation, previous surgery, and secondary glaucoma greatly increase the risk of failure. The majority of surgical patients receive some form of additional chemical antimetabolite therapy, either during surgery by sponge application or post operatively as subconjunctival injections. 5-Fluorouracil or Mitomycin-C are the most commonly used antimetabolite adjuncts to trabeculectomy surgery. In addition, a variety of artificial drainage devices are available that employ a plastic shunt tube to divert the aqueous humor from the anterior chamber into the space behind the eye, where it is resorbed. These glaucoma tube shunts are generally reserved for eyes in which trabeculectomy surgery has failed or in which failure is likely due to extensive scar tissue formation, such as neovascular glaucoma.

Glaucoma at a Glance

Early Symptoms:
Often none

Later Symptoms:
Loss of side (peripheral) vision, blind spots, blindness

Dilated eye exam with eye pressure and visual field testing to test your side vision

Medicine (usually eye drops), laser, or surgery

View Handout