Glaucoma

ANATOMY OR SYSTEM AFFECTED: Eyes

DEFINITION: A group of eye diseases characterized by damage to the optic nerve, often due to an increase in the eye’s intraocular pressure; early diagnosis through regular eye examinations can manage the effects of the disease, while late diagnosis may result in impaired vision or blindness.

CAUSES: Congenital or hereditary factors; anatomic factors (smaller eye length, shallower anterior chambers); drugs; tumor; trauma; inflammation

SYMPTOMS: Often asymptomatic; eye pressure; slow progression toward blindness; at times, pain, nausea, vomiting, severe headaches

DURATION: Ranges from acute to chronic

TREATMENTS: Eye drops, ointments, pills, surgery

Causes and Symptoms

Glaucoma is a group of eye diseases characterized by damage to the optic nerve, most often due to higher-than-normal pressure inside the eye. Damage to the optic nerve can lead to visual impairments or complete blindness. Of all the causes of blindness, glaucoma is among the most common, but it is also the most preventable. If diagnosed early, it can be controlled and the loss of vision avoided. What complicates the problem is that the most common form of glaucoma, primary open-angle glaucoma, shows no symptoms until extensive, irreversible damage has occurred. There is no pain and elevated intraocular pressure may not be present at the time of a physical examination; the first sign that something is amiss may be that peripheral vision and seeing out of the corner of the eye is diminished, while frontal vision remains clear. The second most common form of primary glaucomas, angle-closure glaucoma, occurs there is an increased resistance to aqueous humor outflow from the inner eye. Glaucomas may be considered primary, when the cause is unknown, or secondary, when the cause is known. Causes of secondary glaucoma include inflammation, trauma, neovascularization, or tumors.

To understand glaucoma, it is helpful to understand the structure of the eye. The outer layer of the eye is called the cornea. The inner surface of the cornea is nourished by the aqueous humor, which is also called the aqueous fluid. This secretion from the ciliary body flows into the space behind the iris and then through the pupil into the space in front of the iris. Where the front of the iris joins the back of the cornea is a point called the venous sinus, at the anterior drainage angle. Here the aqueous humor is reabsorbed and transported to the bloodstream. In a normal eye, this drainage process works correctly and the balance between the amount secreted and the amount reabsorbed maintains a constant intraocular pressure. In most forms of glaucoma, the drainage part of the process works inefficiently. For a variety of reasons, some of which are not fully understood, the drainage mechanism can become defective. The upset balance in secretion drainage causes the unwanted increase in intraocular pressure in one eye or both eyes. The iris is pushed forward, further inhibiting drainage of the aqueous fluid. However, not all forms of glaucoma are caused by increased intraocular pressure; normal-tension glaucoma is characterized by damage to the optic nerve while eye pressure remains normal. Normal-tension glaucoma may be caused by reduced blood supply to the optic nerve.

Even a very small elevation in intraocular pressure will affect the eye adversely, causing damage to its most delicate parts. Although the eye as a whole is quite tough, the optic nerve is vulnerable to increased pressure or deterioration due to lack of blood supply. This vital connection between the eye and the brain can be damaged by the higher pressure within the eyeball. The delicate nerve fibers and blood vessels of the optic disc, as the beginning of the optic nerve is called, then die. Once they die, they can never be regenerated or replaced, and vision loss is the result.

The damage that glaucoma inflicts is progressive. In many cases, the defect in drainage does not necessarily worsen, and the pressure, once elevated, does not necessarily continue to increase. Once begun, however, the damage to the optic nerve cells continues until the resulting loss of vision progresses to total blindness. The first nerve fibers to die are the ones near the outer edge of the optic disc, which originates near the periphery of the retina. The first decrease in vision, therefore, is in one’s peripheral vision. Then, as each layer of nerve fibers dies, the visual field progressively narrows.

This slow, progressive route to blindness is typical of open-angle glaucoma, which accounts for two-thirds of primary glaucoma cases. The rise in intraocular pressure does not result from any known underlying reason. Although individuals with a family history of glaucoma are more prone to the disease, it is not directly hereditary. Moreover, not everyone with a family history of glaucoma will develop the disease. For reasons that are not well understood, people of African ancestry suffer from glaucoma at greater rates than those of European ancestry.

In persons of all races, open-angle glaucoma usually begins after the age of forty; however, the aging process does not seem to be a direct cause of glaucoma. Unlike the formation of age-related cataracts, which result from eye changes as one grows older, glaucoma’s development is not explained by the aging process. It can safely be said that glaucoma seems to occur in persons who have a tendency toward inadequate aqueous fluid drainage or who have highly sensitive optic nerves. As persons grow older and their bodies lose their resiliency in general, the drainage problem can reach a point where it begins to raise the intraocular pressure beyond the normal range. Those with untreated open-angle glaucoma are seldom aware of the disease before considerable damage has been done. The progressive destruction of nerve fibers is ordinarily very slow because the elevation of pressure is slight and causes no pain or blurriness of sight. In persons with normal-tension glaucoma, atherosclerosis can potentially reduce blood supply to the optic nerve, causing irreversible damage.

In secondary glaucoma, the drainage defect is caused by some complication of a different condition. The causes of chronic secondary glaucoma include inflammation from an eye infection, an allergic reaction, trauma to the eye, a tumor, or even the presence of a cataract. Medications such as corticosteroids can sometimes cause this type of glaucoma to develop. Whatever the cause, secondary glaucomas exhibit increased pressure, slow nerve destruction, and ultimate loss of vision.

Acute glaucoma is both rare and dramatic in its onset. The increase in intraocular pressure is many times higher than that in open-angle glaucoma. It also occurs very rapidly, sometimes within hours. The anterior drainage angle where drainage is accomplished is almost totally blocked. The eyeball becomes so hard that the elevated pressure can often be felt simply by touching the front of the eye. The great pressure causes terrible pain and immediate damage to the eye. When nausea, vomiting, and severe headaches accompany eye pressure, acute glaucoma should be suspected. Immediate treatment is required to prevent blindness. Acute glaucoma can be either primary or secondary. It is termed primary when a drainage area that has always been abnormally narrow suddenly becomes totally blocked. It is called secondary when it is precipitated by some other eye condition.

The rarest type of glaucoma, congenital glaucoma, is present at birth or develops during early infancy. It results from the incorrect formation of drainage canals while the eye is developing. Because a baby’s eyeball is much smaller and softer than an adult’s, this glaucoma is often recognized by the bulging of the eyes.

Treatment and Therapy

The treatments available for glaucoma include eye drops, ointments, pills, and surgery using both incisions and lasers. In both acute and congenital glaucoma, there is often little time for long-term medication management; patients typically need to be admitted to the hospital and operated on immediately if their eyesight is to be saved. For open-angle glaucoma, medications may be topical—eye drops or ointments, or inserts, thin medicated strips put in to the corner of the eye—or oral (pills and tablets). Prostaglandin analogs and beta-adrenergic antagonists are the most frequent first-line choices to reduce intraocular pressure. If diagnosed early, cases of both chronic primary and chronic secondary glaucomas can often be effectively treated by medications.

If drops or gels do not produce the desired reduction in pressure, pills can be used, not to replace the drops but to supplement them. Beta blockers, carbonic anhydrase inhibitors, or alpha-2-adrenergic agonists in addition to prostaglandin analogs may help to further reduce intraocular pressure.

Although surgery cannot reverse the optic nerve damage that has already occurred, it is often effective in preventing further destruction by alleviating elevated intraocular pressure. One of the most common of these surgical procedures was developed in the mid-nineteenth century. Called an iridotomy, it attempts to provide a better access to the patient’s drainage angle by removing part of the iris. Today, an iridotomy may be completed with incisions or lasers, although laser iridotomy is preferred. The most common forms of laser iridotomy are bilateral laser iridotomy and laser peripheral iridotomy. In laser peripheral iridotomy, which is often used in the treatment of angle-closure glaucoma, a laser makes a small hole in the iris to allow fluid to move more freely within the eye and drain from the fluid channel more easily.

Another common form of glaucoma surgery is called trabeculectomy, which can be performed in several different ways. Argon laser trabeculoplasty is often used to treat open-angle glaucoma. This procedure aims a laser at a special contact lens that is placed in front of the eye, opening the fluid channels of the eye and relieving the intraocular pressure. The passageway created permits the aqueous humor to drain properly from the inner eye.

A different approach to glaucoma control, called laser cyclophotocoagulation, attempts to help the patient by destroying part of the source of the excess fluid, the oversecreting ciliary body. This procedure is usually performed only on older patients who already have severe damage from glaucoma or for whom other surgeries were not successful.

All the above treatments for glaucoma, whether pharmaceutical or surgical, have the potential for serious side effects and complications. Consequently, research continues to seek therapies with better rates of success and fewer complications. Some of the possible complications of surgery include infection, sensitivity to light, bleeding, long-term irritation or inflammation, loss of vision, and the need for more surgery. Risk factors for complications from surgery include obesity, smoking, diabetes, high blood pressure, and bleeding disorders. Nevertheless, glaucoma surgery is a common procedure with a relatively high success rate.

Perspective and Prospects

In 1851, the German doctor Hermann von Helmholtz invented the ophthalmoscope, which enables one to study the interior of the eye. His instrument focused a beam of light into the patient’s eye and then magnified its reflection. If this test revealed early signs of cupping of the optic disc, glaucoma could be diagnosed long before other symptoms have appeared. Today, it is recommended that patients have regular eye exams to detect elevated intraocular pressure so that it be alleviated before loss of vision occurs. An eye exam is recommended every two to four years for patients under the age of forty, one to three years for patients between forty and fifty-four, one to two years for patients between fifty-five and sixty-five, and every six to twelve months for patients over the age of sixty-five.

Intraocular pressure can be measured with an instrument called a tonometer. The two basic varieties are called Schiötz tonometry and applanation tonometry. Both became possible only after biochemists developed anesthetic drops to put in the eye so that the patient would not feel the device touching the very sensitive cornea. The earlier of the two devices, developed in 1905 by the Norwegian physician Hjalmar Schiötz, is a very simple device that is still the most widely used tonometer in the world. With the patient lying down and looking upward, the physician places the hand-sized instrument directly on the cornea. A simple lever is moved by the pressure within the eye to indicate whether that pressure is within the normal range or dangerously high. The Goldman applanation tonometer is considered even more accurate and is often used to confirm the results of the simpler Schiötz device. An orange dye called fluorescein is added to the anesthetic. The patient, in a sitting position, rests the head against a bar to steady it. The doctor uses a tonometer to touch the cornea while simultaneously peering into it with a well-illuminated microscope.

More specialized glaucoma examination may include ophthalmoscopy, gonioscopy, or perimetry. An ophthalmoscopy involves the dilation of the pupil and an examination of the optic nerve with a microscope to detect damage to the nerve. If damage is suspected, the doctor may then recommend other diagnostic exams, such as perimetry and gonioscopy. Perimetry involves visual field tests, which can give a map of the central area where vision is sharp and more acute versus the peripheral area where it is weaker. Since damage to the optic nerve causes a narrowing of the visual field, this mapping is very important. The ability to measure the field has grown from oculokinetic perimetry—using an inexpensive test chart, pencil, record sheet, and human examiner—to the sophisticated automated perimetry, which generates a computer analysis. Gonioscopy involves the placement of a contact lens on the eye. This specialized contact lens has mirrors and facets to provide an illuminated view of the drainage angle, a normally dark corner at a 90 degree angle from the examiner. Excessive narrowing of the angle is an indication of glaucoma.

All these tests, developed through years of ophthalmic research, have given medical science invaluable tools to diagnose glaucoma in its early stages and prevent blindness. Glaucoma is estimated to affect one out of every forty adults over the age of forty years.

Bibliography

Allingham, R. Rand. Shields Textbook of Glaucoma. 6th ed. Philadelphia: Lippincott, 2011. Print.

Chen, C. H. Frontiers of Medical Imaging. Singapore: World Scientific, 2015. Print.

Dowling, John E., and Joseph L. Dowling Jr., Vision: How It Works and What Can Go Wrong. Cambridge: MIT Press, 2016. Print.

Edward, Deepak P., and Thasarat S. Vajaranant. Glaucoma. Oxford: Oxford UP, 2013. Print.

Galloway, N. R., et al. Common Eye Diseases and Their Management. 3rd ed. London: Springer, 2006. Print.

“Glaucoma.” Mayo Clinic, 22 Sept. 2022, www.mayoclinic.org/diseases-conditions/glaucoma/symptoms-causes/syc-20372839. Accessed 2 Apr. 2024.

"Glaucoma." Medline Plus, 22 Aug. 2022, medlineplus.gov/ency/article/001620.htm. Accessed 2 Apr. 2024.

Morrison, John C., and Irvin P. Pollack. Glaucoma: Science and Practice. New York: Thieme, 2003. Print.

Rowe, Fiona. Visual Fields via the Visual Pathway. 2nd ed. Boca Raton: Taylor & Francis, 2016. PRint.

Samples, John R., and Paul N. Schacknow, eds. Clinical Glaucoma Care: The Essentials. New York: Springer, 2014. Print.

Shaarawy, Tarek M., et al. Glaucoma. 2nd ed. London: Elsevier, 2014. Print.

Storgaard, Line. et.al. "Clinical Research: Trends in Treatment Strategies and Drug Development." Frontiers in Medicine, 13 Sept. 2021, doi.org/10.3389/fmed.2021.733080. Accessed 1 Aug. 2023.

Sutton, Amy L., ed. Eye Care Sourcebook: Basic Consumer Health Information About Eye Care and Eye Disorders. 3rd ed. Detroit: Omnigraphics, 2008. Print.

Trope, Graham E. Glaucoma: A Patient's Guide to the Disease. 4th ed. Toronto: U of Toronto P, 2011. Print.