PRIMARY OPEN-ANGLE GLAUCOMAPrimary open-angle glaucoma (POAG) is a silent destroyer of vision. The most common type of the disease, it accounts for 70-80 percent of glaucoma cases worldwide. Among those patients with glaucoma that I see in my practice, a majority have the type called Primary Open-Angle Glaucoma (POAG). The designation primary means that there is no identifiable injury or disease process, such as diabetes or high blood pressure, that is causing the glaucoma. Open angle signifies that the angle formed by the iris and cornea, known as the iridocorneal angle, is open rather than closed. Instances in which the iridocorneal angle is narrow or closed are referred to as primary angle-closure glaucoma. Primary open-angle glaucoma is the most common type, accounting for 70-80 percent of glaucoma cases worldwide. It typically occurs in patients forty years of age and older and is a leading cause of blindness in the USA and in many other countries. Primary open-angle glaucoma usually affects both eyes. It is an especially dangerous form of the disease because it can progress gradually and go unnoticed for years. The only way to detect primary open-angle glaucoma before it becomes a serious problem is through regular eye examinations that specifically assess for glaucoma. MECHANISM OF PRIMARY OPEN-ANGLE GLAUCOMA?The main problem behind primary open-angle glaucoma is elevated intraocular pressure. However, it is important to understand that if your ophthalmologist informs you that your intraocular pressure is high, this alone does not mean that you have glaucoma. Intraocular pressure that is at or above 21 mmHg is a risk factor for glaucoma, but it is not the disease itself. The unifying factor that links all types of glaucoma is damage to the optic nerve that progresses over time and results in a loss of optic nerve fibers. What causes high intraocular pressure in the first place?Elevated intraocular pressure occurs because there is too much aqueous humor in the anterior chamber of the eye. Aqueous humor is produced in a structure called the ciliary body. One way that intraocular pressure potentially can be raised is if aqueous humor is overproduced. While this does occur in some people, this by itself does not appear to be sufficient to substantially raise intraocular pressure. Intraocular pressure also can be elevated through obstruction of aqueous humor drainage. This occurs through a structure called the
trabecular meshwork
and appears to be the main mechanism by which intraocular pressure becomes elevated. The trabecular meshwork acts much like a drain strainer in your kitchen sink to filter out debris before the aqueous humor returns to the blood stream.
It might be tempting to assume that over time the trabecular meshwork would become clogged with debris, which would significantly impede aqueous humor outflow and raise intraocular pressure. This does occur in some cases, such as in pigmentary glaucoma and pseudoexfoliative glaucoma. However, in a majority of primary open-angle glaucoma cases, the fundamental problem appears to be changes in the structural components and integrity of the trabecular meshwork itself rather than an overproduction of particulate matter that becomes lodged in the network.
HOW DOES INTRAOCULAR PRESSURE CAUSE OPTIC NERVE DAMAGE?The optic nerve consists of many fibers. The technical term for these fibers is axons. Each axon has its origin in a specific retinal ganglion cell located in the retina of the eye. The retinal ganglion cells are extensions of the body's central nervous system and are irreplaceable. Two main theories have been forwarded to explain how elevated intraocular pressure causes damage to the optic nerve: the Mechanical Theory and the Vascular theory. Neither fully explains how optic nerve damage occurs in different types of glaucoma. Rather than being mutually exclusive, the two probably work in combination.Mechanical Theory. The essence of the mechanical theory is that intraocular pressure exerts a force from inside the eye to the outside. In this high-pressure environment, the axons of the optic nerve are compressed, causing an alteration in function and death of the cell bodies. The compression is most important in the area where the axons converge to leave the eyeball. This area is known as the lamina cribrosa. The laminia cribrosa organizes optic nerve fibers as they exit the eye and head towards the brain. It is a structure consisting of ten perforated plates that are stacked on top of each other. This creates about 500 channels, through which about one million axons pass through (an average of 2000 axons per channel). When I examine a patient with primary open-angle glaucoma, a characteristic sign is increased cupping in the optic disc. This structure is the location where ganglion cell axons exit the eye to form the optic nerve. Think about a teacup. If you look down at it from above, you will see the outer rim of the cup surrounding a smaller circle that represents its bottom. I see a similar image when I look through the pupil of your eye to see the retina. The optic disc, which is packed with nerve fibers extending from retinal ganglion cells is analogous to the outer rim of the teacup. At the center of the optic disc there is a smaller circle in which the color changes to a brighter yellow. The area representing the bottom of the teacup also is called the optic disc excavation. It is devoid of optic nerve fibers and instead acts as a portal through which important arteries and veins enter and exit the eye. Nerve fibers surround the cup, but none run through it. The optic disc excavation should not occupy an area greater than 35% of the total optic disc. Excavations above 35% indicate a loss of optic nerve fibers and the onset of glaucoma. There also are some glaucoma-related changes that occur to the lamina cribrosa. Some pores become enlarged, causing others to compress. This produces a bulge in the back of the plate. The deformation can pinch or in some instances even sever optic nerve fibers. Vascular Theory. The main premise of the vascular theory is that high pressure inside the eye restricts blood flow to the optic nerve causing it to slowly die from oxygen and nutrient deprivation. The amount of blood delivered to a tissue is known as its blood perfusion pressure (BPP). It is dependent upon the difference between arterial blood pressure (AP) and venous pressure (VP), divided by the degree of resistance (R) along the blood vessels. For example, venous pressure in a glaucoma patient that has an intraocular pressure of 24 mmHg must rise to more than 24 mmHg in order to prevent venous collapse. However, this can significantly affect BPP and the oxygenation of tissues. This is a classic example of how the body's response to one problem can cause other problems. In this case, the optic nerve is vulnerable to damage from both the elevated intraocular pressure and from the reduced blood perfusion pressure. Treatment must therefore focus on lowering intraocular pressure either with eye drops or surgery. WHAT ARE RISK FACTORS FOR PRIMARY OPEN-ANGLE GLAUCOMA?A number of factors alone or in combination can place a person at risk for primary open-angle glaucoma. However, before I discuss them, I want to emphasize that the term risk factor is a population statistic. This means that when population samples of people diagnosed with primary open-angle glaucoma are compared to population samples that do not have it, certain things emerge as being associated with the disease. This does NOT mean that if you are a member of one or more risks groups, it guarantees that you will develop primary open-angle glaucoma. However, it does mean that you should have more frequent eye examinations that monitor the pressure inside your eye and the condition of your optic nerve for signs that you might be developing glaucoma. We only get one pair of eyes. It is important to take care of them. Risk factors for primary open-angle glaucoma can be divided into three groups: major risk factors, associated risk factors, and anecdotal risk factors.Major Risk Factors: These tend to be related to the mechanical theory of damage to the optic nerve.
Associated Risk Factors: These tend to be related to the vascular theory of damage to the optic nerve.
Anecdotal Risk Factors: There is suggestive evidence that these factors could be associated with glaucoma, but more research is needed to demonstrate a link.
HOW OFTEN SHOULD I SEEK CARE?Because primary open-angle glaucoma is a stealth destroyer of eyesight, it is important that everyone have regular eye examinations that specifically check for it. How often you have an examination depends upon your history and risk-factor status. Below are some general guidelines to follow. You should consult with your ophthalmologist for specific guidelines. She or he is the person that knows your eyes the best.
If you are in one or more of the risk categories listed above, you should be screened for glaucoma more often. The frequency should be determined in consultation with your ophthalmologist. WHAT QUESTIONS SHOULD I ASK MY OPHTHALMOLOGIST?It is important that you stay well informed about the condition of your eyesight. Having regular eye examinations is the first step in this process. However, it is important that you go one step further and be an active patient rather than a passive one. Below are some questions that you should ask your ophthalmologist following your examination.
Will I annoy my doctor with these questions?Most doctors welcome questions from their patients. It shows evidence that they are interested in their care and patient engagement often translates into improved adherence to treatment regimens. However, even if your ophthalmologist does show signs of annoyance, that is his or her problem, not yours. Obviously, you need to ask questions respectfully and listen to the answers that you receive attentively. But you should not feel intimidated about asking questions. If you do, then perhaps you should consider changing ophthalmologists. Your eyesight is too important to trust it to a doctor with whom you are not comfortable or who does not listen to you.
REFERENCES:Hattenhauer MG, Johnson DH, Ing HH, et al: The probability of blindness from open-angle glaucoma. Ophthalmology 1998;105:2009–2103. Kaiser HJ, Flammer H, Hendrickson P. Ocular blood flow: new insights into the pathogenesis of ocular diseases. Basel: Karger, 1996. Kerrigan-Baumrind LA, Quigley HA, Pease ME: Number of ganglion cells in glaucoma eyes compared with threshold visual field tests in the same person. Invest Ophthalmol Vis Sci 2000;41:741–748. Kooner KS. Primary Open-Angle Glaucoma. In: Zimmerman TJ and Kooner KS. Clinical Pathways in Glaucoma. New York: Thieme, 2001:23-56.
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This represents the bottom of the teacup in our analogy.