Loretta J. Moss
Stephen F. Austin State University, Spring 2000
Return to Perception: Spring 2000 frontpage
Glaucoma is a common and important health problem. It is one of the leading causes of blindness in Western Society (Hoskins & Kass, 1989). It is responsible for ten percent of all blindness in the United States and continues to be the second or third most common cause of blindness in the world (Bunce, Fraser, & Wormald, 1999). It is estimated that two million people in the United States have been diagnosed as having glaucoma. Glaucoma is known to affect about two percent of Caucasians beginning at the age of 40 with an increasing risk for those over the age of 60. This risk is especially high if a member of the family has glaucoma or diabetes. Further, there is a higher risk of a glaucoma diagnosis for African Americans over the age of 40.
Glaucoma results from increasing intraocular pressure, pressure inside the eye, which can lead to irreparable damage to the retina and the optic nerve, which connects the retina with the back of the brain. Intraocular pressure is determined by the balance between the rate of the aqueous humor production (found between the cornea and the lens) and its resistance to outflow at the angle of the anterior chamber. In most cases, increased resistance to aqueous humor outflow causes elevated intraocular pressure. Lowering intraocular pressure constrains or slows the progress of glaucoma.
There are many conditions that individuals may encounter as a result of glaucoma. Chew et al. (1999) found high intraocular pressure or the presence of glaucoma to be an identification for decreased life expectancy. After minor modifications were made for risk factors such as age, sex, hypertension, diabetes, cigarette smoking, and body mass index, which are known to be associated with higher mortality, this relationship remained present. Thus, the presence of higher intraocular pressure or glaucoma made an independent contribution to the probability of dying. Pain can be another result of the disease and is affiliated with the height of the intraocular pressure and the velocity with which it rises to that level (Hoskins & Kass, 1989). Altered vision is also a possible result of this disease and occurs in many forms. Episodic blurring of vision is frequently arises when rapid increase of intraocular pressure causes corneal edema. Loss of Snellen visual acuity generally appears late in the sequence of glaucoma unless some other problems transpire, such as central retinal vein occlusion. Other symptoms may include things such as a change in the appearance of the eye, halo vision, and redness. Before other symptoms occur, an increased level of intraocular pressure is usually observed. These symptoms and an increase in intraocular pressure are likely to occur in both open-angle glaucoma and angle-closure glaucoma, which are two of the major types of glaucoma.
Visual field defects, defects pertaining to everything a person sees from peripheral vision to central vision, and optic disc damage is the basis of diagnosis in glaucoma (Hoskins & Kass, 1989). If the eye pressure is not within the normal range or if the optic nerve looks unusual, doctors may perform a visual field test that maps out a person's field vision, or perform a test to check whether the angle where the iris meets the cornea is opened or closed. The optic nerve and visual field changes of glaucoma are related to the level of the intraocular pressure and the resistance to damage of the optic nerve axons. However, the level of intraocular pressure is neither an adequate nor an essential basis for glaucoma diagnosis (Horn et al., 1998). There is also a test that is given that measures eye pressure and another test, called a dilated eye exam, is given to examine the inside of the eye (Hoskins & Kass, 1989). The dilated eye exam involves putting drops in the eye that allows the doctor to see the optic nerve and check for possible damage.
Horn et al. (1998) showed that better diagnostic validity of glaucoma can be achieved by a combination of diagnostic methods into one quantitative variable, than when compared to single procedures. More specifically, they found that an increase of knowledge is accomplished in glaucoma diagnosis by affiliating medical and methodological arguments. This combined method may be more successful than repeating only one diagnostic method, in that one specific type of damage to visual function may occur first in one patient, whereas different types of damage may occur first in other patients. The results of their study revealed that if a patient accepts the probability of damage to visual function in glaucoma, sensitivity could be enhanced if procedures are integrated and test different conditions of visual functions.
Open-angle glaucoma is the most common type in the United States. In open-angle glaucoma there is an impeded flow of aqueous humor by way of the Schlemm's canal (Hoskins & Kass, 1989). In conditions such as primary open-angle glaucoma, less dramatic changes in intraocular pressure exist and pain is less likely to occur. Most patients with primary open-angle glaucoma are asymptomatic until late in the course of the disease. For diagnosis and treatment of open-angle glaucoma, intraocular pressure, appearance of disc, visual fields, and tolerance by the optic nerve head of the pressure prevailing in the eye must be monitored (Gorin, 1977).
Medical treatment should be started immediately if intraocular pressure is elevated and there are disc and field changes (Gorin, 1977). Drug therapy used in open-angle glaucoma can be divided into topical and oral preparations. Oral drugs include carbonic anhydrase inhibitors, such as acetazolamide, dichlorphenamide, methazolamide, ethoxzolamide, and glycerin. Topical drugs, such as pilocarpine, are parasympathominetic and can produce side effects due to spasm of the ciliary muscle, which results in blurred vision and myopia. After instillation, pilocarpine consolidates primarily in ocular tissues, such as the ciliary body. It is then expelled gradually to other parts of the eye during the period of its duration of action. Pilocarpine may result in side effects such as sweating, nausea, vomiting, diarrhea, respiratory troubles and many more. Pilocarpine is more effective as an ocular hypotensive agent in lightly pigmented individuals than heavy pigmented individuals. Gorin (1977) suggested that this is due to the fact that the instillation of pilocarpine in darkly pigmented eyes must be two to three times greater before it reaches the receptor site in the muscle.
Dorzolamide and brinzolamide are new medical treatments for glaucoma patients in the form of topical carbonic anhydrase inhibitors that do not cause the intense side effects that are affiliated with the use of oral carbonic anhydrase inhibitors (Lewis & Brinzolamide Primary Therapy Study Group, 1998). However, dorzolamide was shown to have a high incidence of ocular discomfort on instillation while brinzolamide was shown to be safer and more comfortable. Bourne, Egan, Hodge, and McLaren (1998) found that aqueous humor flow rate and intraocular pressure were significantly decreased by dorzolamide. Further dorzolamide suppresses aqueous humor production, which decreases intraocular pressure (Bourne, et al., 1998; Capeans, Gonzalez, Martinez, Perez, & Sanchez-Salorio, 1999). Finally, the drug dorzolamide was shown to improve ocular blood supply as well as decrease intraocular pressure. Brinzolamide was shown to lower and control elevated intraocular pressure as well (Lewis & BPTSG, 1998). The topical carbonic anhydrase drugs showed relevant intraocular pressure reduction, but showed no relevant effects on visual acuity and visual fields. As a result of the effect of the drugs on intraocular pressure, it was suggested that topical carbonic anhydrase inhibitors should be looked upon as a useful drug for treatment of glaucoma.
In angle-closure glaucoma the resistance to outflow of aqueous humor is increased because the angle or periphery of the anterior chamber is closed (Hoskins & Kass, 1989). In acute angle-closure glaucoma, conditions may cause rapid and sustained rises of intraocular pressure and is usually accompanied by pain. Angle-closure glaucoma is considered to be one of the most difficult diagnosis, but it can be diagnosed through an occurrence of elevated intraocular pressure. (Gorin, 1977).
Treatment of angle-closure glaucoma should begin once the disease is diagnosed (Gorin, 1977). To prevent a recurrence in angle-closure glaucoma, such as acute congestive-angle-closure glaucoma, the goal is to reopen the angle. Treatment is given to relieve pain and anxiety before the advent of carbonic anhydrase inhibitors and osmotic agents. Attempts are made to lower intraocular pressure by administering acetazolamide orally followed by oral glycerol. Of the oral osmotic agents, glycerol is the most useful. Gorin (1977) mentioned other osmotic agents that are intravenous agents, such as urea and mannitol. After these intravenous agents are administered patients may become thirsty and are warned not to drink water. If water is consumed, the intake will cause a secondary rise in intraocular pressure, nullifying the hypotensive effect of the urea or the mannitol.
In the United States there are approximately one million people who are unaware that they have glaucoma and each year an additional 5,500 people become legally blind from the disease (Hoskins & Kass, 1989). Bunce, Fraser, and Wormald (1999) found that patients who have highly evolved glaucoma have danger of blindness. It is suggested that people become blind from glaucoma because they seek medical attention too late in the course of the disease or they seek help early but receive suboptimal treatment. The delayed presentation of glaucoma is shown to be a significant and not uncommon risk factor for blindness. Blindness is more likely to advance in patients that already experience visual field loss when treatment begins, compared to those that begin treatment before any visual field loss occurs. The data obtained in this study indicated that certain subgroups of people are at an enormous risk of having highly evolved and irreparable damage, pertaining to their visual field, on their first visit to the doctor.
Many factors in the patient's history may have a bearing on the diagnosis and treatment of glaucoma. Socioeconomic status was shown to be strongly correlated with the risk of a late diagnosis (Bunce et al., 1999). People with a high socioeconomic status were estimated to be at the lowest risk of a late diagnosis. Social factors, such as socioeconomic status, affect access to adequate medical care as well as the patient's compliance with treatment. Also found to be an important component of the disease stage at which medical attention is received was a patient's family history. The patient was more likely to seek early attention if more people in their family have been diagnosed with glaucoma. A last factor that was mentioned in this study pertained to the gender of the patient. It appeared that men are more likely to receive a later diagnosis than women.
The elderly population in the United States is increasing, which implies that more people will be capable of being a victim of glaucoma (Bunce et al., 1999). The meaning of the term glaucoma does not pertain to a singular disease but rather to a cluster of diseases that differ in their clinical presentation, pathophysiology, and treatment (Hoskins & Kass, 1989). These diseases are compiled together on the account that they share certain features, which includes visual field loss and atrophy of the optic nerve head, which are related to the level of intraocular pressure. Blindness from glaucoma in nearly all cases is preventable if the disease is detected early and proper treatment is implemented (Bunce et al., 1999). This implies that detection depends on educating the public about the importance of routine examinations and proper training of professionals to recognize the signs and symptoms of glaucoma. There is no cure for glaucoma but it can be controlled. Future research on diagnosis of the disease using multivariate analysis should be considered in order to help control and prevent blindness that may come as a result of the disease (Horn et al., 1998). Horn et al. suggested that such an analysis can be created if a future study takes into consideration the effects of therapy, which should be dependent on the results of diagnostic measurements.
References
Bourne, W. M., Egan, C. A., Hodge, D. O., & McLaren, J. W. (1998). Effect of dorzolamide on corneal endothelial function in normal human eyes. Investigative Ophthalmology & Visual Science, 39, 23-27.
Bunce, C., Fraser, S., & Wormald, R. (1999). Risk factors for late presentation in chronic glaucoma. Investigative Ophthalmology & Visual Science, 40, 2251-2257.
Capeans, C., Gonzalez, F., Martinez, A., Perez, R., & Sanchez-Salorio, M. (1999). Dorzolamide effect on ocular blood flow. Investigative Ophthalmology & Visual Science, 40, 1270-1275.
Chew, E. Y., D'Agostino, R. B., Hiller, R., Podgor, M. J., Sperduto, R. D., & Wilson, P. W. F. (1999). High intraocular pressure and survival: the Framingham studies. American Journal of Ophthalmology,128, 440-445.
Gorin, G. (1977). Clinical glaucoma . New York: Marcel Dekker, Inc.
Horn, F., Jonas, J. B., Junemann, A., Korth, M., Martus, P., & Wisse, M. (1998). A multivariate sensory model in glaucoma diagnosis. Investigative Ophthalmology & Visual Science, 39, 1567-1573.
Hoskins, H. D., Jr., & Kass, M. (1989). Beckner-Schaffer's diagnosis and therapy of the glaucomas (6th ed.). St. Louis: The C. V. Mosby Company.
Lewis, S. H., & Brinzolamide Primary Therapy Study Group (1998). Clinical efficacy and safety of brinzolamide (azopt^tm), a new topical carbonic anhydrase inhibitor for primary open-angle glaucoma and ocular hypertension. American Journal of Ophthalmology, 126, 400- 408.