Loretta J. Moss
Stephen F. Austin State University, Spring 2000
Return to Perception: Spring 2000frontpage
Glaucoma is a common and important health problem. It is one ofthe leading causes of blindness in Western Society (Hoskins &Kass, 1989). It is responsible for ten percent of all blindness inthe United States and continues to be the second or third most commoncause of blindness in the world (Bunce, Fraser, & Wormald, 1999).It is estimated that two million people in the United States havebeen diagnosed as having glaucoma. Glaucoma is known to affect abouttwo percent of Caucasians beginning at the age of 40 with anincreasing risk for those over the age of 60. This risk is especiallyhigh if a member of the family has glaucoma or diabetes. Further,there is a higher risk of a glaucoma diagnosis for African Americansover the age of 40.
Glaucoma results from increasing intraocular pressure, pressureinside the eye, which can lead to irreparable damage to the retinaand the optic nerve, which connects the retina with the back of thebrain. Intraocular pressure is determined by the balance between therate of the aqueous humor production (found between the cornea andthe lens) and its resistance to outflow at the angle of the anteriorchamber. In most cases, increased resistance to aqueous humor outflowcauses elevated intraocular pressure. Lowering intraocular pressureconstrains or slows the progress of glaucoma.
There are many conditions that individuals may encounter as aresult of glaucoma. Chew et al. (1999) found high intraocularpressure or the presence of glaucoma to be an identification fordecreased life expectancy. After minor modifications were made forrisk factors such as age, sex, hypertension, diabetes, cigarettesmoking, and body mass index, which are known to be associated withhigher mortality, this relationship remained present. Thus, thepresence of higher intraocular pressure or glaucoma made anindependent contribution to the probability of dying. Pain can beanother result of the disease and is affiliated with the height ofthe intraocular pressure and the velocity with which it rises to thatlevel (Hoskins & Kass, 1989). Altered vision is also a possibleresult of this disease and occurs in many forms. Episodic blurring ofvision is frequently arises when rapid increase of intraocularpressure causes corneal edema. Loss of Snellen visual acuitygenerally appears late in the sequence of glaucoma unless some otherproblems transpire, such as central retinal vein occlusion. Othersymptoms may include things such as a change in the appearance of theeye, halo vision, and redness. Before other symptoms occur, anincreased level of intraocular pressure is usually observed. Thesesymptoms and an increase in intraocular pressure are likely to occurin both open-angle glaucoma and angle-closure glaucoma, which are twoof the major types of glaucoma.
Visual field defects, defects pertaining to everything a personsees from peripheral vision to central vision, and optic disc damageis the basis of diagnosis in glaucoma (Hoskins & Kass, 1989). Ifthe eye pressure is not within the normal range or if the optic nervelooks unusual, doctors may perform a visual field test that maps outa person's field vision, or perform a test to check whether the anglewhere the iris meets the cornea is opened or closed. The optic nerveand visual field changes of glaucoma are related to the level of theintraocular pressure and the resistance to damage of the optic nerveaxons. However, the level of intraocular pressure is neither anadequate nor an essential basis for glaucoma diagnosis (Horn et al.,1998). There is also a test that is given that measures eye pressureand another test, called a dilated eye exam, is given to examine theinside of the eye (Hoskins & Kass, 1989). The dilated eye examinvolves putting drops in the eye that allows the doctor to see theoptic nerve and check for possible damage.
Horn et al. (1998) showed that better diagnostic validity ofglaucoma can be achieved by a combination of diagnostic methods intoone quantitative variable, than when compared to single procedures.More specifically, they found that an increase of knowledge isaccomplished in glaucoma diagnosis by affiliating medical andmethodological arguments. This combined method may be more successfulthan repeating only one diagnostic method, in that one specific typeof damage to visual function may occur first in one patient, whereasdifferent types of damage may occur first in other patients. Theresults of their study revealed that if a patient accepts theprobability of damage to visual function in glaucoma, sensitivitycould be enhanced if procedures are integrated and test differentconditions 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 byway of the Schlemm's canal (Hoskins & Kass, 1989). In conditionssuch as primary open-angle glaucoma, less dramatic changes inintraocular pressure exist and pain is less likely to occur. Mostpatients with primary open-angle glaucoma are asymptomatic until latein the course of the disease. For diagnosis and treatment ofopen-angle glaucoma, intraocular pressure, appearance of disc, visualfields, and tolerance by the optic nerve head of the pressureprevailing in the eye must be monitored (Gorin, 1977).
Medical treatment should be started immediately if intraocularpressure is elevated and there are disc and field changes (Gorin,1977). Drug therapy used in open-angle glaucoma can be divided intotopical and oral preparations. Oral drugs include carbonic anhydraseinhibitors, such as acetazolamide, dichlorphenamide, methazolamide,ethoxzolamide, and glycerin. Topical drugs, such as pilocarpine, areparasympathominetic and can produce side effects due to spasm of theciliary muscle, which results in blurred vision and myopia. Afterinstillation, pilocarpine consolidates primarily in ocular tissues,such as the ciliary body. It is then expelled gradually to otherparts 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. Pilocarpineis more effective as an ocular hypotensive agent in lightly pigmentedindividuals than heavy pigmented individuals. Gorin (1977) suggestedthat this is due to the fact that the instillation of pilocarpine indarkly pigmented eyes must be two to three times greater before itreaches the receptor site in the muscle.
Dorzolamide and brinzolamide are new medical treatments forglaucoma patients in the form of topical carbonic anhydraseinhibitors that do not cause the intense side effects that areaffiliated 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 discomforton instillation while brinzolamide was shown to be safer and morecomfortable. Bourne, Egan, Hodge, and McLaren (1998) found thataqueous humor flow rate and intraocular pressure were significantlydecreased by dorzolamide. Further dorzolamide suppresses aqueoushumor production, which decreases intraocular pressure (Bourne, etal., 1998; Capeans, Gonzalez, Martinez, Perez, & Sanchez-Salorio,1999). Finally, the drug dorzolamide was shown to improve ocularblood supply as well as decrease intraocular pressure. Brinzolamidewas shown to lower and control elevated intraocular pressure as well(Lewis & BPTSG, 1998). The topical carbonic anhydrase drugsshowed relevant intraocular pressure reduction, but showed norelevant effects on visual acuity and visual fields. As a result ofthe effect of the drugs on intraocular pressure, it was suggestedthat topical carbonic anhydrase inhibitors should be looked upon as auseful drug for treatment of glaucoma.
In angle-closure glaucoma the resistance to outflow of aqueoushumor is increased because the angle or periphery of the anteriorchamber is closed (Hoskins & Kass, 1989). In acute angle-closureglaucoma, conditions may cause rapid and sustained rises ofintraocular pressure and is usually accompanied by pain.Angle-closure glaucoma is considered to be one of the most difficultdiagnosis, but it can be diagnosed through an occurrence of elevatedintraocular pressure. (Gorin, 1977).
Treatment of angle-closure glaucoma should begin once the diseaseis diagnosed (Gorin, 1977). To prevent a recurrence in angle-closureglaucoma, such as acute congestive-angle-closure glaucoma, the goalis to reopen the angle. Treatment is given to relieve pain andanxiety before the advent of carbonic anhydrase inhibitors andosmotic agents. Attempts are made to lower intraocular pressure byadministering acetazolamide orally followed by oral glycerol. Of theoral osmotic agents, glycerol is the most useful. Gorin (1977)mentioned other osmotic agents that are intravenous agents, such asurea and mannitol. After these intravenous agents are administeredpatients may become thirsty and are warned not to drink water. Ifwater is consumed, the intake will cause a secondary rise inintraocular pressure, nullifying the hypotensive effect of the ureaor the mannitol.
In the United States there are approximately one million peoplewho are unaware that they have glaucoma and each year an additional5,500 people become legally blind from the disease (Hoskins &Kass, 1989). Bunce, Fraser, and Wormald (1999) found that patientswho have highly evolved glaucoma have danger of blindness. It issuggested that people become blind from glaucoma because they seekmedical attention too late in the course of the disease or they seekhelp early but receive suboptimal treatment. The delayed presentationof glaucoma is shown to be a significant and not uncommon risk factorfor blindness. Blindness is more likely to advance in patients thatalready experience visual field loss when treatment begins, comparedto those that begin treatment before any visual field loss occurs.The data obtained in this study indicated that certain subgroups ofpeople are at an enormous risk of having highly evolved andirreparable damage, pertaining to their visual field, on their firstvisit to the doctor.
Many factors in the patient's history may have a bearing on thediagnosis and treatment of glaucoma. Socioeconomic status was shownto be strongly correlated with the risk of a late diagnosis (Bunce etal., 1999). People with a high socioeconomic status were estimated tobe at the lowest risk of a late diagnosis. Social factors, such associoeconomic status, affect access to adequate medical care as wellas the patient's compliance with treatment. Also found to be animportant component of the disease stage at which medical attentionis received was a patient's family history. The patient was morelikely to seek early attention if more people in their family havebeen diagnosed with glaucoma. A last factor that was mentioned inthis study pertained to the gender of the patient. It appeared thatmen are more likely to receive a later diagnosis than women.
The elderly population in the United States is increasing, whichimplies that more people will be capable of being a victim ofglaucoma (Bunce et al., 1999). The meaning of the term glaucoma doesnot pertain to a singular disease but rather to a cluster of diseasesthat differ in their clinical presentation, pathophysiology, andtreatment (Hoskins & Kass, 1989). These diseases are compiledtogether on the account that they share certain features, whichincludes visual field loss and atrophy of the optic nerve head, whichare related to the level of intraocular pressure. Blindness fromglaucoma in nearly all cases is preventable if the disease isdetected early and proper treatment is implemented (Bunce et al.,1999). This implies that detection depends on educating the publicabout the importance of routine examinations and proper training ofprofessionals to recognize the signs and symptoms of glaucoma. Thereis no cure for glaucoma but it can be controlled. Future research ondiagnosis of the disease using multivariate analysis should beconsidered in order to help control and prevent blindness that maycome as a result of the disease (Horn et al., 1998). Horn et al.suggested that such an analysis can be created if a future studytakes into consideration the effects of therapy, which should bedependent on the results of diagnostic measurements.
Bourne, W. M., Egan, C. A., Hodge, D. O., & McLaren, J. W.(1998). Effect of dorzolamide on corneal endothelial function innormal human eyes. Investigative Ophthalmology & Visual Science,39, 23-27.
Bunce, C., Fraser, S., & Wormald, R. (1999). Risk factors forlate 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 intraocularpressure and survival: the Framingham studies. American Journal ofOphthalmology,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'sdiagnosis 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), anew topical carbonic anhydrase inhibitor for primary open-angleglaucoma and ocular hypertension. American Journal of Ophthalmology,126, 400- 408.