Published: August 2010
Vision is essential to the patient’s quality of life and has a significant impact on morbidity. Myriad activities, from reading medication labels to using visual cues to ambulate in a room, arguably make vision one of the most important systems in the body. Declines in the visual system can lead to the inability to live independently, economic hardship, and psychological difficulties.1, 2 In fact, recent research has shown that certain eye disorders are associated with declines in quality of life measures regardless of measured visual acuity. This may be because the visual system is multifaceted, and impairment can cause changes in other aspects such as contrast sensitivity, peripheral vision, color vision, dark and light adaptation, glare, and depth perception.3
The prevalence and disabling effects of eye-related illness such as cataract, glaucoma, age-related macular degeneration, and diabetic retinopathy increase as the population ages. An estimated 3.3 million Americans ages 40 years and older have some visual impairment (best corrected vision between 20/40 to 20/200 in the better-seeing eye). It is estimated that 937,000 Americans are legally blind, with a best corrected vision of less than 20/200 in the better-seeing eye.4 Formalized research reports have validated the significance of vision in the physical well-being of the geriatric patient. For example, the Blue Mountain Eye Study found that visual impairment was strongly associated with two or more falls in elderly adults.5 The Beaver Dam study confirmed these findings, showing that patients older than 60 years who had impaired vision had an increased rate of hip fractures and decreased mobility.6
The leading cause of blindness and visual impairment differs among race categories. Age-related macular degeneration is the most prevalent cause of blindness of among whites, and glaucoma and cataract are the leading causes among African American and Latin American patients. Table 1 summarizes the important causes among these groups. Cataract was the most common contributor of low vision, accounting for approximately one half of the patients with low vision in each category. Overall, the age-adjusted blindness prevalence was higher for African Americans (odds ratio [OR], 2.77) and Latin Americans (OR, 3.13) as compared with whites (OR, 1.00). African American male patients had a significantly higher prevalence of blindness than female patients. The prevalence of visual impairment increases with age, and it incrases dramatically after the age of 75 years.7 Applying the prevalence in race and age category to U.S. census projections for 2020, the number of blind persons older than 40 years in the United States is expected to increase by approximately 70% to 1.6 million, with an additional 3.9 million persons making a total of 5.5 million visually impaired Americans.7
|African Americans||European Americans||Latin Americans|
|Disease||Blindness (%)||Low Vision (%)||Blindness (%)||Low Vision (%)||Blindness (%)||Low Vision (%)|
Blindness is defined as visual acuity less than 20/200 best corrected in the better-seeing eye.
Visual impairment is defined as one-eye vision less than 20/200.
AMD, age-related macular degeneration.
Screening for ophthalmic issues has been shown to have a significant benefit in the elderly population. In a 5-year study of Medicare beneficiaries, those who had regular eye examinations experienced less decline of vision and functional status than those who had less-frequent examinations.8 Ophthalmologists are best qualified to perform comprehensive ophthalmic screening and evaluation for cataracts. The frequency of screenings depends on the patient’s clinical history as well as the findings during the most recent examination. Because the primary line of defense is prevention of these pathologic conditions, this chapter explores the screening measures and the current literature on the prevention of these disorders.
The development of cataracts is a lifelong process involving a change in the chemical composition and disarrangement of lens fibrils. Only when the opacification causes significant visual loss and symptoms should the cataractous lens be removed and replaced with an artificial lens.
Cataract is the leading preventable cause of blindness in the United States and the world today.9 It is responsible for 60% of all Medicare costs related to vision.10 In the United States, an estimated 20.5 million (17.2%) Americans older than 40 years have a cataract in either eye. Women have a significantly higher age-adjusted prevalence of cataract than men in the United States. The number of Americans affected by cataract and undergoing cataract surgery will dramatically increase by 2020 as the U.S. population ages. The total number of persons who have cataract is estimated to rise to 30.1 million by 2020, and those who are expected to undergo cataract surgery will rise to 9.5 million by 2020.11
There are several different types of cataracts, each with its own pathology, anatomic location, and risk factors. Numerous potential risk factors have been associated with cataract formation. However, most of these studies are observational, and a true cause-and-effect relation cannot be proved. Furthermore, many of these studies are limited in their power because they failed to correlate cataract exposure to the risk factor in a standardized fashion.12 The causes of cataracts are multifactorial and include age, diabetes, inflammation, trauma, and drugs such as steroids. Studies of potential risk factors for cataract formation are summarized in Box 1.
|Box 1 Risk factors for Developing Cataracts|
|UVB light exposure|
|No Benefit or Unknown|
Adapted from American Academy of Ophthalmology: Preferred practice pattern: Cataract in the Adult Eye.
The prevention of cataracts has been studied in numerous clinical trials evaluating nutritional or vitamin supplementation. Thus far, no study has shown a significant benefit in delaying the onset and progression of cataract formation.13-15 The Roche European American Cataract trial showed some protective effect from the use of vitamins C and E and beta-carotene, but this was not found in the European arm.16 The American Academy of Ophthalmology (AAO) has no recommendations for nutritional supplements to prevent cataracts or delay progression.
Smoking has been directly linked to cataract formation and shows a dose-response effect. Several studies have shown decreased cataract formation in past smokers as compared with current smokers, illustrating a significant benefit from smoking cessation.17-20 Cumulative exposure to ultraviolet (UV) B radiation has been associated with the development of cataracts, and therefore reduced sun exposure, UVB-protective sunglasses, and brimmed hats should be recommended to patients.21-23 Long-term use of inhaled and oral corticosteroids has demonstrated a higher risk of formation.24, 25 Many studies have also found that diabetes mellitus is a risk factor for cataract formation and that tight glucose control can reduce the progression to cataract formation.26
For screening, patients can be stratified into those without risk factors, those with risk factors, and those with conditions that require intervention. The AAO recommends that patients ages 65 years and older have ophthalmic examinations every 1 to 2 years in the absence of risk factors and those 55 to 64 years have an examination every 1 to 3 years. Patients with risk factors or those with conditions that might require interventions should have more frequent follow-ups, depending on the nature of the cataract and the functional visual impairment it causes.
Glaucoma is a group of diseases with the common characteristic of optic neuropathy associated with visual field loss, with elevated intraocular pressure as the primary risk factor. The two major forms of glaucoma are open-angle glaucoma (OAG) and angle-closure glaucoma (ACG). ACG refers to closure of the angle formed between the iris and cornea, thereby restricting the outflow of aqueous fluid through the trabecular meshwork at the apex of the angle. OAG includes glaucoma conditions where the angle appears normal, with outflow obstruction likely at the level of trabecular meshwork or beyond. Both processes of aqueous outflow restriction lead to buildup of fluid and pressure in the eye, with associated optic neuropathy and visual field loss.
Between 1991 and 1999, the prevalence of glaucoma among Medicare recipients increased from 8.4% to 25.4%. Among patients with glaucoma, those with primary OAG increased from 4.6% to 13.8%, and those with ACG also increased from 0.7% to 2.7%.27 The overall prevalence of OAG in the U.S. population 40 years and older in 2000 was estimated to be 1.86%, with 1.57 million white and 398,000 African American persons affected. After applying race-, age-, and gender-specific rates to the U.S. population as determined in the 2000 U.S. census, it is estimated that OAG affects 2.22 million U.S. citizens. Owing to the rapidly aging population, the number with OAG will increase by 50% to 3.6 million in 2020. African American patients had almost three times the age-adjusted prevalence of glaucoma as white patients.28 Risk factors for OAG include elevated intraocular pressure, older age, positive family history, African or Latin American descent, and thinner central corneal thickness. Other possible risk factors include low diastolic perfusion pressures, diabetes, myopia, and systemic hypertension.29
Screening for OAG can be attempted by intraocular pressure measurement, optic nerve and nerve fiber layer appearance, and visual field testing, all cumbersome approaches to screening. Measuring intraocular pressure alone is not an effective screening tool because many population-based studies have shown persons with primary OAG and an intraocular pressure of less than 22 mm Hg, the usual screening cutoff.30 Another method of attempted screening is to test visual fields. Perimetry based on frequency-doubling technology shows promise as a screening tool to detect moderately glaucomatous eyes. The positive predictive value found in a retrospective series was 32.6% to 45.1%, and the negative predictive value was 98.7%.31
Thus far, no effective screening process has been identified from extensive review of the literature.32 Screening by a combination of positive family history and elevated intraocular pressure showed an 82% sensitivity for OAG.29, 33, 34 The more likely scenario for screening larger populations will be a combination of intraocular pressure measurement, visual field testing, and optic nerve head cupping evaluation.
Age-related macular degeneration (AMD) involves the destruction of the retina and commonly affects central vision or the macula and its supportive tissue underneath. Early manifestations include the appearance of drusen, waste products of metabolism underneath the retina. Vision loss is manifested in the dry, non-neovascular, form with progressive atrophy of the retina and retinal pigment epithelium in a geographic pattern. In the wet or neovascular form, more-rapid visual loss occurs secondary to leakage, bleeding, and fibrotic scarring from neovascular tissue proliferating under the retina.
The overall prevalence of neovascular AMD and geographic atrophy in the U.S. population older than 40 years is estimated to be 1.47%, with 1.75 million Americans having AMD. A survey of Medicare beneficiaries between 1994 and 1998 showed a prevalence of wet macular degeneration of between 0.37% and 1.14%, compared with 1.48% obtained from the Beaver Dam Eye Study.35 The prevalence of AMD increases dramatically with age, with more than 15% of the white women older than 80 years having neovascular AMD or geographic atrophy, or both. More than 7 million persons had drusen measuring 125 γm or larger and were, therefore, at substantial risk for developing AMD. Owing to the rapidly aging population, the number of Medicare recipients with AMD increased from 5.0% to 27.1% between 1991 and 1999. The percentage of patients with AMD is expected to increase by 50% to 2.95 million in 2020.36
Although an estimated 80% of AMD patients have the non- neovascular form, the neovascular form may be responsible for almost 90% of the severe visual loss from AMD.37, 38 Advancing age is a major risk factor for AMD. In the Framingham Eye Study, 6.4% of patients ages 65 to 74 years had signs of macular degeneration. This rate increases to 19.7% in patients older than 75 years.39
Antioxidant vitamin and mineral supplementation of vitamins C and E, beta-carotene, zinc, and copper has been shown by the Age-Related Eye Disease Study (AREDS) to reduce the rate of development of advanced AMD from those with intermediate stage or unilateral advanced AMD. In this patient population, the AREDS vitamin and mineral formula reduced the 5-year risk of progression to advanced AMD by 25% and reduced moderate visual loss by 19%. However, beta-carotene administration has been associated with increased risk for lung cancer in heavy smokers and in persons with asbestos exposure.40
Other risk factors for AMD include cigarette smoking, hyperopia, light iris color, hypertension, hypercholesterolemia, female gender, cardiovascular disease, and low level of dietary antioxidants and other dietary factors.41 Recent studies have highlighted the possible relation between complement factor H mutations and AMD. Homozygous patients with the risk allele have a 7.4-fold increased risk of AMD development and progression.42 Finally, the role of heredity has been supported by many studies.43
Persons without any risk factors for AMD should be evaluated by the standard age criteria set by the AAO. Patients older than 65 years should have yearly examinations, and patients aged 40 to 64 years should have an examination every 1 to 2 years. Patients with early or intermediate retinal changes from AMD should be seen annually. They should also be educated about the symptoms indicating advancement of AMD and the need to contact the ophthalmologist when new changes arise. Follow-up examinations in patients with advanced AMD are also helpful because they can permit evaluation of signs in the contralateral eye, provide an opportunity for the patient to discuss new preventive measures, and reinforce self- monitoring.
Like AMD, diabetic retinopathy manifests itself in two forms, nonproliferative and proliferative (neovascular). Early diabetic retinopathy involves abnormality of existing retinal vessels seen by vascular leakage, retinal hemorrhage, tissue infarction, and nonperfusion. Macular edema, a result of leaking microaneurysms causing fluid accumulation in the macula, represents a visually significant entity in nonproliferative retinopathy. In the proliferative forms, abnormal vessels grow secondary to signals from the ischemic retina. Bleeding into the vitreous (secondary to abnormal neovascularization) causes vision loss. Neovascular proliferation also causes tractional retinal detachment and severe loss of vision when left untreated.
The duration of diabetes is a major risk factor for development of diabetic retinopathy. According to the Wisconsin Epidemiologic Study of Diabetic Retinopathy, 25% of patients with type 1 diabetes develop retinopathy after 5 years, 60% after 10 years, and 80% after 15 years. In patients with type 2 diabetes, 40% of those taking insulin and 24% not taking insulin develop retinopathy within 5 years of diagnosis. After 19 years, these rates increase to 84% and 53%, respectively.44, 45
Although the development of retinopathy in diabetic patients is difficult to prevent, tight glucose control can reduce progression to visually significant diabetic retinopathy. Intensive glucose control has been shown to reduce development of retinopathy by 76% in patients with type 1 diabetes within 3 years. The risk of retinopathy progression is reduced by 54%, and the risk of progression to proliferative disease is reduced by 47%.46 In patients with type 2 diabetes, tighter blood glucose control reduced the need for laser surgery by 29%. Concurrent control of hypertension resulted in a 47% reduction of vision decrease.47 A recent (ACCORD) study on the effects of even more intense glucose control with a goal of hemoglobin A1c of below 6% (vs. 7%) found an increased relative mortality of 22% in the tightly controlled group after a 3.5-year follow up. The question of increased benefit with even tighter glycemic control may be clarified as more data emerge.48
In patients with poorly controlled diabetes, vision fluctuations can occur as changes in serum osmolality affect the refractive qualities of human lenses. This acute phenomenon does not necessarily correlate with the presence of diabetic retinopathy. A stable blood glucose level can ensure proper vision testing as well as proper refraction measurement if corrective lenses are needed.
Regular ophthalmologic examination for patients with diabetes should be emphasized. With treatments for diabetic retinopathy effective in preventing vision loss in 90% of the patients, the numbers of patients referred by primary care physicians are far below those recommended by the American Diabetes Association guideline.49 Between 50% and 60% of Medicare beneficiaries with diabetes were found to receive annual eye examinations within a 15-month survey period.50 The Wisconsin Epidemiologic Study of Diabetic Retinopathy found 11% of patients with type I diabetes and 7% of patients with high-risk proliferative retinopathy had no examination by an ophthalmologist within 2 years.51
Routine medical eye examinations are beneficial to patients, because many changes due to diabetic retinopathy may be visually subtle or affect peripheral visual areas not commonly noticed. For patients with diabetes, the AAO recommends a comprehensive eye examination schedule of initial examination within 5 years after onset of type 1 diabetes, with yearly follow-ups; initial examination at diagnosis of type 2 diabetes, with yearly follow-ups; and examination before pregnancy for all women with diabetes, before conception or early in the first trimester, with follow-ups every 1 to 3 months for severe nonproliferative diabetic retinopathy and every 3 to 12 months if retinopathy is milder.
Routine eye examinations allow patients to receive advice about self-protective activities for disease prevention. Closer monitoring can be planned for patients with worrisome findings on the initial examination such as nonperfusion of the retina without formation of proliferative disease, or edema adjacent to the macula but not clinically significant for laser treatment. Good glucose control should be maintained in conjunction with primary care physicians and possible nutritional consultation.