61: Managing Vision Impairment in Older Adults

Vision impairment is relatively rare in people younger than 65 years of age, but its incidence steadily increases to almost 24% of those 80 years and older. Not surprisingly, vision impairment can have a significant impact on a patient’s quality of life. It is associated with social isolation, anxiety, depression and a loss of independence. It can affect balance, leading to more frequent falls, and has been shown to negatively affect physical activity.

The following 3 levels are used to categorize the severity of vision loss*:

1. Normal vision: Visual acuity ≥20/40

2. Visual impairment: Visual acuity >20/40 but <20/200

3. Legal blindness: Acuity ≤20/200 in the better eye, or total visual field <20 degrees

Although not meeting the definition of vision impairment, there are still a number of changes in the aging eye leading to diminished vision. In all adults, the crystalline lens gradually becomes less flexible and less able to change its curvature (accommodate) with age. This results in the condition known as presbyopia, in which patients lose the ability to focus their eyes on near objects. The ability to see well in dim light also becomes diminished in older adults as a result of a combination of decreases in pupil size and progressive increases in the light absorption of the lens. This age-related reduction in retinal illumination is substantial. A typical 60-year-old’s retina receives only about one-third of the light that a typical 20-year-old receives. As a result of the tendency for opacities to form in the aging lens and cornea, older adults are increasingly sensitive to glare caused by scattered light in the eye. Finally, because of neural changes in the retina, there is an age-related reduction in the ability to adapt to sudden changes in illumination.

Clinical Findings

Signs & Symptoms

Starting in the mid-40s, reading glasses may be required to manage presbyopia. Although distance vision remains stable during this time, by the seventh decade and beyond, distance vision also can be reduced because of changes in refractive error. Difficulty with dim lighting and sensitivity to glare may cause problems with driving at night. Dry eye, especially in older women, is also common. Symptoms include a mild foreign-body sensation, burning, small fluctuations in vision, and even (reflexive) tearing because of mild corneal irritation. Table 61–1 includes suggested vision screening tests for older adults.

Treatment & Prognosis

Although a number of normal, age-related changes have a negative impact on vision, there are simple ways to compensate for many of them. Because dry eye tends to be chronic and associated with many medications used by older adults, nonprescription artificial tears can help relieve symptoms. In epidemiologic studies, 40% to 60% of older adults have vision worse than 20/40 simply because of problems with their eyeglasses, a problem easily remedied through ensuring regular eye examinations. Finally, other ways to compensate for normal age-related losses of vision include providing bright, but indirect (ie, nonglare) lighting, which significantly improves visual function in most older adults.

The leading abnormal ocular changes that cause vision impairment in older adults are cataracts, age related macular degeneration, diabetic retinopathy, and glaucoma.

General Principles in Older Adults

A cataract is a clouding of the lens and is a leading cause of vision impairment in the United States and globally. Cataracts progress gradually, and may require removal. By age 80 years, more than half of all people in the United States either have a cataract or have had cataract surgery. Risk factors for cataracts include advanced age, diabetes, cumulative exposure to ultraviolet B radiation, smoking, current or previous long-term use of corticosteroids, previous eye surgery, or a history of eye injury.

Prevention

Decreasing UV exposure by wearing sunglasses and hats, encouraging smoking cessation and good glycemic control may delay the onset and progression of cataracts. Currently, there is no evidence that medication or nutritional supplementation prevents, delays the progression of, or cures cataracts.

Clinical Findings

Typical symptoms of cataracts include a gradual onset of blurred vision and increased sensitivity to glare (especially when driving at dusk or night). A common sign of a sight-limiting cataract is an insensitivity to subtle color differences such as those caused by food stains on clothing in an otherwise neatly dressed patient. Observing a white haze in the pupil during pupil testing suggests a moderate or worse cataract. With the pupil dilated, the red eye reflex may exhibit focal or diffuse areas of darkness when viewed with the direct ophthalmoscope or a slit lamp.

Differential Diagnosis

Patients with significant cataracts often present with a history of painless, gradual and progressive deterioration of vision and a normal appearing external eye. Other possibilities include uncorrected refractive error, diseases of the macula or optic nerve, or diabetic eye disease. If vision loss is rapid, consider vitreal or retinal hemorrhage, or other vascular disorders. Associated eye pain and/or conjunctival hyperemia should raise concern for uveitis or angle-closure glaucoma.

Complications

Complications due to cataracts are very rare and include lens-induced glaucoma or uveitis. In the case of glaucoma, the lens pushes the iris forward into the anterior chamber angle, and blocks aqueous drainage. In lens-induced uveitis, disruption of the lens capsule causes an immune-related intraocular inflammation, which can also induce glaucoma by blocking aqueous outflow. In both situations, surgical removal of the lens is curative.

Management & Treatment

Cataracts usually develop slowly, and in the early stages an updated spectacle correction often will improve vision. Environmental modifications, such as avoiding high glare situations (eg, night driving) the use of antiglare sunglasses and providing adequate ambient light, can help patients cope. The only treatment for cataracts is removal. Surgery is usually indicated when visual acuity is approximately 20/40 or when a patient’s daily activities are compromised by reduced vision, despite best correction. The decision for surgery should take into account other pathologies, such as macular degeneration or diabetic retinopathy, which may limit postsurgical vision.

Pre- and Postoperative Care

Most older adults can tolerate cataract surgery. Patients should be medically stable and ideally be able to lie supine for 30 minutes. Postoperative care typically requires the administration of antibiotic and antiinflammatory eye drops, as well as follow-up office visits. For patients with comorbidities such as chronic obstructive pulmonary disease, poorly controlled blood pressure, coronary artery disease, or diabetes, the ophthalmologist will typically request a medical evaluation by the patient’s primary care physician. Although preoperative laboratory testing for any medical problems indicated by the history and physical examination is appropriate, studies show that routine medical testing before cataract surgery does not improve outcomes.

Cataract surgery is usually an outpatient procedure. In patients deemed to have a reasonably healthy cornea, the incision is made through the cornea, which results in minimal or no blood loss and usually requires only topical anesthesia and minimal systemic medications. Because of this, anticoagulant or antiplatelet therapy may be continued, based on the preferences of the eye surgeon and primary care physician.

Complications

Serious postoperative complications from cataract surgery are rare (<1.5%). Symptoms of pain or a decrease in vision in the days following surgery suggest intraocular infection (endophthalmitis), and an increase in floaters or flashes of light could signal retinal detachment. Both of these conditions require immediate ophthalmologic consultation. While less vision-threatening, 2 more common complications, cystoid macular edema and the development of opacities on the posterior capsule of the lens, also require consultation because they can reduce visual acuity. Cystoid macular edema occurs at a rate of <3% in the weeks following cataract removal and is typically treated with topical antiinflammatory medications. Posterior capsular opacities (sometimes called secondary cataracts) can develop months to years following lens removal surgery and occur at a rate of 18% to 50%. If the opacity becomes visually significant, a laser is used to ablate the area of membrane that blocks vision.

Prognosis

Age-related cataracts typically progress slowly over time. Through regular evaluations, an optometrist or ophthalmologist can monitor their progress and recommend when the risks of cataract surgery are justified by its potential benefits in terms of ensuring the patient’s visual capacities continue to meet the demands of daily living.

General Principles in Older Adults

Age-related macular degeneration (AMD) is a disease that progressively destroys the macula, impairing central vision. It accounts for 54% of all legal blindness and is the leading cause of irreversible vision loss in people older than the age of 65 years. Although the etiology of AMD is unknown, it is likely an inherited disease with environmental factors contributing. Risk factors include advancing age, white race, a family history of AMD, and smoking. There are 2 forms of AMD: nonneovascular (or dry) and neovascular (or wet). Ninety percent of patients have the dry form of AMD, which causes a gradual loss of vision. Even though wet AMD is less common, leakage from the newly growing vessels results in rapid vision loss, and the majority of cases of legal blindness in older adults.

Prevention

Although there are no definitive preventive treatments for either dry or wet AMD, studies suggest that people who eat a diet rich in green, leafy vegetables and fish may have a lower risk of developing AMD. Smoking doubles the risk of AMD. For patients who have been diagnosed with intermediate or advanced dry AMD, taking high doses of antioxidants and zinc may reduce the risk of developing advanced AMD and experiencing severe vision loss. Because severe vision loss is typically associated with the wet form of AMD, the best prevention of blindness is prompt diagnosis and treatment of neovascularization.

Clinical Findings

In its early stages, AMD has no symptoms. As dry AMD progresses, patients note a gradual blurring of central vision, and increased difficulty reading fine print, recognizing faces or seeing street signs. In contrast, wet AMD often presents as a rapid loss of central vision, with metamorphopsia (images that appear distorted) or central scotomas. Even with advanced wet or dry AMD, patients maintain navigational mobility. In dry AMD, drusen—cream colored lesions that represent a build-up of metabolic waste products within the retina—are seen in the macula. Other signs include pigmentary changes or chorioretinal atrophy of the macula. In wet AMD, abnormal blood vessels grow and hemorrhage, causing macular swelling, loss of retinal function and scarring.

Differential Diagnoses

Other conditions causing a reduction in visual acuity with changes in the appearance of the macula include diabetes and hypertension, each of which might cause retinal hemorrhages and/or the deposition of exudates, which may or may not be in the macula.

Complications, Treatment, & Prognosis

Loss of central vision is the main complication of AMD. In wet AMD, the vision loss quickly becomes severe and represents an ocular emergency requiring urgent consultation. Evaluation and treatment for wet AMD frequently involves visualizing the retinal vasculature with fluorescein angiography and then laser photocoagulation of abnormal blood vessels. Unfortunately, while the laser stops leakage and destroys new blood vessels, it also destroys the underlying retina. The development of antivascular endothelial growth factor (anti-VEGF) medications such as bevacizumab that inhibit neovascularization has markedly changed the management of wet AMD. These drugs are injected intravitreally and may be used alone or in conjunction with laser treatment. With prompt recognition and referral to a retinal specialist ophthalmologist, many patients treated with anti-VEGF intravitreal injections will maintain or even have mildly improved vision. Patients who develop unilateral wet AMD have a 30% 6-year risk of neovascularization in the contralateral eye, so frequent follow-up evaluations are recommended.

For patients with dry AMD, vision loss progresses slowly. In mild cases, there is no treatment. For moderate-to-severe dry AMD, vitamin supplements may be recommended to slow progression. According to a 10-year clinical trial, the Age-Related Eye Disease Study (AREDS), a specific formulation of antioxidants and zinc in supplements reduced risk of developing advanced AMD and subsequent severe vision loss. The AREDS formulation is not a cure, nor does it restore vision loss caused by AMD; it simply may delay the onset of advanced AMD and help maintain stable vision.

General Principles in Older Adults

Diabetic retinopathy is characterized by a progressive series of abnormal changes in the retinal microvasculature. The early phase of the disease is called nonproliferative (or background) retinopathy. Changes in the microvasculature lead to areas of retinal nonperfusion and to increased vasopermeability, which causes the appearance of microaneurysms and hemorrhages. If the disease progresses, proliferative diabetic retinopathy develops when there is a pathologic propagation of fragile retinal vessels that can break and bleed extensively. Overall, approximately 40% of all diabetics have some stage of diabetic retinopathy. The longer one has diabetes, the more likely retinopathy will develop.

Prevention

Good glycemic and blood pressure control are associated with decreased development and progression of diabetic retinopathy. Although diabetic retinopathy may not be completely avoidable, studies show that severe vision loss can be prevented 90% of the time with timely detection and intervention. Therefore, leading eye care organizations and the American Diabetes Association recommend that all diabetic patients should have an annual dilated, funduscopic examination. In the early stages of nonproliferative retinopathy with no macular edema, management consists of emphasizing the importance of glycemic control and follow-up evaluations. In more advanced cases of retinopathy, laser treatment or other medications may be indicated.

Clinical Findings

Diabetic retinopathy may be asymptomatic in its early more treatable stages. Blurred vision may occur if there is macular edema, but if the contralateral eye is unaffected or the vision loss is subtle, patients may not notice changes. In cases of proliferative retinopathy, new blood vessels can bleed extensively, causing blurred vision, or visual field scotomas. Patients who have had extensive laser photocoagulation for treatment of proliferative disease may have an overall constriction of the visual field. Signs of diabetic retinopathy are best evaluated through dilated funduscopy, and can include hemorrhages, exudates or neovascularization. In areas where there is inadequate access to eye care specialists, fundus photographs reviewed via telemedicine can be a sensitive and effective screening tool for identifying patients with diabetic retinopathy who need to be prioritized for referral to specialty eye care. Specialty diabetic eye examinations typically include retinal examination for subtle signs of macular edema, assessing the location and amount of hemorrhages and assessing the vascular abnormalities that help stage the severity of either nonproliferative or proliferative retinopathy.

Differential Diagnosis

Hypertensive retinopathy, vein occlusions, ischemic disorders, inflammatory or infectious disorders or any other disorder that can cause retinal hemorrhages can be considered in the differential diagnosis of diabetic retinopathy.

Complications

Vision loss caused by diabetic retinopathy is caused mainly by macular edema and proliferative retinopathy, and to a lesser extent, by macular capillary nonperfusion. Macular edema occurs when fluid leaks into the central retina, and may occur with either nonproliferative or proliferative retinopathy.

Treatment

Management of nonproliferative diabetic retinopathy (with no macular edema) typically consists of observation by an optometrist or ophthalmologist who has performed a dilated stereoscopic examination of the fundus. In cases where macular edema or proliferative disease is present or likely to occur (such as in severe nonproliferative retinopathy), referral to an ophthalmologist (preferably one specializing in retina) is indicated. Clinical studies show that treatment of a specific subset of macular edema, clinically significant macular edema (CSME), reduces the risk of moderate vision loss. In proliferative retinopathy, blood vessels can bleed extensively into the vitreous and/or undergo fibrous proliferation, causing vitreoretinal traction and tears in the retina. Treatment for both CSME and proliferative retinopathy can include laser and intravitreal injections of anti-VEGF agents.

Prognosis

Current treatment for diabetic eye disease usually does not restore lost vision. Instead, it is aimed at preventing additional vision loss. Studies show that laser treatment for CSME reduces the risk of moderate vision loss by 50% to 70%, and that panretinal laser photocoagulation for proliferative or severe nonproliferative diabetic retinopathy yields a 50% reduction in the risk for severe vision loss.

General Principles in Older Adults

Glaucoma is a progressive, chronic optic neuropathy in which intraocular pressure (IOP) and other currently unknown factors contribute to a characteristic acquired atrophy of the optic nerve that, if left to progress, leads to visual field loss. There are 2 major forms of glaucoma: open angle, in which the intraocular drainage system is open, and closed angle, in which the system is blocked. Primary open-angle glaucoma (POAG) accounts for vast majority of cases of glaucoma. Vision loss caused by glaucoma typically occurs first in peripheral vision, but as the disease advances central vision is lost. Glaucoma is the second leading cause of blindness worldwide, and approximately 50% of those with glaucoma are unaware they have the condition.

In the United States, glaucoma is the leading cause of blindness in African Americans. There is a 3-times-higher prevalence of POAG in African Americans relative to non-Hispanic whites. Studies also suggest that Hispanic/Latinos have a prevalence rate of POAG comparable to African Americans. Besides race, increasing age is also risk factor for glaucoma. POAG occurs in 5.7% of African Americans 73–74 years of age. At age 75 years and older, it increases to 23.2%. Although the prevalence of POAG is much lower in white populations, with older age, it increases from a rate of 3.4% in 73–74-year-olds to 9.4% in those age 75 years and older.

Clinical Findings

Prevention of vision loss from glaucoma is dependent upon early diagnosis and treatment. Unfortunately, because glaucoma is often asymptomatic, most patients fail to notice changes in vision until end-stage disease. Because of this, annual eye examinations are recommended for older adults at higher risk (Table 61–2). For others, an eye examination every 1–2 years is recommended. Clinical examination for glaucoma includes measurement of IOP (tonometry), optic disc assessment, visual field assessment and gonioscopy to assess whether the intraocular drainage system is “open” or “closed.” In gonioscopy, a specialized lens is placed on the patient’s cornea that allows the examiner to visualize the iridocorneal angle between the cornea and the iris where aqueous humor drains. IOP normally ranges from 10–21 mm Hg; however, IOP outside of this range is not pathognomonic for glaucoma—it is simply a risk factor associated with the development and/or progression of the disease.

Optic disc examination is one of the most important ways to evaluate for glaucoma. Glaucomatous atrophy causes increased optic nerve cupping. Although most cases of glaucoma are typically bilateral, the presentation can vary between the 2 eyes. Hence, markedly asymmetric cupping between the 2 eyes can indicate glaucoma. In the earliest stage of glaucoma, optic disc findings are usually observed before visual field losses appear. Nonetheless, periodic visual field assessment using standardized perimetry is important for diagnosing, staging, and monitoring disease progression.

Differential Diagnosis

The differential diagnosis of glaucoma encompasses a variety of conditions that affect the optic nerve. In angle-closure glaucoma, narrowing of the intraocular drainage system raises IOP and induces optic atrophy. If the rise in IOP occurs quickly, patients may complain of pain. Gradual rises in IOP may be asymptomatic. In normal tension glaucoma, glaucomatous optic atrophy occurs in the absence of documented elevated IOP. Other possibilities include optic atrophy caused by retinal vascular disease, ischemic disease, or chiasmal tumors. These conditions can be differentiated from glaucomatous atrophy in that they usually cause optic nerve pallor without optic nerve cupping.

Complications & Treatment

Vision loss in glaucoma typically starts in the periphery and extends inward, ultimately destroying central vision until complete blindness. Treatment of POAG consists of lowering IOP, with the goal of preventing progressive visual field loss by slowing optic nerve atrophy. Therapies to lower IOP may include topical or oral medications, laser surgery, such as trabeculoplasty, or incisional surgical procedures, such as a trabeculectomy with or without an iridectomy. Topical medications are often the first line of treatment and work by either decreasing aqueous production or increasing aqueous outflow. As a result of their effectiveness in lowering IOP, simplicity of once-a-day dosing, and few systemic side effects, prostaglandin analogs are among the most frequently prescribed first-line therapies for glaucoma. All medications used for the treatment of glaucoma may have significant local and systemic effects, and should be included in the older patient’s chronic medication list (Table 61–3).

Although topical medications are typically first-line therapy, surgery may be an option. If 2 or more topical therapies do not adequately control IOP, or if the topical medications are not tolerated well, surgery will be considered. Other indications for surgical care of glaucoma include poor compliance with medications because of memory impairment and if poor manual dexterity prevents eyedrop application. Finally, when compared to the cost of surgery, the annual cost of medications may become prohibitive for some.

Prognosis

Without treatment, glaucoma causes a progressive loss vision that will eventually lead to complete blindness. Patients who are diagnosed before extensive glaucoma optic nerve atrophy and who are able to achieve good IOP control have a good prognosis for vision.

When working with older patients with or without vision impairment, there are 2 simple ways to maximize their vision: increase contrast and provide adequate lighting. Contrast sensitivity refers to the ability to distinguish an object from its background. Low-contrast objects are harder for older persons to detect, becoming markedly more difficult in those with vision impairment. Patients may demonstrate adequate acuity when tested with a high-contrast, black-on-white eye chart, but their performance drops markedly when reading a low-contrast chart with light gray letters on a white background. This latter test much more closely resembles the everyday situation an older adult faces when trying to step off the curb at the edge of a sidewalk. Providing adequate lighting for these patients means using a light source that brightly illuminates the object of regard without shining directly into the their eyes or producing excessive reflections. This typically involves use of an indirect, high-wattage light source.

In addition to receiving medical eye care, patients with vision impairment will often benefit from referral to a low-vision specialist. These eye doctors specialize in maximizing the patient’s remaining functional vision through customized optical devices, such as strong reading glasses, telescopes, magnifiers, and electronic devices that enlarge and project reading material onto a video screen. Their efforts often include collaboration with rehabilitation specialists who, in addition to working directly with visually impaired patients, can recommend the use of nonoptical aids, such as large-print books and newspapers, free library services for access to books on tape, and special telephones, clocks, or dials (eg, oven or cooktop) equipped with large, high-contrast numerals.

The use of corticosteroids, such as cortisone and prednisolone, can increase IOP. Although the majority of patients taking corticosteroids do so without a subsequent elevation in IOP, risk factors for developing increased IOP include a personal or family history of glaucoma, current status as a glaucoma suspect, route of administration and duration of the corticosteroid treatment. Topically or intravitreally applied corticosteroids pose the highest risk. In descending risk are intravenous, parenteral, and inhaled routes of administration. Corticosteroid use for <2 weeks generally does not require special monitoring of IOP. However, any patient taking corticosteroids who uses them chronically or is at risk for glaucoma should have at least an annual eye evaluation.

Most medications that list glaucoma as a contraindication or adverse effect are concerned with the form of glaucoma in which the anterior chamber angle drainage system is narrow. When the patient takes the medication, the drainage system can narrow even further, sometimes to the point of closure, which causes a rise in IOP. Classes of medications that have the potential to induce angle closure are antispasmolytic agents, antihistamines, antiparkinsonian drugs, antipsychotic medications, tricyclic antidepressants, monoamine oxidase inhibitors, and topical mydriatics. These warnings do not apply to most glaucoma patients who have the primary open-angle form of the disease. Rather, they are relevant only to those with the relatively uncommon, narrow-angle form. Narrow-angle glaucoma is typically treated surgically, and consultation with an eye specialist may reveal that the above medications can be used safely.

Red flags indicating the need for urgent referral include significant changes in vision and moderate or worse eye pain. Changes in vision may include a sudden onset of decreased visual acuity (even with correction), a report of distorted vision (in metamorphopsia straight lines appear curved or irregular), or the sudden appearance of a scotoma or a visual field defect.

Careful review of the ocular history is important. In the history, the patient should be questioned about, among other things, which eye is affected and the timing and onset of symptoms such as pain, decrease in vision, photophobia, or discharge. If the primary symptom is pain, ask about a history of recent eye surgery, trauma, chemical injury, photophobia, or recent use of contact lenses. If there is a reduction in vision, ask about the location of the loss. A reduction in central vision suggests macular involvement and may be a result of macular degeneration, diabetic retinopathy, vascular occlusive disease, or optic neuropathy. If the vision loss is peripheral, establish whether it is monocular or binocular. If it is monocular, suspect either a retinal or optic neuropathy. In cases of bilateral loss of vision, consider a neurologic cause or, less likely, concomitant bilateral eye disease (Table 61–4).

Lighthouse (provides more information on visual rehabilitation services, education, research, prevention, and advocacy). http://www.lighthouse.org