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Visual impairment is defined as binocular acuity of 20/40 or worse. Legal blindness is when acuity is worse than 20/200. Older adults with good visual acuity show problems with visual function in real-life situations as testing is usually done in an optimum condition with maximum contrast and illumination with minimal glare. Testing for visual problems with decreased contrast sensitivity, decreased illumination, and increased glare is not practical for primary care providers, and hence it is important that they ask questions routinely to screen for performance under these circumstances. Educating the patient about simple measures to improve the environment may help with their quality of life.
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General Considerations
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Presbyopia is an age-associated progressive loss of the focusing power of the lens. Its incidence increases with age. The cause of this disorder is the ongoing increase in the diameter of the lens as a result of continued growth of the lens fibers with aging. This thickened lens accommodates less responsively to the contraction of muscles in the ciliary body, limiting its ability to focus on near objects.
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Patients presenting with this disorder frequently complain of eye strain or of blurring of their vision when they quickly change from looking at a nearby object to one that is far away. On examination, the only abnormality noted is a decrease in near vision.
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Because presbyopia is due to normal age-related changes of the eye, there is no proven prevention. In patients with normal distance vision, treatment for this disorder is as simple as purchasing reading glasses. For patients requiring correction of their distance vision, options include spectacle correction with bifocal or trifocal lenses, monovision contact lenses in which one eye is corrected for distance vision and the other eye for near vision, or contact lens correction of distance vision and simple reading glasses for near vision. Surgical treatment of presbyopia is an evolving science, including procedures on the cornea, lens, and sclera.
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All patients should be educated to anticipate a decline in near vision with aging. When left uncorrected, problems may occur with reading, driving, or other activities of daily living.
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AGE-RELATED MACULAR DEGENERATION
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ESSENTIALS OF DIAGNOSIS
Slowly progressive central vision loss with intact peripheral vision.
Vision problems in low light intensity and Amsler grid distortion.
Drusen located in the macula of the retina.
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General Considerations
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Age-related macular degeneration (AMD/ARMD) is the leading cause of severe vision loss in older Americans. It is characterized by atrophy of cells in the central macular region of the retinal pigment epithelium, resulting in the loss of central vision. Peripheral vision generally remains intact. AMD is typically classified as early and intermediate (usually dry type) or advanced/late AMD, which is divided into atrophic or nonneovascular (dry) or exudative or neovascular (wet) forms. The exudative form occurs in only 10% of patients with AMD, but it is responsible for the majority of severe vision loss related to the disease.
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Multiple risk factors for this disorder have been studied, including genetic factors, white race, obesity, and cardiovascular disease; only increasing age and tobacco abuse have consistently been associated with AMD. Because smoking has been strongly implicated as a risk factor and continued tobacco use is associated with a worse response to laser photocoagulation, tobacco avoidance and smoking cessation should be highly recommended to all patients. Hypertension has also been linked to a worse response to laser therapy; thus, effective blood pressure control is desirable, as well. Finally, antioxidants play a role in tertiary prevention. Patients with intermediate AMD or unilateral advanced AMD had a ∼25% reduction of their risk for developing advanced AMD if treated with a high-dose combination of vitamin C, vitamin E, β-carotene, and zinc. Patients with early or no AMD did not have the same benefit.
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A. Symptoms and Signs
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Patients may report onset of blurred central vision that is either gradual or acute with difficulty reading in dim light and night driving. Wavy or distorted central vision, known as metamorphopsia; intermittent shimmering lights; and central blind spots, termed scotoma, may all occur. Clinical findings include decreased visual acuity, Amsler grid distortion, and characteristic abnormalities on dilated funduscopic examination. In early disease, the most common findings are drusen: yellowish-colored deposits deep in the retina. In late disease of the atrophic type, areas of depigmentation are seen in the macula. In the exudative form, abnormal vessels (subretinal neovascularization) leak fluid and blood beneath the macula.
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B. Special Examinations
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Fluorescein angiography may be used by a specialist to confirm the diagnosis and to help determine whether a patient has atrophic or exudative AMD.
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An ophthalmologist will play a critical role in care of the patient with known or suspected AMD. Urgent referral to an eye specialist should occur if a patient with suspected or known AMD presents with acute visual changes. Treatment of exudative AMD is a rapidly advancing field with many ongoing clinical trials of surgical and pharmaceutical interventions. Current treatment options include laser photocoagulation, photodynamic therapy (Verteporfin), and intravitreal antiangiogenic therapy [antivascular endothelial growth factor (VEGF)]. No effective treatments exist for patient with dry AMD.
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Vision rehabilitation is the cornerstone to helping patients maximize their remaining vision and maintain their level of function for as long as possible. Low-vision professionals along with social workers can be of great assistance in recommending optical aids and devices and accessing local, state, and federal resources for the visually impaired. Direct-illumination devices, magnifiers, high-power reading glasses, telescopes, closed-circuit television, large-print publications, and bold-lined paper are some of the many devices that can be employed.
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Patient education topics include the importance. (Its use is described at http://www.amd.org.)
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Many patients with mild dry AMD will not experience significant worsening of their vision. It is difficult to predict which patients will develop advancing disease and further loss of central vision. This condition is generally progressive but is not completely blinding. Peripheral vision should not be affected by AMD.
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Bourla
DH
et al.. Age-related macular degeneration: a practical approach to a challenging disease.
J Am Geriatr Soc. 2006; 54 (7):1130–1135.
[PubMed: 16866687]
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Jager
RD
et al.. Age-related macular degeneration.
N Engl J Med. 2008; 358(24):2606–2617.
[PubMed: 18550876]
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Lim
LS
et al.. Age-related macular degeneration.
Lancet. 2012; 379(9827):1728–1738.
[PubMed: 22559899]
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General Considerations
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Glaucoma is the second leading cause of blindness in the United States. Although glaucoma is most often associated with elevated IOP, it is the optic neuropathy that defines the disease. Normal IOP is generally accepted to be between 10 and 21 mmHg. The majority of patients with an IOP of > 21 mmHg will not develop glaucoma, and 30–50% of patients with glaucoma will have an IOP of < 21 mmHg. Despite these facts, it has been clearly shown that as IOP increases, so does the risk of developing glaucoma. Other identified risk factors for glaucoma include family history and advancing age and African-American race. Additional possible risk factors include diabetes mellitus, hypertension, and myopia.
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The AAFP and the USPTF do not recommend screening for glaucoma, citing insufficient evidence to recommend for or against routine screening by primary care clinicians for elevated IOP or early glaucoma. The American Academy of Ophthalmology recommends screening for glaucoma by an ophthalmologist every 1–2 years after age 65.
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A. Symptoms and Signs
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Patients with acute angle-closure glaucoma typically present with unilateral intense pain and blurred vision. Patients may report seeing halos around light sources and complain of photophobia, headache, nausea, and vomiting. Physical examination shows a middilated pupil, conjunctival injection, and lid edema. Patients generally have markedly elevated IOP, usually between 60 and 80 mmHg.
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Primary open-angle glaucoma is a more insidious disease with a long asymptomatic phase. Patients may notice a gradual loss of peripheral vision. Examination may reveal diminished visual fields, elevated IOP, and abnormalities of the optic disk on direct ophthalmoscopy (symmetrically enlarged cup-to-disk ratio, cup-to-disk ratio asymmetry between the two eyes, or a highly asymmetric cup in one eye).
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Intraocular pressure may be measured using a variety of tools. The most readily available tool is the physician’s hand. Palpation of the globe through a lightly closed lid can reveal asymmetric hardness or bilaterally firm eyeballs and provide a very gross measure of IOP. More accurate tools include the Tono-Pen (a handheld applanation tonometer), Goldmann applanation tonometry, and pneumotonometry (puff test).
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Patients with significant risk factors or physical findings that raise concern for glaucoma should be referred to an ophthalmologist for further evaluation and confirmation of diagnosis.
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A. Acute Angle-Closure Glaucoma
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Acute angle-closure glaucoma is a medical emergency that requires immediate referral and treatment.
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B. Primary Open-Angle Glaucoma
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The treatment of primary open-angle glaucoma consists of pharmacologic and surgical interventions aimed at decreasing the IOP. Although elevated IOP is not required for the diagnosis of glaucoma, it has been shown that reduction of IOP in patients with glaucoma slows the progression of disease. Even patients with normal pressures can benefit from reduction in IOP.
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Topical eyedrops or oral medications aimed at decreasing aqueous humor production or increasing outflow are used. Topical agents such as β-blockers and prostaglandin analogs are first-line therapy, and α-adrenergic agents and carbonic anhydrase inhibitors are second-line of therapy. Topical miotics and epinephrine compounds are now infrequently used. Oral medications include carbonic anhydrase inhibitors such as acetazolamide. Topical glaucoma agents have varying degrees of systemic absorption and are capable of producing systemic side effects and drug-drug interactions. Patients should be educated on the importance of routine eye care and of taking medications as prescribed.
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2. Surgical intervention
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When medical management is unsuccessful, surgical intervention is considered. Laser trabeculoplasty and laser or conventional trabeculectomy are the most commonly performed procedures.
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Untreated glaucoma can result in blindness. Rapid treatment of acute angle-closure glaucoma may preserve vision. Treatment of primary open-angle glaucoma can prevent further loss of vision, but typically does not restore lost vision.
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Kwon
YH
et al.. Primary open-angle glaucoma.
N Engl J Med. 2009;360(11):1113–1124.
[PubMed: 19279343]
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General Considerations
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Any opacification of the lens is termed a cataract. Cataract disease is the most common cause of blindness worldwide and the most common eye abnormality in the elderly. Risk factors for cataracts include advancing age, exposure to ultraviolet (UV) B light, glaucoma, smoking, alcohol abuse, diabetes, and chronic steroid use. Diet and vitamins do not play a role in development or progression of the disease. Because cataracts tend to develop slowly, the patient may not be fully aware of the degree of vision impairment.
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Prevention of cataracts is aimed at the modifiable risk factors. Physicians should use steroids at as low a dose as is therapeutic and discontinue them when possible. Patients should be advised on how to minimize UV light exposure as well as the benefits of smoking cessation and control of chronic diseases.
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Patients may report blurring of vision, “ghosting” of images, difficulty seeing in oncoming lights (glare) and difficulty with night driving, and monocular diplopia. The patient may also complain of a decrease in color perception and even note “second sight,” which is an improvement in near vision with a nuclear cataract. Examination of the eye reveals opacification of the lens. Cataracts may be easier to see with dilation of the eye and a direct ophthalmoscope at +5D (diopters) setting held 6 inches from the patient’s eye.
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The treatment of cataracts is predominantly surgical. Although small cataracts may be treated by an updated eyeglass prescription, most patients with significant symptoms from a cataract benefit from surgical removal and replacement of the lens. Factors influencing the timing of surgery include life expectancy, current level of disability, status of other medical illnesses, family and social situations, and patient expectations.
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Family physicians may aid patients in understanding the surgery and assisting with preoperative management. Cataract surgery is a low-risk procedure. Routine use of laboratory testing and electrocardiogram screening has not improved surgical outcome. Individuals should receive a history and physical examination prior to undergoing surgery. Additional testing is recommended only if findings are abnormal. Cataract surgery is often accomplished under local anesthesia with minimally invasive techniques. In this case, there is no need to discontinue anticoagulation for the procedure. Surgeons should be made aware if patients are taking α-blockers as this is associated with a complication called intraoperative floppy iris syndrome.
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Cataracts do not resolve and may progress without treatment. The prognosis with surgical treatment is excellent, and ≤95% of patients obtain improved vision after surgery.
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Eichenbaum
JW. Geriatric vision loss due to cataracts, macular degeneration, and glaucoma.
Mt Sinai J Med. 2012;79(2):276–294.
[PubMed: 22499498]
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ESSENTIALS OF DIAGNOSIS
Asymptomatic, gradual vision loss or sudden vision loss in a diabetic patient.
Characteristic fundoscopic findings of micro aneurysms, flame hemorrhages, exudates, macular edema, and neovascularization.
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General Considerations
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Diabetic retinopathy (DR) is the leading cause of blindness in adults in the United States. It is important to consider diabetic retinopathy as a disease of the aging eye because prevalence increases with duration of diabetes mellitus. The risk of blindness attributable to this disorder is greatest after 30 years of illness. DR is divided into two major forms: nonproliferative (NPDR) and proliferative (PDR), named for the absence or presence of abnormal new blood vessels emanating from the retina, respectively. NPDR can be further classified into mild, moderate, severe, and very severe categories depending on the extent of nerve fiber layer infarcts (cotton-wool spots), intraretinal hemorrhages, hard exudates, and microvascular abnormalities. The severity of proliferative retinopathy can be classified as early, high-risk, and severe depending on the severity and extent of neovascularization.
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Patients with diabetes mellitus type 2 should have a comprehensive eye examination by an ophthalmologist shortly after diagnosis to screen for signs of retinopathy. Meticulous glycemic control decreases the risk of development and progression of retinopathy in all patients with diabetes. In addition, tight control of blood pressure also significantly reduces a patient’s risk of developing retinopathy.
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Many patients presenting with diabetic retinopathy are free of symptoms; even those with the severe proliferative form may have 20/20 visual acuity. Others may report decreased vision that has occurred slowly or suddenly, unilaterally or bilaterally. Scotomata or floaters may also be reported. Funduscopic examination reveals any or all of the following: microaneurysms, dot and blot intraretinal hemorrhages, hard exudates, cotton-wool spots, boat-shaped preretinal hemorrhages, neovascularization, venous beading, and macular edema.
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Fluorescein angiography may be performed by an ophthalmologist to further assess the degree of disease.
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Untreated proliferative retinopathy is relentlessly progressive, leading to significant vision impairment and blindness. In addition to maximizing glucose and blood pressure control, focal and pan-retinal laser photocoagulation surgery or vitrectomy is the mainstay of acute and chronic treatment and may preserve vision in certain patients. There is emerging evidence that intravitreal anti-VEGF treatment can be used in the management of retinopathy. When vision loss has occurred, vision rehabilitation should be initiated, as described earlier in the discussion of AMD. Topics to review with patients include the importance of an annual, comprehensive eye examination, glycemic control, and hypertension management.
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Early diagnosis and treatment, as well as tight glycemic and blood pressure control, improve prognosis and prevents blindness.
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Antonetti
D
et al.. Diabetic retinopathy.
N Engl J Med. 2012; 366(13):1227–1239.
[PubMed: 22455417]
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