Evaluation of Impaired Vision

James W. Hung

Claudia U. Richter

Visual impairment compromises both functional status and quality of life. An increase over the past decade in chronic illnesses such as diabetes that may compromise vision has resulted in an increase in prevalence of nonrefractive visual impairment. Although patients with impaired vision often refer themselves directly to an eye specialist, they may first present to their primary physician. The primary physician should routinely inquire into symptoms of decreased vision and consider incorporating basic vision testing into the comprehensive physical exam, especially in persons at increased risk, such as those with diabetes.

Eye disorders are common, with more than one third of the US population having some ocular abnormality that may affect vision. The prevalence of nonrefractive visual impairment certainly increases with advancing age, but other important risk factors include diabetes of more than 10 years, poverty, lack of education, and lack of health insurance. Prevalence is increasing markedly among persons aged 20 to 39 years, particularly in those with diabetes of more than 10 years.

Sudden visual loss is a medical emergency and should be evaluated by an eye specialist immediately. Gradual diminution of sight may be due to the normal aging process but can also represent treatable eye disease. Some elderly patients may not volunteer that their vision is decreasing because they consider it a natural part of aging. Assessing activities of daily living such as driving or reading may help identify these patients. The primary physician should be capable of a basic vision assessment that helps to ensure proper initial care and appropriate and timely referral.

PATHOPHYSIOLOGY AND CLINICAL PRESENTATION (1, 2, 3, 4, 5, 6, 7, 8, 9 and 10)

Anatomic orientation provides a framework for considering the pathophysiology of visual difficulties, beginning with the eyelid and cornea and working inward to internal structures including the anterior chamber, lens, vitreous, retina, and optic nerve.

Vision can become impaired when there is a change in the refractive state of the eye, opacification of the transparent ocular media, damage to the photoreceptor cells of the retina, or a lesion of the optic nerve, its radiations, or the visual cortex.

Refractive Error

Refractive error is the most common cause of decreased visual acuity. It results from the inability of the eye to focus light precisely on the retina and may be due to irregularities in the cornea, lens, or shape of the globe. Astigmatism is defined as an abnormally curved cornea or lens that causes blurred vision. Refraction with corrective lenses will neutralize the refractive and astigmatic error and improve vision. Myopic, or nearsighted, patients commonly present during their teens and early 20s due to difficulty with distance vision. Hyperopic, or farsighted, patients can present later in life as the ability of the lens to accommodate compensates for this condition. Patients in their 40s often report decreased visual acuity at near distances and suffer from presbyopia, the loss of the accommodative process. They benefit from reading glasses to counteract the loss of the elasticity of the crystalline lens. Over time, cataracts can increase myopia as the lenses opacify and block the transmission of light. Systemic disease can sometimes alter refractive error. Uncontrolled diabetes mellitus can produce swelling of the lens and myopia, which resolves with control of the blood sugar. Additionally some medications such as sulfonamides, thiazides, and anticholinergic agents may induce myopia, causing blurred vision.

Eyelid Disease

Occasionally, visual loss results from eyelids being closed. Acute ptosis with swelling can be due to trauma, insect bites, cellulitis, or angioneurotic edema. Acute blepharospasm secondary to ocular surface pain may be described as an inability to see. Chronic forms of ptosis can be due to congenital, age-related, or systemic conditions such as myasthenia gravis and necessitate appropriate workup and treatment.

Corneal Disease

The cornea is the major refracting surface of the eye, and any change in it can lead to visual disturbances. A corneal abrasion, herpes simplex virus keratitis, or ulcer causes irregularity of the corneal epithelium and opacification of the normally clear cornea. Acute glaucoma causes corneal edema and is associated with pain, nausea, and vomiting due to suddenly elevated eye pressure. Corneal dystrophies or degenerations result in a more gradual reduction in visual acuity, often progressing over a period of years.

Fuchs corneal dystrophy, a condition of bilateral corneal endothelial dysfunction, causes irregularities in the inner layers of the corneal endothelium, leading to corneal edema, loss of transparency, and impaired vision as the cornea becomes cloudy. It is the leading cause of need for corneal transplantation in the United States, with an estimated prevalence of nearly 5% among adults over the age of 40 years. Guttae, the defining clinical feature of the condition, are thickenings and excrescences of the basement membrane underlying the corneal endothelial cells. The most common form of the disease is the age-related variety, but genetic variants encoding for the E-2 protein have been found in such patients, suggesting both a genetic propensity and a potential test for early identification of patients at risk (which would be desirable because the condition can be exacerbated by refractive or cataract surgery).

Anterior Chamber Disease

The anterior chamber may be opacified by inflammatory cells resulting from iritis or red blood cells resulting from a hyphema. Bleeding in the anterior chamber can be from trauma or neovascularization of the iris due to ischemia from diabetics or vascular occlusive disease.

Lenticular Disease

Cataracts—opacification of the lens—are a leading cause of gradual vision loss in older patients. The usual history is one of a painless slow deterioration of eyesight after the sixth decade. However, cataracts may develop earlier. Diabetes and chronic corticosteroid use can accelerate the process. Traumatic cataracts can even develop over a period of hours to days.

Vitreal Disease

Vitreous opacification occurs most often from hemorrhage and less commonly from inflammation or infection. Proliferative
diabetic retinopathy, a retinal hole or detachment, trauma, sickle cell retinopathy, hypertension, and clotting abnormalities may cause vitreous hemorrhage. A vitreous floater may transiently blur vision or may be called a blind spot. Age-related vitreal syneresis with associated posterior vitreous detachment is a common cause of floaters. Given its association with retinal tears and detachment, patients complaining of new-onset floaters should be evaluated by an ophthalmologist.

Retinal Disease

The retinal pathology that can compromise vision ranges from degeneration, inflammation, and trauma to detachment and ischemia. Visual loss may ensue. Neovascularization, the pathophysiologic common denominator of many important retinal diseases, accounts for much of the vision loss in developed nations. It derives, in part, from local ischemia and appears mediated by vascular endothelial growth factor, which triggers increased vascular permeability and angiogenesis. Vision loss ensues from the resultant retinal edema and bleeding from these fragile vessels. Age-related macular degeneration (ARMD), diabetic retinopathy, and retinal vein occlusion are among the common conditions manifesting neovascularization and its consequences.

ARMD occurs in patients older than age 55 years and is a leading cause of legal blindness. Central vision is impaired, whereas peripheral vision remains intact. Funduscopic examination may show a loss of the foveal reflex, macular drusen, atrophy of the retinal pigment epithelium with prominent choroidal vessels, subretinal edema or hemorrhage, or a central fibrous scar. Some 15% of patients with ARMD have treatable disease, presenting with early visual symptoms and a subretinal neovascular net that can be treated. They need to be seen promptly to maximize their chances of effective treatment. Those at particular risk of developing subretinal neovascular nets have soft drusen or a disciform scar in one macula. These patients should screen their central vision daily with an Amsler grid (see Chapter 206).

Central serous retinopathy is an idiopathic spontaneous detachment of the retina in the macular area. Patients range in age from 20 to 50 years. Central vision is reduced, but recovery is usually spontaneous within a few months.

Retinal inflammation, such as that due to histoplasmosis, toxoplasmosis, cytomegalovirus, or herpes virus infections, can involve the macula or produce a vitritis, decreasing vision. Cytomegalovirus retinitis is of concern in HIV-infected patients and important to recognize because it is treatable. Patients with CD4 counts less than 200 are at significantly increased risk of developing cytomegalovirus retinitis. Spread to the eye is hematogenous. Ocular symptoms include new floaters and loss of vision. Funduscopic manifestations include perivascular yellowwhite retinal lesions presenting as a focal white granular infiltrate with or without hemorrhage, expanding in a “brushfire” pattern.

Trauma may cause decreased visual acuity by producing macular edema or a choroidal rupture. Macular edema resolves within a few days, and visual acuity improves. A choroidal rupture causes permanent decreased visual acuity.

Retinal detachment may cause decreased visual acuity when it is extensive or may be noted as a minor field defect when it is small. Flashing lights and a shower of vitreous floaters may presage a retinal detachment. As a detachment extends, the patient may note that the visual field defect progresses like a shade being drawn. A detached retina appears ballooned forward with undulating folds.

Ischemic disease of the retina or optic nerve may lead to sudden visual loss. In central retinal artery occlusion, there is sudden painless profound loss of vision (e.g., cannot see hand movements, cannot perceive light). The patient may have had previous episodes of amaurosis fugax with fleeting blindness lasting only seconds. Ophthalmoscopy reveals a pale optic disk, attenuated arterioles, “boxcar” veins, hazy edematous retina, and a cherry-red spot in the macula. Occasionally, an embolus may be seen at a bifurcation of a retinal arteriole.

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