Visual Impairment — Age-Related Causes and Clinical Approach

Visual Impairment — Age-Related Causes and Clinical Approach RECURS Scale and significance

As many as 75% of older adults have significant visual or auditory dysfunction that is not reported to their physician — therefore adequate screening for these problems is important, and correction of remediable conditions may improve the ability to perform daily activities.

Consequences of untreated visual impairment: limited functional activity, social isolation and depression, falls and fractures, driving cessation, medication errors, and accelerated cognitive decline.

The prevalence of visual problems and blindness increases with age. The four commonest causes of blindness in older adults are cataract, glaucoma, macular degeneration and diabetic retinopathy. Physiological and functional changes of the ageing eye

Presbyopia develops from nuclear sclerosis of the lens and atrophy of the ciliary muscle; the near point of accommodation recedes so that by about age 45 comfortable reading requires corrective lenses.

Latent hyperopia becomes manifest with loss of accommodative reserve; alternatively myopia increases as old lens fibres accumulate in the nucleus, which becomes compact and harder (nuclear sclerosis), increasing the refractive power of the lens.

Diminished tear secretion, especially in postmenopausal women, causes dry eye with irritation and discomfort and may endanger the integrity of the corneal surface; treatment is substitution therapy with frequent artificial tears.

Corneal endothelial cells seldom proliferate in adult life, so the cell population falls with age, leaving an irregular anterior chamber surface where pigment accumulates. Dense pigment accumulation slightly reduces acuity, and progressive endothelial dystrophy may cause corneal oedema requiring corneal transplantation.

Intraocular pressure slowly increases with age. Also: senile miosis, slower dark adaptation, reduced contrast sensitivity, increased glare sensitivity, and impaired blue–yellow discrimination from lens yellowing.

Senile cataract — opacification of the crystalline lens; prevalence 46% at ages 75–85 (Framingham Eye Study). Development is painless, progressive and variable, typically bilateral and often asymmetrical. Patients complain of problems with night driving, reading road signs and difficulty with fine print. The cause is unknown but opacification is associated with breakdown of the γ-crystallin proteins, and ultraviolet light may be a contributing factor. The process may occur in the cortex or the nucleus.

Glaucoma — a group of disorders characterised by increased intraocular pressure, progressive excavation of the optic nerve head with damage to nerve fibres, and a specific loss in the visual field. Prevalence of open-angle glaucoma rises with age to 7.2% at ages 75–85, with much higher rates in men.

Chronic open-angle glaucoma (the commoner variety) has an insidious onset and slow progression: the irido-corneal angle is open but aqueous outflow is diminished, the neuroretinal rim thins from loss of retinal ganglion cell axons, producing optic-nerve cupping. Central acuity may remain normal for a long time while peripheral field defects are characteristic and gradually progressive — initially a paracentral scotoma, which may coalesce, and a nasal step, until the entire field constricts.

Angle-closure glaucoma is acute and relatively infrequent, with a sudden painful attack of raised intraocular pressure and marked loss of vision. Treatment is to normalise the pressure with miotic drops, carbonic anhydrase inhibitors or osmotic agents; the definitive treatment is surgical or laser iridectomy, and because the disease is usually bilateral, prophylactic iridectomy of the second eye is often proposed.

Age-related macular degeneration — the commonest cause of legal blindness (20/200 or worse) in older adults; prevalence 28% at ages 75–85, higher in women. Causes loss of central vision (see Question 12).

Diabetic retinopathy — prevalence rises with age to about 7% at ages 75–85. Visual loss is usually related to vascular changes in and around the macula: leakage of serous fluid causes macular oedema (may respond to laser photocoagulation), haemorrhage within the macula causes more permanent loss, and loss of retinal capillaries causes macular ischaemia with a poor prognosis for recovery.

Other important causes: uncorrected refractive error (the commonest and most easily reversible cause worldwide), giant cell arteritis (sudden painless visual loss — a medical emergency requiring immediate high-dose steroid), retinal artery and vein occlusion, retinal detachment, vitreous haemorrhage, homonymous field defects after stroke, and drug toxicity (ethambutol, hydroxychloroquine, amiodarone).

History: onset (sudden versus gradual), laterality, central versus peripheral loss, pain, redness, glare, floaters and flashes, metamorphopsia, diplopia; difficulty with specific tasks (reading, driving, recognising faces, negotiating stairs); falls history; full medication review; and systemic disease (diabetes, hypertension, symptoms of giant cell arteritis).

Sudden painless visual loss → retinal detachment, vitreous haemorrhage, retinal artery or vein occlusion, giant cell arteritis, wet AMD, occipital stroke — same-day ophthalmology referral. Sudden painful visual loss with a red eye → acute angle-closure glaucoma, uveitis, keratitis.

Ophthalmological screening comprises visual acuity (ability to read newspaper-sized print), ophthalmoscopic examination of lens and fundus, tonometry for intraocular pressure, and visual field testing.

Bedside additions: Snellen chart with pinhole (improvement indicates refractive error), near-vision card, confrontation fields, Amsler grid (central distortion in AMD), pupils for a relative afferent pupillary defect, red reflex, colour vision, and dilated fundoscopy.

Pattern recognition (Essentials Table 13-4): pain, red eye and a fixed pupil → angle-closure glaucoma; glare intolerance with loss of acuity → cataract; loss of peripheral vision with optic disc changes → open-angle glaucoma; sudden visual loss → temporal arteritis or diabetic retinopathy; loss of central acuity with retinal vessel changes and exudates → macular degeneration or diabetic retinopathy.

Systemic evaluation: blood pressure, HbA1c, and ESR/CRP urgently if giant cell arteritis is suspected.

Consider cataract surgery when the cataract progresses to interfering with activities; consider glaucoma when defects in the peripheral visual field are present; and consider AMD when central visual acuity is affected.

Restoring vision after cataract surgery: an intraocular lens corrects central and peripheral vision, increases image size by only 1%, can be used after surgery on one or both eyes, is useful for older adults unable to wear contact lenses, but requires bifocal spectacles and introduces added surgical and postsurgical complications. Contact lenses increase apparent object size by 6% and are difficult for many older people to handle.

Visual impairment is a known risk factor for falls and fractures, and patients who have had cataract surgery have a lower risk of hip fracture.

Glaucoma is usually treated medically first with miotics and β-blocking agents (which have the advantage of not changing pupil diameter), with combination drops and systemic carbonic anhydrase inhibitors in severe cases; surgery or laser therapy is indicated only if disease progresses on maximal medical therapy.

Diabetic retinopathy: initiate intensive blood glucose control and tight blood pressure control to reduce retinopathy in type 2 diabetes; panretinal and focal laser photocoagulation reduce the risk of visual loss in severe retinopathy and macular oedema respectively.

Aids to maximise visual function: magnifying device; lighting intensifiers without glare; tinted glasses to reduce glare; a night light to assist dark adaptation; and large-print newspapers, books and magazines. Refer all patients with AMD for visual rehabilitation.

Beware systemic absorption of ophthalmic medications — these agents may cause other organ system dysfunction and interact with other medications. β-blocker drops can cause bradycardia, bronchospasm and heart failure. Assess the patient's other medical problems and medications, use the minimum dose to achieve the desired effect, and monitor for systemic toxicity.

Screen for and treat depression, which commonly follows the loss of quality of life. Recognise Charles Bonnet syndrome — formed visual hallucinations with retained insight in the visually impaired — and reassure rather than misdiagnose psychosis or dementia.