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Home , Arcus senilis, Geographic atrophy

The ageing eye Most people’s eyes change as they age.

RIZWANA CASSIM AMOD, MB ChB, BMedSc (Hons) Pharmacology, MMedOphth, FCOphth (SA), BBus & Admin (Hons) Senior Specialist and Head of Retinal Surgery Unit, Tygerberg Academic Hospital and Faculty of Health Sciences, Stellenbosch University Rizwana Amod is a retinal specialist, practising full-time at Tygerberg Hospital. Her main interests in are retinal trauma surgery, surgery for diabetic , age-related (AMD) and infectious disease of the eye. Her long-term vision for ophthalmology is to help eradicate serious .

As people age, most will inevitably encounter some changes in their with contact lenses the options include monovision, where one vision that may be attributed solely to the ageing process. These eye is corrected for distance vision and the other for near vision processes are distinct from age-related eye diseases, although the or bifocal contact lenses. Refractive surgery for has not visual changes they produce may be similar. One of the truest signs yet been perfected. of ageing is the gradual loss of and the onset of presbyopia. With an increasing elderly population, age-related eye diseases are Ageing causes laxity of the eyelids due to involutional changes of becoming the leading causes of vision impairment in the developed the skin, orbicularis and levator muscles, tarsus and the canthal world. Many elderly patients are afflicted by more than one ageing tendons. These changes contribute to the aetiology of several eye condition, and these have a tremendous impact on their mental disorders such as lower lid inversion (), lower lid and social health and overall quality of life. Enormous strides are eversion () and aponeurotic of the upper lid. These being made in understanding and preventing eye diseases. This conditions usually necessitate surgical correction. article will focus on both the normal ageing processes of the eye and the common eye diseases that afflict the ageing patient. As the ages, the lens continues to grow and becomes thicker due to the increasing deposition of outer cortical lens Normal ageing of the e ye fibres. This is accompanied by a gradual yellowing of the lens and The natural quality of vision gradually declines with the anatomical a change in the refractive index – even before the development and physiological processes that occur with ageing of the human of . As a result, the sensitivity of the eye to shorter blue eye and . These changes include presbyopia, changes wavelengths of light and the ability to discriminate blues and blue- in the eyelids and tearfilm, and changes in the various intraocular greens becomes reduced.2 structures contributing to the integrity of the visual system. Presbyopia The clarity of the cornea is maintained throughout life by the Presbyopia refers to the reduced ability to focus at close range as corneal endothelial cells. With ageing, the density of the endothelial a result of loss of accommodation. It is the most common ocular cells decreases and their morphology changes, rendering the aged affliction in the world and is due to the decreased elasticity of the cornea more vulnerable to the stress of injury or intraocular crystalline lens and reduced tone that occurs with surgery. ageing. The extent to which the lens power can be increased with Ageing and degeneration of the peripheral cornea is more benign accommodation slowly declines over the years and the innate and commonly manifests as the prominent white ring of arcus ability to focus on objects located at varying distances becomes senilis. increasingly difficult. Aberrations of the corneal surface also increase with age, resulting The average adolescent can comfortably accommodate up to 14D, in , glare and reduced contrast. Referral to an and by age 45 this drops to about 4D and is completely gone by the optometrist for refraction is often beneficial. Dry eye also manifests age of 50 - 55.1 The rate of decline of accommodative amplitude frequently due to diminished aqueous tear production and this is occurs with very little inter-individual variability and is considered treated with tear supplements. to be one of the most reliable biomarkers of human age known.2 Presbyopia usually manifests after 40 - 45 years of age. Patients Vitreous usually complain of increasing difficulty with near visual tasks such Progressive liquefaction of the vitreous gel occurs, manifesting as reading fine print and find that small objects need to be held as the occasional . These are benign and tend to be more further from the eye in order to be seen clearly. of an annoyance than a . However, the age- related separation of the vitreous gel from the , i.e. posterior Treatment of presbyopia vitreous detachment (PVD), may also manifest with and In the early stages of presbyopia simply extending the arms and may be complicated by retinal tears and . Hence improving the lighting is adequate for reading. Later, help in the any new-onset floaters and visual disturbances (flashes) mandate form of reading glasses (plus lenses) becomes necessary. If distance referral to an ophthalmologist for a dilated fundal examination and corrective lenses are worn then the presbyopic correction may be careful scrutiny of the peripheral retina. incorporated as bifocal or multifocal spectacle lenses. If corrected

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Retina • An untreated mature white cataract is Age-related macular degeneration Ageing causes a general decline in retinal easily visible through the . Age-related macular degeneration (AMD) function (colour and contrast) due to the is defined as central vision loss attributable gradual loss of neuronal elements and an Morphological types of age-related to degenerative atrophic and/or neovascular accumulation of waste material under the cataract (Fig. 1) changes in the macula. The macula is the retina, called liposfuscin. Regeneration of highly specialised central area of the retina • Nuclear sclerosis – progressive yellowing rhodopsin in photoreceptors slows down used for fine visual acuity and colour vision.6 of the centre of the lens. and there is reduced retinal illuminance Damage to this makes reading, writing and due to the gradual reduction in pupil size • Cortical – peripheral spokes and driving very difficult. (senile ), giving rise to night vision radial water clefts. AMD is the leading cause of irreversible problems. Therefore a 60-year-old receives • Posterior subcapsular cataract – opacity visual impairment in the elderly worldwide, about one-third of the light a 20-year-old just beneath the posterior lens capsule. affecting an estimated 14 million people.6 receives – similar to wearing medium- The disease tends to be bilateral although density sunglasses in bright light.3 one eye may be affected long before the Treatment other. The risk to the second eye is around As yet no effective method exists to prevent 50% within 5 years. Age-related e ye disease or halt the development of cataract. Good visual acuity depends on the integrity Studies to evaluate the role of nutritional The exact aetiology of AMD is not known of the various structures in the eye and visual supplements (carotenoids) or antioxidants but advancing age is a major risk factor. A pathways. Therefore it is natural to expect (vitamins C and E) to delay cataract have number of studies have linked smoking to that maintenance of good visual acuity been inconclusive.2 In the early stage the the development of AMD. Other associated into old age is an exception rather than induced refractive change from the cataract risk factors include ultraviolet exposure, the rule. As the average life expectancy in can often be corrected with spectacles and nutritional factors and genetic susceptibility. developed countries is climbing, age-related may delay the need for surgery. Compelling evidence is emerging that the eye diseases are becoming increasingly innate immune system and the complement common, creating an enormous economic Surgery factor H gene play a vital role in the 6 burden. These include cataract, , Surgery is indicated when: pathobiology of AMD. age-related macular degeneration and the retinal complications of vascular diseases. • visual improvement is likely or Clinical features • the cataract is a risk to the eye, e.g. Early AMD is characterised by the Age-related cataract precluding a view of the retina in retinal presence of yellow deposits () and Cataract refers to opacity of the crystalline disease or the cataract is inducing pigmentary abnormalities in the macula. lens of the eye and is the leading cause inflammation or angle closure glaucoma. It is usually asymptomatic or causes mild of treatable visual impairment affecting visual impairment. It denotes the risk of Tremendous advances have been made in approximately 16 million people worldwide. progression to late AMD (Fig. 2). cataract surgery in the last decade. Surgery Risk factors for developing cataract include is performed under topical anaesthesia increasing age, genetics, diabetes, ultraviolet via a small (< 3 mm) self-sealing corneal exposure, nutrition, steroid use, smoking incision. High-frequency ultrasound and trauma.4 (phaco-emulsification) is used to remove the cataract and a foldable intraocular lens Symptoms (IOL) is then positioned within the capsular • Cataract typically produces gradual loss bag. Usually monofocal IOLs selected for of vision in the affected eye. optimal distance vision are implanted and • Scattering of light by the cataract may reading glasses are used for near vision. The cause monocular . newer multifocal and accommodating IOLs allow for unaided near and distance vision. • Subcapsular cataracts may cause Visual rehabilitation after cataract surgery troublesome glare, especially when Fig. 2. Age-related macular degeneration. driving. is rapid and in the absence of co-morbid ocular disease, 92% of patients achieve a 5 Signs vision of 6/12 or better. Complications Late AMD is divided into two types, i.e. wet of cataract surgery are infrequent, with a (neovascular) and dry (non-neovascular) • Loss of the red reflex or the presence of 0.01% risk of blindness from infection. Late opacities in the red reflex. based on the clinical appearance of the secondary deterioration of vision may result macula. from new retinal pathology or opacification of the posterior lens capsule. The opaque • Dry AMD is most common and accounts posterior capsule is easily excised using a for 85% of all cases of late AMD. It photo-disruptive Nd:YAG laser and the develops slowly and causes gradual loss visual axis is cleared. of central vision. It is characterised by of the retinal pigment Glaucoma epithelium (RPE). There is no treatment for dry AMD and patients usually require Glaucoma describes a group of conditions vitamins and low-vision aids. characterised by progressive damage with elevated • Wet AMD is less common and accounts for Fig. 1. Senile cataract. (IOP) being the major risk factor (see the 10 - 15 % of all cases of late AMD. The onset article on glaucoma, p. 464 of this issue). is fairly rapid with an acute drop in central vision and distortion (metamorphopsia). October 2007 Vol.25 No.10 CME 485

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Wet AMD is characterised by the development of new vessels beneath the retina (choroidal neovascular membranes (CNV)), serous elevation (detachment) of the neurosensory retina and/or pigment epithelium and macular haemorrhages. End-stage disease demonstrates macular scarring.

Neurospecial investigations •  confirms and localises the presence of CNV. Two major forms of CNV membranes may be defined, i.e. classic (well-defined) and occult (poorly defined). • Optical coherence tomography (OCT) Fig. 4. Optical coherence tomography demonstrating a macular hole. involves non-invasive retinal imaging of this formulation in patients with bilateral technology depicting the layers of the Retinal vein occlusion (branch early AMD is less certain. retina and the underlying RPE. It is used (BRVO) or central (CRVO)) as an adjunct to fluorescein angiography to Beta carotene is thought to confer a higher Retinal vein occlusions are the most diagnose, monitor and guide treatment. risk of lung cancer to smokers and is common retinal vascular disease after contraindicated. Cessation of smoking is diabetic retinopathy (Fig. 5). These patients Management of AMD also strongly advised. present with acute vision loss or floaters. Typical ophthalmoscopic features include There is neither a cure nor a means to Current and upcoming therapies for AMD dilated and tortuous veins, intraretinal prevent AMD. Early detection is crucial as are outlined in Table I. The optimal timing haemorrhages, cotton-wool spots, lipid all interventions are largely palliative and and specific combination of therapy are not exudates and retinal oedema. In CRVO directed purely at minimising the vision loss yet known. Factors influencing the choice these changes are widespread and in BRVO associated with neovascular (wet) AMD. of regimen include the angiographic lesion they are localised to the quadrant. An Amsler grid may be given to patients for type, the lesion composition and location early detection of any change in their central and the patient affordability. vision. This test is performed monocularly, wearing their near correction. The grid is Macular hole (Fig. 4) held at 33 cm and any distortion is noted Senile macular holes occurs spontaneously (Fig. 3). Any new distortion or field loss in the macula of elderly patients and result requires urgent specialist referral. in loss of central vision (). They are believed to be caused by focal shrinkage of the vitreous and traction in the foveal area. They usually affect one eye although there is a 10% chance that the other eye will eventually be affected. Formation of the hole tends to occur in stages and may arrest at any stage. A stage 4 macular hole refers Fig. 5. Central retinal vein occlusion. to a full-thickness hole in the presence of a PVD. Management Treatment is directed at: Vascular disease and the • diagnosis and management of the underlying cause and ageing e ye • prevention and management of Age-related systemic vascular diseases are complications, i.e. macular oedema and important risk factors for the development of neovascularisation; complications depend ischaemic retinal diseases and the associated on the extent of ischaemia and whether a complications. Common presenting diseases collateral circulation is established. include diabetes, hypertension, carotid artery Fig. 3. The Amsler grid with distortion. disease, hyperlipidaemia, systemic vasculitis In CRVO, severe ischaemia usually results and hypercoagulability states. Management in neovascularisation of the (NVI), of the ocular disease is directed towards the often complicated by neovascular glaucoma High-dose antioxidants and zinc have been underlying cause and possible concurrent – a serious and blinding disease. In BRVO postulated to prevent AMD and their role antiplatelet therapy to reduce systemic neovascularisation of the (NVD) was explored in a large multicentre study cardiovascular risk.7 and elsewhere in the retina (NVE) occurs (AREDS). The outcomes suggest that high- and may result in vitreous haemorrhage. dose supplements (Table I) can help to delay Diabetes Treatment of neovascularisation is with the progression of AMD in patients with Manifests as diabetic retinopathy and/or retinal laser photocoagulation to prevent either CNV in one eye, geographic atrophy (see article on diabetes and the further complications. Laser treatment or bilateral drusen, and long-term use is eye, p. 476 of this issue). of macular oedema is only indicated in recommended in these patients. The benefit selected cases of BRVO. However, ongoing

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novel treatment options are being proposed, including intravitreal injections of vascular Table I. Current treatment options for wet AMD endothelial growth factor (VEGF) inhibitors or triamcinolone and decompression Treatment options Indications Outcomes surgery. Vitamin therapy (AREDS formulation) Anterior ischaemic optic neuroathy 500 mg vitamin C, • Severe AMD in fellow Risk of developing (AION) – arteritic and non-arteritic 400 IU vitamin E, eye (foveal atrophy, CNV) advanced AMD in AION is an infarction of the optic nerve 15 mg beta-carotene • Moderate AMD (large the fellow eye at 5 head caused by occlusion of the short and 80 mg zinc drusen; extrafoveal atrophy) years reduced by posterior ciliary arteries. It is characterised Copper 2 mg 20 - 25% by profound unilateral visual loss, optic disc NB! Beta carotene swelling, relative afferent pupil defect and contraindicated in altitudinal visual field loss. smokers

Argon laser • Extrafoveal CNV Reduced risk of • Non-arteritic (NAION) may occur in (thermal laser) • Limited role in juxtafoveal severe visual loss isolation or in association with systemic membranes Risk of recurrence vascular disease. The risk to the other eye 50% is 5% per year. The management is to treat the vascular risk factors and initiate Photodynamic therapy Subfoveal and juxtafoveal CNV: Stabilises lesion: antiplatelet agents such as aspirin. (PDT) IV Visudyne over 10 mins • all small membranes • limits size of • Arteritic AION is due to giant cell arteritis Non-thermal diode laser • predominantly classic scotoma (temporal arteritis/giant-cell arteritis (689 nm) for 83 secs • 100% occult lesions • limits more vision (GCA)) and typically affects patients over loss the age of 70. The common presenting Re-treatment features include temporal headache required at with scalp tenderness, jaw claudication 3-monthly intervals manifesting as pain on chewing, VEGF inhibitors Any lesion type or location • Stabilises vision polymyalgia rheumatica and fever, weight PegaptinibNa (Macugen) • May improve loss and malaise. Bavacizumab (Avastin) vision Ranizibumab (Lucentis) • Frequent Management Serial injections in eye injections – small Vision loss from GCA is an ophthalmo- 4 - 6- weekly indefinitely risk (< 1%) of logical emergency as the risk of blindness in cataract, infection, the fellow eye is almost 40% within 10 days retinal detachment 7 if left untreated. The diagnosis of GCA is Macular translocation Subfoveal CNV – preferably • Successful made on clinical grounds and verified with Retina repositioned no previous laser cases have visual an elevated erythrocyte sedimentation rate surgically so macula lies improvement (ESR) (> 60 mm/hr) and /or C-reactive on healthy RPE/ • Complication rate protein. high • Risk of total visual Treatment with high-dose steroids is usually loss instituted on clinical grounds while awaiting biopsy of the superficial temporal artery to confirm the diagnosis. Table II. Indications for urgent referral Vision Role of the GP in age- • Acute vision loss not correctable with pinhole related e ye disease • Acute-onset visual phenomena – floaters, flashes Many elderly patients do not actively seek • New-onset visual field defect medical attention and accept that poor • Central scotoma, metamorphopsia or diplopia vision is an inevitable consequence of Anterior segment ageing. General practitioners therefore have • Presence of RAPD an important role to play in screening for, • Dull cornea or positive staining with fluorescein appropriately referring and co-managing • Hard eye, shallow anterior chamber visual impairment in older patients. These • Neovascularisation of iris responsibilities include: Posterior segment • To assess the severity and urgency of • Total loss of red reflex visual symptoms and refer appropriately • Disc swelling, pallor (Table II). • New haemorrhages – retinal or vitreous • To become thoroughly familiar with the • Neovascularisation of retina or disc examination of the ageing eye and the clinical morphology of common diseases (Table III). Regular dilated fundal

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Table III. Examining the ageing eye – specific features Conclusion Visual acuity tests As the average life expectancy increases • Snellen visual acuity with pinhole vision worldwide, age-related eye diseases are • Near vision assessment, colour vision becoming increasingly important and Eyelids account for significant morbidity. Age is an • Entropion or ectropion, horizontal lid laxity important predictor of visual impairment • Elevated lid crease and ptosis and active screening for visual loss in the elderly should become part of the • Relative afferent pupil defect routine examination. Prompt referral to the ophthalmologist for the treatment of Anterior segment visual disorders may considerably reduce • , dry eye, corneal opacities morbidity from . • Assessment of IOP (digital/tonometry) Red reflex References • Opacities, loss of red reflex 1. Kaufman PL. Accommodation and Presbyopia Optic nerve in Adlers Physiology of the Eye. Missouri: Mosby, 1999: 9. • Cupping, disc haemorrhages, nerve fibre layer 2. Meyer CH, Sekundo W. Nutritional • Disc swelling, pallor, vasculature supplementation to prevent cataract Retinal vasculature formation. Dev Ophthalmol 2005; 38: 103- • Tortuousity, venous beading, new vessels 119. Retinal pathology 3. Hammond CJ, Sneider H, Spector TD, Gilbert CE. Factors affecting pupil size after dilation: • Haemorrhages, hard exudates, cotton wool spots, macular oedema, degeneration, The twin eye study. Br J Ophthalmol 2000; 84: retinal detachment 1173-1176. Visual fields 4. West SK, Valmadrid CT. Epidemiology of • Distortion on Amsler grid risk factors for age-related cataract. Surv • Altitudinal defect, central scotoma Ophthalmol 1995; 39(4): 323-334. 5. Desai P, Minassian DC, Reddy A. National examination in high-risk patients elective surgery to avoid complications cataract surgery survey 1997- 8: a report of results of clinical outcomes. Br J Ophthalmol evaluating the retina, macula and optic and cancellation of surgery. 1999; 83(12): 1336-1340. disc. • General medical evaluation, screening 6. Kanski JJ. Clinical Ophthalmology. Oxford: • Important role in continued prescription and co-management of patients with Butterworth-Heinemann,1994:3. of long-term eye drops and monitoring eye manifestations of systemic diseases. 7. Gehrs KM, Anderson DH, Johnson for systemic side-effects which may not LV, Hageman GS. Age related macular • Supportive management for visually degeneration – emerging pathogenetic be evident to the ophthalmologist. impaired patients in their occupation and therapeutic concepts. Ann Med. 2006; • Patients with high-risk factors, e.g. and daily activities and facilitating the 38(7):450-71. family history of primary open- best use of their remaining vision. 8. Ramkissoon YD, Sagoo MS, Charteris D. angle glaucoma (POAG), should be Managing disorders of the ageing eye. The • Ongoing advice and encouragement to Practitioner 2007; 251(1693)50,54,56. informed of their risk and referred to maintain ocular health, stop smoking an ophthalmologist for screening. and avoiding co-morbidities like falls, • Control of systemic risk factors hip fractures, accidents and depression. (hypertension and diabetes) prior to

In a nutshell • Active screening for visual loss in the elderly should become routine. • The evaluation of visual impairment should include visual symptoms, visual acuity testing and detection of visual field changes. • Dilated fundal examination in high-risk groups is mandatory for early detection and timeous referral of treatable eye diseases. • Presbyopia usually presents adults over 40 years of age and is easily treated with reading glasses. • Cataracts are detected by the vision loss and opacities in the red reflex. • Early POAG is asymptomatic and the diagnosis is based on raised IOP > 21 mmHg, increased cupping of the optic disc and visual field changes. • Wet AMD is not curable or preventable and current treatments are largely directed at minimising visual loss. • The management of retinal vascular diseases is directed towards early detection, treating the systemic cause and instituting antiplatelet therapy. • Retinal vascular occlusions may be complicated by neovascularisation and macular oedema. • In giant-cell arteritis, treatment with high-dose steroids should not be delayed because the risk of fellow eye blindness is very high.

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