Visual Impairment in the Elderly PDF

4.1 History and visual assessment in the elderly Elderly patients often give a very helpful and detailed history, with the result that a presumptive diagnosis can be made on history taking alone and then verifi ed by examination. Some elderly patients are slower at performing assessment tasks and sh...

4.1 History and visual assessment in the elderly Elderly patients often give a very helpful and detailed history, with the result that a presumptive diagnosis can be made on history taking alone and then verifi ed by examination. Some elderly patients are slower at performing assessment tasks and should be encouraged. It should also be noted that the elderly, especially those with age-related macular degeneration (AMD), can have trouble mastering the art of the ‘pinhole’ and may benefi t from refraction, irrespective of the fact that a pinhole fails to improve on the acuity recorded with habitual correction in place. Although few eyes that have survived 65 or more years of life are free from at least some slight sign of deterioration, degeneration, or past or present disease, 14.5% of patients aged 70–74 years have corrected vision of less than 6/7.5 [LogMAR 0.1], yet have no clinically reported degenerative or disease conditions.1 The eyes are found to be clinically normal. When examining eyes in the elderly it is important to understand which changes may be regarded as a physiological part of ageing. The known changes with ageing in the various structures of the eye are listed in Table 4.1. 4.2 Age-related macular degeneration 4.2.1 Aetiology AMD, fi rst described in 1885, is a progressive disabling bilateral condition that is responsible for 30–49% of new blind registrations per year in the UK.2,3 Although the condition is common, until recently the underlying aetiology remained an enigma. Numerous potential risk factors such as age, sex, race, height, social status, hypertension, cardiovascular and cerebrovascular disease, refractive error, personal attributes such as eye colour, skin characteristics, light exposure and nutritional factors have been implicated in the causation of AMD. The only defi nitive contributory evidence that has been found is for cigarette smoking, hypertension and hereditary factors.4–7 It appears likely that AMD is a multifactorial disease triggered by environmental infl uences in those who are genetically predisposed. The genetic factors implicated are described in Section 4.2.4. The prevalence of AMD ranges from 0.2% in those aged 50–54 years, to 1.5% in those aged 70–74 years, to 16.4% in those aged 80 years or more.8 4.2.2 Clinical features Clinically, AMD is a heterogeneous disease and is classifi ed into two subgroups: a ‘dry’ or ‘atrophic’ form (80%) and an exudative or ‘wet’ form (20%).3 Exudative AMD, although much less common, is responsible for the majority of cases of severe loss of central vision. Symptoms of AMD are listed in Table 4.2. Drusen are the hallmark of AMD and, on ophthalmoscopic examination, appear as small, bright, sharply defi ned, circular points lying beneath the retinal vessels, confi ned mostly to the posterior pole. Drusen can vary in size and shape, and occasionally present a crystalline appearance resulting from calcifi cation. Histologically, hard drusen have been identifi ed at the macula in 83% of normal adult Table 4.1 Non-pathological Changes in the Eye with Age Cornea Corneal sensitivity to touch is decreased Increase in ‘against the rule’ astigmatism Anterior Anterior chamber depth decreases with age chamber Iris Senile miosis Pigment desquamation into the anterior chamber Lens Increase in axial thickness by about 28% Increase in the amount of yellow pigment leading to decreased sensitivity at the violet end of the spectrum Decrease in accommodation, possibly due to a decrease in capsular elastic force Little evidence to support atrophy or sclerosis of the ciliary muscle Vitreous Chromatic aberration decreases with age Index of refraction of the vitreous increases Liquefaction and syneresis occur Retina Visual acuity decreases as age increases. In most cases, pathology is found but in about 10% of patients aged 75–85 years vision is less than 6/7.5 [LogMAR 0.1] and they are entirely free from ocular disease Visual fi eld size decreases Loss of ability to discriminate hues, especially at the violet end of the spectrum. Mesopia and scotopia occur at lower levels of ambient illumination Absolute level of dark adaptation achieved is lower Delayed recovery to glare Loss of contract sensitivity at low frequencies Decrease in retinal illuminance Decline in acuity with target velocity with increasing age Variability in visual performance increases with age  Table 4.2 Symptoms of AMD ‘Dry’ AMD ‘Wet’ AMD Reduced near vision and reading speed Acute distortion of vision (metamorphopsia) Central or paracentral scotoma Sudden loss of central vision ‘Jumbling’ of words and letters Red discoloration of vision Formed visual hallucinations Formed visual hallucinations Ocular pain due to massive subretinal haemorrhage eyes. Most drusen cause little disturbance and often remain undetected.9 Drusen have been noted to occur in the fundi of persons as young as 30 years of age, and have been noted to lie within 1500 μm from the fovea, even at this age.10 With time, drusen tend to enlarge and undergo atrophy. ‘Dry’ AMD As the changes in ‘dry’ AMD progress, the photoreceptors, retinal pigment epithelium and, in some cases, the choriocapillaris are lost in the atrophic areas. The advanced stage of ‘dry’ AMD is known as geographic atrophy. Geographic atrophy often starts in the perifoveal region and, over a period of years, the atrophy tends to expand in a horseshoe-like fashion around the central fovea, usually closing on the temporal or nasal side and then fi nally invading the foveola.11 As AMD progresses, it has been noted that hard drusen undergo softening to form soft drusen. Patients with soft drusen are more likely to progress to ‘choroidal neovascularisation’. The pathway for the clinical management of patients with drusen is shown in Figure 4.1. Although severe visual loss is possible in ‘dry’ AMD, severe loss of central vision (i.e. LogMAR 1.0 – 200 μm b - juxtafoveal >18) 10% risk of CNVM in 5 years  Drusen with pigmentary changes 58% risk of CNVM in 5 years Visual loss in a CNVM 60% of eyes show more than six lines of visual loss at 18 monthsa Risk of second eye becoming involved by 13% per year disciform scar Risk of a PED developing a CNVM 25% at 10 years Risk of a PED developing GA 75% at 10 years Loss of central vision to 21 mmHg), with either visual fi eld loss and/or optic disc cupping. Practical advice Assessment of the drainage angle by gonioscopy is important as chronic angle closure glaucoma (CACG) may masquerade as COAG. The underlying pathological mechanism in COAG is abnormal resistance to fl ow in the trabecular meshwork – the cause of which remains unknown. Important risk factors for glaucoma include myopia, diabetes mellitus, hypertension and a positive family history. Genetic investigation of the glaucomatous process is now well under way. The candidate gene Trabecular meshwork inducible glucocorticoid responsive gene product (TIGR) has been shown to be responsible for some familial glaucoma.30,31 Several genetic loci are known for juvenile-onset glaucoma (OMIM #137750), adult-onset glaucoma (OMIM #137760), primary infantile glaucoma (OMIM #231300) and glaucoma- associated pigment dispersion syndrome (OMIM #600510).8 Treatment options for COAG are numerous, ranging from surgical drainage with or without antimetabolites to retard healing, laser trabeculoplasty and drug therapy. Recently there have been several new additions to the medical management of COAG, reducing signifi cantly the need for surgical treatment. Despite increased public awareness and meticulous screening by optometrists, some patients still present late for treatment. A further and rather diffi cult subset of patients is those with ‘normal tension glaucoma’. These patients present with typical glaucomatous fi eld loss and optic disc cupping but with normal IOP. It is important to be wary of the diagnosis of normal tension glaucoma in case a more sinister problem, such as a compressive neurological lesion, is overlooked. 4.4.2 Acute angle closure glaucoma Acute angle closure glaucoma (AACG) characteristically presents in the elderly. In contrast to the asymptomatic patient with COAG, these patients are acutely unwell – so much so that they may be misdiagnosed as having an acute abdominal problem. The onset is rapid, although a full-blown episode can be preceded by episodes of subacute angle closure that have aborted spontaneously. In retrospect, the patient may recall having noted episodes of blurred vision associated with coloured haloes around lights. The symptoms of AACG include severe ocular pain with headache, a red eye and blurring of vision. As the pressure rises, the patient becomes progressively nauseous and then begins to vomit. Clinical examination reveals a red beefy eye and a mid-dilated pupil, often with a greenish hue. The cornea may be oedematous and the eye stony hard to touch. After treatment and resolution of the attack, areas of lenticular infarction (glaucomenfl ecken) may become apparent. These indicate previous episodes. Medical therapy should be started immediately and, once the IOP has settled, treatment should be completed by bilateral peripheral iridectomies or laser iridotomies. Patients who are hypermetropic and who have enlarged cataractous lenses appear to be most at risk. The incidence of AACG varies depending on race. An overall incidence for Caucasians is 0.1%; however, a recent study from France reported an incidence of 3.8 per 100 000 population.32 AACG, if treated promptly, should not lead to visual impairment. 4.4.3 Visual prognosis and the implications One of the most diffi cult issues to deal with when speaking to the glaucomatous patient about rehabilitation concerns mobility and driving. Whereas the patient with moderate to advanced bilateral AMD generally recognises that visual loss is likely to make driving hazardous, particularly in conditions of poor visibility, those with glaucoma are often oblivious to fi eld loss and unaware of the risks until such time as they are involved in an accident or have a ‘near miss’. Low vision aids and advice on alternative eye movement strategies will not help with mobility tasks, including driving, and advice on the legal consequences of driving with impaired vision must be given. For all other central visual tasks, advice on lighting, contrast and, in particular, the use of contrast enhancement will prove benefi cial. 4.5 Diabetic retinopathy Diabetic retinopathy, in particular maculopathy, is a cause of signifi cant visual morbidity in the elderly. By the age of 60 years, most patients with insulin-dependent diabetes mellitus (IDDM) and proliferative retinopathy have usually reached a stable state – be it that of bilateral regressed neovascularisation and good central vision following laser treatment, or of long-term poor vision due to maculopathy. Patients with type 2 diabetes may require ongoing treatment for maculopathy. A summary of the fi ndings in diabetic retinopathy is given in Chapter 3. 4.6 Central retinal vein occlusion 4.6.1 Clinical presentation Central retinal vein occlusion (CRVO) presents with sudden blurring of vision in one eye. Most patients with CRVO are aged 50 years or more, and 50–70% suffer from hypertension, diabetes mellitus or cardiovascular disease. A recent study on risk factors for CRVO33 reported an increased risk for CRVO with systemic hypertension, diabetes mellitus and open angle glaucoma. Treatment of these conditions has no effect on ocular complications, although meticulous treatment of the underlying condition can prevent complications as well as CRVO in the second eye.33 The risk of CRVO is reported to be decreased by increased levels of activity and increased levels of alcohol consumption. In women the risk of occlusion was found to be decreased with use of postmenopausal oestrogens and increased with a higher erythrocyte sedimentation rate. Cardiovascular disease, treatment for diabetes, lower albumin/globulin ratios and higher γ-globulin ratios are associated with higher risk of ischaemic versus non-ischaemic CRVO. Systemic hypertension is a risk factor for both ischaemic and non-ischaemic CRVO. The clinical fi ndings in patients with CRVO fall within a spectrum ranging from mild to severe. The mildest changes are those of venous stasis with dilated veins and widespread dot and blot haemorrhages; the most severe are those of a profoundly ischaemic retinal vein occlusion where massive intraretinal haemorrhages, multiple cotton-wool spots, prominent disc swelling and retinal oedema are present. The prognosis and complications in these eyes are directly proportional to the degree of ischaemia present, and CRVO is therefore classifi ed into two groups: ischaemic and non-ischaemic. From a clinical viewpoint it is thus necessary to assess the degree of capillary non-perfusion in each patient and to determine whether poor central vision is due to macular non-perfusion and damage to the retinal pigment epithelial cells or due to macular oedema. Figure 4.6 outlines the clinical assessment and management of CRVO. Approximately 30% of CRVOs are non-perfused or ischaemic, and neovascular glaucoma ensues in 40–60% of these. At the onset of CRVO, the iris vessels may be dilated; however, this sign is not necessarily indicative of rubeosis iridis. 4.6.2 Laser treatment of CRVO Controversy regarding the need for prophylactic photocoagulation (PRP) of ischaemic CRVOs for the prevention of neovascular glaucoma has existed for some time. The Central Retinal Vein Occlusion Study, which reported in 1995, was designed to answer two questions:34 1 Is PRP useful in preventing iris neovascularisation and neovascular glaucoma in eyes with CRVO? 2 Does grid laser help in terms of visual acuity in CRVO? The study group concluded:34  CRVO 30% Ischaemic 70% Non-ischaemic (>10DD of retinal non-perfusion ) (7 en car ls CR W art sy au sy >1 e ea ar 5 d or op di O ati di 00 s o al VO eri m m LL le ca m pr se tic ov , tis pt pt s ar E art tio m/ ot d dis as o o ei e te ce N eri c. cul L ntr O RA ar P Is C a or al C ha PD sys TI c o s ru ret R We B , te C N ed S m P ? h nt er b ina rel m; CRor uc an or in Di a ro fo e l VOm l ati C ed d rh cr ab N vei al V ret ag ea et o C ve W S n or A in es N es se n- o aff S, Pi pl L oc nk Pa Bl in o is nt er co clu H u an v pil in in te Bil B C c ro en tto sio ea cr m d lo da d r e at P T h l t n- n; b C s ed ch s ea h n er ch sc pu wo se o al ec an ar on NV w e es p pill ol oll d a p tro , m u ar sp e N l ne Hy H R s B y ot N o R w pedi a ef s; vis V o re ea Fig ve rmsc e ra ES ual A fi d ss ur R, ss etrdr m ct go d ur ac el e el; opus or iv od e an uit d 4. VA ia/ en rh e s ce y. 7 , 4.8 Central retinal artery occlusion 4.8.1 Clinical presentation Occlusion of the central retinal artery (CRAO) presents with sudden unilateral painless loss of vision. The cause, especially in the elderly, is usually embolic, with a common source being the carotid arteries.37 CRAO is often preceded by episodes of amaurosis fugax (temporary loss of vision in one eye). The typical clinical appearance of a CRAO is of retinal pallor with a cherry-red spot at the macula. Intraretinal haemorrhage is usually minimal. If the cause is embolic, the embolus is usually visible and lodged at an arterial bifurcation. Less common aetiologies include occlusive disorders such as temporal arteritis, collagen vascular diseases and syphilis. If the embolus is lodged in a more peripheral artery, visual fi eld loss may be sectorial. Investigations are usually limited to clinical examination with cardiac and carotid artery auscultation, and an ESR measurement to rule out temporal arteritis. The presence and severity of carotid artery disease can be quantifi ed by carotid doppler studies. 4.8.2 Management of central retinal artery occlusion CRAO is an ophthalmic emergency. If the embolus can be dislodged within the fi rst hour, the visual loss can be lessened. Emergency measures include: Digital massage Intravenous acetazolamide Inhalation of a 95% oxygen–5% carbon dioxide mixture Anterior chamber paracentesis (reduction of intraocular pressure by the removal of aqueous humour). In practice, however, the patient either presents late or the embolus is impossible to dislodge despite these measures. As with many of the conditions mentioned in this chapter, a fundamental role of the optometrist is to be vigilant for signs and symptoms indicative of second eye involvement and to initiate rapid re-referral. Practical advice As the risk of permanent blindness following amaurosis fugax is approximately 10% in 5 years and the risk of stroke is 20% in 5 years, these patients should be investigated urgently. Some hospitals offer a rapid access TIA (transient ischaemic attack) clinic. 4.9 Anterior ischaemic optic neuropathy Anterior ischaemic optic neuropathy (AION) is due to arteritic or non-arteritic occlusion of the posterior ciliary arteries.38 Loss of vision is sudden and usually progressive for 24–48 hours. The most common causes include temporal arteritis (10%) and nonarteritic atherosclerotic optic neuropathy. Patients with arteritic optic neuropathy tend, on average, to be 10 years older than those with the non-arteritic form. The non-arteritic form is more common in men, in contrast to the arteritic type, which is more prevalent in women. Coronary bypass and cataract surgery have also been implicated in the pathogenesis of AION. Management of the arteritic form of AION is as for temporal arteritis. There is no proven effi cacious management of the non-arteritic type. 4.10 Cerebrovascular accidents and visual function Cerebrovascular accidents are a signifi cant cause of visual disability. The most common sign is homonymous hemianopic or quadrantopic visual fi eld loss, although oculomotor abnormalities and perceptual irregularities may also be present. Sometimes a patient can present with visual symptoms being unaware that he or she has had a cerebrovascular event. After excluding ophthalmic pathology, it is imperative that the patient be referred for investigation of the stroke. During the recovery phase of a stroke it is important that ophthalmic symptoms and signs are not overlooked. A signifi cant proportion of patients will have diffi culty with vision due to uncorrected refractive errors, wrong glasses being worn during rehabilitation, diplopia and progressive comorbidities such as AMD, diabetic retinopathy, glaucoma and cataract.39 It is imperative that information on ophthalmic status and the magnitude of visual impairment is provided to those responsible for overall medical and rehabilitation management, as these problems will complicate other aspects of rehabilitation management. 4.11 Low vision management of the elderly Low vision management of the elderly has to be seen within the context of their overall health status. Those who have age-related ophthalmic pathology in the absence of other health problems often do very well with conventional illuminated stand magnifi ers and portable hand magnifi ers, provided they have come to terms with vision loss and the fact that new spectacles or surgery will not reverse the condition. As motivation and confi dence in handling improves, spectacle magnifi ers and telescopic aids can be added to the armoury. Those who were avid readers may fi nd a CCTV or Easyreader system invaluable. Those with complex health problems, and in particular age-related degeneration of the higher functions, will fi nd low vision aid usage diffi cult. Elderly confused patients with Alzheimer’s disease cannot use low vision aids, and their families need to be advised on practical, high contrast, colour and size issues. Those with handling problems such as arthritis of the hands or spine need ergonomically suitable low vision aids. However, those with Parkinson’s disease may benefi t from a spectacle mounted device and a reading stand. It is important to remember that almost all elderly people, before the onset of visual impairment, will have been used to wearing distance and/or reading glasses or bifocals. The refractive error does not disappear with the onset of visual impairment, although it may become insignifi cant. Advice on the need for, and use of, spectacles needs to be given carefully. The elderly visually impaired are the group that optometric practitioners deal with most. In this group, the visual impairment is often asymmetrical and for some time unilateral. Most patients cope well with this situation, although occasionally some patients fi nd it diffi cult to accept. Those who develop bilateral problems vary greatly in their ability to cope. Some manage very well and simply adjust their lifestyle and use visual aids with great motivation whilst accepting their limitations. A small minority are never able to come to terms with their problem and often retreat into their homes and lead a lonely isolated existence. Important factors in success in using visual aids include family and social support and the patient’s general health and motivation.