Age-related eye disorders are a leading cause of visual impairment in the UK.¹ Cataract, glaucoma, age-related macular degeneration and diabetic retinopathy all increase in prevalence with age, and many individuals are affected by more than one condition.

Visual impairment in older people reduces their quality of life and increases the risk of other comorbidities such as falls, hip fractures, accidents and depression.

Minimising the individual and socioeconomic burden of age-related eye disease requires patient education and support, clinical awareness, screening, appropriate access to eye care specialists and timely treatment.

GPs, optometrists and care of the elderly physicians have an important role in identifying potentially treatable visual impairment in older people, who may feel that poor vision is an inevitable consequence of ageing.

A minimum standard is a test of visual acuity using a Snellen chart, with an acuity of 6/12 or worse denoting visual impairment.

Normal ageing of the eye

The human eye and visual system undergoes a normal ageing process, which results in gradual deterioration in visual function independent of age-related eye disease. Key changes are described below.

Presbyopia: Reduced ability to focus at close range (loss of accommodation) caused by decreased elasticity of the crystalline lens and reduced ciliary body tone. By the age of 45 years, most people require reading glasses.

Reduced pupil size: Decrease in pupil size with advancing age (senile miosis) reduces retinal illuminance, such that a 60 year old receives about one third of the light compared with a 20 year old.

Cornea: The prominent white ring of arcus senilis is caused by age-related deposition of cholesterol and lipid in the peripheral cornea. Changes in corneal epithelium, stroma and endothelium reduce corneal clarity and contribute to increased light scatter and lower contrast sensitivity. In addition, the curvature of the cornea alters with age, changing astigmatism and refractive error.

Lens: Yellowing of the lens reduces sensitivity to shorter 'blue' wavelengths of light, and also increases light scatter even before the development of cataract.

Vitreous: Progressive liquefaction of the vitreous gel occurs with advancing age, causing harmless floaters. However, subsequent separation of the vitreous gel from the retina (posterior vitreous detachment) can cause retinal tears and retinal detachment. New onset of floaters and flashes therefore warrants referral to an ophthalmologist.²

Retina: Regeneration of rhodopsin within photoreceptors becomes slower with advancing age, causing delayed dark adaptation and difficulty in seeing at night. In addition, gradual loss of neuronal, photoreceptor and retinal pigment epithelial elements together with accumulation of waste material under the retina (lipofuscin) lead to a general decline in retinal function.

Eyelids: Involutionary changes of the skin, orbicularis and canthal tendons result in eyelid laxity, wrinkles and redundant skin folds (dermatochalasis). In the lower lid, horizontal laxity contributes to lid margin eversion (ectropion) or inversion (entropion). In the upper lid, attenuation or disinsertion of the levator muscle aponeurosis can cause ptosis.

Refractive error: In the UK, more than 30 per cent of visual impairment in the over-75s may be caused by untreated refractive error.¹ Patients aged more than 60 years should be advised that they are entitled to regular free NHS eye examinations. In addition, free NHS domiciliary eye examinations are available to those unable to attend community optometric practice (for example nursing home residents).

Age-related cataract

Cataract refers to opacity of the crystalline lens of the eye associated with reduced vision. The vast majority of cataract is age related, and cataract is the most common cause of treatable visual impairment in older people. In the UK, prevalence of cataract increases from 11 per cent in the 65-69 age group to 33 per cent in the 75-79 age group, rising to 56 per cent in those aged 85 years or more.³ Other risk factors include diabetes, ethnic group, lifetime ultraviolet exposure, nutrition, steroid use, smoking, trauma and alcohol consumption.⁴

Symptoms

Cataract typically produces gradual loss of vision in one or both eyes, with patients reporting blurred or dull vision. Slowly progressing cataracts may mean that patients are unaware of their very poor eyesight, and it is important to consider reduced vision as a cause of falls in older people.

Scattering of light by cataract may cause monocular diplopia or troublesome glare, particularly when driving at night. The impact of visual symptoms on daily activities, including occupation, reading, crossing the road and driving, must be assessed.

Examination

Visual acuity testing is the standard for quantifying visual impairment, but provides little information on visual disability from cataract-related glare or contrast sensitivity disturbance. Checking vision through a pinhole may indicate potential visual improvement following cataract surgery as the pinhole can neutralise up to 6 dioptres of refractive error. Lens opacity can usually be detected by viewing the red reflex using a hand-held direct ophthalmoscope; however, slit-lamp examination and fundoscopy are essential to exclude ocular comorbidity.

Cortical cataracts are characterised by peripheral spokes and water clefts caused by osmotic imbalances in lens epithelial cells. Nuclear sclerosis is progressive yellowing of the centre of the lens resulting from accumulation of protein aggregates, which increase the refractive index (figure 1a, attached). Posterior subcapsular cataract occurs just beneath the posterior lens capsule and is associated with steroid use or diabetes (figure 1b, attached).

If left untreated, lens opacity can increase until a white mature cataract forms (figure 1c, attached).

Non-surgical management

Refractive change from early cataract can often be corrected with updated spectacles and may delay the need for surgery. Studies to evaluate the effects of nutritional supplements (carotenoids) or antioxidants (vitamins C and E) on cataract have been inconclusive.⁵ Smoking increases the risk of cataract and stopping smoking may slow progression.

Who should be referred for cataract surgery?

A common misconception among patients is that a cataract has to be 'ripe' before surgery is possible. However, routine referral to consider cataract surgery is justified whenever vision deteriorates below a patient's requirements. Cataract surgery is also undertaken:

• If lens opacity precludes assessment or treatment of retinal disease

• For second eye surgery to improve binocular visual function

• To treat cataract-related inflammation or glaucoma

• As a means of correcting high refractive error.

41135791Poorly controlled hypertension and diabetes should be addressed before referral as they increase the risk of complications and may result in cancellation of surgery.

Box 1, above, shows information that it would be helpful to include when referring patients for cataract surgery.

Modern cataract surgery

Cataract extraction is routinely performed by phakoemulsification (high frequency ultrasound) via

a small (3.2mm) self-sealing corneal incision. The natural lens capsule is left intact to allow placement of a foldable intraocular lens implant in an anatomically correct position behind the iris. The vast majority of procedures are performed as day cases under local anaesthesia, allowing rapid visual rehabilitation. Complications are infrequent (1:1000 risk of blindness from infection or haemorrhage) and most can be treated.

Following cataract surgery 80 per cent of eyes without ocular comorbidity achieve a final best corrected visual acuity of 6/9 or better (92 per cent better than 6/12).⁶ However, spectacles may still be necessary to correct residual refractive error, and reading glasses are normally required as traditional monofocal intraocular lens implants have a fixed focus.

Newer multifocal or accommodating intraocular lenses allow better unaided near vision. Secondary deterioration of vision can occur months to years after surgery in over 20 per cent of patients as a result of opacification of the posterior lens capsule; however, YAG laser posterior capsulotomy can improve vision again.

The earliest symptoms of posterior capsule opacification (PCO) are gradual blurring of vision or glare. This is similar to the onset of the original cataract, hence it is sometimes termed 'secondary cataract'. While history may be suggestive of PCO, retinal pathology must be excluded, especially in the elderly where other comorbidity may exist.

Glaucoma

IOP is determined by the balance between aqueous humour production and outflow. An IOP of 21mmHg is considered the upper limit of normal.⁷ Aqueous humour is produced by the ciliary body and passes through the pupil into the anterior chamber. Exit of aqueous humour from the anterior chamber occurs largely through the trabecular meshwork in the angle formed by the iris and cornea. The remainder drains directly via a uveoscleral route.

Glaucoma describes a group of conditions characterised by optic nerve damage associated with elevated IOP (usually >21mmHg). Primary open-angle glaucoma (POAG) and acute angle closure glaucoma (AACG) are the most common forms of the disease seen in clinical practice and in older people.

Primary open-angle glaucoma

POAG is a chronic, painless, progressive condition affecting four per cent of those over 65 years of age in the UK. Most are asymptomatic until significant visual impairment has occurred. Visual loss usually begins with characteristic peripheral visual field defects, which, if left untreated, may progress to tunnel vision and blindness. Early detection is therefore important to prevent irreversible visual loss.

Examination

Raised IOP, glaucomatous optic nerve damage manifest as disc 'cupping', characteristic thinning of the neuroretinal rim of the optic disc caused by loss of retinal ganglion cell axons (figure 2a, attached)and corresponding visual field defects (figure 2b, attached) are key clinical findings in POAG. Glaucoma may also occur in patients with normal IOP - so-called normal tension glaucoma.

The positive predictive value of optometrist referrals for suspected glaucoma is less than 50 per cent but may be increased by specific training in glaucoma detection, including standardised criteria for assessment of intraocular pressure, optic disc 'cupping' and perimetry.

Management

The goal of management in POAG is to prevent significant visual impairment from glaucoma in the patient's lifetime. Current medical and surgical therapies aim to lower IOP in order to halt or slow progression of optic nerve damage. The reduction in IOP required to preserve vision varies according to the level of IOP, the amount of optic nerve damage and visual field loss at presentation, as well as the rate of progression. Regular review of these parameters therefore allows the response to treatment to be determined.

Eye drops: Topical IOP-lowering medication is first-line treatment for POAG, and is usually continued indefinitely. More than one type of eye drop may be required for satisfactory IOP reduction.

Currently available preparations and notable side-effects are summarised in table 1,attached. It is important to note that ß-blockers are contraindicated in asthma and COPD, and can cause significant respiratory or cardiovascular side-effects as a result of systemic absorption.

Laser: Argon laser trabeculoplasty applies burns to the trabecular meshwork to increase the drainage of aqueous humour. It is usually only used in certain types of open angle glaucoma as its effect is usually not great and diminishes with time. It is a useful adjunct in cases where drops alone are failing and surgery is not possible.

Cyclodiode laser applied to the ciliary body through the sclera can also be used to reduce aqueous humour production, especially when other modalities of treatment have failed or in special cases.

Surgery: Trabeculectomy may be required if IOP is unresponsive to medical and/or laser therapy or when large reductions in pressure are required. A channel is fashioned for aqueous humour to bypass the trabecular meshwork and drain directly from the anterior chamber into the subconjunctival space.

A natural scarring reaction may obliterate the drainage channel; however, the use of antimetabolite agents (fluorouracil or mitomycin) during surgery can double the success rate. For those with refractory glaucoma, tube drainage devices are used.

Acute angle-closure glaucoma

AACG is characterised by closure of the drainage angle between the cornea and the base of the iris, often initiated by apposition of the iris to the lens (pupil block), which prevents the flow of aqueous humour into the anterior chamber of the eye. The iris is therefore pushed forward by a build-up of aqueous humour behind it and further occludes the drainage angle. A rapid rise in IOP follows and patients usually present with a painful red eye and reduced vision, often noting coloured haloes around lights due to corneal oedema.

Symptoms of headache, nausea and vomiting may predominate and lead to investigation of abdominal disease, delaying the diagnosis of AACG.

Longsighted (hypermetropic) and Oriental eyes with shallow anterior chamber anatomy are predisposed to AACG, which may also be triggered by pupil dilatation, including that occurring as an antimuscarinic side-effect of systemic drugs.

Examination

The eye is usually stony hard to palpation, showing conjunctival injection with a cloudy cornea and mid-dilated pupil. Diagnosis is confirmed by high IOP (typically >50mmHg) and a shallow anterior chamber on slit-lamp examination.

Management

AACG is an ophthalmic emergency requiring urgent treatment to lower IOP rapidly and reduce the risk of irreversible optic nerve damage. Acetazolamide, a systemic carbonic anhydrase inhibitor, is usually given in addition to pilocarpine to constrict the pupil and reverse pupil block. Once the acute episode is controlled, laser iridotomy is performed to create a channel through the peripheral iris (peripheral iridotomy) to allow aqueous humour to flow freely into the anterior chamber and prevent pupil block recurring.

Primary care management of glaucoma

Patients with a family history of POAG or AACG, especially if hypermetropic, should be informed of their increased risk and advised to attend an optometrist or ophthalmologist for screening.

Screening is recommended for patients over the age of 40, but can be earlier depending on risk factors including family history (first degree relatives of affected patients have three to ten times the risk of developing POAG) and ethnicity - Afro-Caribbeans tend to develop the condition approximately a decade earlier.

The GP has an important role in continuing prescription of long-term eye drops and monitoring for systemic side-effects of treatment (particularly in older people), which may not be evident to the patient or ophthalmologist (see table 1, attached).

Some patients develop raised IOP secondary to steroid treatment (steroid responders), so any patient taking high-dose topical steroids (face/scalp creams, eye drops) or systemic steroids should have an IOP check one month after starting treatment and annually thereafter. Any patient with suspected AACG should be referred for an immediate ophthalmic opinion.

Age-related macular degeneration

The macula is the small central area of retina containing the fovea, which consists of mainly cone photoreceptors used for fine focus, reading and colour vision. Age-related macular degeneration (AMD) is a major cause of irreversible visual impairment in older people, affecting an estimated 20 per cent of those aged 75 years or more in developed countries.

Early AMD, also known as age-related maculopathy (ARM), is usually asymptomatic or causes mild visual impairment. ARM is characterised by pigmentary abnormalities of the retinal pigment epithelium (RPE) and yellow deposits (drusen) beneath the RPE, which denote risk of progression to late AMD.

Late AMD occurs as so-called 'dry' and 'wet' varieties:

• Dry AMD is typically slowly progressive, causing gradual loss of central vision, and accounts for 85 per cent of all cases of late AMD. It is characterised by atrophy of the RPE and overlying retina.

• Wet AMD is defined by the development of new vessels beneath the retina (choroidal neovascular membranes, CNVM) which leak fluid and/or bleed (figure 3a, attached). Patients experience acute decline in central vision and/or distortion (metamorphopsia). Diagnosis must be confirmed by fluorescein angiography, which can identify two major forms of CNVM: classic (figure 3b, attached) and occult. Eventually the overlying macula becomes scarred, representing the end stage of the wet form of AMD (disciform scar).

Management

The loss of central vision from AMD has a huge impact on quality of life, especially with bilateral disease (patients with wet AMD in one eye have around a 50 per cent chance of the other eye becoming affected within five years). Management for most patients is supportive, including provision of low vision aids to allow the best use of remaining vision. Current treatments for AMD are largely directed at minimising visual loss in wet AMD caused by CNVM, with new and evolving therapies likely to improve visual prognosis of this disease.

Conventional argon laser: Ablation of CNVM with thermal laser is indicated for wet AMD where lesions are away from the fovea (juxtafoveal and extrafoveal). Although the risk of severe visual loss is significantly reduced, the recurrence rate is 50 per cent with this treatment.

Photodynamic therapy (PDT): Subfoveal CNVM may be selectively targeted (without further damaging the overlying retina) using a non-thermal diode laser (689nm) following intravenous administration of a photo-activated drug (verteporfin). Current NICE guidance recommends PDT for the treatment of subfoveal 100 per cent classic CNVM with vision of 6/60 or better. Funding is also provided for treatment of predominantly classic (>50 per cent) lesions if part of a trial.

Re-treatment is often required but the risk of moderate visual loss at two years in these subgroups is reduced from 69 per cent to 41 per cent. PDT may also be of some benefit for lesions composed of occult or minimally (<50 per cent) classic CNVM, but the NHS does not currently fund these indications.

Intravitreal VEGF inhibitors: A number of inhibitors of vascular endothelial growth factor (VEGF) administered as regular intravitreal injections, especially ranibizumab and bevacizumab, have shown efficacy for the treatment of all angiographic types of CNVM in wet AMD and may even improve vision;⁸ previous treatments such as PDT only reduce risk of further vision loss.

Wet AMD occurs in a minority (15 per cent) of all cases of late AMD (dry AMD is much more common), but the degree of visual impairment and speed of onset is generally greater for wet AMD. There are 214,000 people in the UK with visual impairment, eligible to be registered blind, caused by AMD. This figure is expected to rise to 239,000 by 2011.

• Pegaptanib results in 70 per cent of patients losing less than three lines of visual acuity compared with 55 per cent of controls (all lesion types, NNT 6.7). It received US Food and Drug Administration (FDA) marketing approval in December 2004 and is currently being appraised by NICE, with guidance expected later this year.

• Ranibizumab is an anti-VEGF antibody fragment that not only minimises visual loss but is also the first treatment that would potentially improve vision in patients with wet AMD. The drug has recently been licensed in the UK, but awaits NICE appraisal before use in the NHS.

• Bevacizumab is a monoclonal antibody, initially developed for use in metastatic colon cancer, from which ranibizumab is derived. Both agents appear to show similar results in the treatment of wet AMD. Serial intravitreal injections every four to six weeks are, however, associated with small (less than one per cent) but significant risks, including endophthalmitis, retinal detachment and cataract.

Macular translocation surgery: Macular translocation for wet AMD is available in the UK on an investigational basis at present.⁹ The surgery involves repositioning the macula such that the fovea comes to lie on healthy RPE and choroid, away from the visually destructive subretinal CNVM. While up to two-thirds of patients may experience visual improvement, significant complications such as retinal detachment may lead to visual loss.

Antioxidants: In patients with late AMD in one eye, antioxidant supplements have been shown to have some protective effect on the other eye.

The Age-Related Eye Disease Study¹⁰ (AREDS) was a large multi-centre study with approximately 3,600 participants. The average follow-up was 6.3 years. The aim was to investigate whether daily high-dose antioxidant supplements (containing 500mg vitamin C, 400iu vitamin E, 15mg ß-carotene and 80mg zinc) could decrease the progression from early disease (ARM) to late neovascular AMD. Copper 2mg was added to prevent anaemia.

In patients with at least moderate disease in one eye (for example large drusen, extra-foveal atrophy) and those with advanced wet AMD in the other eye, the risk of developing advanced AMD in the study eye at five years was 28 per cent for placebo, 23 per cent for antioxidants alone, 22 per cent for zinc alone and 20 per cent for zinc and antioxidants. Therefore, in high-risk ARM there was a proven preventative effect for antioxidants and zinc. This treatment is the only proven benefit for patients with ARM.

It is important to note that ß-carotene is contraindicated in smokers, but preparations without ß-carotene are available to reduce the theoretical risk of lung cancer. The benefit of antioxidants in patients with bilateral early AMD/drusen is less certain, as is the increase in macular pigment density with high dietary intake of lutein and zeaxanthin.

Primary care management

Patients with rapid onset of blurred or distorted vision require same-day referral for ophthalmology review to exclude treatable wet AMD or other acute pathology. Those with dry AMD tend not to describe acute visual loss and may be referred less urgently - initial review by an optometrist may be useful in these circumstances.

Smokers are at higher risk of developing AMD than non-smokers or ex-smokers, so ongoing advice and encouragement to give up smoking is important. Awareness of the increased risk of depression, anxiety and falls is important in patients with visual loss. Knowledge that AMD does not damage peripheral vision is reassuring to many patients who fear total blindness.

Ocular problems associated with other medical conditions

Diabetic retinopathy

Diabetes accounts for 10 per cent of new cases of blindness per year in the US. Almost a quarter of people with type 2 diabetes will have signs of diabetic retinopathy by 13 years' duration.¹¹ Patients may be asymptomatic and the presence of diabetes may reveal itself on fundus examination or they may complain of reduced vision (gradual or sudden) or floaters.

Signs of non-proliferative diabetic retinopathy include microaneurysms, dot haemorrhages, cotton-wool spots, hard exudates and intraretinal microvascular abnormalities (figure 4, attached).

Neovascularisation of the optic disc, retina or iris constitutes the proliferative stage, for which panretinal laser photocoagulation is required in order to reduce the chance of severe loss of vision by 50 per cent.¹² If the neovascularisation leads to non-clearing vitreous haemorrhage, then vitrectomy is usually indicated to remove the blood and apply laser treatment to the retina at the same time.

Diabetic maculopathy with clinically significant macular oedema should also be treated with laser, reducing the chance of severe loss of vision.¹³ Laser treatments are aimed at stabilising vision, but emphasis needs to be placed on tight glycaemic, blood pressure and cholesterol control.¹⁴

Hypertension

Hypertension is implicated in other eye problems such as retinal vascular occlusions, may worsen conditions such as diabetic retinopathy or affect the retina in its own right as hypertensive retinopathy.

Retinal findings in hypertensive retinopathy include 'silver wiring' changes of retinal arterioles, arteriovenous crossing changes, dot and blot haemorrhages, retinal exudates, cotton-wool spots and occasionally optic disc swelling. AV nipping occurs in about 6 per cent of patients over 50 years, and is correlated with hypertension. Often patients with hypertension are asymptomatic, but may present to eye casualty departments with a painless unilateral red eye from a subconjunctival haemorrhage.

The aim of treatment is to normalise blood pressure.

Hypercholesterolaemia

Patients with abnormal lipid profiles may present with xanthelasma around the eyelids, but often these abnormalities are picked up in the investigation of vascular ocular diseases, such as retinal arterial occlusion, retinal vein occlusion or anterior ischaemic optic neuropathy.

Although there is a link between xanthelasma and hyperlipidaemia, only half of patients have elevated serum lipids - however, younger individuals with xanthelasma have a greater likelihood of hyperlipidaemia and hypercholesterolaemia than older patients. Histology reveals lipid-laden macrophages in the dermis. Xanthelasma may be treated with laser or excised, but serum lipids should be lowered with lifestyle changes (diet and exercise) and statins if necessary.

Retinal vein occlusion

Occlusion of the retinal venous system is classified into branch retinal vein occlusion (BRVO) and central retinal vein occlusion (CRVO), depending on which vein is affected. Both conditions present with reduced vision or floaters. In CRVO, presentation can be with the severe pain and raised IOP of neovascular glaucoma. This so-called '100-day glaucoma' occurs around three months after the vision is lost from the CRVO, when iris neovascularisation occurs in cases where perfusion is severely compromised.

Other, more common signs of vein occlusion are intraretinal haemorrhages, cotton-wool spots, lipid exudates and retinal oedema. In BRVO these signs occur in the corresponding retinal quadrant, whereas in CRVO these changes are widespread throughout the retina (figures 5a and 5b, attached).

Neovascularisation of the retina or optic disc is more common in BRVO than CRVO, and sectoral panretinal photocoagulation is warranted to prevent visual loss from vitreous haemorrhage. In CRVO, panretinal photocoagulation is recommended when iris neovascularisation occurs to prevent neovascular glaucoma.

Both BRVO and CRVO may lead to macular oedema, but macular laser treatment is indicated only in cases secondary to BRVO, where at least three months have elapsed since onset, visual acuity is below 6/12 and fluorescein angiography demonstrates a perfused capillary network around the fovea. In non-perfused cases of macular oedema following BRVO and all cases of CRVO there is no proven effective treatment.

Medical conditions implicated in vein occlusion include hypertension, diabetes, hypercholesterolaemia and other hypercoagulability states. Investigations and systemic management are directed towards these, and antiplatelet therapy is recommended to reduce systemic cardiovascular risk.¹⁵

Retinal artery occlusion

Retinal arterial occlusions are caused by thrombotic or embolic occlusive events and result in painless severe loss of vision. Systemic risk factors are similar to those for vein occlusion, but systemic examination may additionally reveal irregularity of the pulse, cardiac abnormality or carotid bruit warranting carotid Doppler scanning.

Arterial occlusions are also divided into branch retinal artery occlusion (BRAO) and central retinal artery occlusion (CRAO). Signs include oedema and whitening of the retina, either around the arterial branch in BRAO or throughout the retina with a central 'cherry-red spot' in CRAO.

Emergency care is directed at assessing risk factors, and giant cell arteritis should be ruled out. In CRAO, lowering the IOP and vasodilating the arterioles (by rebreathing into a paper bag to raise the blood CO₂ tension) and ocular massage to dislodge the embolus can be tried, but is rarely successful after a few hours have elapsed since the onset of CRAO.

Anterior ischaemic optic neuropathy

Anterior ischaemic optic neuropathy (AION) is classified by aetiology into arteritic (arising as a manifestation of giant cell arteritis) or non-arteritic (NAION), caused by vasculopathic risk factors such as hypertension, diabetes and hypercholesterolaemia. Optic disc swelling, relative afferent papillary defect and altitudinal visual field loss are all signs associated with this group of disorders.

Profound unilateral loss of vision is the presenting feature of both types of AION, but in arteritic cases the history includes severe temporal headache, jaw claudication, tongue pain, intermittent fever, night sweating, anorexia, weight loss, malaise and polymyalgia.

In all cases investigations should be directed at this condition, which presents with raised erythrocyte sedimentation rate (in nine per cent of cases of giant cell arteritis the ESR may be normal) and raised C-reactive protein. A full blood count should also be conducted to check for anaemia.

Biopsy of the superficial temporal artery may be undertaken, but immunosuppressive treatment with high-dose steroids should not be delayed if giant cell arteritis is suspected on clinical grounds as the risk of bilateral blindness is up to 40 per cent within ten days if left untreated.

Appropriate clinical assessment to exclude other causes of high ESR and contraindications to systemic steroid treatment must be actively sought.

Long-term management is often undertaken in collaboration with the GP or rheumatologist.

The management of NAION is to treat the underlying vasculopathic risk factors and initiate antiplatelet agents such as aspirin. The risk to the other eye is up to 50 per cent, so it is imperative to address these systemic factors.

Conclusion

Age-related eye disorders account for significant morbidity among older people, many of whom are undiagnosed and untreated. Older people should be encouraged to undergo regular eye examinations by an optometrist and those with visual impairment should be referred early to an ophthalmologist.