Oxford Handbook of Geriatric Medicine (2 edn)
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The ageing eye
Vision is a complex activity which involves eye function, cognition, reasoning, and memory. With increasing age the chance of visual impairment increases because of:
Changes due to senescence
Changes due to cumulative exposure to environmental toxins
Changes in associated functions (cognition, hearing, etc.)
Increasing incidence of many eye diseases
Visual impairment is not inevitable—there is considerable diversity both in visual decline and in compensatory adaptations. There is a tendency for patients to blame failing vision on age, and so not to seek help. However some changes may be age related (but corrective action may be available, eg glasses) or else impairment may herald the onset of treatable disease. Prompt identification and treatment may make all the difference between independence and dependence. Distinguishing what is ‘normal’ and when to refer to a specialist is key.
Changes in vision with age
Visual acuity often decreases
Multifactorial—changes in macula, lens, and cornea
May be corrected (eg glasses)
Consider eye disease if deterioration is rapid
Visual fields—peripheral vision less sensitive
Although formal field-testing normal—consider cerebrovascular disease if distinct homonymous field defect
Multifactorial—pupil smaller, lens cloudier, and peripheral retina less sensitive
Near vision decreases
Accommodative power diminishes due to increasingly rigid lens
Presbyopia (a lack of accommodation range) is part of normal ageing, begins in middle age and can be corrected with glasses
Colour vision
Retinal receptors unchanged
Alterations in colour perception may relate to yellowing of the lens altering the light reaching the retina
Light adaptation slower
Rods and cones may be slower to react to changes in illumination, and the pupil may let in less light, requiring brighter lighting for good vision
Causes difficulty with night driving in particular
Glare may be a problem as the lens, cornea, and vitreous become less clear, and minute particles scatter light
Contrast sensitivity decreases
Due to changes in cornea, lens, and retina
Floaters
Due to aggregation of collagen fibrils in vitreous
Usually normal, but if sudden onset, or large quantity, may indicate retinal detachment or vitreous haemorrhage
Visual impairment
▸.5% of the UK population has visual impairment not amenable to correction by glasses alone. There is considerable social and psychological impact, yet it is underreported and optimal help is often not delivered.
Causes
(From blind registration data):
Macular degeneration (49%)
Glaucoma (15%)
Diabetes (6%)
Cardiovascular disease (5%)
83% of people who register are >65 years old. Low-vision clinics are available in most hospitals.
Interventions
Include:
Change glasses prescription (benefits 10–20%)
Explain the disease (often does not cause total blindness, eg with macular degeneration; improve understanding of future)
Psychological support (often combined with hearing loss in older people—beware social withdrawal. Acknowledge problem, discuss fears)
Discuss blind registration
In some cases, consider guide dogs and learning Braille
Take specific history of certain activities and provide practical advice:
Reading—what do they actually need to read? Advise about good light, magnifiers, large print books, photocopy recipes to larger size.
Writing—use black pen on white paper, consider a Millard writing frame or bold line paper, discuss specific tasks such as cheques and pension books.
Television—sitting closer, black and white sets may improve contrast
Telling the time—talking watches and clocks
Cooking—improving lighting in kitchen by removing net curtains, tactile markers for cookers, electronic fullness indicators on cups
Telephoning—large button telephones
Social interaction—sit with back to the window to improve light on a visitor's face, discuss accessible holidays
Further reading
Blind registration
Done by ophthalmologists. Copy of the form goes to social services, GP and the office for national statistics.
Generally there is under-registration—probably due to stigma and a sense that this is the end of the fight, rather than the start of new help and opportunity.
Definitions
Partially sighted <6/60 in both eyes or reduced fields (eg homonymous hemianopia)
Blind need not mean no vision. Statutory definition is that the person should be ‘so blind as to be unable to perform any work for which eyesight is essential’. Pragmatically it is vision <3/60 or very diminished fields
Benefits to individual
Financial—including personal income tax allowance, disability living allowance or attendance allowance, working tax credit or pension credit, extra housing or council tax benefits, carers’ allowance, help towards care home fees, free NHS sight test, free NHS prescriptions, lower television licence fee, car parking and public transport concessions, exemption from directory enquiries fees
Easier access to help from social services
Loan of cassette recorder and talking books and newspapers (also available without registration)
Magnifiers (glasses or contacts, hand magnifiers, stand magnifiers, illuminated magnifiers, reading telescopes). Consider portability, cosmetic aspects, and posture required to use
Larger print (books, enlarge frequently used items with photocopier)
Contrasting colours—eg black on white
Use to emphasize written word, door handles, stair edges, etc.
Use white cups for dark drinks
Put contrasting strips round light fittings
Remove net curtains
Use high power bulbs (eg 150W not 60W incandescent; a wider range of high luminescence ‘low energy’ lamps is now available)
Use directable light sources (eg angle poise lamps)
Visual hallucinations
Management varies with the cause.
Organic brain disease
Lewy body dementia (occur in 50–80%; usually well formed, eg animals). Also occurs in dementia of Parkinson's disease. Can respond dramatically to cholinesterase inhibitors
Anoxia, migraine and delirium—treat the underlying cause
Focal neurological disease (especially occipital and temporal lobe—range from unformed lines and lights, etc. to complex)
Occipital lobe seizures—treat with anticonvulsants
Drugs
Common with dopamine agonists and anticonvulsants (usually mild and unformed). Try reducing the dose, watching for rebound in symptoms
Overdose of anticholinergic drugs such as antihistamines or tricyclic antidepressants
Use of amphetamines and LSD
Alcohol withdrawal
Psychiatric disease
Visual hallucinations occasionally occur with schizophrenia (auditory more common).
Charles Bonnet syndrome
Diagnosis of exclusion
No other psychiatric symptoms or diseases present
Occurs with bilateral visual loss (typically secondary to cataracts or glaucoma) as a ‘release phenomenon’
These are usually well formed, vivid, and occur in clear consciousness
Insight is usually present
Duration is usually seconds to a minute or so
May be simple (flashes, shapes) or complex (recognisable images)
Non-threatening—the patient's reaction is often one of curiosity or amusement
Probably under-estimated as patients reluctant to tell doctors for fear of being labelled as ‘mad’
Not related to psychiatric problems
Reassurance is often all that is required, but symptoms may be improved by enhancing vision
Cataract
Term used to describe any lens opacity. The most common cause of treatable blindness worldwide. In the UK it is largely a disease of the older population: 65% of people in their 50s and everyone >80 have some opacification. This is probably caused by cumulative exposure to causative agents rather than senescence per se.
Causes
Exposure to environmental agents (eg UV light, smoke, blood sugar)—more exposure with increasing age
Ocular conditions (trauma, uveitis, previous intraocular surgery)
Systemic conditions (eg diabetes, hypocalcaemia, Down's syndrome)
Drugs (especially steroids—ocular and systemic)
Symptoms
Painless visual loss which varies depending on whether unilateral/bilateral and severity/position of the opacity
Commonly begins with difficulty in reading, recognizing faces, and watching television
May be worse in bright light or be associated with glare around lights
Signs
Reduced visual acuity—usually gradual
Diminished red reflex on ophthalmoscopy
Change in the appearance of the lens (appears cloudy brown or white when viewed with direct light)
Beware co-existing conditions: pupil responses are normal, and the patient should be able to point to the position of a light source
Management
Optimizing visual conditions
▸New glasses prescription may delay need for surgery.
Surgical removal of opacified lens
No effective medical treatment
When to treat?
Tailor treatment to the individual. Depends on visual requirements of patient, severity of cataract, and presence of other ocular disease (worsens outcome from surgery). Roughly speaking <6/18 in both eyes is likely to benefit from surgery, but an elderly person who does not read much may be quite content with this visual level. Conversely, someone who wishes to continue driving, or needs precise vision for other reasons may wish for surgery much sooner. Previously surgeons waited for the cataract to ‘ripen’ to aid extraction—this is no longer the case. Have a frank discussion about risks and benefits with each individual.
What the surgery involves
Usually done as a day case under local or topical anaesthesia
Patient must be able to lie fairly flat and still. Patients with dementia may need sedation or general anaesthesia (altering risk/benefit); consider heart failure, chest disease and spinal deformity—can they lie flat? If not, then the surgeon may be able to adapt the procedure
It is not necessary for patients to discontinue medications. The procedure may be done safely while a patient is taking aspirin, and even warfarin
Generally a safe and well tolerated procedure
Phacoemulsification is most commonly used in the UK (small cut in eye to access lens that is then liquefied with an ultrasonic probe). A replacement lens is then folded into the empty lens capsule. Sutures are not usually needed
Other methods (extracapsular and intracapsular extraction) are less commonly used
Postoperatively the patient will wear an eye shield (usually at night) for a period, and use steroid and antibiotic eye drops
Surgery is done on one eye at a time. The poorer-seeing eye is usually done first. Second eye surgery may be done once outcome from the first eye is assessed
Outcome
With no ocular comorbidity, 85% have a visual acuity of >6/12 at discharge. Outcome is worse with other eye diseases, eg glaucoma, and in patients with diabetes and cerebrovascular disease.
As the replacement lens has a fixed focus and is usually chosen to allow clear distance vision, the patient will usually require glasses for reading. A new prescription should be made up a few weeks after surgery, once postoperative inflammation has settled. If second eye surgery is planned then glasses are usually issued once both surgeries are completed.
Glaucoma
Third most common cause of blindness worldwide.
▸Leading cause of preventable blindness in the UK. Early detection can slow/halt progression.
Definition
Visual loss due to a combination of loss of visual fields and cupping of the optic disc. Usually associated with a rise in intraocular pressure sufficient to cause damage to the optic nerve fibres (either direct mechanical damage, or by inducing ischaemia).
Intraocular pressure
Ciliary body (posterior) makes aqueous, which flows anteriorly through the pupil and drains via the trabecular network in the anterior chamber angle of the eye
Balance of production and drainage determines pressure
Wide range of pressures seen in normal adults (detected with tonometry)—average 15.5mmHg, normal <21mmHg
The pressure at which ocular damage occurs is probably highly variable between people
Can develop glaucoma with ‘normal pressure-normal tension glaucoma’ (may be high for that person/other factors such as ischaemia may be relevant). More common in older patients. Fluctuating BP may be contributory
Can have ‘high’ pressures without glaucoma—‘ocular hypertension’
Symptoms depend on rate and degree of rise in pressure. Generally asymptomatic unless advanced or acute
Primary (‘chronic’) open-angle glaucoma
Most common
Failure of outflow of aqueous causes slow rise in pressure, allowing adaptation, so subtle symptoms
No pain, corneal cloudiness, or haloes
Slow loss of visual field, typically in an arc shape (‘arcuate scotoma’) with preservation of central vision (macula has more nerve cells so is relatively protected). Progresses to tunnel vision, and then blindness
Risk factors
Age (1% in 5th decade, rising to 10% in 9th decade)
African Caribbean origin (four times risk)
Blood relatives with glaucoma
Screening
Target those at higher risk
Combination of ophthalmoscopy (looking for disc ‘cupping’), automated perimetry testing (for minor field defects) and tonometry (for intraocular pressure) is best
Most cases picked up by optometrists
Encourage regular eye tests, and include careful fundoscopy in physical examination
Treatment
Topical treatments (eye drops): β-blockers, eg timolol (decrease aqueous secretion. Can cause systemic β-blockade); prostaglandin analogues eg latanoprost (improve drainage, may darken iris); α-agonists (decrease aqueous production); carbonic anhydrase inhibitors, eg dorzolamide (decrease aqueous secretion); parasympathomimetics, eg pilocarpine (constrict pupil so will reduce visual field—not commonly used)
Oral treatments: carbonic anhydrase inhibitors, eg acetazolamide very powerful, with many side effects including electrolyte imbalance and paraesthesia of extremities
Surgical treatment: trabeculectomy—operation to improve aqueous outflow. Argon laser trabeculoplasty (applied to the trabecular meshwork) may be effective. Cyclodiode laser to the ciliary body (decreases production) is used in refractory cases
Support group: International Glaucoma Association (
www.iga.org.uk)
Acute angle closure glaucoma
▸Emergency sight-threatening condition—requires urgent referral and treatment.
Apposition of lens to the back of the iris prevents outflow of aqueous with a rapid rise in pressure
Causes red, painful eye with vomiting, blurred vision, and haloes around lights (due to corneal oedema)
May be precipitated by pupil dilation, eg at dusk. Pupil constricts when asleep so episodes at night may be aborted by sleep
Very rarely can be precipitated by anticholinergic drugs
More common in older patients, women, and longsighted individuals—beware of the vomiting older woman with a red eye
On examination cornea is usually cloudy and visual acuity significantly reduced (eg counting fingers)
Treat urgently with iv acetazolamide, topical glaucoma treatment, and laser iridotomy to restore flow. Treat other eye prophylactically with laser iridotomy to prevent pupillary block
Age-related macular degeneration
Age-related macular degeneration (AMD) is the most common cause of adult blind registrations in UK and USA.
▸New treatments for early stages make detection crucial.
Definition
As it sounds—age-related degenerative changes affecting the macula (central part of the retina responsible for clear central vision).
Two types:
90% dry with gradual onset of symptoms (drusen and atrophy of the retinal pigment epithelium)
10% wet, where symptoms relate to leaking vessels causing distortion or sudden loss of central vision due to sub-macular haemorrhage (choroidal neovascularization—new vessels can leak, bleed, and scar causing visual loss in a few months)
Prevalence
Increases with age
25–30 million worldwide
Up to 30% of >75s may have early disease, and 7% late disease
Risk factors
Cause unknown
Age, smoking, family history are strongly associated
Female sex, Caucasian race, hypertension, blue eyes, other ocular conditions (lens opacities, aphakia) and low dietary antioxidants
Symptoms
Asymptomatic in early stages, progressing to loss of central vision
May also have decreased contrast and colour detection, flashing lights and hallucinations
Distortion of straight lines is a feature of wet AMD
Peripheral vision is normal in absence of other pathology
Detection
Regular ocular examination
Use of Amsler grid in high risk patients (Fig. 22.1)
Amsler grid.
Prognosis
Dry AMD progresses slowly and rarely causes blindness
Wet AMD may progress rapidly (blind in under 3 months) and accounts for 90% of AMD blind registrations. Sudden onset of distortion of central vision should prompt urgent referral
Bilateral disease—42% with wet AMD will develop this within 5 years
Prevention
Smoking is the most important modifiable risk factor
A diet rich in fruit and vegetables reduces risk
A combination of β-carotene, vitamins C and E, and zinc is effective in preventing severe visual loss in established moderate-severe AMD
A multicentre study showed that antioxidant vitamins halted progression of dry AMD in around 30% of patients
Management
Appropriate for subset of wet AMD only
Halts progression so early treatment is desirable
Fluorescein angiography should be done within a few days of onset of symptoms to determine the type and location of neovascular areas
Treatment options for neovascular AMD include:
Photodynamic therapy—this targets sub-foveal neovascular areas (whilst preserving normal retina) by using photosensitive drug (verteporfin) along with a non-thermal activating laser. Used in early disease, this therapy can slow or halt progression
Anti-angiogenic therapy—eg ranibizumab—a recombinant, humanized, monoclonal antibody that neutralizes all active forms of vascular endothelial growth factor A. NICE recommends its use for wet AMD under certain conditions (eg no permanent damage to the central fovea). The cost of ranibizumab beyond 14 injections in the treated eye is met by the manufacturer
Laser photocoagulation is sometimes used for extra-foveal lesions
Test one eye at a time
Usual reading glasses should be worn, and the grid held at comfortable reading distance
Ask the patient to look at the central spot, and not to look away
Assess the following:
Can all four corners of the grid be seen?
Are any of the lines missing, wavy, blurred, or distorted?
Do all of the boxes appear the same size and shape?
Any abnormalities may indicate macular pathology and should prompt referral to an ophthalmologist
The eye and systemic disease
Two of the top four causes for blind registration are due to systemic disease—diabetes and vascular disease. Eye disease develops as a late complication of prolonged poor control in both cases, and the important message is to strive to prevent these problems in the first place.
Diabetes
Causes retinopathy, cataracts, and ‘microvascular’ cranial nerve palsies.
Retinopathy
Associated with increasing duration of diabetes—at 20 years, 80% will have some retinopathy
All patients with diabetes require dilated annual screening (either photographic, or by appropriately trained professional). Direct ophthalmoscopy alone is inadequate
Appearance: microaneurysms, haemorrhages, (background retinopathy) progressing to cotton wool spots, blot haemorrhages and tortuous vessels (pre-proliferative retinopathy) then new vessels (proliferative retinopathy). Exudates and macular oedema are indicators of maculopathy
Early detection of problems (especially when near the macula) should prompt referral to an ophthalmologist. Sight-threatening retinopathy requires laser treatment to limit progression
▸A diabetic person diagnosed at age 70 may well live 20 years, so tight control is desirable. Meticulous control of diabetes and hypertension has been shown to reduce all complications including retinopathy.
Vascular disease
Affects the eye directly with hypertensive retinopathy, and more indirectly when cerebrovascular disease impacts on vision. Associated with ‘microvascular’ cranial nerve palsies
Early detection and control of risk factors for vascular disease will ameliorate this problem (see 
‘HOW TO . . . Protect your patient from another stroke’, p.195). Tight blood pressure control, smoking cessation, lipid lowering, diabetic control, and appropriate anti-platelet use should all be targeted at the older age group as aggressively as the younger patients
There is little in the way of treatment for the disease once it is established
Appearance: silver wiring, arteriovenous nipping, and arteriolar narrowing progressing to exudates, cotton wool spots, haemorrhages and papilloedema
Giant cell arteritis
See ‘Giant cell arteritis’, p.474.
Drugs and the eye
Many drugs that are frequently used in the older patient can cause ocular side effects. Older people are more vulnerable to developing side effects, but are least likely to report them (attributing it to part of getting older).
Direct toxicity
Chloroquine and hydroxychloroquine (used in treatment of rheumatoid arthritis and other connective tissue diseases as well as malaria) cause a toxic maculopathy in large prolonged doses
Phenothiazines used for a long time (to treat psychosis) may cause retinal damage
Tamoxifen (for breast cancer treatment) may cause maculopathy
Amiodarone (for arrhythmias) may cause cataracts
Ethambutol (anti-tuberculous) can cause optic neuritis and red/green colour blindness
Altering accommodation
Causes blurred vision
Antihistamines
Some antihypertensives
Decreasing pupil size
Causes less light accommodation.
Opiates
Miotic drops used for glaucoma
Steroids
Oral steroids over time can cause cataracts
Topical and oral steroids may raise the intraocular pressure
Eyelid disorders
Eyelids provide physical protection to the eyes and ensure normal tear film and drainage. Disorders are common in older people, are often uncomfortable and yet are under-recognized and under-treated.
Entropion
In-turning of the (usually) lower lid. Occurs as orbicularis muscle weakens with age (or with conjunctival scarring distorting the lid). Lashes irritate the eye and may abrade the cornea, causing red eye. Lubricants and taping of the eye may relieve symptoms. Surgery (under local anaesthesia) provides definitive correction.
Ectropion
Eversion of the eyelid. Occurs with orbicularis weakness, scarring of the periorbital skin or seventh nerve palsy. Distortion prevents correct drainage of tears and correct tear film, leading to watery eye with conjunctival dryness. Treat with ointment to protect conjunctiva. Surgery (local anaesthesia) corrects.
Ptosis
Drooping of upper eyelid. When severe can cover pupil and impair vision.
Causes: aponeurotic (defects in levator aponeurosis), mechanical (lid lesion, lid oedema), neurological (third nerve palsy—look for pupil and eye movement problems, Horner's syndrome), myogenic (congenital levator dystrophy, muscular dystrophies, myasthenia gravis, chronic progressive external ophthalmoplegia).
▸Do not ignore ptosis in older people—it may not be longstanding; look for signs of underlying disease.
Dry eyes
Common in older people as tear secretion diminishes. Eyes feel gritty, but are not red. Diuretics may exacerbate. Most common cause is blepharitis (inflamed lid margins with blocked meibomian gland orifices and crusting); usually worse in those with rosacea, eczema, and psoriasis.
Treat blepharitis with hot compresses (5min bd), lid massage (upwards towards lid margin lower lid, downwards towards lid margin upper lid, eyelid cleaning targeting the base of eyelashes at the lid margin (warm water ± baby shampoo on a cotton wool bud). Antibiotic ointment not usually required unless staphylococcal infection suspected. Treat dry eyes with artificial tears or ointment (gives considerable relief).
Eyelid tumours
Most common (90%) is basal cell carcinoma. Slow growing, non-metastasising but locally invasive. Often ignored by patient. More common in fairer skins after chronic sun exposure. Waxy nodule with telangiectatic vessels on surface and pearly rolled border (rodent ulcer) is usual appearance. Treatment is with surgical excision (Moh's micrographic surgery preserves most tissue and may be appropriate in some) or radiotherapy.
Varicella zoster infection
Facial shingles. Involvement of the ophthalmic division of the trigeminal nerve will cause vesicles and crusting periorbitally (see ‘Varicella zoster infection’, p.624).
