Eyes
Age-Related Changes
1. Eyes appear sunken due to loss of periorbital fat.
2. Arcus senilis (deposition of calcium and cholesterol salts in a ring at the edge of the cornea) is common but not clinically significant.
3. The muscles in the iris weaken so the pupil becomes small (miosis) and less light reaches the retina. The pupil is slow to react to light and accommodation becomes impaired.
4. Dark adaptation slows because of the reduced rate of regeneration of rhodopsin.
5. The sclera appears more yellow due to dehydration and lipid deposition.
6. The conjunctiva contains fewer mucus-secreting cells so becomes drier. Conjunctival vessels are more fragile leading to conjunctival haemorrhages.
7. The vitreous contains more floaters and cholesterol deposits. It may become more liquid, increasing the risk of retinal detachment.
8. Presbyopia, the deterioration of vision with age, occurs because the lens becomes inelastic, so that focusing on near objects becomes difficult.
9. Entropion (in-turned lashes) is common and causes irritation of the cornea. It must be corrected surgically to avoid corneal damage.
10. Ectropion (out-turned lashes) is very common and the most frequent cause of epiphora (watery eye). Again, this can be surgically corrected. The everted eyelid can be mistaken for ‘red eye’.
Examination of the Fundus in Old Age
Age-related miosis can make it difficult to examine the fundi of older people. Short-acting eye drops are recommended, usually tropicamide 0.5% (rapid onset and effects last 4–6 h). Reversal with pilocarpine is usually unnecessary and can be painful. The risk of acute closed-angle glaucoma is minimal, but beware the small eyeball with a shallow anterior chamber and small-diameter cornea.
Loss of Vision
Approximately 70,000 persons over the age of 65 years in the UK are registered as partially sighted, i.e. about 1% of the elderly population. Figure 15.1 lists the causes of blindness in older people. Many more are visually disabled but remain unregistered. Registration of disability is essential for special benefits and visual aids.
Figure 15.1 Causes of blindness in old age. Source: ABPI (1991) The Challenges of Ageing. ABPI, London.
Criteria for being Registered Blind/Partially Sighted
- Severely sight impaired/blind:
Visual acuity (VA) of less than 3/60 with a full visual field.
VA between 3/60 and 6/60 with severe field reduction, such as tunnel vision.
VA of 6/60 or above, but with a much reduced field of vision, especially in the lower part of the field.- Sight impaired/partially sighted:
VA of 3/60 to 6/60 with a full field of vision.
VA of up to 6/24 with a moderate reduction of field of vision or central vision that is blurry.
VA of up to 6/18 if a large part of the field, for example a whole half field or a lot of peripheral vision, is missing.Causes of visual impairment
Slow loss:
• Age-related macular degeneration, 45%: central vision is lost but peripheral vision is maintained.
• Cataracts, 33%.
• Retinopathy (diabetes mellitus), 17%.
• Open-angle glaucoma (chronic), 15%: central vision is maintained until late in the disease.
Sudden loss:
• Acute glaucoma.
• Vitreous haemorrhage, more common in diabetics.
• Central retinal artery occlusion, secondary to embolus from carotid bifurcation or mitral valve.
• Venous occlusion: more common in patients with hypertension or hyperviscosity.
• Retinal detachment.
• Ischaemic optic atrophy, secondary to giant-cell arteritis or atherosclerosis.
NB: If one eye is affected, the other is at risk.
Advantages of being Registered Blind
- Fifty percent reduction in television licence fee; free for over 75s anyway!
- Blue badge scheme for the driver.
- Free eye tests; free for over 60 year olds anyway.
- Free loan of equipment from Low Visual Aid clinics.
The Painful Eye
1. Closed-angle glaucoma (acute).
2. Infection:
Conjunctivitis.
Uveitis.
Herpes zoster: when the ophthalmic branch of the facial nerve is affected, there may be involvement of the forehead, eyelids and conjunctiva. The patient must see an ophthalmologist urgently.
Conjunctivitis. Uveitis. Herpes zoster: when the ophthalmic branch of the facial nerve is affected, there may be involvement of the forehead, eyelids and conjunctiva. The patient must see an ophthalmologist urgently.3. Trauma, e.g. corneal abrasion or a foreign body.
Primary Open Angle/Chronic Glaucoma
- A silent and progressive disease which may result in blindness if not treated.
- Accounts for 15% of blindness fulfilling criteria for registration in the UK.
- Risk factors include increasing age, family history, African or Caribbean descent, diabetes, myopia and hypertension.
- There may be cupping and atrophy of the optic disc.
- Early cases are best detected by regular eye tests, with ocular-pressure measurement.
- Affects peripheral vision first, only affecting central vision late in the disease.
- May affect one eye more than the other.
- Treatment is aimed at reducing the intraocular pressure:
Once daily prostaglandin agonists give excellent results, e.g. latanaprost. Intraocular pressure is reduced by increased drainage of aqueous humour via the trabecular meshwork.
Beta-blockers, e.g. timolol eye drops and alpha2 adrenergic agonists, e.g. brimonidine eye drops, reduce the production of aqueous humour by the ciliary body.
Carbonic anhydrase inhibitors act on the carbonic anhydrase in the ciliary body, e.g. dorzolamide. They are less effective than other treatments so are often used as adjuncts.
Educate the patient about the efficacy of treatment and the high risk of blindness without it, to engage them in persevering with eye drops for life.- If treatment with eye drops fails, trabeculoplasty with an argon laser or surgical trabeculectomy will improve aqueous flow.
Acute Glaucoma
- Less common than chronic glaucoma.
- More common in females because the anterior chamber is more shallow.
- Most common in 6th and 7th decades.
- Easier to detect because it presents with sudden painful loss of vision in a red eye.
- Often associated with ipsilateral headache and vomiting.
- The patient may describe haloes around lights secondary to corneal oedema.
- The patient may report a precipitating event such as exposure to very dim light or mydriatic treatments such as anticholinergics and sympathomimetics.
- The pupil is mid-dilated and non-reactive.
- Visual acuity is reduced.
- Slit lamp examination may show corneal oedema and an irregular pupil.
- The intraocular pressure will be increased.
- Emergency treatment is IV and oral acetazolamide or IV mannitol plus topical beta-blocker eye drops. Steroid drops reduce inflammation.
- Analgesia and anti-emetics reduce the distress of the patient which also helps reduce the pressure.
- Laser iridotomy reduces the pressure acutely.
Table 15.1 Summary of differences between acute and chronic glaucoma
| Acute – closed-angle | Chronic – open-angle | |
| Symptoms | Sudden pain in eye, blurred vision, vomiting and prostration | Insidious loss of vision, leading to tunnel vision; family history common |
| Signs | Painful red eye with reduced vision. Eye tense, irregular fixed pupil, cornea and conjunctiva congested | Painless normal looking eye. |
| Raised pressure on tonometry, scotoma on field testing; cupped disc | ||
| Pathology | Sudden impairment of anterior-chamber drainage – may be precipitated by anticholinergics and mydriatics | Gradual increase in intraocular pressure – idiopathic |
| Treatment | Constrict pupil, analgesia, carbonic anhydrase inhibitor – urgent action needed | Prostaglandin, beta-blocker and/or pilocarpine drops, drainage operation |
Table 15.1 summarizes the differences between acute and chronic glaucoma.
Age-Related Macular Degeneration (AMD)
- Affects people aged 50 and over, and becomes more common with advancing age.
- The most common cause of visual impairment in the industrialized world.
- Affects 1.5 million people in the UK currently, and predicted to rise to 1.9 million by 2020 because of the ageing population.
- As the macula is the area damaged, central vision is affected more, with peripheral vision being preserved.
- Loss of central vision means loss of face recognition and difficulty reading.
- AMD is usually bilateral, but may affect one eye earlier or more than the other.
- Age-related maculopathy: mild or moderate non-exudative changes in the macula.
Risk factors for AMD
Increasing age
Female preponderance
Positive family history
Smoking (inhibits complement factor H)
Hypertension
White ancestry, especially with light-coloured eyes
Obesity
Cataract surgery
Sun exposure
Diet low in vitamins A, C and E, and zinc
AMD is divided into two broad types:
1. ‘Dry’ or non-exudative AMD, characterized by atrophic and hypertrophic changes and drusen (yellow extracellular deposits of proteins, lipids and debris) in the retinal pigment epithelium (RPE) underlying the macula.
- Develops slowly over months or years.
- No treatment, but encourage to stop smoking; some evidence that antioxidant supplements (vitamins A, C and E with zinc and copper) may be protective.
- Geographic atrophy (patchy loss of RPE cells) may signal development of wet AMD.
- Ten to twenty percent of patients progress to the wet type.
2. Wet AMD or exudative AMD, characterized by choroidal neovascularization. Tissue hypoxia stimulates the release of vascular endothelial growth factor (VEGF). This in turn stimulates the production of new vessels growing into the choroid which are fragile and ‘leaky’.
- More rapidly progressive and causes more visual impairment.
- New treatments have been developed to inhibit VEGF: pegaptanib sodium (a direct antagonist) and ranibizumab (a monoclonal antibody). Both are given as monthly intraocular injections and need to be continued for at least 2 years to preserve vision. ‘Rationing’ of these expensive treatments by imposing strict eligibility criteria (likely to increase in the current economic climate) creates controversy,
- NICE (2011) only recommended ranibizumab. Criteria for treatment include best corrected vision 6/12 and 6/96, no permanent structural damage of fovea (central macula), lesion less than 12 disc areas, evidence of disease progression and response to initial treatment.
- Side-effects: conjunctival haemorrhage, eye pain, vitreous floaters, vitreous haemorrhage, retinal detachment and increased intraocular pressure.
- Ranibizumab improves vision in 40% of cases and prevents further deterioration of sight in most patients.
- NICE supports photodynamic therapy for wet AMD with definite choroidal neovascularization. Verteporfin (a light-sensitive drug given intravenously) sticks to the new vessels and is activated using a cold laser to seal the vessels.
- Exciting developments in the genetics of AMD point to a single nucleotide polymorphism in complement factor H (CFH) gene on chromosomes 1 and 10. CFH is an inhibitor of the complement pathway and abnormal CFH leads to inflammation.
- If vision is severely impaired, refer to the Low Vision Service.
Table 15.2 summarizes the differences between dry and wet AMD.
Table 15.2 Differences between dry and wet AMD
| Dry AMD | Wet AMD | |
| Frequency | 80–85% | 10–15% |
| Symptoms | Asymptomatic until late stage | Rapid loss of central vision over days to weeks |
| May notice loss of central acuity | Metamorphopsia | |
| Peripheral vision preserved | Decreased colour and contrast sensitivity | |
| Sudden deterioration of vision suggests progression to wet AMD | Slow dark adaptation | |
| Appearance | Focal hyperpigmentation, drusen, geographic atrophy | Larger more confluent drusen, more pigmentation and new vessels, scarring |
| Management | Stop smoking | Intravitreal ranibizumab |
| Increase dietary antioxidants | Photodynamic therapy |
Driving
- Legally, the patient must be able to read a car registration plate at 20 m, in good light with glasses if appropriate.
- A patient with visual field defects, regardless of cause (e.g. glaucoma, stroke or pituitary disease), should not drive unless allowed by the ophthalmologist.
Cataracts
- So called because the world appears blurred as if seen behind a waterfall.
- Arise because of protein breakdown and dehydration of the lens.
- Are very common and easily detected and corrected, resulting in marked improvement of quality of life.
- In the USA 300,000–400,000 cases occur annually.
- Responsible for around 36% of cases of blindness in Africa.
- Short-sighted patients may report an improvement in near vision (‘second sight’) because progression temporarily increases the power of the lens. As the cataract progresses further, near vision is lost again.
- Other visual problems include reduced contrast sensitivity and increased glare from daylight or car headlights at night.
Types
1. Central – early visual loss.
2. Peripheral – late visual loss and vision impaired by scattering of bright light.
Multifactorial pathogenesis.
Causes
- Ageing.
- Hereditary.
- Diabetes mellitus.
- Hypertension.
- Iatrogenic, e.g. steroids.
- Alcohol.
- Environmental – bright sunshine (increased incidence in the tropics).
- Nuclear cataracts seem to be related to smoking.
Examination
Thorough assessment of both eyes is essential to exclude problems, e.g. AMD which will not be resolved by cataract extraction, to ensure a good outcome from surgery. This includes acuity, fields, assessment of pupillary reflexes, indirect and direct ophthalmoscopy and slit lamp examination.
Treatment
Surgery
Timing depends on individual need, e.g. earlier in those who read a lot, but may be delayed in those whom the distortion, change in magnification and reduced visual fields caused by wearing glasses post-operatively would be a hindrance.
Contraindications
1. Early stages.
2. Where vision is compromised by other ocular co-morbidities such as AMD or severe retinopathy.
3. In the presence of severe mental impairment.
4. Avoid oral alpha-blockers such as tamsulosin in the month prior to cataract surgery to avoid ‘floppy iris’ syndrome.
Surgical Procedure
- Usually done as a day case under local anaesthetic.
- The anterior chamber of the eye is incised. Phacoemulsification is the process of fragmenting the opacified lens by ultrasound. This debris is removed, leaving the lens capsule intact. An artificial lens is inserted into the capsule.
- The power of the new lens is selected to optimize vision so that the patient does not have to wear thick aphakic spectacles.
Complications of Treatment
1. Dilatation of the pupil may precipitate glaucoma.
2. Lens implant: possible failure and risk of infection.
3. Posterior capsular opacification: may occur several months after the cataract extraction and is treated by Yittrium Aluminium Garnet (YAG) laser capsulotomy.
Giant-Cell Arteritis (GCA)
See also Chapter 9.
Clinical Features
1. This is a vision-threatening disease: a systemic vasculitis of large and medium sized arteries. Arteritis affecting the posterior ciliary arteries can cause ischaemic optic neuropathy leading to blindness.
2. May present with loss of vision which is sometimes transient (amaurosis fugax), or with abnormal purple vision (photopsia).
3. Associated with headache, usually localized to the temples, plus scalp tenderness when combing the hair. Jaw ache when chewing secondary to ischaemia of the masseter muscles, occipital headache secondary to occipital artery claudication, or more rarely tongue claudication also occur.
4. The patient is often systemically unwell and febrile.
5. Often overlaps with polymyalgia rheumatica: proximal limb girdle ache, early morning stiffness.
6. Fundus examination is usually normal, but if there is visual loss, it may reveal a pale swollen optic nerve head.
7. Diagnosis is supported by a raised ESR and CRP and confirmed by temporal artery biopsy (ultrasound of the temporal artery improves the diagnostic yield).
8. Alkaline phosphatase is often elevated.
9. The histology remains characteristic of GCA for up to 4 weeks after commencing steroids, so do not wait for biopsy result before treating.
10. The treatment is high-dose oral steroids: 1 mg/kg.
11. Evidence suggests that co-prescribing aspirin 75 mg for the first month reduces the increased risk of stroke associated with inflammation.
12. The disease often lasts for up to 2 years. The steroids should be weaned down slowly according to the clinical picture and fall in ESR and CRP.
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