Eye Problems in General Practice

MR Besharati MD

Shahid Sadoughi University

Topics to be discussed

• Lacrimal disorders

• Blepharitis

• Degenerative changes of cornea and sclera

• Age related maculopathy

• Hypertensive eye disease

• Cataract

• Glaucoma

• Diabetic eye disease

Lacrimal system

• Stable tear film essential for maintenance corneal clarity

• Nutritional and protective functions

• Deficient tear film causes corneal and conjunctival damage

Tear film• Superficial lipid layer derived

from meibomian glands• Aqueous tears derived from

lacrimal gland contain immunoglobulins and lysozyme

• Thin mucus layer created by goblet cells allow adherence aqueous tears to cornea

• Tears flow from lacrimal gland to lacrimal puncta mainly along lower lid margin

• Upper lid has essential function in applying mucus to corneal surface and ensuring even spread of tears

Lacrimal system – ‘dry eye’

• Keratoconjunctivitis sicca = aqueous tear deficiency

• Common in elderly• Chronic gritty sensation,

eyes not unduly red, stringy mucus, transient blurred vision

• Associated with systemic disease eg RA

• Associated with drugs – especially diuretics

Investigation of ‘dry eye’

• Tear film break up time (BUT)

• Rose bengal staining• Schirmer’s test –

absorbent paper strips placed in lower fornix, <10 mm wet in 5 minutes = deficiency

Treatment ‘dry eye’

• Artificial tear drops• Simple eye ointment

at night (prolonged lubrication)

• Acetylcysteine eye drops useful if filamentary keratitis

• Treat associated blepharitis

Lacrimal disorders – ‘watering eye’

• Tears are produced by lacrimal glands

• Flow along lid margins, spread by blinking

• Enter upper and lower puncta to lacrimal sac

• Flow down nasolacrimal duct to nose

‘watering eye’

• Excessive production of tears – can be paradoxical in dry eyes

• Punctal malposition• Punctal stenosis• Blockage of lacrimal sac

or nasolacrimal duct – syringing, -dacrocystorhinostomy

Blepharitis

• Generalised eyelid inflammation– Staphylococcal or

seborrheic dermatitis

• Itchy red burning eyelid margins

• Scales on lashes and crusty secretions on lids

• Recurrent and may be associated with bacterial conjunctivitis

Blepharitis

• Regular cleaning– Apply hot wet flannel

firmly against closed eye – Use moistened cotton

wool bud to wipe away secretions

• Local antibiotic –chloramphenicol or fusidic acid

• Add 1% hydrocortisone if persistent inflammation

Corneal degeneration

• Arcus senilis occurs in 60% patients aged 50 and nearly all over 80

• Vogt’s white limbal girdle

• Lipid keratopathy• Band keratopathy

Age-related macular degeneration

• Leading cause of blindness in over 50s

• Over ½ million people in UK affected by AMD

• 190,000 new cases AMD in UK per year

What is AMD?

• Degenerative condition of central retina

• Dry AMD (85%) – atrophic form

• Wet AMD responsible for 15% sufferers but 90% blindness – neovascular form with new abnormal vessels at the macula

• High risk of second eye involvement within 5 years of first

AMD – risk factors

• Age (wet AMD usually presents in patients over 50)

• Genetics – hereditary link. Screening of blood relatives has debatable value

• Race/gender – white females• Smoking increases wet and dry

AMD• Hypertension• Post-menopausal women not on

HRT more likely to develop neo-vascularisation

AREDS (Age Related Eye Disease Study)

• Performed by National Eye Institute

• Antioxidants including Vit A and Vit E

• Zinc and copper• Beneficial in

preventing progression to sight-threatening AMD

Dry AMD• 85% cases

• Slow progression, not usually severe

• Difficulty with reading and fine visual tasks

• Distortion and metamorphosia uncommon

• Drusen, pigmentation and atrophy of retina

• No proven treatment

• Low vision services helpful

Wet AMD

• 15% cases• More severe, rapid visual loss,

3-6 months if untreated• Choroidal neovascularisation –

abnormal vessels leak fluid into macula, causing retinal surface to become uneven with blurring and distortion of central vision

• Scar tissue creates irreversible blind spots

AMD - symptoms

• Recent change in visual function, in particular ability to read, recognise faces, difficulty with changing light conditions

• On waking, dark patch in vision which quickly fades

• Distortion of the shape of familiar objects especially kinking of lampposts/windows (and not double vision or ghosting associated with cataract)

AMD -Signs

• Decreased acuity with Snellen chart

• No improvement in acuity with pinhole (in macular disease)

• Amsler grid testing

• Fundoscopy – subretinal fluid, exudate, haemorrhage or pigment epithelial elevation

Rehabilitation• Provision and training in use of

optical aids

• Increase wattage of household bulbs

• Mark cooker controls with tactile dots etc

• Registration as blind or partially sighted in order to access local social support

• Put in touch with community voluntary services or relevant support groups

Hypertensive eye disease

• Severity of hypertension– degree of hypertensive

vascular change

– retinopathy

• Duration of hypertension– degree of arteriosclerotic

vascular change

– retinopathy

Hypertensive features

• Characterised by vasoconstriction and leakage

• Diffuse arteriolar narrowing

• Focal arteriolar narrowing• Severe hypertension may

lead to obstruction of precapillary arterioles and cotton-wool spot formation

Hypertensive features

• Abnormal vascular permeability leads to haemorrhages, retinal oedema and hard exudates

• Deposition of hard exudates around the fovea may lead to their radial distribution as a macular star

• Swelling of the nerve head occurs in malignant hypertension

Arteriosclerotic features

• Thickening of vessel wall with hyaline degeneration and narrowing of the lumen

• Arteriovenous crossing change / AV nipping

• Copper wiring

• Silver wiring – heightened reflex from opaque arterioles

Cataract

• A common cause of visual loss

• Most important cause of blindness worldwide

• Lens opacification

Symptoms of cataract

• Difficulty reading

• Vision worsens in bright light (especially with central opacity)

• Monocular diplopia

• Haloes around lights

• Improved near vision (nuclear sclerotic cataract can improve converging power of lens)

Signs of cataract

• Reduction in acuity (unilateral/bilateral)

• Diminished red reflex• Change in appearance

of lens

Types of cataract

• Senile • Traumatic• Metabolic• Toxic• Secondary• Hereditary

Treatment of cataract

• No effective medical treatment

• Decision to operate is a quality of life issue

• Various surgical options

Chronic open angle glaucoma

• Uncommon under age 40

• Major cause of blindness in the elderly

• Asymptomatic

• Gradual and painless visual loss

• Central vision preserved until late in the disease progression

Signs of glaucoma

• Raised intraocular pressure ( >21 mmHg)

• Pathological cupping of optic disc – gradual loss of nerve fibres at disc resulting in a pale disc with an enlarged cup

• Visual field loss

Causes of chronic open angle glaucoma

• Impairment of aqueous outflow from the anterior chamber of the eye

• Caused by alteration in function of trabecular meshwork overlying canal of Schlemm

• Aetiology unknown- indirect ischaemic theory and direct mechanical theory

• Familial tendancy

Medical treatment

• Pilocarpine drops 1-4% – act via ciliary muscle to open drainage channels

• Adrenaline drops 0.5-2% increase outflow aqueous humour

• Timolol drops 0.25-0.5 % and other beta blockers reduce aqueous humour production

• Acetozolamide capsules 250 mg reduce rate aqueous humour production

Laser / surgical options

• Laser trabeculoplasty – laser burns to trabecular meshwork result in increased aqueous flow

• Surgical drainage eg trabeculectomy – portion of sclera adjacent to the cornea is removed to create a fistula

• Long –term monitoring with applanation tonometry (= pressure gauge) and perimetry(=field testing)

Diabetic eye disease

• Background retinopathy

• Maculopathy• Proliferative

retinopathy

Diabetic background retinopathy

• Blot haemorrhages• Hard exudates

• Vision normal

Diabetic Maculopathy

• Hard exudate at fovea

• Vision irreversibly damaged

Diabetic proliferative retinopathy

• New vessel formation at optic disc in response to ischaemia

• Irreversible reduction in visual acuity

• Risks of vitreous haemorrhage and retinal detachment

Goals for treatment

• Good diabetic control can prevent new vessel formation

• Concurrent diseases such as hypertension, renal disease, anaemia, hyperlipidaemia, can accelerate retinopathy and need to be treated

• Pre-symptomatic screening and early photocoagulation

Screening for diabetic retinopathy

• Allows laser photocoagulation to be used for maculopathy and proliferative retinopathy

• May be done by regular eye examination

• Increasing use of retinal photography

• ?? Retinal photography in primary care