1 / 48

Eye Problems in General Practice

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.

jacob
Download Presentation

Eye Problems in General Practice

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Eye Problems in General Practice MR Besharati MD Shahid Sadoughi University

  2. Topics to be discussed • Lacrimal disorders • Blepharitis • Degenerative changes of cornea and sclera • Age related maculopathy • Hypertensive eye disease • Cataract • Glaucoma • Diabetic eye disease

  3. Lacrimal system • Stable tear film essential for maintenance corneal clarity • Nutritional and protective functions • Deficient tear film causes corneal and conjunctival damage

  4. 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

  5. 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

  6. 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

  7. Treatment ‘dry eye’ • Artificial tear drops • Simple eye ointment at night (prolonged lubrication) • Acetylcysteine eye drops useful if filamentary keratitis • Treat associated blepharitis

  8. 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

  9. ‘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

  10. 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

  11. 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

  12. Corneal degeneration • Arcus senilis occurs in 60% patients aged 50 and nearly all over 80 • Vogt’s white limbal girdle • Lipid keratopathy • Band keratopathy

  13. 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

  14. 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

  15. 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

  16. 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

  17. 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

  18. 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

  19. 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)

  20. 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

  21. 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

  22. Hypertensive eye disease • Severity of hypertension • degree of hypertensive vascular change • retinopathy • Duration of hypertension • degree of arteriosclerotic vascular change • retinopathy

  23. 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

  24. 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

  25. 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

  26. Cataract • A common cause of visual loss • Most important cause of blindness worldwide • Lens opacification

  27. 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)

  28. Signs of cataract • Reduction in acuity (unilateral/bilateral) • Diminished red reflex • Change in appearance of lens

  29. Types of cataract • Senile • Traumatic • Metabolic • Toxic • Secondary • Hereditary

  30. Treatment of cataract • No effective medical treatment • Decision to operate is a quality of life issue • Various surgical options

  31. 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

  32. 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

  33. 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

  34. 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

  35. 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)

  36. Diabetic eye disease • Background retinopathy • Maculopathy • Proliferative retinopathy

  37. Diabetic background retinopathy • Blot haemorrhages • Hard exudates • Vision normal

  38. Diabetic Maculopathy • Hard exudate at fovea • Vision irreversibly damaged

  39. 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

  40. 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

  41. 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

More Related