Chronic Visual LossA global and Australian perspective

Dr Nicholas Cheng (HMO2)

Worldwide Causes of Blindness and Visual Impairment

Key Facts•285 million visually impaired

▫ 39 million blind

▫ 246 million with low vision

•Major causes:▫ Uncorrected refractive error 42%

▫ Cataract 33%

▫ Glaucoma 2%

•90% live in the developing world

World Health Organisation. Visual Impairment and Blindness. June 2012. Available from http://www.who.int/mediacentre/factsheets/fs282/en/

80% of visual impairment can be avoided or cured

Worldwide Causes of Blindness and Visual Impairment

World Health Organisation. Global data on visual impairments 2010.. Available from http://www.who.int/blindness/GLOBALDATAFINALforweb.pdf

Who is this?

Australian Causes of Blindness and Visual Impairment

Eye Research Australia – Clear Insight. The economic impact and cost of vision loss in Australia. Available from http://www.cera.org.au/uploads/CERA_clearinsight.pdf

Case 1• Inspired by a recent ophthalmology lecture, you decide to

undertake a volunteering role with a non-profit eye health organisation.

• With the aid of an interpreter you interview your first patient.

• A 65yo man presents complaining of gradually increasing difficulty with both near and distance vision.

• He has been experiencing glare around lights and feels he needs stronger glasses.

• PHx: Type II diabetes, HTN

Cataract

Symptoms:•Slowly progressive over years

•Glare, haloes, worsening myopia

•Risk factors:▫ Daylight (UV), Degeneration (Age), Diabetes, Drugs

(cigs + steroids), Damage (Trauma)

▫ Congenital cataract – Autosomal dominant, birth trauma, maternal infection, galactosaemia

Signs: Lens opacity

Types of cataract

Batterbury M, Bowling B. Ophthalmology: An illustrated colour text. 3rd ed. Edinburgh: Churchill Livingstone; 2009.

Management of Cataract

Modern phacoemulsification cataract surgery•Timing depends on degree of functional impairment

•Sometimes medical indications such as visualising fundal pathology

•Preop evaluation▫ VA, screen lids/ocular adnexa, cornea, fundoscopy

Management of CataractModern Phacoemulsification Surgery

Management of CataractModern Phacoemulsification Surgery•Anaesthesia

▫ Majority LA + peribulbar/sub-Tenon block

▫ Can do GA or topical

•Intraop complications▫ Rupture of lens capsule

▫ IOL dislocation

▫ Choroidal rupture

•Postop complications▫ Most devastating is endophthalmitis – Wary of acute painful

red eye postop

▫ Posterior capsule opacification

Case 2• Still overseas, a family brings in a blind man asking if

anything can be done.

• The man describes recurrent episodes of red eye, irritation and mucopurulent discharge over many years taking days-weeks to resolve

Previously

Now

Chlamydial Conjunctivitis

•Symptoms: Chronic conjunctivitis – Subacute

•Signs: Mucopurulent discharge, Large follices predom in inferior fornix

•Ix: PCR•Rx: Azithromycin 1g single dose,

reportable disease

Trachoma•Chronic conjunctivitis•Common cause of blindness worldwide

and in Aboriginal communities of Australia

•Cxs:▫Cicatricial change with entropion,

trichiasis, dry eye and secondary corneal ulceration and scarring

•Rx: WHO SAFE – Surgery, Abx, Face washing, Enviro improvement

Case 3• You return home from your trip, exhausted but happy. No

more eyes for a while.• While discussing your trip with your aunt, she mentions

that she too is having some eye problems.• She has been noticing increasing difficulty reading the

newspaper, with distortion of the writing. Her distant vision seems to be ok though.

Age-Related Macular Degeneration (AMD)

Atrophic (Dry) AMD90%

Neovascular (Wet) AMD – 10%

Slowly progressive atrophy of photoreceptors, RPE and choriocapillaris

Choroidal neovascular membrane growing (CNV_ through Bruch’s membrane into retina

Symptoms

Gradual loss of central vision bilatMetamorphopsia

Rapid progression over weeksMetamorphopsiaBlurring of central vision

Signs Hyperpigmentation or depigmentation of RPEGeographic atrophy – choroid visibleMacular drusen

CNV – elevated lesionMacular oedema – from leakage

Ixs Fluoroscein angiography – window defect, unmasking of choroid

Fluoroscein angiographyOCT

Dry AMD

Drusen

Geographic atrophy

Geographic atrophy responsible for majority of visual loss

Wet AMD

Choroidal neovascular membrane

Wet AMD

Batterbury M, Bowling B. Ophthalmology: An illustrated colour text. 3rd ed. Edinburgh: Churchill Livingstone; 2009.

Age-Related Macular Degeneration (AMD) Management

Atrophic (Dry) AMD Neovascular (Wet) AMD

• Visual aids• AREDS Multi-vitamins• Monitoring • Lifestyle modification –

stop smoking

Anti-VEGF•Lucentis = Ranibizumab 0.5mg monthly•Avastin = Bevacizumab

Focal laser photocoagluationPhotodynamic therapy

Age-Related Macular Degeneration (AMD) Management

High-dose multivitamins•New Study AREDS2•No benefit in early AMD, but can retard progression in moderate to severe AMD•25% decreased progression over 5 years

Components•Beta carotene – Now could be substituted for lutein/zeaxanthin•Vitamin C•Vitamin E•Zinc oxide

Case 4• A 60yo woman initially presents to her optometrist

complaining of gradual worsening of her peripheral vision. The optometrist performs this test and refers her to you, her GP, for a referral to an ophthalmologist.

What is this test?

Case 4

•You are tempted to just write the referral, but glance up to see your direct ophthalmoscope in the corner of the room.

•You decide you will have a look at her fundus to see the cause of her problem.

MCQs

•Which of these can be used as mydriatics?▫Tropicamide 0.5%▫Phenylephrine▫Cocaine 10%▫Cyclopentolate ▫Atropine

Parasymp Antagonist – 2-6hours

Sympathetic Agonist

Sympathetic Agonist

Parapsymp Antagonist – 24hours

Parapsymp Antagonist – 7-14days

Case 4• You are tempted to just write the referral, but glance up to

see your direct ophthalmoscope in the corner of the room.

• You decide you will have a look at her fundus to see the cause of her problem.

GlaucomaEssentially a characteristic optic neuropathyTriad of:1.Raised IOP

▫ Normal IOP 10-21mmHg

2.Optic disc cupping – ▫ Normal <0.3 but variation, look for asymmetry ≥0.2

3.Peripheral field changes

Glaucoma

MiVision. Glaucomatous Discs. 2009. Available from http://www.mivision.com.au/the-optometrist-s-practitioner-patient-manual-glaucomatous-disc/

GlaucomaSymptoms:•Largely asymptomatic until late•Peripheral field loss•Risk factors:

▫ High IOP, Diabetes, Age, High myopia, Thin corneas, FHx, Sterioids

Evaluation:1.Fundoscopy

▫ Optic disc cupping – “ISNT” Inferior rim usually biggest

2.Tonometry▫ Raised IOP

3.Perimetry ▫ Visual field testing

Measuring IOPGoldmann tonometer (contact) Tonopen (contact)

Pneumotonometry (non-contact)

Anatomy of Glaucoma

Kanski JJ. Clinical ophthalmology: A systematic approach. 6th ed. Edinburgh; New York: Butterworth-Heinemann/Elsevier; 2007.

Name the structure

Trabecular meshwork (a+b)

Canal of Schlemm

MCQs

•Aqueous humor:1.Is produced by the ciliary processes2.Is produced by the trabecular meshwork3.Is produced by the canal of Schlemm4.Is responsible for glaucoma5.Exits the eye through the posterior

chamber

MCQs

•A man is worried about developing glaucoma, as his uncle has just been diagnosed. Which of the following is true?1.If he has a pressure IOP of 18mmHg he

cannot have glaucoma2.Field loss is confirmative of glaucoma3.A raised IOP is confirmative of glaucoma4.Visual loss in glaucoma is related to nerve

fibre damage

Glaucoma MysteriesOcular hypertension= Raised IOP without symptoms (visual field loss) or signs (optic disc cupping) of glaucoma

Normal tension glaucoma= Symptoms and signs of glaucoma without a rise in IOP

Pathogenesis of Glaucoma• Retinal ganglion cell death• Exact mechanism still

uncertain▫ Mechanical (high IOP) vs

Ischaemic vs Both• Mechanical

▫ Raised IOP directly damages nerve fibres

• Ischaemic:▫ Compromise of

microvasculature

US Pharmacist. An Overview of Glaucoma Management for Pharmacists. 2010. Available from http://www.uspharmacist.com/continuing_education/ceviewtest/lessonid/106698/

Types of Glaucoma1. Primary

▫ Open angle▫ Angle closure

2. Secondary▫ Open angle – eg. neovascular,

pigmentary3. Congenital

Types of Glaucoma1. Primary open angle

glaucoma (POAG) = Chronic – Most common

2. Primary angle closure glaucoma (PACG) = Acute

Kanski JJ. Clinical ophthalmology: A systematic approach. 6th ed. Edinburgh; New York: Butterworth-Heinemann/Elsevier; 2007.

Glaucoma ManagementAim: Either decrease production or increase drainage of aqueous humor1.Pharmacological - ABCPP

▫ Alpha-agonists

▫ Beta-blockers

▫ Carbonic anhydrase inhibitors

▫ Prostaglandins

▫ Parasympathetic agonists

2.Surgical▫ Trabeculoplasty

▫ Trabeculectomy

Glaucoma Management - PharmDrug Class Mechanism Examples SEs

Prostaglandins ↑ outflow (uveoscleral)

• Latanoprost = Xalatan

• Traveprost = Travatan

• Brimatoprost = Lumigan

• Eyelash growth• Transient red eyes• Increased Iris

pigmentation

β-blockers ↓ production Non specificTimolol = Timoptol β1 specific Betaxolol = Betoptic

Resp•Asthma/COPDCVS•Bradycardia, heart block

Adrenergic agonists

↓ production↑ outflow (uveoscleral)

Brimonidine = Alphagan • Red eye• Dry mouth• Tiredness, Drowsy

Parasympathetic agonist

↑ outflow (trabecular)

Pilocarpine MiosisHeadacheReduced peripheral visionReduced night vision

Carbonic anhydrase inhibitors (CAIs)

↓ production Acetozolamide (Diamox)Brinzolamide (Azopt)

• ParaesthesiaGIT• Anorexia• DiarrhoeaRenal• HypoK• Metabolic acidosis

Glaucoma Management - SurgicalLaser Trabeculoplasty

•Laser to trabecular meshwork to increase outflow

Trabeculectomy

•Surgical fistula between anterior chamber angle and sub-Tenon’s space

•Creation of drainage bleb

Case 5

Diabetic RetinopathyDiabetic Retinopathy Hypertensive Retinopathy

Keith-Wagener-Barker ClassificationBackground Retinopathy1.Microaneurysms 2.Dot and Blot Haemorrhages (intraretinal)3.Flame haemorrhages (nerve fibre layer)4.Hard exudates (chronic retinal oedema)

Grade 1 – Mild to moderate narrowing or sclerosis of arterioles

1. Copper / Silver wiring (focal constriction + sclerosis of arterioles)2. Arteriolar narrowing

Pre-Proliferative Retinopathy = Infarction1.Cotton wool spots (nerve fibre layer infarcts)2.Venous beading (2 of 4 quadrants)3.IRMAs – arteriovenous shunts

Grade 2 – Moderate to marked narrowing of arterioles1.AV nipping2.Exaggerated light reflex

Proliferative Retinopathy1.New vessels at disc (NVD)2.New vessels elsewhere (NVE)

Grade 3 – Retinal arteriolar narrowing and focal constriction1.Retinal haemorrhages (flame haemorrhages)2.Cotton wool spots3.Retinal oedema

Maculopathy1.Background retinopathy at the macula2.Macular oedema

Grade 41.Papilloedema

Advanced Disease1.Rubeosis iridis2.Vitreous haemorrhage3.Retinal detachment

Background DRMicroaneurysms

Dot and blot haemorrhages

Flame haemorrhages

Glycosmedia. Diabetic retinopathy. 2000. Available from http://www.glycosmedia.com/education/diabetic_retinopathy/aims.php

Pre-proliferative DRCotton wool spots Venous changes

Glycosmedia. Diabetic retinopathy. 2000. Available from http://www.glycosmedia.com/education/diabetic_retinopathy/aims.php

Proliferative DRNew vessels at the disc (NVD)

New vessels elsewhere (NVE)

MCQs

•What is the most common cause of visual disability in diabetics?1.Macular ischaemia2.Vitreous haemorrhage3.Macular oedema4.Glaucoma5.Retinal detachment

MaculopathyMacular oedema + hard exudate

Angiogram

Maculopathy

Normal OCT Macular oedema

Diabetic RetinopathyRisk Factors:•Duration of diabetes, poor metabolic control, HTN

▫ After 10 years – 50% DR▫ After 30 years – 90% DR

Pathogenesis:•Microangiopathy

▫ Microvascular occlusion and leakage▫ Subsequent neovascularisation

Diabetic Retinopathy NHMRC GuidelinesScreening

All patient with diabetes

•At diagnosis and at least every 2 years

High risk patients without DR (long duration, poor control, HTN, hyperlipid)

•Screen annually

Patient with NPDR

•Screen 3-6 monthly

Diabetic Retinopathy ManagementGeneral

•Good glycaemic control, control HTN, hyperlipidaemia

•Regular screening

Severe preproliferative DR / Proliferative DR

•Pan-retinal photocoagulation

Macular oedema

•Focal argon laser photocoagulation

•New treatments: anti-VEGF (Lucentis = ranibizumab, Avastin = bevacizumab) in sub-population (central retinal thickness >400microm) NICE Guidelines

Diabetic Retinopathy Management

PRPFocal laser

Case 6

• 29yo man presents with difficulty seeing at night, and feeling he is losing peripheral vision

Retinitis Pigmentosa• Retinal dystrophy affecting rods more than cones• Prevalence 1:5000• Hereditary - Can be AD, AR, X-linked• Sxs:

▫Bilateral loss of peripheral vision▫Difficulty with night vision▫Glare (cataract)

• Ex: Triad of:▫Arteriolar attenuation▫Bone-spicule pigmentation – RPE changes▫Waxy disc pallor

Retinitis Pigmentosa• Mx:

▫ No current cure▫ Supplemental Vit A may retard progression▫ Bionic Eye

SUMMARY•Chronic visual loss causes a high burden

globally•Predominant causes of chronic visual loss

vary across the world▫AMD, DR, Glaucoma, Cataract in developed world▫Cataract, refractive error, corneal opacities in

developing world•Exciting new treatments for previously

untreatable conditions▫Anti-VEGF▫Bionic Eye

Extra Slides

Case 4LE R

E

Medrounds. Peripheral vision. 2006. Available from http://www.medrounds.org/glaucoma-guide/2006/08/section-6-d-peripheral-vision-visual.html

Sxs: Headache, nausea, vomiting, Pain +++, Blurred vision, haloes

Acute Angle Closure Glaucoma

•Signs: VA 6/60 – Think outside in▫Cornea – cloudy

▫Anterior chamber – shallow, aqueous flare and cells

▫Pupil - mid-dilated non-reacting

▫High IOP

•Rx: Acetozolamide 500mg IV or PO, topical timolol 0.5%, pilocarpine 1%

•Definitive Rx: YAG laser iridotomy