Chronic Visual Loss A global and Australian perspective Dr Nicholas Cheng (HMO2)
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Transcript of Chronic Visual Loss A global and Australian perspective Dr Nicholas Cheng (HMO2)
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Chronic Visual LossA global and Australian perspective
Dr Nicholas Cheng (HMO2)
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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
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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
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Who is this?
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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
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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
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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
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Types of cataract
Batterbury M, Bowling B. Ophthalmology: An illustrated colour text. 3rd ed. Edinburgh: Churchill Livingstone; 2009.
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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
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Management of CataractModern Phacoemulsification Surgery
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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
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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
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Chlamydial Conjunctivitis
•Symptoms: Chronic conjunctivitis – Subacute
•Signs: Mucopurulent discharge, Large follices predom in inferior fornix
•Ix: PCR•Rx: Azithromycin 1g single dose,
reportable disease
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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
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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.
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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
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Dry AMD
Drusen
Geographic atrophy
Geographic atrophy responsible for majority of visual loss
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Wet AMD
Choroidal neovascular membrane
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Wet AMD
Batterbury M, Bowling B. Ophthalmology: An illustrated colour text. 3rd ed. Edinburgh: Churchill Livingstone; 2009.
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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
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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
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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?
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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.
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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
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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.
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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
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Glaucoma
MiVision. Glaucomatous Discs. 2009. Available from http://www.mivision.com.au/the-optometrist-s-practitioner-patient-manual-glaucomatous-disc/
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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
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Measuring IOPGoldmann tonometer (contact) Tonopen (contact)
Pneumotonometry (non-contact)
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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
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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
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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
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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
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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/
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Types of Glaucoma1. Primary
▫ Open angle▫ Angle closure
2. Secondary▫ Open angle – eg. neovascular,
pigmentary3. Congenital
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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.
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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
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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
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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
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Case 5
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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
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Background DRMicroaneurysms
Dot and blot haemorrhages
Flame haemorrhages
Glycosmedia. Diabetic retinopathy. 2000. Available from http://www.glycosmedia.com/education/diabetic_retinopathy/aims.php
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Pre-proliferative DRCotton wool spots Venous changes
Glycosmedia. Diabetic retinopathy. 2000. Available from http://www.glycosmedia.com/education/diabetic_retinopathy/aims.php
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Proliferative DRNew vessels at the disc (NVD)
New vessels elsewhere (NVE)
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MCQs
•What is the most common cause of visual disability in diabetics?1.Macular ischaemia2.Vitreous haemorrhage3.Macular oedema4.Glaucoma5.Retinal detachment
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MaculopathyMacular oedema + hard exudate
Angiogram
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Maculopathy
Normal OCT Macular oedema
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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
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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
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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
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Diabetic Retinopathy Management
PRPFocal laser
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Case 6
• 29yo man presents with difficulty seeing at night, and feeling he is losing peripheral vision
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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
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Retinitis Pigmentosa• Mx:
▫ No current cure▫ Supplemental Vit A may retard progression▫ Bionic Eye
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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
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Extra Slides
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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
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Sxs: Headache, nausea, vomiting, Pain +++, Blurred vision, haloes
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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