Chronic Visual Loss
A 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%
80% of visual
impairment can be
avoided or cured
▫ 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/
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 Cataract
Modern Phacoemulsification Surgery
Management of Cataract
Modern 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) AMD
90%
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 bilat
Metamorphopsia
Rapid progression over weeks
Metamorphopsia
Blurring of central vision
Signs
Hyperpigmentation or
depigmentation of RPE
Geographic atrophy – choroid
visible
Macular drusen
CNV – elevated lesion
Macular oedema – from leakage
Ixs
Fluoroscein angiography – window
defect, unmasking of choroid
Fluoroscein angiography
OCT
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
•
•
•
•
Visual aids
AREDS Multi-vitamins
Monitoring
Lifestyle modification – stop
smoking
Neovascular (Wet) AMD
Anti-VEGF
• Lucentis = Ranibizumab 0.5mg
monthly
• Avastin = Bevacizumab
Focal laser photocoagluation
Photodynamic 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% Parasymp Antagonist – 2-6hours
▫ Phenylephrine Sympathetic Agonist
▫ Cocaine 10% Sympathetic Agonist
▫ Cyclopentolate Parapsymp Antagonist – 24hours
▫ Atropine 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.
Glaucoma
Essentially a characteristic optic neuropathy
Triad 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/theoptometrist-s-practitioner-patient-manual-glaucomatous-disc/
Glaucoma
Symptoms:
• 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 IOP
Goldmann tonometer (contact)
Tonopen (contact)
Pneumotonometry (non-contact)
Anatomy of Glaucoma
Name the
structure
Canal of
Schlemm
Trabecular
meshwork
(a+b)
Kanski JJ. Clinical ophthalmology: A systematic approach. 6th ed. Edinburgh; New York:
Butterworth-Heinemann/Elsevier; 2007.
MCQs
• Aqueous humor:
1. Is produced by the ciliary processes
2. Is produced by the trabecular meshwork
3. Is produced by the canal of Schlemm
4. Is responsible for glaucoma
5. 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 glaucoma
2. Field loss is confirmative of glaucoma
3. A raised IOP is confirmative of glaucoma
4. Visual loss in glaucoma is related to nerve fibre
damage
Glaucoma Mysteries
Ocular 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 Glaucoma
1. Primary
▫
▫
Open angle
Angle closure
2. Secondary
▫
Open angle – eg. neovascular, pigmentary
3. Congenital
Types of Glaucoma
1. 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 Management
Aim: Either decrease production or increase drainage of
aqueous humor
1.
2.
Pharmacological - ABCPP
▫
Alpha-agonists
▫
Beta-blockers
▫
Carbonic anhydrase inhibitors
▫
Prostaglandins
▫
Parasympathetic agonists
Surgical
▫ Trabeculoplasty
▫ Trabeculectomy
Glaucoma Management - Pharm
Drug Class
Mechanism
Examples
Prostaglandins
↑ outflow (uveoscleral)
•
•
•
β-blockers
↓ production
Non specific
Timolol = Timoptol
β1 specific
Betaxolol = Betoptic
Resp
• Asthma/COPD
CVS
• Bradycardia, heart
block
Adrenergic
agonists
↓ production
↑ outflow (uveoscleral)
Brimonidine = Alphagan
•
•
•
Parasympathetic
agonist
↑ outflow (trabecular)
Pilocarpine
Miosis
Headache
Reduced peripheral vision
Reduced night vision
Carbonic
anhydrase
inhibitors (CAIs)
↓ production
Acetozolamide (Diamox)
Brinzolamide (Azopt)
• Paraesthesia
GIT
• Anorexia
• Diarrhoea
Renal
• HypoK
• Metabolic acidosis
Latanoprost = Xalatan
Traveprost = Travatan
Brimatoprost = Lumigan
SEs
•
•
•
Eyelash growth
Transient red eyes
Increased Iris
pigmentation
Red eye
Dry mouth
Tiredness, Drowsy
Glaucoma Management - Surgical
Laser 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 Retinopathy
Diabetic Retinopathy
Hypertensive Retinopathy
Keith-Wagener-Barker Classification
Background Retinopathy
1. 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
Pre-Proliferative Retinopathy = Infarction
1. 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 arterioles
1. AV nipping
2. Exaggerated light reflex
Proliferative Retinopathy
1. New vessels at disc (NVD)
2. New vessels elsewhere (NVE)
Grade 3 – Retinal arteriolar narrowing and focal
constriction
1. Retinal haemorrhages (flame haemorrhages)
2. Cotton wool spots
3. Retinal oedema
Grade 4
1. Papilloedema
Maculopathy
1. Background retinopathy at the macula
2. Macular oedema
Advanced Disease
1. Rubeosis iridis
2. Vitreous haemorrhage
3. Retinal detachment
1. Copper / Silver wiring (focal constriction + sclerosis
of arterioles)
2. Arteriolar narrowing
Background DR
Microaneurysms
Flame haemorrhages
Dot and blot haemorrhages
Glycosmedia. Diabetic retinopathy. 2000. Available from
http://www.glycosmedia.com/education/diabetic_retinopathy/aims.php
Pre-proliferative DR
Cotton wool spots
Venous changes
Glycosmedia. Diabetic retinopathy. 2000. Available from
http://www.glycosmedia.com/education/diabetic_retinopathy/aims.php
Proliferative DR
New vessels at the disc (NVD)
New vessels elsewhere (NVE)
MCQs
• What is the most common cause of visual
disability in diabetics?
1. Macular ischaemia
2. Vitreous haemorrhage
3. Macular oedema
4. Glaucoma
5. Retinal detachment
Maculopathy
Macular oedema + hard
exudate
Angiogram
Maculopathy
Normal OCT
Macular oedema
Diabetic Retinopathy
Risk 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 Guidelines
Screening
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
Management
General
• 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
Focal laser
PRP
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 4
LE
RE
Medrounds. Peripheral vision. 2006. Available from
http://www.medrounds.org/glaucomaguide/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