Chronic visual loss

Chronic VisualChronic Visual
Disturbance and VisualDisturbance and Visual
LossLoss
Setareh ZiaiSetareh Ziai
April 2April 2ndnd
, 2009, 2009
sziai@ottawahospital.on.casziai@ottawahospital.on.ca

Where is the problem?Where is the problem?
LMCC ObjectivesLMCC Objectives
 Pre-retinal:Pre-retinal:

cornea (dystrophy, scarring, edema)cornea (dystrophy, scarring, edema)

lens (age-related, traumatic, steroid-induced)lens (age-related, traumatic, steroid-induced)

glaucomaglaucoma
 Retinal:Retinal:

DM (diabetic retinopathy, macular edema)DM (diabetic retinopathy, macular edema)

vascular insufficiency (arterial or venous occlusion)vascular insufficiency (arterial or venous occlusion)

tumourstumours

macular degenerationmacular degeneration
 Post-retinal:Post-retinal:

anterior to optic chiasm (if optic nerve = monocular)anterior to optic chiasm (if optic nerve = monocular)
• compressive optic neuropathy (intracranial masses, thyroid eye disease)compressive optic neuropathy (intracranial masses, thyroid eye disease)
• toxic/nutritional (nutritional deficiencies, alcohol/tobacco amblyopia)toxic/nutritional (nutritional deficiencies, alcohol/tobacco amblyopia)

optic chiasm lesions (pituitary adenoma)optic chiasm lesions (pituitary adenoma)

Where is the problem?Where is the problem?
 Pre-retinal:Pre-retinal:

cornea (dystrophy, scarring, edema)cornea (dystrophy, scarring, edema)

lens (age-related, traumatic, steroid-induced)lens (age-related, traumatic, steroid-induced)

glaucomaglaucoma
 Retinal:Retinal:

DM (diabetic retinopathy, macular edema)DM (diabetic retinopathy, macular edema)

vascular insufficiency (arterial or venous occlusion)vascular insufficiency (arterial or venous occlusion)

tumourstumours

macular degenerationmacular degeneration
 Post-retinal:Post-retinal:

anterior to optic chiasm (if optic nerve = monocular)anterior to optic chiasm (if optic nerve = monocular)
• compressive optic neuropathy (intracranial masses, thyroid eye disease)compressive optic neuropathy (intracranial masses, thyroid eye disease)
• toxic/nutritional (nutritional deficiencies, alcohol/tobacco amblyopia)toxic/nutritional (nutritional deficiencies, alcohol/tobacco amblyopia)

optic chiasm lesions (pituitary adenoma)optic chiasm lesions (pituitary adenoma)

Diagnosis based on:Diagnosis based on:
- focused ophthalmological historyfocused ophthalmological history
-
monocular vs. binocularmonocular vs. binocular
-
acute vs. chronicacute vs. chronic
-
painful vs. painlesspainful vs. painless
- exam: … start with gross examinationexam: … start with gross examination
-
VAVA
-
slit lamp biomicroscopy +/- fluoresceinslit lamp biomicroscopy +/- fluorescein
-
dilated fundus examinationdilated fundus examination
- VF testingVF testing
- fluorescein angiography +/- other testsfluorescein angiography +/- other tests

 **Remember for exam:**Remember for exam:

sometimes, chronic visual loss in ONE eye issometimes, chronic visual loss in ONE eye is
noted incidentally some time later due tonoted incidentally some time later due to
occlusion of normal eye…: CHRONIC LOSSocclusion of normal eye…: CHRONIC LOSS
OF VISION CAN PRESENT ACUTELY!!OF VISION CAN PRESENT ACUTELY!!

Corneal CausesCorneal Causes
- dystrophydystrophy
- scarringscarring
- edemaedema

The CorneaThe Cornea
- allows light to enter the- allows light to enter the
eyeeye
- provides most of the eye’s- provides most of the eye’s
optical poweroptical power
- 0.5-0.8 mm thick- 0.5-0.8 mm thick
- transparent due to its- transparent due to its
uniformity, avascularityuniformity, avascularity
andand deturgescencedeturgescence

Corneal DystrophiesCorneal Dystrophies
- rare inherited disordersrare inherited disorders
- progressive, usuallyprogressive, usually bilateralbilateral
- can affect any of the three layers of thecan affect any of the three layers of the
corneacornea
- affect transparencyaffect transparency
- age at presentation: first to fourth decadesage at presentation: first to fourth decades

Corneal DystrophiesCorneal Dystrophies
- divided into:divided into:
-
anterior dystrophiesanterior dystrophies::
- epitheliumepithelium
- may present with recurrent corneal erosionsmay present with recurrent corneal erosions
-
stromal dystrophiesstromal dystrophies::
- usually present with visual lossusually present with visual loss
- if very anterior, can cause erosions and painif very anterior, can cause erosions and pain
-
posterior dystrophiesposterior dystrophies::
- endotheliumendothelium
- vision loss secondary to edema (endothelial dysfx)vision loss secondary to edema (endothelial dysfx)

Corneal ScarringCorneal Scarring
- multiple causes:multiple causes:
-
traumatrauma
-
infectious (eg., herpes)infectious (eg., herpes)
-
post-surgicalpost-surgical

Corneal EdemaCorneal Edema
- most often caused by dysfunction of themost often caused by dysfunction of the
corneal endothelium:corneal endothelium:
-
dystrophydystrophy
-
traumatrauma
-
infectious (eg., herpes)infectious (eg., herpes)
-
post-surgicalpost-surgical

CornealCorneal
TransplantationTransplantation

If the corneal stromaIf the corneal stroma opacifiesopacifies due todue to
trauma or infection, or if there istrauma or infection, or if there is
swellingswelling or anor an irregularityirregularity of theof the
surface of the cornea, light cannotsurface of the cornea, light cannot
properly reach the retina.properly reach the retina.
In some cases, a cornea from aIn some cases, a cornea from a
deceased donor can be transplanted.deceased donor can be transplanted.

Corneal TransplantationCorneal Transplantation

Lens-Related CausesLens-Related Causes
(cataract)(cataract)
- age-relatedage-related
- traumatictraumatic
- steroid inducedsteroid induced

The LensThe Lens
- biconvex, avascular,- biconvex, avascular,
transparent structuretransparent structure
- sits inside a thin- sits inside a thin
capsule, attached to thecapsule, attached to the
ciliary body by theciliary body by the
zonuleszonules
- provides the- provides the
remainder of the eye’sremainder of the eye’s
optical power (alongoptical power (along
with the cornea)with the cornea)
Lens

 cataractscataracts are due to the opacification ofare due to the opacification of
this normally clear structurethis normally clear structure

Age-Related CataractAge-Related Cataract
- often affect the nucleus of the lens first:often affect the nucleus of the lens first:
-
yellowing, followed by a browning of the lensyellowing, followed by a browning of the lens
-
eventually, liquefactioneventually, liquefaction
- causes myopic changes (increasedcauses myopic changes (increased
refractive index of the lens)refractive index of the lens)

Traumatic CataractTraumatic Cataract
- most common cause ofmost common cause of unilateral cataractunilateral cataract
in young individualsin young individuals
- most often caused by direct penetratingmost often caused by direct penetrating
injury to the lensinjury to the lens
- can also be caused by:can also be caused by:
-
concussionconcussion
-
ionizing radiation to ocular tumoursionizing radiation to ocular tumours
-
infrared radiation (glassblowers)infrared radiation (glassblowers)

Steroid-Induced CataractSteroid-Induced Cataract
- bothboth systemicsystemic andand topicaltopical steroids can besteroids can be
the culpritsthe culprits
- posterior part of lens affected firstposterior part of lens affected first
- children may be more susceptiblechildren may be more susceptible
- if lens changes develop, dose should beif lens changes develop, dose should be
reduced to the minimum necessaryreduced to the minimum necessary
- early opacities may regress withearly opacities may regress with
discontinuation of therapydiscontinuation of therapy

GlaucomaGlaucoma
 disease of thedisease of the optic nerveoptic nerve, often, often
caused by ancaused by an increase in intraocularincrease in intraocular
pressurepressure due to poor drainage ofdue to poor drainage of
aqueous from the trabecularaqueous from the trabecular
meshwork…meshwork…

GlaucomaGlaucoma
 if left untreated, glaucoma can lead toif left untreated, glaucoma can lead to
permanentpermanent damage to the optic nervedamage to the optic nerve
and resultantand resultant visual field lossvisual field loss
 can progress to blindnesscan progress to blindness

GlaucomaGlaucoma
 by definition, glaucoma is a trimodalby definition, glaucoma is a trimodal
disease, characterized by:disease, characterized by:

increased IOPincreased IOP

optic nerve changesoptic nerve changes

visual field changesvisual field changes

Goldmann Applanation TonometerGoldmann Applanation Tonometer

GlaucomaGlaucoma
 classification:classification:

primaryprimary: open-angle, angle-closure: open-angle, angle-closure

secondarysecondary: inflammatory, traumatic,: inflammatory, traumatic,
neovascular, steroid-induced etc…neovascular, steroid-induced etc…

congenitalcongenital

Risk Factors for GlaucomaRisk Factors for Glaucoma
 ageage
 african-american heritageafrican-american heritage
 high IOPhigh IOP
 family historyfamily history
 myopiamyopia

Symptoms of GlaucomaSymptoms of Glaucoma
 often asymptomaticoften asymptomatic
 with late disease,with late disease, constriction ofconstriction of
peripheral, and later central visual fieldperipheral, and later central visual field
 with very high IOP, can have blurrywith very high IOP, can have blurry
vision and halos around lightsvision and halos around lights

Glaucoma: Optic NerveGlaucoma: Optic Nerve
ChangesChanges
 increased cup:disc ratioincreased cup:disc ratio
 thinning of neural rimthinning of neural rim
 progressive loss of nerve fiber layerprogressive loss of nerve fiber layer
 flame hemorrhages on discflame hemorrhages on disc

Primary Open AnglePrimary Open Angle
GlaucomaGlaucoma
 most common (90%)most common (90%)
 usually bilateral (can be asymmetric)usually bilateral (can be asymmetric)
 prevalence increases with ageprevalence increases with age
 angle is open, eye is quietangle is open, eye is quiet
 increased resistance to aqueous drainageincreased resistance to aqueous drainage
at the level of the trabecular meshwork isat the level of the trabecular meshwork is
thought to be the main pathophysiologicthought to be the main pathophysiologic
featurefeature

Treatment optionsTreatment options
 goal is to stabilize the IOP to protectgoal is to stabilize the IOP to protect
the optic nerve against further damagethe optic nerve against further damage
 options:options:

dropsdrops

laserlaser

surgerysurgery

Glaucoma - MedicationsGlaucoma - Medications
 mechanism of action:mechanism of action:

decrease aqueous production:decrease aqueous production:
• beta blockers: timololbeta blockers: timolol
• alpha agonists: brimonidinealpha agonists: brimonidine
• carbonic anhydrase inhibitors: diamoxcarbonic anhydrase inhibitors: diamox

increase aqueous outflow:increase aqueous outflow:
• miotics: pilocarpinemiotics: pilocarpine
• epinephrineepinephrine
• prostaglandin analogs: latanoprostprostaglandin analogs: latanoprost

Glaucoma - LasersGlaucoma - Lasers
 usually when medical managementusually when medical management
failsfails

ALTALT (argon laser trabeculoplasty),(argon laser trabeculoplasty), SLTSLT
(selective laser trabeculoplasty): for open(selective laser trabeculoplasty): for open
angle glaucomasangle glaucomas

peripheral iridotomyperipheral iridotomy: for angle-closure: for angle-closure
glaucomasglaucomas
 high success ratehigh success rate

Glaucoma - SurgeryGlaucoma - Surgery
 usually when medical management andusually when medical management and
laser treatments faillaser treatments fail

trabeculectomy:trabeculectomy: sub-conjunctival shunt ofsub-conjunctival shunt of
aqueousaqueous

drainage devices (valves)drainage devices (valves)

cyclodestruction:cyclodestruction: last resort – destructionlast resort – destruction
of ciliary bodyof ciliary body

THE RETINATHE RETINA
- neural tissue lining- neural tissue lining
the inside of the eyethe inside of the eye
- converts the visual- converts the visual
image into aimage into a
neurochemicalneurochemical
message and sends itmessage and sends it
to the brainto the brain
- is made up of 10- is made up of 10
anatomic layersanatomic layers

DiabetesDiabetes
- diabetic retinopathydiabetic retinopathy
- diabetic macular edemadiabetic macular edema

Diabetic RetinopathyDiabetic Retinopathy
microangiopathymicroangiopathy
affects pre-capillary arterioles, capillariesaffects pre-capillary arterioles, capillaries
and post-capillary venulesand post-capillary venules
features offeatures of::
microvascular occlusionmicrovascular occlusion
leakageleakage
clinically, can be divided into:clinically, can be divided into:
background DR (nonproliferative)background DR (nonproliferative)
preproliferative DRpreproliferative DR
proliferative DRproliferative DR

Diabetic Retinopathy: EpidemiologyDiabetic Retinopathy: Epidemiology
239 million people by 2010239 million people by 2010
doubling in prevalence since 1994doubling in prevalence since 1994
diabetes will affect:diabetes will affect:
28 million in western Europe28 million in western Europe
18.9 million in North America18.9 million in North America
138.2 million in Asia138.2 million in Asia
1.3 million in Australasia1.3 million in Australasia
• #1 cause of blindness in patients 20-64 yrs#1 cause of blindness in patients 20-64 yrs
• prevalence increases withprevalence increases with duration of diabetesduration of diabetes andand
patient agepatient age
rare to find DR in children < 10 yrs, regardless of durationrare to find DR in children < 10 yrs, regardless of duration
risk of developing DR increases after pubertyrisk of developing DR increases after puberty

EpidemiologyEpidemiology
Wisconsin Epidemiologic Study of Diabetic RetinopathyWisconsin Epidemiologic Study of Diabetic Retinopathy
Between 1979-1980Between 1979-1980
1210 patients with Type 11210 patients with Type 1
1780 patients with Type 21780 patients with Type 2
predominantly white populationpredominantly white population
After 20 yrs, DR present in:After 20 yrs, DR present in:
99% of Type 199% of Type 1
60% of Type 260% of Type 2

WESDR: Frequency of retinopathy inWESDR: Frequency of retinopathy in
subjects with type 1diabetessubjects with type 1diabetes

WESDR: Frequency of retinopathy inWESDR: Frequency of retinopathy in
subjects with type 2 diabetessubjects with type 2 diabetes

Diabetic Retinopathy: Risk FactorsDiabetic Retinopathy: Risk Factors
duration of diabetesduration of diabetes: most important risk: most important risk
factorfactor
poor metabolic controlpoor metabolic control
pregnancy: can be associated with rapidpregnancy: can be associated with rapid
progressionprogression
HTNHTN
nephropathynephropathy
smokingsmoking
obesityobesity
hyperlipidemiahyperlipidemia

Classification of Diabetic RetinopathyClassification of Diabetic Retinopathy
Classified intoClassified into 2 stages2 stages
Nonproliferative Diabetic Retinopathy (NPDR)Nonproliferative Diabetic Retinopathy (NPDR)
early stageearly stage
also known as background DR (BDR)also known as background DR (BDR)
further categorized based upon extent of DRfurther categorized based upon extent of DR
mild, moderate, severe, very severemild, moderate, severe, very severe
Proliferative Diabetic Retinopathy (PDR)Proliferative Diabetic Retinopathy (PDR)
more advanced stagemore advanced stage
•
***Macular edema***Macular edema
• May be presentMay be present at any stage of DRat any stage of DR

NPDRNPDR
typicallytypically asymptomaticasymptomatic
fluctuatingfluctuating visual acuity:visual acuity:
fluctuating blood sugarfluctuating blood sugar
decreaseddecreased visual acuity:visual acuity:
CSMECSME
macular ischemiamacular ischemia
review these patients annuallyreview these patients annually

Proliferative Diabetic RetinopathyProliferative Diabetic Retinopathy
more likely to becomemore likely to become
symptomatic than earlysymptomatic than early
NPDRNPDR
may have decreasedmay have decreased
vision, sudden vision loss,vision, sudden vision loss,
floaters, cobwebs, flashes,floaters, cobwebs, flashes,
dull eye achedull eye ache
PDR can also affect visualPDR can also affect visual
function by affecting thefunction by affecting the
macula with resultingmacula with resulting
macular ischemia and/ormacular ischemia and/or
edemaedema

Proliferative DRProliferative DR
affects 5-10% of the diabetic populationaffects 5-10% of the diabetic population
neovascularizationneovascularization is the hallmarkis the hallmark
NVD: neovascularization of the discNVD: neovascularization of the disc
NVE: neovascularization elsewhereNVE: neovascularization elsewhere
new vessels are not only extremely fragilenew vessels are not only extremely fragile
((intraretinal or vitreous hemorrhageintraretinal or vitreous hemorrhage), but), but
often associated with fibrous proliferation,often associated with fibrous proliferation,
leading to an increased risk ofleading to an increased risk of tractional retinaltractional retinal
detachmentdetachment

Advanced PDRAdvanced PDR
 Tractional retinalTractional retinal
detachmentdetachment
resulting fromresulting from
contraction ofcontraction of
the fibrovascularthe fibrovascular
proliferativeproliferative
tissue on thetissue on the
retinaretina

Panretinal Photocoagulation for High-riskPanretinal Photocoagulation for High-risk
PDRPDR
 goal is to inducegoal is to induce
involutioninvolution (or at(or at
leastleast arrestarrest) of new) of new
vessels by creatingvessels by creating
areas of retinalareas of retinal
ischemiaischemia
 1200-3000 burns1200-3000 burns
 4 sessions4 sessions

Vitrectomy for VitreousVitrectomy for Vitreous
Hemorrhage / TRDHemorrhage / TRD

Diabetic Macular Edema (DME)Diabetic Macular Edema (DME)
retinal edemaretinal edema threateningthreatening oror involvinginvolving thethe
maculamacula
diagnosis is made by slit-lamp exam,diagnosis is made by slit-lamp exam,
confirmed by fluorescein angiography and/orconfirmed by fluorescein angiography and/or
OCTOCT
important observations include:important observations include:
locationlocation of retinal thickening relative to theof retinal thickening relative to the
foveafovea
presence and location ofpresence and location of exudatesexudates

Treatment of CSMETreatment of CSME
 argon laser applicationargon laser application
 intravitreal steroid injectionintravitreal steroid injection
 intravitreal anti-VEGF injectionintravitreal anti-VEGF injection
 pars plana vitrectomypars plana vitrectomy

Ophthalmological Follow-UpOphthalmological Follow-Up
 Diabetic ScreeningDiabetic Screening
Type 1 diabeticsType 1 diabetics::
Dilated funduscopic exam (DFE) 5 yrs after diagnosisDilated funduscopic exam (DFE) 5 yrs after diagnosis
Newly diagnosed patients with Type 1 diabetes rarelyNewly diagnosed patients with Type 1 diabetes rarely
have retinopathy during the first 5 yrshave retinopathy during the first 5 yrs
Type 2 diabeticsType 2 diabetics::
Type 2 diabetics typically diagnosed yrs after initialType 2 diabetics typically diagnosed yrs after initial
onsetonset
DFE at the time of diagnosisDFE at the time of diagnosis
Significant portion of newly diagnosed Type 2Significant portion of newly diagnosed Type 2
diabetics have established DR at the time ofdiabetics have established DR at the time of
diagnosisdiagnosis

Vascular InsufficiencyVascular Insufficiency
- arterial occlusions (CRAO, BRAO)arterial occlusions (CRAO, BRAO)
- venous occlusions (CRVO, BRVO)venous occlusions (CRVO, BRVO)

 most of the retina is supplied by themost of the retina is supplied by the
central retinal arterycentral retinal artery (branch of the(branch of the
ophthalmic artery, which is the first branchophthalmic artery, which is the first branch
of the ICA)of the ICA)
 if this supply is interrupted (embolus,if this supply is interrupted (embolus,
thrombosis, inflammation, vasculitis orthrombosis, inflammation, vasculitis or
compression), the retina becomescompression), the retina becomes
ischemicischemic
 irreversible damage occurs afterirreversible damage occurs after
approximately 90 minutesapproximately 90 minutes
CRAOCRAO

CRAOCRAO
 presentation is with sudden andpresentation is with sudden and
profound loss of visionprofound loss of vision
 RAPD is presentRAPD is present
 orange reflex from the choroid standsorange reflex from the choroid stands
out at the fovea, and contrasts with theout at the fovea, and contrasts with the
surrounding pale retina (surrounding pale retina (cherry-redcherry-red
spotspot))
 must r/o temporal arteritismust r/o temporal arteritis

CRAOCRAO
 most commonly the result ofmost commonly the result of
atherosclerosis (atherosclerosis (thrombosisthrombosis)) but maybut may
also be caused by calcificalso be caused by calcific emboliemboli
 often inoften in olderolder patients, with a hx ofpatients, with a hx of
arteriosclerosisarteriosclerosis
 may have had a hx of amaurosis fugaxmay have had a hx of amaurosis fugax
(transient visual loss)(transient visual loss)

CRAOCRAO
 OPHTHALMOLOGIC EMERGENCY!!OPHTHALMOLOGIC EMERGENCY!!
 treatment:treatment:

decrease IOPdecrease IOP

paracentesisparacentesis

ocular massageocular massage
 goal: to send the embolus distallygoal: to send the embolus distally
 **remember to r/o giant cell arteritis! (**remember to r/o giant cell arteritis! (ESR, CRP, pltESR, CRP, plt))
 poor prognosis:poor prognosis: 60%60% << 20/40020/400

BRAOBRAO
 sudden and profoundsudden and profound altitudinal oraltitudinal or
sectoralsectoral visual field lossvisual field loss
 similar causes as CRAOsimilar causes as CRAO
 identify and treat associated medicalidentify and treat associated medical
conditions (HTN, DM,conditions (HTN, DM,
hypercholesterolemia, smoking,hypercholesterolemia, smoking,
vasculitis etc…)vasculitis etc…)

BRAOBRAO
 retinal cloudiness in ischemic arearetinal cloudiness in ischemic area
 +/- visible embolus+/- visible embolus
 also has a poor prognosis, unless thealso has a poor prognosis, unless the
obstruction can be dislodged within aobstruction can be dislodged within a
few hoursfew hours

 thrombosis of thethrombosis of the central retinal veincentral retinal vein
 sudden loss of vision in affected eyesudden loss of vision in affected eye
 severity of symptoms varies…severity of symptoms varies…
 non-ischemic:non-ischemic: 75%75%
 IschemicIschemic
 most characteristic finding:most characteristic finding: retinalretinal
hemorrhageshemorrhages
CRVOCRVO

CRVOCRVO
 underlying associationsunderlying associations

advancing ageadvancing age

systemic conditions: HTN, DM, smoking,systemic conditions: HTN, DM, smoking,
obesity, hyperlipidemiaobesity, hyperlipidemia

glaucomaglaucoma

inflammatory diseases: sarcoidosis, Behcetinflammatory diseases: sarcoidosis, Behcet
diseasedisease

thrombophilic disorders:thrombophilic disorders:
hyperhomocysteinaemia, antiphospholipidhyperhomocysteinaemia, antiphospholipid
antibody syndromeantibody syndrome

CRVOCRVO
 Treatment:Treatment:

treat associated medical conditionstreat associated medical conditions

decrease IOP if elevateddecrease IOP if elevated

pan-retinal photocoagulationpan-retinal photocoagulation
(laser) if:(laser) if:
• neovascularization (iris, angle,neovascularization (iris, angle,
retina)retina)
• ……especially if ischemic CRVOespecially if ischemic CRVO

 thrombosis of a branch of thethrombosis of a branch of the centralcentral
retinal veinretinal vein
 visual loss depends on thevisual loss depends on the amount ofamount of
macular drainage compromised by themacular drainage compromised by the
occlusionocclusion (peripheral occlusions may be(peripheral occlusions may be
asymptomatic)asymptomatic)
 characteristic findings incharacteristic findings in one sectorone sector of theof the
retina:retina:
 dilatation and tortuosity of veinsdilatation and tortuosity of veins
 retinal hemorrhagesretinal hemorrhages
 retinal/macular edemaretinal/macular edema
 cotton-wool spotscotton-wool spots
BRVOBRVO

 obstruction often at arterio-venousobstruction often at arterio-venous
crossings: arteries and veins sharecrossings: arteries and veins share
adventitial sheath… thickening of theadventitial sheath… thickening of the
arteriole (arteriole (arteriosclerosisarteriosclerosis) compresses) compresses
the vein, eventually causing an occlusionthe vein, eventually causing an occlusion
 often associated with:often associated with:

hypertension (75%)hypertension (75%)

diabetes (10%)diabetes (10%)
BRVOBRVO

 prognosisprognosis: depends on amt of venous: depends on amt of venous
drainage involved by the occlusion anddrainage involved by the occlusion and
severity of macular ischemia:severity of macular ischemia: within 6 mos,within 6 mos,
about 50% of eyes have a VA of 20/30 orabout 50% of eyes have a VA of 20/30 or
betterbetter
 main complications:main complications:

chronic macular edemachronic macular edema

neovascularizationneovascularization
 laser photocoagulationlaser photocoagulation may be helpful inmay be helpful in
above casesabove cases
BRVOBRVO

Retinal TumoursRetinal Tumours

 ocular tumours:ocular tumours:
 ciliary bodyciliary body::
• melanomamelanoma
 choroidchoroid::
• melanomamelanoma
• hemangiomahemangioma
• metastasesmetastases
 primary ocular lymphomaprimary ocular lymphoma
 retina and optic nerveretina and optic nerve::
• retinoblastomaretinoblastoma
• astrocytomaastrocytoma
• hemangiomahemangioma

Choroidal MelanomaChoroidal Melanoma
 most common primary intraocularmost common primary intraocular
tumour in adultstumour in adults
 presentation usually in 6th decade:presentation usually in 6th decade:

asymptomatic vs. visual field defect and/orasymptomatic vs. visual field defect and/or
decreased visual acuitydecreased visual acuity
 signs:signs:

raised, usually pigmented lesion visible atraised, usually pigmented lesion visible at
the back of the eyethe back of the eye

may be associated with retinal detachmentmay be associated with retinal detachment

optic nerve may be involvedoptic nerve may be involved

Choroidal MelanomaChoroidal Melanoma
 treatment:treatment:

consider size, location, activity of tumour,consider size, location, activity of tumour,
state of fellow eye, general health/age of pt,state of fellow eye, general health/age of pt,
pt’s wishes/fearspt’s wishes/fears
• brachytherapybrachytherapy
• external radiotherapyexternal radiotherapy
• transpupillary thermotherapytranspupillary thermotherapy
• local resectionlocal resection
• enucleationenucleation
• exenterationexenteration
• palliativepalliative (may include chemo)(may include chemo)

Choroidal MetastasesChoroidal Metastases
 ……with choroidal melanoma, don’t forgetwith choroidal melanoma, don’t forget
general medical investigations!general medical investigations!

mets TO the choroid:mets TO the choroid:
• most frequently frommost frequently from bronchusbronchus in both sexesin both sexes
and theand the breastbreast in women, rarely kidney or GIin women, rarely kidney or GI

CXR, rectal exam, mammographyCXR, rectal exam, mammography

mets FROM the choroid:mets FROM the choroid:
• liverliver

hepatic u/s, GGT, ALPhepatic u/s, GGT, ALP
• lungslungs (rarely affected before liver)(rarely affected before liver)

CXRCXR

 usually present with visual impairmentusually present with visual impairment
only IF tumour is near the maculaonly IF tumour is near the macula
 signssigns::

fast-growing, creamy coloured lesionfast-growing, creamy coloured lesion

most often in posterior polemost often in posterior pole

usually not very elevated (infiltrates laterally)usually not very elevated (infiltrates laterally)

 treatmenttreatment::

observe: if asxic or receiving systemic chemoobserve: if asxic or receiving systemic chemo

radiation: external beam or brachyradiation: external beam or brachy

transpupillary thermotherapytranspupillary thermotherapy

systemic therapy for the primarysystemic therapy for the primary

enucleation: for painful blind eyeenucleation: for painful blind eye
 prognosis is poorprognosis is poor……

median survival: 8-12 mos for all pts, 15-17median survival: 8-12 mos for all pts, 15-17
mos for those with breast camos for those with breast ca

RetinoblastomaRetinoblastoma
 most common malignant tumour of the eyemost common malignant tumour of the eye
in childhood (1:20 000)in childhood (1:20 000)
 mean age ofmean age of presentationpresentation: 8 mos if: 8 mos if
inherited, 25 mos if sporadicinherited, 25 mos if sporadic

60% present with leukocoria (white pupillary60% present with leukocoria (white pupillary
reflex)reflex)

strabismus (20%)strabismus (20%)

occasionally: painful, red eyeoccasionally: painful, red eye

if inherited: often bilateralif inherited: often bilateral

 malignant transformation of primitivemalignant transformation of primitive
retinal cells before their final differentiationretinal cells before their final differentiation
 can be caused bycan be caused by germinal mutationsgerminal mutations (can(can
be passed on to the next generation), orbe passed on to the next generation), or
can becan be sporadicsporadic (66% of cases)(66% of cases)

 this is athis is a clinical diagnosisclinical diagnosis, but, but CSFCSF andand
bone marrowbone marrow should be examined to checkshould be examined to check
for metastatic disease if ON involved or iffor metastatic disease if ON involved or if
there is evidence of extraocular extensionthere is evidence of extraocular extension
 rx:rx:

smallsmall: cryotherapy, photocoagulation: cryotherapy, photocoagulation

mediummedium: brachytherapy, external beam, chemo: brachytherapy, external beam, chemo

large/advanced caseslarge/advanced cases: chemoreduction + local: chemoreduction + local
treatment, enucleationtreatment, enucleation

metastatic diseasemetastatic disease: chemo (intrathecal if cells: chemo (intrathecal if cells
in CSF)in CSF)

 prognosis:prognosis:

depends on extent of disease at diagnosisdepends on extent of disease at diagnosis

overall mortality ~ 5-15%overall mortality ~ 5-15%

~ 50% of children with the germinal mutation~ 50% of children with the germinal mutation
will eventually develop a second primarywill eventually develop a second primary
tumour (eg.,tumour (eg., osteosarcomaosteosarcoma of the femur orof the femur or
pinealoblastomapinealoblastoma))

Macular DegenerationMacular Degeneration

MaculaMacula
 1.5 mm1.5 mm in diameterin diameter
 central vision:central vision: BEST VISUAL ACUITYBEST VISUAL ACUITY
 colour visioncolour vision
 progressive destruction of the macularprogressive destruction of the macular
area:area:
MACULAR DEGENERATIONMACULAR DEGENERATION

 most common cause of irreversiblemost common cause of irreversible
visual loss in the developed worldvisual loss in the developed world
 exists in two forms:exists in two forms:

non-exudativenon-exudative (dry) macular(dry) macular
degenerationdegeneration

exudativeexudative (wet) macular(wet) macular
degenerationdegeneration

Non-exudative MacularNon-exudative Macular
DegenerationDegeneration
 lipid products arising fromlipid products arising from
photoreceptor outer segments arephotoreceptor outer segments are
found under retinafound under retina

can be seen with ophthalmoscope!can be seen with ophthalmoscope!

calledcalled « drusen »« drusen »

Exudative MacularExudative Macular
DegenerationDegeneration
 new vessels from the choroid grow intonew vessels from the choroid grow into
the sub-retinal space; form athe sub-retinal space; form a sub-sub-
retinal neovascular membraneretinal neovascular membrane
 subsequentsubsequent hemorrhagehemorrhage into the sub-into the sub-
retinal space or even through the retinaretinal space or even through the retina
into the vitreous is associated withinto the vitreous is associated with
profound loss of visionprofound loss of vision

 symptoms:symptoms:

since fovea is responsible for fine visualsince fovea is responsible for fine visual
resolution, any disruption will causeresolution, any disruption will cause
severe visual impairmentsevere visual impairment
• blurry/reduced visionblurry/reduced vision
• distorted vision (distorted vision (metamorphopsiametamorphopsia))
• reduction (micropsia) or enlargementreduction (micropsia) or enlargement
(macropsia) of objects(macropsia) of objects
• VF loss (VF loss (scotomascotoma))

 rx:rx:

non-exudativenon-exudative (usually slowly(usually slowly
progressive):progressive):
• no actual medical treatmentno actual medical treatment
• use low vision aidsuse low vision aids
• high dose antioxidants MAY behigh dose antioxidants MAY be
beneficial (eg., vitalux)beneficial (eg., vitalux)

 rx:rx:

exudativeexudative (can be rapidly progressive and(can be rapidly progressive and
devastating):devastating):
• intravitreal injections of anti-VEGFintravitreal injections of anti-VEGF
factors: bevacizumab, ranibizumabfactors: bevacizumab, ranibizumab
• photodynamic therapy (injection ofphotodynamic therapy (injection of
photosensitizer into systemic circulationphotosensitizer into systemic circulation
followed immediately by laser targetingfollowed immediately by laser targeting
new vessels in macular area)new vessels in macular area)
• combination of above treatmentscombination of above treatments

OPTIC NERVEOPTIC NERVE
 1.2 million cells1.2 million cells
 80 % visual fibres80 % visual fibres
 20 % pupillary fibres20 % pupillary fibres
 carries visualcarries visual
information frominformation from
the eye to the brainthe eye to the brain

OPTIC CHIASMOPTIC CHIASM
crossover of nasal fiberscrossover of nasal fibers
above the pituitaryabove the pituitary
internal carotids are justinternal carotids are just
laterallateral
from optic chiasm:from optic chiasm:
optic tract to theoptic tract to the
lateral geniculate bodylateral geniculate body
optic radiationoptic radiation to theto the
primary visual cortexprimary visual cortex

Anterior to OpticAnterior to Optic
ChiasmChiasm
- compressive optic neuropathiescompressive optic neuropathies
- toxic/nutritional optic neuropathiestoxic/nutritional optic neuropathies

Compressive OpticCompressive Optic
NeuropathiesNeuropathies
 INTRACRANIAL MASSES:INTRACRANIAL MASSES:

optic nerve gliomaoptic nerve glioma
• typically affects young women, end of first decadetypically affects young women, end of first decade
• associated with NF-1associated with NF-1

optic nerve sheath meningiomaoptic nerve sheath meningioma
• most frequent in middle-aged womenmost frequent in middle-aged women
• unilateral, gradual visual impairmentunilateral, gradual visual impairment

anyany other orbital or chiasmal tumourother orbital or chiasmal tumour
compressing any part of the optic nervecompressing any part of the optic nerve
 THYROID EYE DISEASETHYROID EYE DISEASE

Thyroid Eye DiseaseThyroid Eye Disease
 may occur in the absence of biochemicalmay occur in the absence of biochemical
evidence of thyroid dysfxevidence of thyroid dysfx
 autoimmune reaction (IgG Abs) causing:autoimmune reaction (IgG Abs) causing:

inflammation of EOMs: pleiomorphic cellularinflammation of EOMs: pleiomorphic cellular
infiltration associated with increased secretioninfiltration associated with increased secretion
of GAGs and osmotic imbibition of waterof GAGs and osmotic imbibition of water
• muscles can become up to 8 times their originalmuscles can become up to 8 times their original
size!!size!!
 no relation to severity of thyroid dysfx!no relation to severity of thyroid dysfx!

 main findings: (not all are always present!)main findings: (not all are always present!)

soft tissue involvementsoft tissue involvement

lid retractionlid retraction

proptosisproptosis

optic neuropathyoptic neuropathy

restrictive myopathyrestrictive myopathy

 vision loss from:vision loss from:

exposure keratopathyexposure keratopathy
• due to severe proptosis resulting in incomplete liddue to severe proptosis resulting in incomplete lid
closure → chronically exposed cornea → cornealclosure → chronically exposed cornea → corneal
ulceration & exposure keratopathyulceration & exposure keratopathy

optic neuropathyoptic neuropathy
• affects 5% of ptsaffects 5% of pts
• compression of ON or its blood supply bycompression of ON or its blood supply by
congested (enlarged) EOMscongested (enlarged) EOMs
• can lead to severe,can lead to severe, permanentpermanent visual impairmentvisual impairment
• rx with steroids, surgery if neededrx with steroids, surgery if needed

Toxic/Nutritional OpticToxic/Nutritional Optic
NeuropathiesNeuropathies
 nutritional deficienciesnutritional deficiencies
 alcohol-tobacco amblyopiaalcohol-tobacco amblyopia

Nutritional DeficienciesNutritional Deficiencies
 pts with extremely poor diets, often in associationpts with extremely poor diets, often in association
with alcohol-tobacco amblyopiawith alcohol-tobacco amblyopia
 usually due to B12 deficiency in combination withusually due to B12 deficiency in combination with
cyanide toxicitycyanide toxicity
 symmetrical VF losssymmetrical VF loss
 if early, can be treated with high-dose vitaminsif early, can be treated with high-dose vitamins
and restoration of « well-balanced diet »and restoration of « well-balanced diet »
 eventually leads to optic atrophy and permanenteventually leads to optic atrophy and permanent
vision lossvision loss

Alcohol-Tobacco AmblyopiaAlcohol-Tobacco Amblyopia
 affects heavy drinkers, cigar and pipe smokers: deficient inaffects heavy drinkers, cigar and pipe smokers: deficient in
protein and the B vitaminsprotein and the B vitamins
 symptomssymptoms: insidious, bilateral, progressive visual: insidious, bilateral, progressive visual
impairment + dyschromatopsiaimpairment + dyschromatopsia
 signssigns: symmetrical VF defect, may have pale (or normal): symmetrical VF defect, may have pale (or normal)
discsdiscs
 rxrx: 1000 units of hydroxocobalamin qweekly X 10 wks +: 1000 units of hydroxocobalamin qweekly X 10 wks +
multivitamins + « well-balanced diet »multivitamins + « well-balanced diet »
 pxpx::

good in early cases if comply with rxgood in early cases if comply with rx

advanced cases: optic atrophy and permanent visualadvanced cases: optic atrophy and permanent visual
lossloss

Optic Chiasm LesionsOptic Chiasm Lesions
- pituitary adenomapituitary adenoma

Pituitary AdenomaPituitary Adenoma
 presentation usually in early adult life orpresentation usually in early adult life or
middle agemiddle age
 symptoms:symptoms:

h/ah/a

visual symptoms: very gradual onset (oftenvisual symptoms: very gradual onset (often
not noticed by pt until very well-established)not noticed by pt until very well-established)
• VF defectVF defect: usually, bitemporal hemianopia, worst in: usually, bitemporal hemianopia, worst in
the superior field, and extending inferiorlythe superior field, and extending inferiorly
• colour desaturationcolour desaturation across vertical midlineacross vertical midline
• optic atrophyoptic atrophy: in 50% of cases with field defects: in 50% of cases with field defects
caused by pituitary lesionscaused by pituitary lesions

 investigations:investigations:

MRI: coronal, axial and sagittal sections beforeMRI: coronal, axial and sagittal sections before
and after gadolinium injectionand after gadolinium injection

CT: demonstrates enlargement or erosion ofCT: demonstrates enlargement or erosion of
the sellathe sella

endocrinological investigation: PRL, FSH, TSH,endocrinological investigation: PRL, FSH, TSH,
GHGH

 treatment options:treatment options:

observationobservation

medical: dopamine agonists (bromocriptine)medical: dopamine agonists (bromocriptine)

surgerysurgery

radiotherapy: often used as an adjunctradiotherapy: often used as an adjunct

gamma knife stereotactic radiotherapygamma knife stereotactic radiotherapy

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