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0P21 Ophthalmology Toronto Notes 2023
Table 8. Anatomic Classification of Uveitis
Anterior Uveitis (Iritis) Intermediate Uveitis Posterior Uveitis
Complications Inflammatory glaucoma
Posterior synediiae
Adhesions ol posterior iris to anterior lens capsule
Indicated by an irregularly shaped pupil
If occurs360\ can lead to angle closure glaucoma
Peripheral anterior synechiae (rare)
Adhesions of iristo cornea
Can lead tosecondary angle closure glaucoma
Cataracts (usually posteriorsubcapsular)
Band keratopathy - superficial corneal calcification (seen in chronic iritis)
Macular edema with chronic iritis
Cystoid macular edema (30% ol cases),
cataract, and glaucoma
Macular edema
Vitritis
Neovascularization
Visual field lossfscotoma
Mydriatics:dilate pupil to prevent formation ol posteriorsynechiae and to Systemic or sub- tenon/inlravitrealsteroids
and immunosuppressive agents
Vitrectomy, cryotherapy, or laser
photocoagulalion lo the '
snowbank'
Steroids:sub- lenon, inlravitreal,or systemic il indicated
(e.g.threat of vision loss)
Vitreous biopsy ilsuspected masquerade/malignancy
treatment
decrease pain from ciliary spasm
Steroids:topical, sub-lenon. or systemic
Systemic analgesia
If recurrent episodes, medical workup may be indicated lo rule out
secondary causes
Lens
• consists of an outer capsule surrounding a soft cortex and a firm inner nucleus
Cataracts
Definition
• any opacity of the lens, regardless of etiology
• most common cause of reversible blindness worldwide
• types: nuclear sclerosis, cortical, and posteriorsubcapsular
lortical
Etiology
• acquired
• age-related (over 90% of all cataracts)
• cataract associated with systemic disease (may have juvenile onset)
DM
metabolic disorders (e.g. Wilsons disease, galactosemia, or homocystinuria)
hypocalcemia
traumatic (may be rosette-shaped)
intraocular inflammation (e.g. uveitis)
toxic (steroids,phenothiazines)
radiation
• congenital
high myopia
present with altered red reflex or leukocoria
• treat promptly to prevent amblyopia
Clinical Features
• gradual, painless, progressive decrease in VA
• glare, dimness, halos around lights at night, monocular diplopia
• “second sight" phenomenon: patient is more myopic than previously noted, due to increased refractive
power of the lens (in nuclear sclerosis only)
patient may read without previously needing reading glasses
• diagnosis by slit-lamp exam
• may impair view of retina during fundoscopy
-Posterior
I subcapsular
Nuclear sclerosis
I
I
u
@
TYPES OF CATARACTS
Cortical
• Radial or spokc-likc
I opacification in the
1 cortex of the lens, either
' anteriorly or posteriorly
• Associated with aging
and diabetes
o
Nuclear Sclerosis
• Yellow to brown
("brunosccnfl
discolouration ol the
central pan of the lens
• Age-related
Postihor Subcapsular
• Usiallymthe postenor
of tie lens, adjacent to
thecapsule
• Asociated with steroid
use intraocular
infbmmation.diabetes,
traima,radiation aging
Treatment
• medical: no role for medical management
• surgical:definitive treatment
indicationsfor surgery
to improve visual function in patients whose vision loss leads to functional impairment
to aid management of other ocular disease (e.g. cataract that prevents adequate retinal exam
or laser treatment of DR)
congenital or traumatic cataracts
phacoemulsification (phaco = lens)
most commonly used surgical technique
postoperative complications: RD, endophthalmitis, dislocated IOL, macular edema,
glaucoma, posterior capsular opacification
©Tobi Lam 2012
Figure 16. Types of cataracts
J
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OP22 Ophthalmology Toronto Notes 2023
Dislocated Lens (Ectopia Lentis)
Etiology
• associated with Marfan Syndrome, Ehlers-Danlos type VI, homocystinuria,syphilis,lens coloboma
(congenital cleft due to failure of ocular adnexa to complete growth)
• traumatic
Clinical Features
• decreased VA
• may get monocular diplopia
• iridodonesis (quivering of iris with movement)
• phacodonesis (observed movement of the lens)
• direct ophthalmoscopy may elicit abnormal red reflex
Complications
• cataract,glaucoma, and uveitis
Treatment
• surgical lens replacement
Vitreous
• dear gel (99% water plus collagen fibrils, glycosaminoglycans, and hyaluronic acid) that fills the
posterior segment of eye
• normally adherent to optic disc, vitreous base (pars plana/ora serrata), and along major retinal blood
vessels
Posterior Vitreous Detachment
Etiology
• central vitreous commonly shrinks and liquefies with age (syneresis)
• during syneresis, vitreous fibrils condense causing vitreousfloaters
• liquid vitreous moves between posterior vitreous gel and retina
• vitreous is peeled away and separates from the internal limiting membrane of the neurosensory retina
posterior to the vitreous base
Clinical Features
• floaters,flashes oflight
Complications
• traction at sites of firm adhesion may result in retinal tear with or without subsequent
rhegmatogenous retinal detachment
• retinal tears/detachment may cause vitreous hemorrhage if bridging retinal blood vessel is torn
• complications more common in high myopes and following ocular trauma (blunt or perforating)
Weiss Ring:formed by glial tissue around
the optic disc that remains attached to
the detached posterior vitreous
Floaters: “bugs", “cobwebs”, or “spots”
of vitreous condensation that move with
eye position
Although most floaters are benign, new
or markedly increased floaters or flashes
of light require a dilated fundus exam to
rule out retinal tears/detachment
Treatment
• acute onset of PVD requires a dilated fundus exam to rule out retinal tears/detachment
• no specific treatment available for floaters/flashes of light
Vitreous Hemorrhage
Definition
• bleeding into the vitreous cavity
Etiology
. PDR
• retinal tear/dctachment
. PVD
• retinal vein occlusion
• trauma
Any time a vitreous or retinal
hemorrhage isseen in a child, must
consider child abuse
n
Clinical Features
• sudden loss of VA
• may be preceded by “shower" of many floaters and/or flashes of light
• ophthalmoscopy: no red reflex if large hemorrhage,retina not visible due to blood in vitreous
LJ
+
Treatment
• ultrasound (B-scan) to rule out RD
• expectant: in non-urgent cases (e.g. no RD), blood usually resorbs in 3- 6 mo
• surgical: vitrectomy ± RD repair ± retinal endolaser for bleeding sites/retinal tears
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OP23Ophthalmology Toronto Notes 2023
Endophthalmitis and Vitritis E
Definition
• intraocular infection:acute,subacute, or chronic
Etiology
• most commonly as postoperative complication:risk following cataract surgery is <0.1%
• also due to penetrating injury to eye (risk is 3-7%), endogenous spread, and intravitrea) injections
• etiology usually bacterial, may be fungal
Clinical Features
• painful, red eye, photophobia,discharge
• severely reduced VA,lid edema, proptosis, corneal edema, anterior chamber cells/flare, hypopyon,
reduced red reflex
• may have signs of a ruptured globe (severe subconjunctival hemorrhage, chemosis, hyphema,
decreased lOP.etc.)
Remember to inquire about tetanus
status in post-traumatic endophthalmitis
Treatment (see Ocular Trauma, OP41)
• OCULAR EMERGENCY:presenting vision indicates prognosis
• LP or worse: admission, immediate vitrectomy, and intravitrea!antibiotics to prevent loss of vision
• HM or better:vitreous tap for culture and intravitreal antibiotics
• topical fortified antibiotics
Retina Peripheralfethta
V
• composed of two parts ( Figure 2,OP2)
• neurosensor)'retina: comprises 9 of the 10 retinal layers, including photoreceptors and ganglion
cell layer
RPE layer: external to neurosensory retina
• macula:rich in cones (for colour vision), most sensitive area of retina
• fovea: centre of macula, responsible for detail, fine vision, lacks retinal vessels
• optic disc: collection of retinal nerve fibre layers forming optic nerve (CN II)
• ora serrata: irregularly-shaped, anterior margin of the retina (cannot be visualized with direct
ophthalmoscope, but possible with indirect ophthalmoscope/scleral depression)
isFovea Opt! irve
Macula /
Figure 17. Retina Central/Branch Retinal Artery Occlusion
Etiology
• occlusion of blood flow from the following causes results in loss of vision due to oxygen starvation of
the retinal tissues and eventual cell death
• emboli from carotid arteries or heart (e.g. arrhythmia, endocarditis, valvular disease)
thrombus
GCA/temporal arteritis
Hallmark of CRAO
"Cherry-red spot" located at centre
of macula (visualization of unaffected
highly vascular choroid through the thin
fovea)
Clinical Features
• sudden, painless (except in GCA),severe monocular loss of vision
. RAPD in CRAO or large BRAO
• patient may have experienced transient episodes in the past (amaurosisfugax)
• fundoKopy
“cherry-red spot"
retinal edema
cotton wool spots(retinal infarcts)
• cholesterol emboli (Hollenhorst plaques) - usually located at arteriole bifurcations
Treatment for a CRAO must be initiated
within 2 h of symptom onset for any
hope of restoring vision
The "blood and thunder" appearance on
fundoscopy is very specific for CRVO
Treatment
• OCULAR EMERGENCY: attempt to restore blood flow within 2 h (irreversible retinal damage if >90
min of complete CRAO)
• massage the globe (compress eye with heel of hand for 10 s, release for 10 s, repeat for 5 min) to
dislodge embolus
. decrease 10F
• topical p-blocker
IV acetazolamide
IV mannitol (drawsfluid from eye)
drain aqueousfluid - anterior chamber paracentesis (carries risk of infection, lens puncture)
• YAG laser embolectomy
• intra-arterial or intravenous thrombolysis
• hyperbaric oxygen therapy
There is an 8-10% risk of developing
CRVO or BRVO in the other eye
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OP21 Ophthalmology Toronto Notes 2023
Central/Branch Retinal Vein Occlusion
Etiology
• second most frequent “vascular” retinal disorder after DR
• exact cause is not known; possible arteriosclerotic changesin the central retinal artery transform the
artery into a rigid structure and impinge upon the central retinal vein as they share a common sheath
• predisposing factors: atherosclerotic vascular disease, HTN, DM, glaucoma, hyperviscosity (e.g.
sickle cell disease, polycythemia rubra vera, lymphoma, leukemia), drugs (e.g. oral contraceptive pill,
diuretics)
Effect of Beradnimab vs.Aflibercept on Visual
Acuity among Patients with Macular Edema due
to Centra!Retinal Vein Occlusion - The SC0RE2
landomiied Clinical Trill
JAMA 2017:317(20) 2072 2087
Purpose lo mrestigitewhether heuatiiunab
(used off label) is non inleilot to alhbeiceptfor the
treatment of macular edema secondary lo central
retinal or bemiretieialvein occlusion.
Methods:362 patients with macular edema doe to
central retinal or hemiretinalueinocclusion were
randomized toeither the beracizumab-treatment
group or the allibercept-treatment group.
Results:At 6 ano,the meanU letterscore (VMS) was
69.3(a mean increase from baselineof 18.6)in the
bencumabgroupand 69.3 (a mean increase from
base lire of 18.9) in Ihc alldieicepl group (P•0.001
lor aoniaferiority). Mrerse events were rare bul were
simitar between the two giaups.
Conclusion: After 6 mo of treatment, bevacizumab
was non-inferior to aflibercept with respect toU.
Cost differences between the drugs has important
economic implications.
Clinical Features
• painless,monocular, gradual, orsudden vision loss
. ± RAPD
• fundoscopy
“blood and thunder"
appearance
diffuse retinal hemorrhages, cotton wool spots, venous engorgement,swollen optic disc, macular
edema
• two fairly distinct groups
• venousstasis/non-ischemic retinopathy
no RAPD, VA -20/80
mild hemorrhage, few cotton woolspots
resolvesspontaneously over weeks to months
may regain normal vision if macula unaffected
hemorrhagic/ischemic retinopathy
usually older patient with deficient arterialsupply
RAPD, VA -20/200, reduced peripheral vision
more hemorrhages, cotton wool spots, venous congestion
poor visual prognosis
Integrated Results from Ihc COPERNICUS and
6AIIK0Studies
Clin Ophthalmol 2012:11:15331940
Purpose: Comparing theeffectsof nlraullrtal
affibtitcpllosham Injection lor macular edema
caused by CRV0.
Methods:COPERNICUS (n*187) and GALILEO (n
-171)
were pa raid,double-blind, Phase IN RCTs.In the
COPERNICUS trial, patients# the sham group crossed
orer to the treatment group at 24-52wk ofthetriat
Patients in the GALILEO trial receiving thesham
treatment continued to receive sham injections every
4 wt between 24 wt and 52 w k.
CoiKlasioa: Prompt treatment with Intrav ideal
aflrbticept rsan effective treatment for macular
td«MMowing CRVO.
Complications
• neovascularization of retina and iris(secondary rubeosis), may lead to secondary glaucoma
• vitreous hemorrhage
• macular edema
Treatment
• retinal laser photocoagulation, anti
-VEGF, and/or corticosteroid injection
Retinal Detachment
Definition
• cleavage in the plane between the neurosensory retina and the RPE
• three types
rhegmatogenous (most common)
caused by a tear or hole in the neurosensory retina, allowing fluid from the vitreous to pass
into the subretinal space
tears may be caused by PVD, degenerative retinal changes, trauma, or iatrogenic
complications
« incidence increases with advancing age, in high myopes, and after ocular surgery/trauma
• tractional
caused by vitreal, epiretinal, orsubretinal membrane pulling the neurosensory retina away
from the underlying RPE
found in conditionssuch as DR, RVO,sickle cell disease,ROP, and ocular trauma
exudative
caused by vascular transudation of fluid or damage to the RPE resulting in fluid accumulation
in the subretinalspace
main causes are intraocular tumour, posterior uveitis, centralserous retinopathy
Clinical Features
• sudden onset
• flashes of light
• due to mechanicalstimulation of the retinal photoreceptors
• floaters
• hazy spotsin the line of vision which move with eye position
due to drops of blood from torn vessels bleeding into the vitreous
• curtain of blackness/peripheral field loss
• darkness in the field of vision where the retina has detached
• loss of central vision (if macula “off")
• decreased IOP (usually 4-5 mmHg lower than the other, unaffected eye)
• ophthalmoscopy: detached retina is grey-white from retinal edema, and loss of red reflex
. ± RAPD
n
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OP25Ophthalmology Toronto Notes 2023
Treatment
• prophylactic:symptomatic tear (flashes or floaters) can be sealed off with laser/cryotherapy
• therapeutic: Ifficacy and Safety of Widely Died Treatments
Ior Macular Edema Secondary to Retinal Vein
Occlusion:ASystematic Review
BMC Ophthalmol 2014:14:17
Purpose:1o assess Use efficacy of widely used
treatmentslor macular edema|ME) secondary to
retinal vein occlusion (RVO). ME secondary to(VO can
cause rision loss due to CRVO or a BRVO.
Outcomes:Mean change in BCVA from haseine and/
or number of patientsgaining at least10 lettersfrom
haseine to 0 moor equivalent time point
Resnlts:14 unique RCIs identified. Rambiiumab
0.5 mg produced greater improvements in BCVAat
6 mo compared tosham m BRVO (mean difference 11
letters;95% Cl 7.83-14.17) and CRVO (mean difference
14 letters:95% Cl 10.51-17.(9). Improvements m
BCM were alsoobserved with deumethasone 0.7
mg mtravitieal implant (IVI) compaied with sham
in patieotswith BRVO or CRVO (mean difference 2.5
letters;95% Cl 0.7-4.3).The difference wassignificant
with BRVO alone, bot notCRVO alone, At 3S mo in
o large prospective RCI.a greatci proportion of
patients with BRVO gained >15 letters with laser
therapy vs.no treatmeot(OR 3.16;95% Cl1JS-8.00).
whereas no difference was observed ina 9 mo
endpoint in a smaller study, three studiesshowedoo
benefit lor laser therapy m CRVO.
Conclusion: Bath IVt rani rumab and
Betamethasone show significant improvements over
previously accepted standard of care(laser therapy)
for the treatment of BRVO and CRVO.
rhegmatogenous
scleral buckle procedure
pneumatic retinopexy
pars plana vitrectomy plus injection of gas ( injection of silicone oil in cases of recurrent
detachment, air travel, or inability to posture postoperative)
tractional
vitrectomy ± membrane removal/scleral buckling/injection of intraocular gas orsilicone oil
as necessary
• exudative
management is nonsurgical; any underlying disease should be treated if possible
Complications
• loss of vision, vitreous hemorrhage, recurrent RD
• RD is an emergency, especially if the macula is still attached (“macula on")
• prognosis for visual recovery'varies inversely with the amount of time the retina is detached and
whether the macula is attached or not
Retinitis Pigmentosa
Definition
• hereditary degenerative disease of the retina manifested by photoreceptor degeneration (rods affected
to a greater extent than cones) and atrophy
• many forms of inheritance,most commonly autosomal recessive (60%)
Clinical Features
• night blindness,decreased peripheral vision (“tunnel vision”),decreased central vision (macular
changes),glare (from posteriorsubcapsular cataracts, common)
Investigations
• fundoscopy: areas of “ bone-spicule" pigment clumping in mid-periphery of retina, narrowed retinal
arterioles, pale optic disc
• electrophysiological tests:electroretinography (ERG) and electrooculography (HOG)
Treatment
• gene treatments have the potential to reverse the condition; cataract extraction improves visual
function
• vitamin A supplementation can reduce progression of disease in some patients;avoid vitamin E
supplementation
• Voretigene neparvovec-rzyl (Luxturna*) is an l
'DA-approved novel gene therapy for children and adult
patients with biallelic RPE65 mutation-associated retinal dystrophy
Supciotemporal retina Is the most
common site for horseshoe tears
Retinitis Pigmentosa Inherited Forms
. AutosomaI recessive:most common
• Autosomal dominant best prognosis
• X-linked: worst prognosis
Triad of Retinitis Pigmentosa
APO
Age-Related Macular Degeneration Arteriolar narrowing
Perivascular bone spicule pigmentation
Optic disc pallor
Definition
• leading cause of irreversible blindness in industrialized countries, associated with increasing age.
usually bilateral but asymmetric
Classification
• Non-Exudative/“Dry” (Non-Neovascular) AMD
• most common type of AMD (90% of cases)
slowly progressive loss of visual function
drusen:yellow deposits between the RPE and Bruch’s membrane
geographic atrophy:coalescence of RPE atrophy, clumps of focal hyperpigmentation or
hypopigmentation
• may progress to neovascular AMD
• Exudative/“ \Vet” (Neovascular) AMD
10% of AMD cases; however, responsible for 80% of AMD-related vision loss
choroidal neovascularization: drusen predisposes to breaks in Bruch’s membrane causing
subsequent growth and proliferation of new, fine choroidal vessels
• may lead to serous detachment of overlying RPE and retina, hemorrhage, and lipid precipitates
into the subretinalspace
• can also lead to an elevated subretinal mass due to fibrous metaplasia of subretinal fibrovascular
proliferation that progresses to disciform scarring and severe central vision loss
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OP26 Ophthalmology Toronto Notes 2023
Risk Factors
• female
• increasing age
• family history
• smoking
• White individuals
• blue irides
Clinical Features
• variable degree of progressive central vision loss
• metamorphopsia (distorted vision characterized by straight parallel lines appearing convergent or
wavy) due to macular edema
Investigations
• Amsler grid: held at normal reading distance with glasses on, assesses macular function
• fluorescein angiography: assesses type and location of choroidal neovascularization - pathologic new
vessels leak dye
• OCT retinal imaging: assesses the amount of intraretinal and subretinal exudation
Treatment
• non-neovascular “dry” AMD
• monitor, Amsler grid allows patients to check for metamorphopsia
• low vision aids(e.g. magnifiers, closed-circuit television)
anti
-oxidants, green leafy vegetables
sunglasses/visors
• see Age-related Eye Disease Study 2 (AREDS2) in sidebar
• neovascular “wet” AMD
see Common Medications, OP44
intravitreal injection ofanti
-VEGF
pegaptanib (Macugen*), ranibizumab (Lucentis*), bevacizumab (Avastin*), allibercept
(Eylea*), brolucizumab (Beovu*) (see VEUP Inhibitors, OP45 )
no definitive treatment for disciform scarring
• photodynamic therapy with verteporfin (Visudyne*)
IV injection of verteporfin, followed by low-intensity laser to area of choroidal
neovascularization
Age-Related Eye Disease Study 2 (AREDS2)
Lutein * Zeaianthin and Omega -3Fatty Acids
I or AMD:The Age-Related Eye Disease Study 2
IARE0S2) Raedomiied Clinical Trial
JAMA 20I3;309(19|:?0D5-201S
See landmark Ophthalmology Trials table for
more information on Age- Related Eye Disease
Study 2 (ARE0S2).which details whettier adding
lutein -leaiaothin,docosalreianoic acid (DHA)
-
eitosapentanoK acid|EPA|
. or both to the AREDS
formulation decreases the riskof developing
advanced AMO and to evaluate the effect of
eliminating J carotene, lowering line doses, or
both in the AREDS formulation in patients at risk for
advanced AMD.
Ten Year follow Up of Age-Related Macular
Degeneration in the Age-Related Eye Disease
Study:AREDS Report No. 36
JAMA Ophthalmol 2014:132(3)r272-27?
Study:Ra'
darued clinical trial.
Purpose: To describe ID yr progression ratesto
intermediate or adcanced AMD.
Patients Age related eye disease study (AREDS)
participants were obsened for an additional S yr
after RCf completion.Participants ages S5-80 yt
with no AMO or AMD of varying severity (n -4757)
were followed up in the AREDS trial for a median
duration of 6.5 yr.When the trial ended,3549 of
the 42D3sunr.vtig participants were followed foe 5
additional yr.
Intervention: Treatment with antioidant vita- s
and minerals.
Main Outcome Oe velppment of vary-uig stages of
AMD and changesin VA.
Results:
(he risk of progression to advanced AMD
increased with increasing age (F0.01|and severity
of drusen.Women (P-0.005) and currentsmokers
(P'
O.OOI) were at increased risk of neovascular
AMD.In the oldest participants with the mostsevere
AMD status at baselme.the ilskt of developing
neovascular AMD and cential geographic atrophy by
10 y r were 48.fi, and 26.0%.respectively.Slim larly.
rates of progression to large drusen increased with
increasing severity of drusen at base me.with
20.9% of participants with bilateral medium drusen
progressing to large drusen and 13.8% to advanced
AMD in 10 yr.Median VA at 10 yr in eyesthat had large
drusen at baseline but never developed advanced
AMD was 20/25:eyes that developed advanced AMO
hadamedianVAof 20
'
200.
Conclusion: Thenatural history of AMDdemonstrates
relentless loss of vision in persons who developed
advanced AMD.
Glaucoma
Definition
• progressive, irreversible,pressure-sensitive optic neuropathy involving characteristic structural
changes to optic nerve head with associated visual field changes
• commonly associated with high IOP, but not required for diagnosis
Background
• aqueous is produced by the ciliary body and drains into the episcleral veins via the trabecular
meshwork and Canal of Schlemm
• an isolated increase in IOP is termed ocular hypertension (OHT) - should be followed for increased
risk of developing glaucoma
• IOP >21 mniHg increases the risk of developing glaucoma
• Central corneal thickness is important when interpreting the 10P (e.g. thicker cornea will result in
overestimation of the IOP)
• loss of peripheral vision most commonly precedes central vision loss
• structural changes commonly precede functional changes
Investigations
• VA testing
• slit-lamp exam to assess anterior chamber depth; gonioscopy to assess angle (open or closed)
• ophthalmoscopy to assess the disc features
• tonometry to measure IOP
• automated perimetry (formal visual field testing)
• pachvmetry to measure corneal thickness
• OCT of the retinal nerve fibre layer (NFL) at the optic nerve to monitor for loss of NFL
• OCT'
of the macular ganglion cell layer-inner plexiform layer ((iCIPL) to monitor for loss of (»CIPL
• follow- up includes optic disc examination, IOP measurement. OCT of the retinal NFL and macular
GC1PL and visual field testing to monitor course of disease
r -t
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OP27 Ophthalmology Toronto Notes 2023
Optic norvo lie,id damago Visual fiold changes
Average IOP:15±3 mmHg
Normal COR: s0.4
Suspect glaucoma if CDR >0.6. CDR
differs between eyes by >0.2.or cup
approaches disc margin
f /
,
Pallor and cupping of optic disc (C D ratio 02 Small paracentral scotoma -03)
w 1. Ciliary body processes
2.Flow into anterior chamber
3.Pretrabecular
4. Trabecular and Canal ol Schlernm 4
^
5.Post-trabecular
Figure 19. Aqueous flow and sites of
potentialresistance
Concentric enlargement (C:D ratio 0.5)
Arcuate defect J
Superior expansion
Temporal central island
I
a
Q
o
Advanced/total cupping
Figure 18. Glaucomatous damage
Primary Open-Angle Glaucoma
Definition
• most common type, >95% of all glaucoma cases
• unobstructed open-angle, resistance is within the trabecular meshwork
• insidious and asymptomatic,screening is critical for early detection
Risk Factors tor POAG
A FIAT
Age
Family history
Major Risk Factors
• ocular hypertension (IOP >21 mmHg)
• age: prevalence at 40 yr is 1-2% and at 80 yr is 10%
• ethnicity:African descent
• familial (2-3x increased risk); polygenic
• thin central cornea (OHTS trial)
IOP
African descent
Thin cornea
Open- and Closed-Angle Glaucoma
Minor Risk Factors
• myopia
• HTN
• DM
• hyperthyroidism (Graves’ disease)
• chronic corticosteroid use (topical significantly higher risk than oral)
• previous ocular trauma
• anemia/hemodynamic crisis (ask about blood transfusions in past)
Clinical Features
• asymptomatic initially
• insidious, painless, gradual rise in IOP due to restriction of aqueous outflow
• bilateral, but usually asymmetric
• earliest signs are optic disc changes
increased CDR (vertical CDR >0.6)
• significant CDR asymmetry between eyes (>0.2 difference)
POAG PACG
Common (9S%) Rare (St,)
MoiecommoninBack Mote common in
d-d Hispanic individuals Asian at dIndigenous
Canadians
Chronic course Acute or chronic onset
Painless eye without Painfulredeye
redness
Moderately highIOP tilremely high IOP
Normal corneaand pupil Hatycotnea
Mid-dilatedpupil
unreactrre to light
•N7, abdominal pain
N: ns around r; He '
:. d I rt
r »
L J
+
Ho MV
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OP28 Ophthalmology Toronto Notes 2023
thinning, notching of the neuroretinal rim
flame-shaped disc hemorrhage
360° of peripapillary atrophy
Nl-
'
L defect
large vessels become nasally displaced
retinal Nl-
'
L vertical thinning on OCT
GC1PL thinning on OCT
•visual field loss
•slow, progressive, irreversible loss of peripheral vision
•paracentral defects, arcuate scotoma, and nasal step are characteristics (see Figure 18,OP27)
•late loss of central vision if untreated
Elevated I0P Is the only modifiable risk
factor that has been proven to prevent
progression of glaucoma. Treating
patients with ocular hypertension but
no signs of glaucoma has also been
shown to reduce the risk of developing
glaucoma.
The Ocular Hypertension Treatment Study
Arch Ophthalmol Chic 2002:120:70T 713
S ee landmark Ophthalmology Inalstable lor more
information on Ihe Ocular Hypertension Treatment
Study, witch details the safety and efficacy of
topical ocular hypotensive Dedication in delayingor
preventing the onsetof MiG.
Treatment
•medical treatment:decrease IOP by increasing the drainage and/or decreasing the production of
aqueous (seeTable 14, Glaucoma Medications, OP44 )
increase aqueous outflow
topical prostaglandin analogues
topical a2-adrenergics
topical cholinergics/parasympathomimetics
• decrease aqueous production
topical 0-blockers
topical and oral carbonic anhydrase inhibitors
topical a2-adrenergics
•laser trabeculoplasty, cyclophotocoagulation in order to achieve selective destruction of ciliary body
(for refractory cases)
•trabeculectomy:creation of a new outflow tract from anterior chamber to under the conjunctiva
forming a bleb
•minimally invasive glaucoma surgery (MIGS): implantation of IOP lowering drainage devices (e.g.
iStent, Xen, Hydrus); high safety profile, primarily used for modest IOP reductions in patients with
mild-to-moderate glaucoma
•tube shunt (Ahmed, Baerveldt):for advanced stages of glaucoma
•serial optic nerve head examinations,IOP measurements,OCT of retinal Nl-
'
L and GC1PL, and visual
field testing to monitor disease course
Normal Tension Glaucoma
Definition
• glaucomatous optic neuropathy with IOP in normal range
• often found in women >60 yr, but may occur earlier
• associated with migraines, peripheral vasospasm,systemic nocturnal hypotension, and sleep apnea
• damage to optic nerve may be due to vascular insufficiency
Treatment
• treat reversible causes
• lower intraocular pressure
Secondary Open-Angle Glaucoma
Rule of Fours
1/4 of general population using topical
steroid for 4 wk, 4x/d wifi develop an
increase in IOP
Definition
• increased IOP secondary to ocular/systemic disorders that obstruct the trabecular meshwork
including:
• steroid-induced glaucoma: topical, periocular, and even systemic or inhalational routes can
induce open angle glaucoma, primarily due to reduced facility of aqueous outflow
• traumatic glaucoma: both blunt and penetrating injuriesleave damaged tissues and scarring that
may obstruct drainage channels and potentially raise IOP immediately after the injury or years
later
pigmentary glaucoma: a result of pigment dispersion syndrome, which is characterized by
aberrant iridozonular contact leading to iris pigment dispersion throughout the anteriorsegment
and deposition into the trabecular meshwork
• pseudoexfoliation glaucoma: a result of pseudoexfoliation syndrome, an age-related systemic
disorder where extracellular fibrillar deposits progressively accumulate over various tissues,
including the anterior segment of the eye
A. Open-angle
with normal
aqueous flow ^
aqueous flow
B. Closed-angle
with abnormal
Primary Angle-Closure Glaucoma 1.Aqueous flow
2.Ciliary body
3.Correa
4.Lens
5. Blocked trabecular meshwork 9
Figure 20. Normal open-angle vs.
angle-closure glaucoma
Definition I +
• 5% of all glaucoma cases
• peripheral iris bows forward obstructing aqueous access to the trabecular meshwork
• sudden forward shift of the lens-iris diaphragm causes pupillary block and results in impaired
drainage,leading to a sudden rise in IOP
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OP29 Ophthalmology Toronto Notes 2023
Risk Factors
hyperopia:small eye, big lens-large lens crowds the angle
• age >70 yr
• female
• family history
• more common in people of Asian and Inuit descent
• mature cataracts
• shallow anterior chamber
• pupil dilation (topical and systemic anticholinergics,stress, darkness)
Clinical Features
• red, painful eye with acute presentation = RED FLAG
• unilateral, hut other eye at increased risk
• decreased V'A, vision acutely blurred from corneal edema
• halos around lights
• nausea and vomiting,abdominal pain
• fixed, mid-dilated pupil
• marked increase in IOP;may be noticeable even to palpation (>40 mniHg)
• shallow anterior chamber ± cells in anterior chamber
§( 1
Angle-Closure Glaucoma
BACH
Tx with miotics and 3-blockers
Adrenergics
Cholinergics
Hyperosmotic agents
Collaborative Normal TrillionGlaucoma Study
Curr Opin Ophthalmol 2003:14:86 90
Irealmentalmedat toutrmg I0P by 30%*
patients
Willi normaltension glaucoma tends to reduce the
rate of visual field loss.Due to variability in disease
progression and a significant group that shows no
visualfield lossat5yt despite no treatment,further
studies are needed to delineatewhich subgroups may
benefit most from treatment
Complications
• irreversible loss of vision within hours to days if untreated
• permanent peripheral anteriorsynechiae,resulting in permanent angle closure
Treatment
• OCULAR EMERGENCY: refer to ophthalmologist for acute angle-closure glaucoma
• medical treatment (see Table 14,Glaucoma Medications, OP44 )
• aqueoussuppressants and hyperosmotic agentssuch as oral glycerine or IV mannitol
• miotic drops(pilocarpine) to reverse pupillary block
• multiple topical lOP-lowering agents
• laser iridotomy is definitive
Secondary Angle-Closure Glaucoma
Uveitis
• inflamed iris adheres to lens (posterior synechiae)
Neovascular Glaucoma
• abnormal blood vessels develop on surface of iris (rubeosis iridis), in the angle, and within the
trabecular meshwork
• due to retinal ischemia associated with PDR or CRVO
• treatment with laser therapy to retina reduces neovascularstimulus to iris and angle vessels
Pupils
• pupil size is determined by a delicate balance between the sphincter and dilator muscle tone
• sphincter muscles are innervated by the parasympathetic nervoussystem carried by CN 111
• dilator muscles are innervated by the sympathetic nervoussystem (SNS)
first-order neuron = hypothalamus-» brainstem -» spinal cord
second-order/preganglionic neuron = spinal cord -> sympathetic trunk via internal carotid artery
-> superior cervical ganglion in neck
• third-order/postganglionic fibres originate in the superior cervical ganglion, neurotransmittcr is
norepinephrine
• see Neurology, f igure 8, N8
5Targets of Retinal Signals
• Pretectal nucleus (pupillary reflex/eye
movements)
• Lateral geniculate body of thalamus
• Superior colliculus (eye movements)
• Suprachiasmatic nucleus
(optokinetic)
• Accessory optic system (circadian
rhythm)
Pupillary Light Reflex
• light shone directly into eye travels along optic nerve (CN II, afferent limb) -> optic tracts -> midbrain
• impulses enter bilaterally in midbrain via pretectal area and Edinger-Westphal nuclei
• nerve impulses then travel down CN III (efferent limb) bilaterally to reach the ciliary ganglia, and
finally to the irissphincter muscle, which results in the direct and consensual light reflexes
• receptors involved:
al- pupillary dilator muscle contraction (mydriasis)
(J2 - ciliary muscle relaxation (non-accommodation);increased aqueous humour production
M3 - pupillary'sphincter contraction (miosis); increased ciliary muscle contraction
(accommodation)
LJ
+
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OP30 Ophthalmology Toronto Notes 2023
Pupil Abnormalities
Denervation Hypersensitivity
• when postganglionic fibres are damaged, the under-stimulated end-organ attempts to compensate by
developing an increase of neuroreceptors and becomes hypersensitive
• postganglionic parasympathetic lesions (i.e. Adie's pupil)
• pupil will constrict with pilocarpine 0.125% (cholinergic agonist), normal pupil will not
pupil constricts to a near target ( light-near dissociation )
• postganglionic sympathetic lesions (i.e. Horner’ssyndrome)
Horner's pupil will dilate with apradonidine 0.5-1%, normal pupil will not ( reversal of anisocoria)
Local Disorders of Iris
• posteriorsynechiae (adhesions between iris and lens) due to iritis can present as an abnormally
shaped pupil
• ischemic damage (e.g. post-acute angle-closure glaucoma ) usually occurs at 3 and 9 o’clock positions
resulting in a vertically oval pupil that reacts poorly to light
• trauma (e.g. blunt trauma or post-intraocular surgery)
Anisocoria
• unequal pupil size
• idiopathic/physiologic anisocoria
• 20% of population
round, regular, <1 mm difference
pupils reactive to light and a near target
• responds normally to mydriatics/miotics
post eye surgery, or extensive retinal laser treatment
[ Patient with Anisocoria J
Relevant history and examination with specific attention to:
•History of ocular trauma
•Check old photographs ( ptosis, ocular deviation, long standing anisocoria)
•Use of topical medications
•Exposure to toxins and drugs
a Associated ocular and neurologic symptoms/signs
Which pupil is abnormal?
Examino pupils in light and dark
I T 1
Anisocoria accentuated
by light
(large pupil is abnormal)
Anisocoria accentuated
by darkness
(small pupil abnormal)
Anisocoria equal in
light and dark
ptosis/Ophthalmoplegiaj Isolated
Sluggish to light
Light near dissociation
Oilation lag
Ptosis
Brisk reaction
to light
I
^
Test with apraclomdmc j palsy ^
Usc of 0.1% pilocarpincj Third nerve
T T i
Small pupil does
not dilate
Both pupils dilate
symmetrically
Large pupil
constricts
Large pupil docs
not constrict
V
Adie s tonic pupil ( Use of 0 1% pilocarpine j
Horner'
ssyndrome
[ Mmimal/no constriction ]
1 f
— Physiologic anisocoria | Pharmacologic anisocoria
r 1
Patient Must Fixate on Distant Target
Figure 21. Approach to anisocoria
Reproduced with permission from:Kedar S.Biousse V.Newman NJ.Approach to the patient with anisocoria.In:UpToDate.Rose.BD (editor).
UpToDate.Waltham. MA. 2011. Copyright 2011 UpToDate.Inc. For more information visitwww.uptodate.com.
L J ,
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0P31 Ophthalmology Toronto Notes 2023
Table 9. Summary of Conditions Causing Anisocoria
Features Site of Lesion Light and
Accommodation
Anisocoria Effect of
Pilocarpine
ABNORMAL MIOTIC PUPIL (impaired pupillary dilation)
Horner's Syndrome Round,unilateral. Sympathetic system Both brisk
ptosis,anhidrosis,
pseudoenophlhalmos
Argyll-Robertson Irregular,usually Midbrain
bilateral
Greater indark N/A
Poor in light:better to
accommodation
N/A
Pupil
ABNORMAL MYDRIATIC PUPIL (impaired pupillary constriction)
Adie's Tonic Pupil Irregular,larger in Ciliary ganglion
bright light
Poor in light,better to Greater inlight
accommodation
Constricts
(hypersensitivity to
dilute pilocarpine)
CNIIIPalsy Round Superficial CN III Constricts
*
fixed(acutely) at Greater inlight
7-9mm
Pharmacologic Fixed at 7 8 mm Greater inlight
Dilation
Round,uni- or
bilateral
Iris sphincter Will not constrict
Dilated Pupil (Mydriasis)
Sympathetic Stimulation
• fight or flight response
• mydriatic drugs:epinephrine, phenylephrine
Parasympathetic Under-Stimulation
• cydoplegics/mydriatics: atropine, tropicamide, cydopentolate (parasympatholytic)
• CN Ill palsy
eye deviated down and out with ptosis present
» etiology includes microvascular ischemia (associated with vascular risk factors), vasculitis(e.g.
GCA), compression (e.g. pituitary adenoma or posterior communicating artery aneurysm), or
midbrain stroke
CN III palsy with pupillary involvement
may be associated with a posterior
communicating artery aneurysm
*
Midbrain
Acute Angle-Closure Glaucoma
• fixed, mid-dilated pupil
Adie’s Tonic Pupil
• 80% unilateral, F>M
• pupil is tonic or reacts poorly to light (both direct and consensual) hut constricts with accommodation
• caused by benign lesion in ciliary ganglion; results in denervation hypersensitivity of
parasy mpathetically innervated constrictor muscle
dilute (0.125%)solution of pilocarpine will constrict tonic pupil but have no effect on normal
pupil
• long-standing Adie’
s pupils are smaller than unaffected eye
Trauma
• damage to irissphincter from blunt or penetrating trauma
• iris transillumination defects may be apparent using ophthalmoscope or slit-lamp
• pupil may be dilated (traumatic mydriasis) or irregularly shaped from tiny sphincter ruptures
TJasilar
artery Posterior
communicating
artery CN III
Norniel
Post. comm, artery
— Parasymp.
Somatic motor
Externally Compressive CN III Lesion
Constricted Pupil (Miosis)
Senile Miosis
• decreased sympathetic stimulation with age
Parasympathetic Stimulation
• local or systemic medicationssuch as:
• cholinergic agents:pilocarpine, carbachol
opiates, barbiturates
Horner’s Syndrome
• lesion in sympathetic pathway
• difference in pupil size greater in dim light, due to decreased innervation of adrenergics to iris dilator
muscle
• associated with ptosis and anhidrosis of ipsilateral face/neck (in pre-ganglionic lesions)
• apraclonidine (strong a-2 and weak a-1 blocker) is the most common pharmacologic diagnostic test,
in which denervation hypersensitivity resultsin dilation of the Horner pupil but not the normal pupil
(leading to reversal of anisocoria)
mydriasis
A.Post. comm.
artery
.Hi
'
.1
uryVII
Central Vascular CN III Lesion
J
^
G> Andreea Margineanu 2012
^
Figure 22. CN III lesions with and ~l
~
without mydriasis
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OP32 Ophthalmology Toronto Notes 2023
• application of cocaine 4-10% (blocks reuptake of norepinephrine) to eye does not result in dilation of
the Horner’s pupil, whereas the normal pupil will dilate, thereby confirming the diagnosis
• hydroxyamphetamine 1% (stimulates norepinephrine release) will dilate pupil if central or
preganglionic lesion, not postganglionic lesion
• cocaine and hydroxyamphetamine are rarely used in practice due to issues with availability
• causes: mostly idiopathic but other causesinclude brainstem infarct (lateral medullary syndrome),
Pancoast tumour, neck surgery, and carotid artery dissection
• must rule out carotid artery dissection in acute Horner’s syndrome (<14 d old)
Iritis
• miotic pupil initially
• can become irregularly shaped pupil due to posteriorsynechiae
• later stages non-reactive to light
§< !
Homer’s MAP
Miosis
Anhidrosis
Ptosis
Argyll-Robertson Pupil
• both pupils irregular and <3 mm in diameter, ± ptosis
• does not respond to lightstimulation
• responds to accommodation (light-near dissociation)
• suggestive of neurosyphilis or other conditions(DM, encephalitis, MS, chronic alcoholism,CNS
degenerative diseases)
Relative Afferent Pupillary Defect
Normal Pupillary Response
Direct response Consensual response
<jfh.
Constriction of Constriction ol
stimulated eye unstimulated eye
1.Swinging Light Test
Normal eye Pathological eye
Constriction of both pupils to normal
\
2. Swinging Light Tost
Normal eye Pathological eye
Aqueduct
Pretectal nucleusEdinger-Westphal - fj
nucleus (III) ( (
, ."0>
Constriction of both pupils to normal
\
Oculomotor nerves dill
Optic chiasm s 3. Swinging Light Test
Normal eye Pathological eye
<jSK,
Pupils appear to dilate = positive RAPO
Optic nerve (111-
iSCilliary : -
ganglion 3
I
t
_
Constrictor muscles a
ol pupil Rapidly swing light to pathological eye ,,
Figure 23. Relative afferent pupillary defect
• also known as Marcus Gunn pupil
• impairment of direct pupillary response to light caused by a lesion in visual afferent (sensory)
pathway, anterior to optic chiasm
• differential diagnosis: any unilateral or asymmetric optic neuropathy (e.g. optic neuritis, ischemic
optic neuropathy, compressive optic neuropathy) orsevere retinopathy (e.g. CRAG, large RD, GRVO)
• does not occur with media opacity'(e.g. corneal edema, cataracts) or if optic neuropathy issymmetric
(since it is relative)
• pupil reacts poorly to light and better to accommodation
• test:swinging flashlight
if light is shone in the affected eye, direct and consensual response to light is decreased
• if light is shone in the unaffected eye,direct and consensual response to light is normal
• if the light is moved quickly from the unaffected eye to the affected eye, “paradoxical” dilation of
both pupils occurs
observe red reflex, especially in patients with dark irides
Cataracts never produce a RAPD
Differentiate
6
RAPD from physiologic
pupillary athetosis (“hippus"),which is
rapid,rhythmic fluctuations of the pupil,
with equal amplitude in both eyes
n
LJ
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OP33Ophthalmology Toronto Notes 2023
Malignancies
• uncommon site for 1° malignancies
• see Retinoblastoma,UP40
Lid Carcinoma a
Etiology
• basal cell carcinoma (90%)
spread via local invasion, rarely metastasizes
ulcerated centre (rodent ulcer), indurated base with pearly rolled edges, telangiectasia
• squamous cell carcinoma (<5%)
spread via local invasion, may also spread to nodes and metastasize
• ulceration, keratosis of lesion
• sebaceous cell carcinoma (1-5%)
often masquerades as chronic blepharitis or recurrent chalazion
highly invasive, metastasizes
• other:Kaposi’ssarcoma,malignant melanoma, Merkel cell carcinoma, metastatic tumour
Treatment
• incisional or excisional biopsies
• may require cryotherapy, radiotherapy, chemotherapy, immunotherapy
• surgical reconstruction
To Find Small Ocular Melanoma
TFSOM
Thickness >2 mm
Subretinal Fluid
Symptoms- vision changes
Orange pigment
Margin within 3mm of optic disc
Uveal Melanoma
Etiology
• most common lu intraocular malignancy in adults
• more prevalent in White individuals
• arise from uveal tract,90% choroidal melanoma
• hepatic metastases predominate
Clinical Features
• classic appearance of a pigmented dome-shaped mass extending from the ciliary body or the choroid
• diagnosis necessitates expertise of an ophthalmologist/ocular oncologist
• despite treatment, has the possibility of remaining dormant and resurfacing with metastasis years
later
Treatment
• investigations:ocular ultrasound, fluorescein angiography, OCT, and systemic cancer investigations
• depending on the size of the tumour, either radiotherapy ( brachytherapy vs. external beam), or
enucleation
Metastases
•most common intraocular malignancy in adults
•most commonly from breast and lung in adults, neuroblastoma in children
•usually infiltrate the choroid, but may also affect the optic nerve or extraocular muscles
•may present with decreased or distorted vision, irregularly shaped pupil, iritis,and hyphema
Treatment
•local radiation, chemotherapy
•enucleation if blind, painful eye, or large tumour
Ocular Manifestations of Systemic Disease
HIV/AIDS
ri
LJ
•up to 75% of patients with AIDS have ocular manifestations
External Ocular Signs
•Kaposi’
ssarcoma
secondary to human herpes virus8 (HH V-8), causes bright red conjunctival lesion and
subconjunctival hemorrhage
differential diagnosis:subconjunctival hemorrhage (non-clearing), hemangioma
•multiple molluscum contagiosum
•herpessimplex/zoster keratitis
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