5. Toronto Notes 2011 Dl1fermtialDlagnolesofCommon Pre8entaliom/Oclllarl!mergmci5/0cularI!Jam.inalion Ophthalmology OPS
Ocular Problems in the Elderly
• blepharitis
• ptosis
• entropion, ectropion
• dry eyes, epiphora (excessive tearing)
• presbyopia
• cataracts
• glaucoma
• age-related macular degeneration
• retinal artery/vein occlusion
• temporal arteritis (arteritic ischemic optic neuropathy)
Ocular Problems in the Contact Lens Wearer
• superficial punctate keratitis (SPK)/dry eyes
• solution hypersensitivity
• tight lens syndrome
• corneal abrasion
• giant papillaryconjunctivitis
• sterile corneal infiltrates (immunologic)
• infected ulcers (Pseudomonas, Acanthamoeba)
Ocular Emergencies
These require urgent consultation to an ophthalmologist for management
Sight Threatening
• lid/globe lacerations
• corneal ulcer
• gonococcal conjunctivitis
• acute iritis
• acute angle-closure glaucoma
• central retinal artery occlusion (CRAO)
• intraocularforeign body
• retinal detachment (especiallymacula threatening)
• endophthalmitis
Life Threatening
• proptosis (rule out cavernous sinus fistula or thrombosis)
• CN III palsy with dilated pupil (intracranial aneurysm or neoplastic lesion)
• papilledema (must rule out intracranial mass lesion)
• orbital cellulitis
• giant cell (temporal) arteritis
• leukocoria - white pupil (must rule out retinoblastoma)
The Ocular Examination
Note: Sometimes vision maybe blurry secondary to eye drops/ointment/mucus or
applying too much pressure when patching. Encourage the patient to blink before starting the
exam and wait until the patient's vision is clear before continuing.
VISION ASSESSMENT
• always testvisual acuity first
• test best corrected visual acuity (BCVA) whenever possible (i.e. corrective lenses)
• test each eye individually, starting with the right eye, and covering the untested eye
• assess distance and near vision
• improvement with a pinhole indicates an uncorrected refractive error
Visual Acuity- Distance
• Snellen Fraction (Figure 5) = testing distance (usually 20 feet or 6 metres)
smallestline patient can read on the chart
• e.g. 20/40 =what the patient can see at 20 feet (numerator), a person can see at
40 feet (denominator)
Exlmple1
sc
V20140-1
20180 +2 20125 PH
Exli1J11Ie2
cc
VCFJ'
HM
NDIII: RIGHT EYEvisual acuity
always listed on top.
V Vision
Sl: Wrthout correction
1:1: Wrth coi1'8Ction
20/40 ·1 All wa:upt one llllter of
20/40
20/88+2 All of20180 plus two
letters of 20170
PH Visulllacuity wi1h pinhole
correction
I:F Counting fingers
HM Hand motion
Figura 5. Ophthalmalagy
Nomenclature for Visual Acuity
6. OP6 Ophthalmology
.....',
..
• OD oculusdut.r right wr-
• OS ocululi sinister lsft eyu
• OU =oculus uterqua =both eyes
.....' ,
..
A SnaUen viSUIIIacuity of2Qf2D aquabls
111 "normal" vision.
.....',
..
Infantand Child Villlll Acuity
• 6-12 months - 201120
• 1-2yell'$-2CV80
• 2-4 ye.,.. - 201'20
CFjCF
RIGHT m fields d111W1'1 on right side;
LEFT EYE fiulds drawn on lull side
{as ifseen through patient's eyes).
CF Able to count fingers in
spacified quadrant with
peripheral vision
Gross visual field deficit in
specified quadrant using
peripheral vision
Figure 6. Ophthalmology
Nomenclaturefor Visual Fialds by
Confrontation
.....',
..
For patients with dlllk iris11, IIISt the
pupils using an ophthalmoscopefocusad
onlha rad rellex. Thiswill provide a
b.u.rviM'than using a panlight.
....',
a.anglngliutiun from dilltance tu
_, r•• ilthe "near rwlllx"":
1. Eye convaroence
2. Pupil constriction
3. Lens accommodation
The Ocular Examination Toronto Notes 2011
• testing hierarchy for lowvision: Snellen acuity (20/x) -+ counting fingers at x distance (CF) -+
hand motion (HM) -+light perception with projection (LP with projection) -+ light perception
(LP) -+ no light perception (NLP)
• legal blindness is BCVA that is in the better eye, or a limit to the binocular central field
ofvision <20 degrees
• minimum visual requirements to operate a non-commercial automobile in Ontario are: with
both eyes open and examined together, 20/50 BCVA, a visual field of120 continuous degrees
along the horizontal meridian, and a visual field of15 continuous degrees above and below
fixation
Visual Acuity- Near
• use pocket vision chart (Rosenbaum Pocket VISion Screener)
• record Jaeger (]) or Point number and testing distance (usually 30 em) e.g. ]2 @ 30 em
• conversion to distance visual acuity possible (e.g. immobile patient, no distance chart available)
Visual Acuity for Infanta, Children, Non-English Speakers, and Dysphasics
• newborns
• visual acuity cannot be tested
• 3 mos-3 yrs (can only assess visual function, not acuity)
• test each eye fur fixation using an interesting object
• noted as "CSM• = central, steady and maintained
• 3 years until alphabet known
• pictures or letter cards/charts such as the HOTV or Sheridan-Gardner test (children point to
the optotypes on a provided matching card)
• tumbling "En chart
Colour Vision
• test with Ishihara pseudoisochromatic plates
• record number ofcorrectly identified plates presented to each eye, specify incorrect plates
• important for testing optic nerve function (e.g. optic neuritis, chloroquine use, thyroid
ophthalmopathy)
• note: red-green colour blindness is sexlinked and occurs in 7-10% ofmales
VISUAL FIELDS
• test "visualfields byconfrontation" (4 quadrants, each eye tested separatdy) for estimate of
visual field loss (Figure 6)
• accurate, quantifiable assessment with automated visual field testing (Humphrey or Goldmann)
or Tangent Screen
• use Amsler grid (each eye individually) to test for central or paracentral scotomas (island-like
gaps in the vision}, for patients with AMD
PUPILS
• use reduced room illumination with patient focusing on distant object to prevent "near reflex"
• examine pupils for shape, size, symmetry and reactivity to light (both direct and consensual
response)
• test for relative afferent pupillary defect (RAPD) with swinging flashlight test
• test pupillary constriction portion ofnear reflexby bringing object close to patient's nose
• "normal• pupil testing often noted as "PERLA" = pupils equal, round, and reactive to light and
accommodation
ANTERIOR CHAMBER DEPTH
• shine light tangentially from temporal side
• shallow anterior chamber: >2/3 ofnasal side ofiris in shadow (Figure 9}
EXTRAOCULAR MUSCLES
Alignment
• Hirschberg corneal reflex test
• examine in primaryposition ofgaze (e.g. straight ahead) with patient focusing on distant
object
• shine light into patient's eyes from -30 em away
• corneal light reflex should be symmetric and at the same position on each cornea
• strabismus testing as indicated (cover test, cover-uncover test, prism testing)
(see Strabismus, OP38)
7. 'IbroDloNota2011
Movement
• examine movement ofeyeball throughsix cardinal positionsofgaze (Figure8)
• askpatientifdiplopiais presentinanypositionofgaze
• ohllerve for horizontal, vertical or rotatorynystagmus (rhythmic, oscillatingmovements ofthe
eye)
• resolvinghorizontal nystagmus at endgazeis usuallynormal
• see sideboxfor cranialnerve Innervationofextraocularmuscles
EXTERNAL EXAMINATION
• thcfuurTh
• lymph nodes (preauricular, submandibular)
• ll.d8
•lashes
• lacrimal system
SUT·LAMP EXAMINATION
1. l'owllrlliWib;h !orVDff)
2. Slit limpjoyltic:k canlnll
3. l..oeki1gknob
ol. Ocular
5. Mllgnilicatian kmb
I. Brightnass lll;.stmantllw«
1. Slit beam hllittrt11$1&1mantknob
I. Slit beamwidlh lldjJstmentknob
9. Palient-P"ilirilutiwne
1D. Fanll,.j lltAp
11. l'aliantchiueat
12. Cl*l reathe9rt knob
Figura 7. Slit-L..mp
Tha aph'llllholagy nolll: Sitlimp 111111m
,....-....., '* LU ok
injectad SC ok
1+ .... I( cle.-
2+ calli AC d+q
:::..::
Dllllailris/Antaiorawfm:e
oflans
0
lale: RIGHTEYE dnrwn onlhe left, LEfT EYE
cnwnonlha right(88 i looking atpatient'•
face).
Ill L.ids,luha, lacrimal
SC: Sclera. conjllllltiva
I Cornea
AC Anteriorchamller
d+• Daap (notshllowland quia! lno eels
inAC)
IS
Allyabnormalityorpathology is4hwn on
1118sketch II1118approprilllllocation, and is
labellllla.g.1richilail.oon.iunetivitisl
apisclaritiii'ICIIritia. canwalllllruia111ulcar,
foraign body, etc.)
• systematicallyaamine allstructuresoftheanteriorsegment+anteriorvitreous
• lids (includingupper lidewrsion ifnecessary), lashes, andlacrimalsystem
• conjunctiva andsclera
• cornea
• iris
OphthalmolOBY 01'7
SR 10
LR
'
.,
, /Sit
Milo Ji5 •LR
IR SO
C ShorryH. Lli 200&
Figura I. Dill•oatic Pasil:ia• Df
GilD1D llallltB Prim1ry Ac:tia• of
EaGIJMacle
...... ',
.
• CN Ill - Suplliot Madill IIIII lnillriar
11actus. lnflliorOlllique
• CN IV- Superior ISO)
• CNVI - l.attnll Rectu•!LR)
---
Sbalow
Light
10Un:8
---+
9. Ellimetian ofAllteriar
Cha•b• hptll
..... ,
Cellini Comaln--...
A¥11111111CCT = 550 IIIII
Alhi:k CDRIIIIIJIIIIrllllirnlllaiiDP by
GAT
Athin com811Dda11181irnlllaiiOP by
GAT
8. OP8 Ophthalmology
T,&
114
Not.: RIGHT EYE lOP alwav- lill'led
ontop.
Nate mllhod usedto maasura lOP
(Goldmann, Tonopen. airpulll.
Figure 10. Tonometry
Dllirad MynPatlam 1111 GAT
NOla: Thick Myers oV81'86linatethe lOP
and 1111a of&KCBSS fluoi8ScBin
.... ,
..
Ouic:k Tipa on Direc:t Ophthlln•copy
1. Examine in adarkroom
2.Ask patienttofol:u1 on a dimnt
object
3. Mall:h ophthalmoscopa light apar1ure
to siza of pupil (i.e. smaller apartura
for Llldilallld 8Yfl)
4. Uu modanlta light intan1ity
5. Useyour lefVriglrt eye and hand
to examine patient'• left/right eye
mpactivaly
6. Gat in cloHI Proximityto patient's
eye is keywith hand rastinq on
patient's cheek
@MIN
(nannal disc, macula, nualll
C:D 0.3 C:D 0.4
Nn: RIGHT EYE drawn on1he left,
LEFT EYE drawn on the right(as if
looking Ill patient'sface(.
C:D Cup:Disc ratio
X FCIVBI
Ally abnolllllllily or pathology of1he
fundus is drawn on tile sketch in the
appropriate location. and is labelled
(e.g. hemorrhages, neovasculariillllion,
cotton-wool epa._, d111sen,
retinaltear/dlllachmant, ate.).
Figura 11. Fundus
....,,
..
StructiiNI Reaponsllllefor Rafracti¥1
Power
1. Cornu (113)
2. Lens (113)
..... ,
..
Diopter (D) - measurement of
rufTaclive power of a len1, equal to 1he
reciprocal of1he focalleng1h in meters
"Nagalive"lam concaw, coiTlll:bi
for myopia
"Polilive" lens =convex, col'l'8ctlfor
hyparopil
Ocular Examination/Optics
• anterior chamber (for depth, cells and flare)
• to observt: cells and flare
I. Darkroom
2. High power beam
3. 1mm beam height
4. Thin beam
5. Highest magnification
Toronto Notes 2011
6. Approach at angle and focus on anterior chamber (space between cornea and lens)
•lens
• anterior vitreous
• when necessary, use:
• fluorescein dye - stains Bowman's membrane in de-epithelialized cornea; dye appears green
with cobalt blue filterered light
• Rose Bengal dye - stains devitalized corneal epithelium
• special lenses (78 or 90 diopter) used with the slit-lamp allow a binocular, stereoscopic view of
the fundus andvitreous
TONOMETRY
• measurement ofintraocular pressure (lOP) (Figure 10)
• normal range is 10-21.5 mmHg (average 15 mmHg)
• commonly measured by:
• Goldmann applanation tonometry (GAT) -gold standard, performed using the slit-lamp
with special tip (prism)
• Tonopen - benefit is portability and use ofdisposable probe tips. Use when cornea is
scarred/assymetric (GAT inaccurate)
• air puff(non-contact and least reliable)
• use topical anesthetic for Goldmann and Tonopen
OPHTHALMOSCOPY/FUNDOSCOPY
• performed with:
• direct ophthalmoscope (monocular with small field ofview, onlyposterior pole visualized)
• slit-lamp with 78 or 90 diopter lens (binocular view, visualization to mid-periphery ofretina)
• indirect ophthalmoscopy with headlamp and 20 or 28 diopter lens (binocular view,
visualization ofentire retina to oraserrata/edge ofretina)
• best peformed with pupils dilated (see Table 8 for list ofmydriatics and cycloplegics)
1.assess red reflex
• light reflected offthe retina produces a "red reflex" when viewed from -1 foot away
• anything that interferes with the passage oflight will diminish the red reflex (e.g. large
vitreous hemorrhage, cataract)
2.examine the posterior segment ofthe eye (Figure 11)
• vitreous
• optic disc (colour, cup:disc ratio, sharpness ofdisc margin)
• macula (-2 disc diameters temporal to disc), fovea (foveal light reflex)
• retinal vessels
• retinal background
• contraindications to pupillarydilatation
• shallow anterior chamber - can precipitate acute angle-closure glaucoma
• iris-supported anterior chamber lens implant
• potential neurologic abnormality requiring pupil evaluation
• use caution with cardiovascular disease - mydriatics may cause tachycardia
Optics
REFRACTION
• two techniques used
• Flash/Streak Retinoscopy- refractive error determined objectively bythe examiner by use of
lenses and retinoscope
• Manifest- subjective trial using phoropter (device the patientlooks through that is equipped
with lenses)
• a typical lens prescription would contain:
• sphere powerin diopters (D), negative lens for myopes, positive lens for hyperopes
• cylinder power (in D) to correct astigmatism (always positive value), axis of cylinder in
degrees
• (bifocal/progressive reading lens) for presbyopes
• e.g. -1.50 + 1.00 x 120 degrees, add +2.00
9. Toronto Notes 2011 Optics
REFRACTIVE EYE SURGERY
• pennanentlyalters cornealrefractive properties by ablating tissue to changecurvature ofthe
cornea
• used for correction ofmyopia, hyperopia, and astigmatism
• common types includephotorefractivekeratectomy(PRK) and LASIK (see Surgical
ophthalmology, OP43)
• potential risks/side-effects: infection, undercorrection/overcorrection, decreased night vision,
cornealhau, dryeyes, regression, complete sever ofcorneal flap (LASIKonly)
Table Z. Optics
Pllllopllysialogy Clinical Flllu11s Trtllment Complications
Elmwtrupia • Image ofdisllrrt objects focus • Norefnlctiw em1r
Myopia
lfrperopil
exactly on 1he retina (Figure 12)
• Globetoo long relrtiw ID
refractive mechanisms, or
refractive mechanismstoo
strong
• "Nearsightedness" • Correctwi1h • Retinal tear/
• Usually presentsillst or nagative ciopter/ detachment,
2nd decede,atabilims in concava'"negative" macular hole,
2nd end 3rd decade; nnly lenses to diverge light openangle
• rays from distant object
focus in front ofretina -+ blurring
of(distance) vision (Figure 12)
begins after age 25 except in rays (Figure 13) glaucoma
patientswi1h diabiii8S • Refractive eyesurgery • Corrf)lications
orcalllracts not pr8V8111ed
• Blurring ofdislllnce wi1h refractive
vision; near viision usually correction
unaffected
• Prevalence of 30-40%in U.S.
populatim
• Globetoo short relative to
refractive mechanisms, or
refractive mechanismstoo
weak
• "Farsightedness" • When syrqJtomatic.
• You1h: usuallydo not require correctwi1h positive
glasses (still have sufficient Oiopter/COI1V8lll""plus"
accommodative abilityto lense& to COIIV8rge light
• rays from distant object
focus behild retina -+ blurring of
near ± distant vision (Figure12)
focus imageonretina), rays (Figure 13)
butmay develop • Refractive eyesurgery
• May be developmenllll ordue
ID any etiology 1hBIshoriBns
globe
accommodative esotropia
(see Stnlbismus, OP38)
• 30s-40s: blurring ofnear
vision due ID decreased
accommodation, may need
reading glasses
• >50s: blurring ofdislllnce
vision due ID severely
decreased accommodation
• rays not refracted uniformly • Affects approxinately30%
in all meridians due to of population, wi1h
non-spherical surface ofcom811S prevalence inCIIIIISing
or (e.g_ wi1hage
football-shaped) • Mild astigmatism
• Two types: unnoticeable
• Ragular- cuMIIuru • Hijler amount& of
uniformly differentin astigmatism may cause
meridians at rightanglesto blurry vision, s!JJinting,
each other as1henopia, orheadaches
• 1111111ular-distorllld cornea
causedby injury, karBioconus
(cone-shaped cornea),
corneal scar, orsevere
dryeye
• Normal aging process • Ifinitiallyemmetropic,
(>40 yeali) person beginstil hold
• Hardening/reduced reading material farther
of1he lens results in decreased away, but distancevision
accommodative ability remains unaffected
• Accommodative power is 140 at • Ifinitiallymyopic, person
age 10, diminishesto 3.50 by 40 removes distlrlce glasses to
• Near images cannotbe focused read
onto 1he retina (focus is behind • Ifinitiallyhyperopic,
1he retina as in hyperopia) ofpre5byapia
occur earlier
• Correctwi1h cylildrical
lens (ifregular),
trycontact lens (if
irregular)
• Refractive eyesurgery
• Correctwi1h positive
diopter/convex!"plus·
lenses for reading
• Angl&-closure
glaucoma,
particulal1y later
in life as lens
AliSDII'Ielropil • OiffwaJce in refractive em1rs
between eyes
• Second most
common cause
of amblyopia i1
children
Ophthalmology OP9
==@F
Emmetropil
==@F
Myopia
Hyperopia
Figura 12. Emmetropia and
Refractive Enors
]?@F
Hyperopia corrected wi1h
positive COIMIIlJiniJIBns
Myopia COIT8CI8d wi1h
negative divefvilg lens
Figura 13. Correction of Refractive
Errors
10. OP10 Ophthalmology
.....,,
Orbillll cellulitis islif&-1hrelll8ning if
untrllllllld (morllllity of 17-2D'l(,without
antibiotic U&B). Promptdiagnosis and
treatment is essential.
The Orbit
The Orbit
Globe Displacement
Table 3. EXDphthelmos (proptosis) end Enophthalmos
Dlfinition
IIIVIIItigatians
Exaphtllllmos (proptosis)
• Anteriordisplacement (protrusion) crf the globe
• Exophthalmos generally refers toan endocme
etiologyor protrusion of >1Bmm {as measured by
aHBrtelaxophthalmometer)
• Ploptosis generally refers to Dlher etiologies (e.g.
cellulitis) or protrusion of <1Bnm
• CT/MRI head/orbits, LJ!rasound orbits, thyroidfunction
tests
Toronto Notes 2011
Enaphlllalmas
• Posteriordisplacement [retraction) crfthe globe
• CTJMRI orbits
Etiology • Note: ruleout pseudoexophthalmos (e.g. lid retraction) • •Blow-out"fracture {see Ocular Trau11111. OP42)
• Graves" disease [unilateral or bilalllral, mostccmmon
causa in adults)
• Orbital cellulitis most conmon cause in
children)
• Primary orsecondary orbital tumours
• OrbitaVretrobulbar hemorrhage
• Cavernous sinus lhronilosis orfistula
Preseptal Cellulitis
• infection ofsoft tissue anterior to orbital septum
Etiology
• usuallyfollows periorbital trauma or dennal infection
Clinical Features (Table 4)
• tender, swollen and erythematous lids
• ± low-grade fever
• Orbital flit atrophy
• Congarital abnonnality
• MeiBsllltic disease
• NORMAL visual acuity, pupils, extraocular movements (EOM)
• NO exophthalmos or RAPD
• may lead to orbital cellulitis
Treatment
• warm compresses
• systemic antibiotics (suspect H. influenzae in children; S. aureu.s or Streptococcus in adults)
• e.g. amoxilin-clavulanic add
• ifsevere or child <1 year treat as orbital cellulitis
Orbital Cellulitis
• OCULAR. and MEDICAL EMERGENCY
• inflammation oforbital contents posterior to orbital septum
• common in children, elderly and immunocompromised
Etiology
• usually secondaryto sinus/facial/tooth infections or trauma
Clinical Features (Table 4)
• decreasedvisual acuity, red eye
• pain with and without movement
• headache and fever
• lid erythema, tenderness, and edema with difficulty opening eye
• conjunctival injection and chemosis (conjunctival edema)
• proptosis, limitation ofocular movements (ophthalmoplegia)
• ±RAPD
Treatment
• admit, blood cultures x2, orbital CT, IV antibiotics (ceftriaxone +vancomycin) for 1week
• surgical drainage ofabscess with close follow-up, especially in children
11. Toronto Notes 2011 TheOrbit/LacrimalApparatus
Complications
• optic nerve inflammation, cavernous sinus thrombosis, meningitis and brain abscess with
possible loss ofvision, death
Tabla 4. Differentiating Between Prasaptal and Orbital Cellulitis
Finding Freseptal Cellullis
Fever
Lid edema
Chemosis
Proptosis
Pain on eye movement
Ocular mobility
Vision
RAPD
Leukocytosis
ESR
findings
May be present
Moderateto severe
-or mild
Normal
Normal
Abnnt
Moderate
Nonnal or elevated
Skin infection
Lacrimal Apparatus
• tear film made up ofthree layers
Orbital Celulitil
Present
Severe
Marked
+
+
Decreased
Dininished ±diplopia
Maybn88n
Marked
Elevated
dental abscess
• an outer oilylayer (reduces evaporation): secretedby the Meibomian glands
• a middle waterylayer (forms the bulkofthe tear film): constantsecretion from conjunctival
glands and reflex secretionby lacrimalgland with ocular irritation oremotion
• an inner mucinous layer (aids with tear adherance to cornea): secretedbyconjunctivalgoblet
cells
• tears drain from the eyes through upperand lower lacrimalpuncta -+ superior and inferior
canaliculi -+ lacrimal sac -+ nasolacrimalduct -+ nasal cavitybehind inferiorconcha (Figure 3)
Dry Eye Syndrome (Keratoconjunctivitis Sicca)
Etiology
• idiopathic - tear production normallydecreases with aging
• blepharitis
• ectropion - downward and outwardturning oflower eyelid
• decreased blinking (CN VII palsy)
• diminished cornealsensitivity (e.g. neurotrophic keratitis)
• systemic diseases: rheumatoid arthritis, Sjogren's syndrome, sarcoidosis, amyloidosis, leukemia,
lymphoma
• medications: anticholinergics, diuretics, antihistamines, oral contraceptives
• vitamin A deficiency
Clinical Features
• dryeyes, red eyes, foreign bodysensation, blurredvision, tearing
• slit-lamp exam: decreased tear meniscus, decreased tear breakup time (TBUT, normally should
be 10 seconds), superficial punctate keratitis (SPK)
• stains withfluorescein/Rose Bengal
• Schirmer's test: measures tear quantity on surface ofeye in 5 minute time period (<10 nun of
paper strip wetting in 5 minutes is considered a dry eye)
Complications
• erosions and scarring ofcornea
Treatment
• medical: nonpreserved artificial tears up to qlh and ointment at bedtime (preservative toxicity
becomes significantifused more than q4h)
• procedural: punctal occlusion (punctal plug insertion), lid taping, tarsorrhaphy (sewlids
together) if severe
• treat underlyingcause
Ophthalmology OP11
12. OP12 Ophthalmology
.....,,
Excessive tearing can be caused by dry
eyes- if lhatear quality is insufficient.
"reflextearing" mil'(occur.
Lacrimal Apparatus Toronto Notes 2011
Epiphora (Excessive Tearing)
Etiology
• emotion
• environmental stressor (cold, wind, pollen, sleep deprivation)
• ectropion, entropion, trichiasis
• conjunctivitis
• corneal foreign body, keratitis
• dryeyes (reflex tearing)
• lacrimal drainage obstruction (aging, rhinitis, dacryocystitis, congenitalfailure of canalization)
• paradoxical lacrimation (crocodile tears)
Investigations
• using fluorescein dye, examine for puncta! reflux bypressing on canaliculi
• Jones dye test - fluorescein placed in conjunctival cul-de-sac, and cotton applicator placed in
nose to detect flow (ie. rule out lacrimal drainage obstruction)
Treatment
• lid repair for ectropion or entropion
• eyelash removal for trichiasis
• puncta! irrigation
• nasolacrimal duct probing (infants)
• tube placement temporary (Crawford) or pennanent (Jones)
• surgical: dacryocystorhinostomy (DCR) - forming a new connection between the lacrimal sac
and the nasal cavity
Dacryocystitis
• acute or chronic infection ofthe lacrimal sac
• most commonly due to obstruction ofthe nasolacrimal duct
• commonly associated with S. aureus, S. pneumoniae, Pseudomonas species
Clinical Features
• pain, swelling. redness over lacrimal sac at medial canthus
• tearing, crusting. ± fever
• digital pressure on the lacrimal sac may extrude pus through the punctum
• in the chronic fonn, tearing maybe the only symptom
Treatment
• warm compresses, nasal decongestants, systemic and topical antibiotics
• ifchronic, obtain cultures by aspiration
• once infection resolves, consider dacryocystorhinostomy (see SurgicalOphthalmology, OP43)
Dacryoadenitis
• inflammation ofthe lacrimal gland (outer third ofupper eyelid)
• acute causes: S. aureus, mumps, EBV, herpes zoster, N. gonorrhoeae
• chronic causes: lymphoma, leukemia, sarcoidosis, tuberculosis, thyroid ophthalmopathy
Clinical Features
• pain, swelling. tearing, discharge, redness ofthe outer region ofthe upper eyelid
• chronic form is more common and may present as painless enlargementofthe lacrimal gland
Treatment
• supportive: warm compresses, oral NSAIDs
• systemic antibiotics ifbacterial cause
• ifchronic, treat underlying disorder
13. Toronto Notes 2011 Lida andLashes
Lids and Lashes
Lid Swelling
Etiology
• commonly due to allergy, with shrivellingof skinbetween episodes
• dependent edema on awakening (e.g. CHF, renal or hepatic failure)
• orbital venous congestion due to mass or cavernous sinus fistula
• dermatochalasis (loose skin due to aging or heredity)
• lid cellulitis, thyroid disease (e.g. myxedema), trauma, chemosis
Ptosis
• drooping ofupper eyelid
Etiology
• aponeurotic: disinsertion or dehiscence oflevator aponeurosis (most common)
• associated with advancing age, trauma, surgery, pregnancy, chronic lid swelling
• mechanical
• incomplete opening ofeyelid due to mass or scarring
• neuromuscular
• myastheniagravis (neuromuscular palsy), myotonic dystrophy
• CN III palsy
• Homer's syndrome
• congenital
• pseudoptosis (e.g. dermatochalasis, enophthalmos, contralateral exophthalmos)
Treatment
• surgery
Trichiasis
• eyelashes turned inwards
• may result from chronic inflammatorylid diseases (e.g. blepharitis), Stevens-Johnson
syndrome, trauma, burns
• patient complains ofred eye, foreign body sensation, tearing
• may result in corneal ulceration and scarring
Treatment
• topical lubrication, eyelash plucking. electrolysis, cryotherapy
Entropion
• lid margin turns in towards globe causing tearing, foreign body sensation and red eye
• most commonly affects lower lid
• may cause abrasions with secondary corneal scarring
Etiology
• involutional (aging)
• cicatricial (herpes zoster, surgery, trauma, burns)
• orbicularis oculi muscle spasm
• congenital
Treatment
• lubricants, evert lidwith tape, surgery
Ectropion
• lid margin turns outward from globe causing tearing and possiblyexposure keratitis
Ophthalmology OP13
....,
Te.ting t.r Entropio•
Fon:1d lid closur1: Ask plllilr'llto tigiDn
lidthan open. In lllllropion, lid roll&
inwerds.
Te.ting t.r Ectropio•
Sn1pbacktest: Pul eyelid inferiorly. In
ectropion, lid --vfrom globe.
14. OP14 Ophthalmology Ucla and Lashes Toronto Notes 2011
Etiology
• involutional (aging)
• paralytic (CN VII palsy)
• cicatricial (bums, trauma, surgery)
• mechanical (lid edema, tumour, herniated fat)
• congenital
Treatment
• topical lubrication, surgery
Hordeolum (Stye)
• acute inflammation ofeyelid gland - either Meibomian glands (internal lid) or glands of
Zeis (modifiedsweat gland) or Moll (modified sebaceous glandin external lid)
• infectious agent is usually S. aureus
• painful, redswellingoflid
Treatment
• warm compresses,lidcare, gentle massage
• topical antibiotics (e.g. erythromycin ointment BID)
• usuallyresolves in 2-5 days
Chalazion
• chronic granulomatous inflammation ofMeibomian gland often preceded by an internal
hordeolum
• acute inflammatorysigns are usually absent
• differential diagnosis: basal cellcarcinoma, sebaceouscell adenoma, Meibomian gland carcinoma
Treatment
• warm compresses
• ifno improvement after 1 month, consider incision and curettage
• chronic, recurrent lesion must be biopsied to rule outmalignancy
Blepharitis
• inflammation oflid margins
Etiology
• two main types
• staphylococcal (S. aureus): ulcerative, dryscales
• seborrheic: no ulcers, greasyscales
Clinical Features
• itching, tearing, foreign bodysensation
• thickened. red lid margins, crusting, discharge with pressure on lids ("toothpaste sign")
Complications
• recurrent chalazia
• conjunctivitis
• keratitis (from poor tear £1m)
• corneal ulceration and neovascularization
Treatment
• warm compresses and lidscrubswith diluted "baby shampoo"
• topical or 8}'5temicantibiotics as needed
• ifsevere, an ophthalmologist mayprescribe a short course oftopicalcorticosteroids
Xanthelasma
• eyelidxanthoma (lipid deposits in dermis oflids)
• appear as pale, slightly elevatedyellowish plaques orstreaks
• mostcommonlyonthe medial upper lids, often bilateral
• associated with hyperlipidemia (approximately50% ofpatients)
• common inthe elderly, more concerningin the young
Treatment
• excision for cosmesis only, recurrences common
15. Toronto Notes 2011 Conjunctiva
Conjunctiva
• thin, vascular mucous membrane/epithelium
• bulbar conjunctiva: lines sclera to limbus (junction between cornea and sclera)
• palpebralconjunctiva: lines inner surface ofeyelid
Pinguecula
• yellow-white subepithelial deposit ofhyaline and elastic tissue adjacent to the nasal or temporal
limbus
• associated with sun and wind exposure. aging
• common, benign, sometimes enlarge slowly
• may be irritating due to abnormal tear film formation over the deposits
• surgery for cosmesis only
• irritative symptoms may be treated with lubricating drops
Pterygium
• fibrovascular triangular encroachment ofepithelial tissue onto the cornea, usually nasal
• may induce astigmatism, decrease vision
• excision for chronic inflammation, threat to visual axis, cosmesis
• irritative symptoms may be treated with lubricating drops
• one-third recur after excision, lower recurrence with conjunctival autograft (5%)
Subconjunctival Hemorrhage
------------------------
• blood beneath the conjunctiva, otherwise asymptomatic
• idiopathic or associated with trauma. Valsalva maneuver, bleeding disorders, hypertension
• give reassurance ifno other ocular findings, resolves in 2-3 weeks
• ifrecurrent, consider medicalJhematologic work-up
Conjunctivitis
Etiology
• infectious
• bacterial, viral, chlamydia!, fungal, parasitic
• non-infectious
• allergic: atopic. seasonal, giant papillary conjunctivitis (contact lens wearers)
• toxic: irritants, dust, smoke, irradiation
• secondaryto another disorder: dacryocystitis, dacryoadenitis, cellulitis, Kawasaki's disease
Clinical Features
• red eye (conjunctival injection often with limbal pallor), chemosis, subepithelial infiltrates
• itching, foreign body sensation, tearing, discharge, crusting oflashes in the morning, lid edema
• preauricular and/or submandibular nodes
• follicles: pale lymphoid elevations ofthe conjunctiva
• papillae: fibrovascular elevations ofthe conjunctiva with central network offinely branching
vessels (cobblestone appearance)
ALLERGIC CONJUNCTIVITIS
Atopic
• associated with rhinitis, asthma, dermatitis, hay fever
• small papillae, chemosis, thickenedand erythematous lids, corneal neovascularization
• seasonal (pollen, grasses, plant allergens)
• treatment: cool compresses, antihistamine, mast cell stabilizer
Giant Papillary ConJunctivitis {GPC)
• immune reaction to mucus debris on lenses in contact lens wearers
• large papillae form on superior palpebral conjunctiva
• treatment: clean, change or discontinue use ofcontact lens
Ophthalmology OP15
...,"
• Enlarged lymph nodes suggest
infactious etiology, especially viral or
chlamydia! conjunctivitis
• Tamporal conjunctival lymphatics
drain to preauricular nodes, and
to submandibular nodes
...,"
• Follicles 11r11 usually se1111 in viral and
chlamydia! conjunctivitis
• Papillae are usually seen in allervic
and bae1llrial conjunctivitis
.....,"
Typ..af Dillcharg•
Allergic: mucoid
Viral: watery
Bactarial: purulent
Chlamydia!: mucopurulant
16. OP16 Ophthalmology Conjunctiva/Sclera Toronto Notes 2011
Vemal Conjunctivitis
• large papillae (cobblestones) on superior palpebral conjunctiva with corneal ulcers andkeratitis
• seasonal (warm weather)
• occurs in children, lasts for 5-10 years and then resolves
• treatment: consider topical steroid, cyclosporine (not in primary care)
VIRAL CONJUNCTIVITIS
• serous discharge, lid edema, follicles
• subepithelial corneal infiltrates
• maybe associated with rhinorrhea
• preauricular node often palpable andtender
• initially unilateral, often progresses to the other eye
• mainly due to adenovirus - highly contagious fur up to 12 days
Treatment
• cool compresses, topical lubrication
• usually self-limiting (7-12 days)
• proper hygiene is very important
BACTERIAL CONJUNCTIVITIS
• purulent discharge, lid swelling, papillae, conjunctival injection, chemosis
• common agents include S. aureus, S. pneumoniae, H. influenzae and M. cata"halis
• in neonates or ifsexuallyactive must consider N. gonorrhoeae (invades cornea to cause keratitis)
• Chlamydia trachomatis is the most common cause in neonates
Treatment
• topical broad-spectrum antibiotic
• systemic antibiotics ifindicated, especiallyin neonates and children
• usually a self-limitedcourse of10-14 days ifno treatment, 1-3 days with treatment
CHLAMYDIAL CONJUNCTIVITIS
• caused by Chlamydia trachomatis
• affects neonates on day 3-5, sexually active people
• causes trachoma and inclusion conjunctivitis
Trachoma
• leading infectious cause ofblindness in the world
• severe keratoconjunctivitis leads to corneal abrasion, ulceration, and scarring
• initially, follicles on superior palpebralconjunctiva
• treatment: topical and systemictetracycline
Inclusion Conjunctivitis
• chronic conjunctivitis with follicles and subepithelial infiltrates
• most common cause ofconjunctivitis in newborns
• prevention: topical erythromycin at birth
• treatment: topical and systemictetracycline, doxycycline or erythromycin
Sclera
• the white fibrous outerprotective coat ofthe eye
• continuous with the cornea anteriorly and the dura ofthe optic nerve posteriorly
• episclera is a thin layer ofvascularized tissue between the sclera and conjunctiva
Episcleritis
• immunologically mediated inflammation ofepisclera
• one-third bilateral; simple (80%) or nodular (20%)
• more frequent in women than men (3:1)
Etiology
• mostly idiopathic
• in 1/3 ofcases, associated with collagen vascular diseases, infections (herpes zoster, herpes
simplex, syphilis), inflammatory bowel disease, rosacea, atopy
17. Toronto Notes 2011 Sclera/Cornea
Clinical Features
• asymptomatic usually, mayhave mild pain and red eye
• sectoral ordiffuse injection ofradially-directed vessels, chemosis, small mobile nodules
• blanches with topical phenylephrine (constricts superfidal conjunctivalvessels)
Treatment
• generallyselflimited, recurrent in 2/3 ofcases
• topical steroid for 3-5 days ifpainful (prescribed and monitored byophthalmologist)
Scleritis
• usuallybilateral: diffuse, nodular or necrotizing
• anterior scleritis: maycause scleralthinning
• posterior scleritis: maycause exudativeretinal detachment
• more common in women and elderly
Etiology
• may be a manifestation ofsystemic disease
• collagenvascular disease, e.g. systemic lupus erythematosus (SLE), rheumatoidarthritis (RA),
ankylosing spondylitis (AS)
• granulomatous, e.g. tuberculosis (TB), sarcoidosis, syphilis
• metabolic, e.g. gout, thyrotoxicosis
• infectious, e.g. S. aureus, S. pneumoniae, P. aeruginosa, herpes zoster
• chemical or physical agents, e.g. thermal, alkali or acid burns
• idiopathic
Clinical Features
• severe pain, photophobia, red eye, decreased vision
• pain is bestindicator ofdisease progression
• inflammation ofscleral, episcleral and conjunctivalvessels
• may have anteriorchamber cells/flare, corneal infiltrate, scleral thinning
• sclera may have a blue hue best seen in natural light, due to scleral thinning and visualization of
underlying choroid pigment
• scleral edema or thinning
• failure to blanch with topical phenylephrine
Treatment
• systemic NSAID or steroid (topical steroids are not effective)
• treat underlyingetiology
Cornea
• function
• transmission oflight
• refraction oflight (2/3 oftotal refractive power ofeye)
• barrieragainst infection, foreign bodies
• transparencydue to avascularity, uniform structure and deturgescence (relative dehydration)
• Slayers (anteriorto posterior): epithelium, Bowman's membrane, stroma. Descemet's
membrane, endothelium (dehydrates the cornea; dysfunction= corneal edema)
• extensive sensory fibre network {Vl distribution); therefore abrasions and inflammation
(keratitis) are very painful
Foreign Body
• foreign material in or on cornea
• may have associated rust ringifmetallic
• patientsmay note tearing, photophobia, foreign body sensation, red eye
• signs include foreign body, conjunctival injection, epithelial defect that stains with fluorescein,
corneal edema, anteriorchamber cells/flare
Complications
• abrasion, infection, scarring, rust ring, secondaryiritis
Treatment
• remove under magnification using local anesthetic and sterileneedle or refer to ophthalmology
(dependingon depth and location)
• treat as per corneal abrasion
Ophthalmology OP17
... ,
•t-----------------,
To dilfarentiall bl!waan apisclaritis and
&eleritis, place adrop of phenylephrine
2.5% {Mydfrin*; AK-Dilata*) in the
affected ay&. Re-axamine the vascular
pattam 10-15 minutas latar. Episclend
veuels should bl1111ch. Scleral Y8Sials
do not.
... "
..-----------------,
Sclaramalacia l'llrflln.ns
• Anteriornecrotizing scleritis
inflammation and asymplllmatic
• Strongly associllled with rheuiMioid
arthritis
• May resun in acinithinning
• Traumatic plllfomion can easily occur
- axamina wvevervuently
... "
..-----------------,
Foreign body behind lid may cause
multiple vertical corneal epithelilll
abrasions dua to blirling.
18. OP18 OphthalmoloBf
Topic;alanlllgelics1houldonly ba Ulld
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Cornea 1'oroDio 2011
Corneal Abrasion
• epithelialdefectusuallyduetotrauma (e.g. fingema.ils, papez;twigs), contactlens (Figure 14)
Clinical Features (Table 5)
• pal.n.redness,tearing, photophobia. foreign bodysensation
• de-epithelialized area stains with fluorescein dye
• painrellevedwith topical anesthetic
Complications
• infection.ulceration, recurrent erosion,seoond.aryiritis
Treatment
• topical antibiotic (drops or ointment)
• considertopical NSAID, cycloplegic (relieves pain andphotophobiabyparalyzingdllary
muscle), patch
• mostalmsions dearspontaneouslywithin 24-48 hours
Recurrent Erosions
• recurrentepisodes ofpain, photophobia.foreign bodysensationwitha spontaneous
corneal epithelialdefect
• usuallyoccurs uponawakening
• 8580ciated with improperadherence ofepithelial cells tothe underlying basement membrane
Etiology
• previous traumatic cornealabr.!sl.on
• corneal dystrophy
• idiopa.thk
Treatment
• asfur cornealabrasionuntilre-epithelializationoccurs
• topical hypertonic saline oinbnent. topical lubrication
• bandagecontactlens, anteriorstromalpunctureorphototherapeu.tickeratectomyfor
chronic recurrences
Corneal Ulcer
Etiology
• localnecrosisofcomealtissueduetoinfection (Figure 14)
• infectionisusuallybacterial, rarelyviral, fungal or protozoan (Atanthamoeba)
• secondarytD cornealexpomre. abrasion,foreign body,conbld:leiU11Uie(50% ofulcen)
• also associated withconjunctivitis,blepharitis,keratitis, vitamin A d.c:ficiency
Clinical Features
• pain, photophobia,tearing, foreign bodysensation,decreasedvisual acu1ty(Ifcentralulcer)
• corneal opacitythat necroses andforms anexcavatedulcerwithinfiltrativebase
• overlyingcorneal epithelialdefectthatstainswithfluorescein
• maydevelopcornealedema.conjunctivalinjection, anteriorchambercells/flare,hypopyon,
cornealhypoesthesia (inviral keratitis)
• bacterialulcersmayhavepurulentdischarge.viral ulcersmayhavewaterydischarge
Complications
• decreasedvision, cornealperforation,lrl.tis, endophthalmitis
Treatment
• urgentreferralto ophthalmology
• culture first
• topical antibi.alics everyhour
• nwsttreatvigorouslytoavoidcomplications
21. Toronto Notes 2011 The Uveal Tract/Lens
Treatment {by ophthalmologists)
• mydriatks: dilate pupilto prevent fonnation ofposterior synechiae and to decrease pain
from ciliary spasm
• steroids: topical, subconjunctival or systemic
• systemic analgesia
• medical workup may be indicated
Posterior Uveitis (Choroiditis)
• inflammation ofthe choroid
Etiology
• bacterial: syphilis, tuberculosis
• viral: herpes simplex virus, cytomegalovirus in AIDS
• fungal: histoplasmosis, candidiasis
• parasitic: toxoplasmosis (most common cause), toxocara
• immunosuppression may predispose to anyofthe above infections
• autoimmune: Beh¢s disease (triad oforal ulcers, genital ulcers, and posterior uveitis)
• malignancies (masquerade syndrome): metastatic lesions, malignant melanoma
Clinical Features
• painless as choroid has no sensory innervation
• often no conjunctival or scleral injection present
• decreased visual acuity
• floaters (debris and inflammatory cells)
• vitreous cells and opacities
• hypopyon formation
Treatment
• steroids: retrobulbar or systemic ifindicated (e.g. threat ofvision loss)
Lens
• consists ofan outer capsule surrounding a soft cortex and a firm inner nucleus
Cataracts
• any opacity ofthe lens
• most common cause ofreversible blindness worldwide
• types: nuclear sclerosis, cortical, posterior subcapsular (Figure 17)
Etiology
• acquired
• age-related (over 90% ofall cataracts)
• cataract associated with systemic disease (may have juvenile onset)
• diabetes mellitus
• metabolic disorders (e.g. Wilson's disease, galactosemia. homocystinuria)
• hypocalcemia
• traumatic (may be rosette shaped)
• intraocular inflammation (e.g. uveitis)
• toxic (steroids, phenothiazines)
• radiation
• congenital
• present with altered red reflex or leukocoria
• treat promptlyto prevent amblyopia
Clinical Features
• gradual, painless, progressive decrease in visual acuity
• glare, dimness, halos around lights at night, monocular diplopia
• "secondsight" phenomenon - patient is more myopic than previously noted, due to increased
refractive power ofthe lens (in nuclear sclerosis only)
• patient may read without previously needed reading glasses
• diagnose by slit-lamp exam, and bynoting changes in red reflex using ophthalmoscope
• may impair view ofretina during fundoscopy
Ophthalmology OP21
Posterior
subcapsular
Nudear sclerosis
(._jC.:.
TYPES OF CATARACTS
Nuclur Sclerosis
• Yallow ID brown l"brwlascent1
discoloLnlion of the central part of
1ha lens
• Aae-rallll&d
• Radial or spok&-likll opacification in
1ha cortBX ofthe luns, eilhar
antariorly or posteriorly
• Associated with aging 111d diabetes
Posterior Sullcap•ul•
• Usually inthe posterior of the lens,
adjacentIDthe c11psule
• Associlltad with steroid use,
intraocular inflammation, diabetn,
trauma. radiation. aging
Figure 17. Types of Cataracts
i
.!!
0
22. OP22 Ophthalmology
..... ,
Flllltars ="bugs", "cobwebs" or
"spDIJ"that ch111ge with eye position.
..... ,
..
Weiq" Ring-glial tissue around the
optic disc remails attached to posterior
vilnloUi.
New ora marked inc11asa in flollllrs
ancl/or flashes af light requires adilated
fundus exam to rule out retinaltlJIIJrs/
detacllment.
Lens/VitreoUB
Treatment
• medical: attempt correction ofrefractive error
• surgical: definitive treatment
• indications for surgery
Toronto Notes 2011
• to improvevisual function in patients whose visual lossleads to functional impairment
(patients maybe inclined to postpone surgeryas long as one eye has sufficientvision)
• to aid management ofother ocular disease (e.g. cataractthat prevents adequate retinal
exam orlasertreatment ofdiabetic retinopathy)
• congenitalortraumaticcataracts
• phacoemulsification (phaco =lens)
• most commonlyused surgical technique (see Surgical Ophthalmology. OP43)
• post-operative complications
• retinal detachment, endophthalmitis, dislocatedIOL, macular edema, glaucoma
• with newfoldable IOI:s that have truncated edges, <10% ofpatients get posterior capsular
opacification (PCO), which is treated with YAG laser
Prognosis
• excellentifnot complicated byother oculardisease
Dislocated Lens (Ectopia Lantis)
-------------------
Etiology
• associated with Marfan's Syndrome, Ehlers-Danlos type VI, homocystinurla, syphilis, lens
coloboma (congenitalcleft due to failure ofocular adnexa to complete growth)
• traumatic
Clinical Features
• decreasedvisual acuity
• may get unilateral diplopia
• iridodenesis (quivering ofiris with movement)
• direct ophthalmoscopy mayelicit abnormal red reflex
Complications
• cataract, glaucoma, uveitis
Treatment
• surgical correction ± lens replacement
Vitreous
• clear gel (99% water plus collagenfibrils, glycosaminoglycans and hyaluronic acid) that fills the
posterior segment ofeye
• normallyadherent to optic disc, pars plana, and along major retinal bloodvessels
• centralvitreous commonlyshrinks andliquefieswith age (syneresis)
• during syneresis,the molecules that held water often condense, causing vitreous floaters
• :O.oaters are usually harmless, but retinal tear/detachment and hemorrhagic diseases must be
ruled out
Posterior Vitreous Detachment (PVD)
Etiology
• normal aging process ofvitreousliquification (syneresis)
• liquidvitreous moves between posterior vitreous gel and retina
• vitreous is peeled away and separates from the retina
Clinical Features
• :O.oaters, flashes oflight
Complications
• traction at areas ofabnormal vitreoretinal adhesions may cause retinal tears/detachment
• retinal tears/detachment maycause vitreous hemorrhageiftear bridgesbloodvessel
• complications more common inhigh myopes and following ocular trauma (blunt or perforating)
Treatment
• acute onsetofPVD requires a dilated fundus exam to rule outretinal tears/detachment
• no specifictreatment available for floaters/flashes oflight
23. Toronto Notes 2011 Vitreous/Retina
Vitreous Hemorrhage
----------------------------------
• bleeding into the vitreous cavity
Etiology
• proliferative diabetic retinopathy (PDR)
• retinal tear/detachment
• posterior vitreous detachment (PVD)
• retinal vein occlusion
• trauma
Clinical Faaturas
• sudden loss ofvisual acuity
• may be preceded bymany floaters and/or flashes oflight
• ophthalmoscopy: no red reflexiflarge hemorrhage, retina not visible due to blood invitreous
Treatment
• ultrasound (B-scan) to rule out retinal detachment
• expectant: in non-urgent cases (e.g. no retinal detachment), blood usually resorbs in 3-6 months
• surgical: vitrectomy ± retinal detachment repair ± retinal endolaser to possible bleeding sites/
vessels
Endophthalmitis and Vitritis
• intraocular infection: acute, subacute or chronic
Etiology
• most commonly a postoperative complication; risk following cataract surgery is <0.196
• also due to penetrating injuryto eye (risk is 3-7%), endogenous spread. and intravitreal
injections
• etiologyusuallybacterial. may be fungal
Clinical Faaturas
• verypainful. red eye, photophobia, discharge
• severely reduced visual acuity, lid edema, proptosis, corneal edema, anterior chamber cells/flare,
hypopyon, reduced red reflex
• may have signs of a ruptured globe (severe subconjunctival hemorrhage, hyphem.a,
decreased intraocular pressure, etc.)
Treatment
• OCULAREMERGENCY: presenting vision best indicates prognosis
• LP or worse - admission, immediate vitrectomy and intravitreal antibiotics to prevent loss of
vision
• HM or better -vitreous tap for culture and intravitreal antibiotics
• topical fortified antibiotics
Retina
• composed oftwo parts (Figure 2)
• neurosensory retina- comprises 9 ofthe 10 retinal layers, including the photoreceptors and
the ganglion cell layer
• retinal pigment epithelium (RPE) layer - external to neurosensory retina
• macula: rich in cones (for colour vision); most sensitive area ofretina; looks darker due to lack
ofretinal vessels and thinning ofretina in this region; 15° temporal and slightlybelow the optic
disc
• fovea: centre ofmacula; responsible for acute, fine vision
• optic disc: slightlyoval vertically, pinkish colour with centrally depressed yellow cup (normal
cup:disc ratio is <0.5), retinal artery and vein pass through cup
• ora serrata: irregularly-shaped, anterior margin ofthe retina (can only be visualized with
indirect ophthalmoscopy ofthe far peripheral retina, or through a Goldmann 3 mirror lens)
Ophthalmology OP23
.
Any time avitreous or retinal
hemorrhage is seen in a child, must rule
outchid abusa.
.....,,
Common causes of vitreous hemorrhage
are prolifanrtiVB diabetic retinopathy and
retinal tem.
.....,,
Rememberto inquire about
tutanuallatu1 in poll-traumlllic
endophthllmitis.
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endoplllhllmitis:
• lllli'lvilalantibioticsprDrad IMirl)'lblmic
l11tililltics
• 1{11r8ctomy'indicalldonlrhilion LPonwrsa
24. OP24 Ophthalmology
Treatmentfor aCllntral ratinal1118ry
occlusion !CRAOI must be initiated
within 2 hours of symptom onsatfor .,y
hope ofres!Dring vision.
llllldlVail Oa:luian Sludy IIIVDII
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foiiiMing BRVO.Thetrublwrtalso._lha
riska1vmeoushem0111ge.
.....,,
,.}-----------------,
The "blood and thunder"" appeiii'BIIce on
fundoscopy is very characbristic of a
cenlrBI retinal vein occklsion {CRVOI.
Retina Toronto Notes 2011
Central Retinal Artery Occlusion (CRAO)- - - -
Etiology
• emboli from carotid arteries or heart (e.g. arrhythmia, endocarditis, valvular disease)
• thrombus
• temporal arteritis
Clinical Features
• sudden, painless (except in temporal arteritis), severe monocular loss ofvision
• relative afferent pupillary defect (RAPD)
• patient willoften have experienced transient episodes in the past (amaurosis fugax)
• fundoscopy
• "cherry-redspot" at centre ofmacula (visualization ofunaffected highly vascular choroid
through the thin fovea)
• retinal pallor
• narrowed arterioles, boxcarring (segmentation ofblood in arteries)
• cotton-wool spots (retinal infarcts)
• cholesterol emboli (Hollenhorst plaques) - usually located at arteriole bifurcations
• after -6 weeks: cherry-red spot recedes and optic disc pallor becomes evident
Treatment
• OCULAR EMERGENCY: attempt to restore blood flow within 2 hours
• the sooner the treatment =better prognosis (irreversible retinal damage if>90 min ofcomplete
CRAO)
• massage the globe (compress eye with heel ofhand for 10 s, release for 10 s, repeat for 5 min)
to dislodge embolus
• decrease intraocular pressure
• topical beta-blockers
• inhaled oxygen-carbon dioxide mixture
• IV Diamox- (carbonic anhydrase inhibitor)
• IV mannitol (draws fluid from eye)
• drain aqueous fluid- anterior chamber paracentesis (carries risk ofendophthahnitis)
• treat underlying cause to prevent CRAO in fellow eye
• follow up 1month to rule out neovascularization
Branch Retinal Artery Occlusion (BRAO)- - - - - - - - -
• onlypart ofthe retina becomes ischemic resulting in a visual fieldloss
• more likely to be ofembolic etiologythan CRAO; need to search for source
• management: ocular massage to dislodge embolus ifvisual acuity is affected
Central/Branch Retinal Vein Occlusion (CRVO/BRVO)
• second most frequent "vascular" retinal disorder after diabetic retinopathy
• usually a manifestation ofa systemic disease (e.g. hypertension, diabetes mellitus)
• thrombus occurs within the lumen ofthe blood vessel
Predisposing Factors
• arteriosclerotic vascular disease
• hypertension
• diabetes mellitus
• glaucoma
• hyperviscosity (e.g. polycythemia rubra vera, sickle-cell disease, lymphoma, leukemia)
• drugs [e.g. oral contraceptivepill (OCP), diuretics]
Clinical Features
• painless, monocular, gradual or sudden visual loss
• ±RAPD
• fundoscopy
• "blood and thundera appearance
• diffuse retinal hemorrhages, cotton-wool spots, venous engorgement, swollen optic disc,
macular edema
• two fairly distinct groups
• venous staaWnon-ischemic retinopathy
• no RAPD, VA approximately20/80
• mild hemorrhage, few cotton wool spots
• resolves spontaneously over weeks to months
• may regain normal vision ifmacula intact
25. Toronto Notes 2011 Retina
• hemorrhagic/ischemic retinopathy
• usually olderpatient with deficient arterial supply
• RAPD, VA approximately20/200, reduced peripheralvision
• more hemorrhages, cotton wool spots, congestion
• poorvisual prognosis
Complications
• degeneration ofretinal pigmentepithelium
• neovascularization ofretina and iris (secondaryrubeosis), leadingto secondaryglaucoma
• vitreous hemorrhage
• macular edema
Treatment
• no treatment available to restore vision in CRVO/BRVO
• treat underlyingcause/contributing factor
• fluorescein angiographyto determine extentofretinal non-perfusion= riskofneovascularization
• retinal laser photocoagulation, intravitrealcorticosteroidor anti-VEGF injectionto reduce
neovascularization and preventneovascular glaucoma
Retinal Detachment (RD)
• cleavagein the plane between the neurosensory retina and the retinal pigment epithelium (RPE)
• three types
• rhegm.atogenous (most common)
• caused by a tear or hole in the neurosensory retina, allowing fluid from the vitreous to
pass into the subretinalspace
• tears maybe causedbyposteriorvitreous detachment (PVD), degenerative retinal
changes, trauma oriatrogenically
• incidence increaseswith advancing age, inhigh myopes andafter ocularsurgery/trauma
• tractional
• caused bytraction (dueto vitreal, epiretinal or subretinal membrane) pullingthe
neurosensory retina awayfrom the underlying RPE
• found in conditions such as diabetic retinopathy, CRVO, sickle cell disease, retinopathy of
prematurity (ROP), and oculartrauma
• exudative
• caused by damage to the RPE resultingin fluid accumulation in the subretinal space
• main causes are intraocular tumours, posterior uveitis, central serous retinopathy
Clinical Features
• sudden onset
• flashes oflight
• due to mechanicalstimulation ofthe retinal photoreceptors
• floaters
• hazyspots in the line ofvision which move with eye position, due to drops ofblood from
tom vessels bleeding into the vitreous
• curtain ofblackness/peripheral fieldloss
• darkness in one field ofvision when the retina detaches inthatarea
• loss ofcentral vision (ifmacula "off")
• decreased lOP (usually 4-5 mmHg lowerthan the other, normal eye)
• ophthalmoscopy: detached retina is grey-white with surface bloodvessels, loss ofred reflex
• ±RAPD
Treatment
• prophylactic: symptomatic tear (flashes or floaters) can be sealed offwith laser/cryotherapy, with
the goal ofpreventing progression to detachment
• therapeutic
• rhegm.atogenous
• scleral buckleprocedure (see Surgical Ophthalmology, OP43)
• pneumatic retinopexy (see Surgical Ophthalmology, OP43)
• both above treatments are used in combination withlocalization ofretinal tears/holes
and subsequent treatment with diathermy, cryotherapy or laserto create adhesions
between the RPE and the neurosensory retina
• vitrectomyplus injection ofsilicone oil in cases ofrecurrent detachment
• tractional
• vitrectomy ±membrane removal/scleral buckling/injection ofintraoculargas as
necessary
• exudative
• treat underlyingcause
Ophthalmology OP25
"" I
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in other eyu.
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26. OP26 Ophthalmology
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the 111tin1 ISSOCimd with dialmic
retinopathy and hypertension
Retina Toronto Notes 2011
Complications
• loss ofvision, vitreous hemorrhage, recurrent retinal detachment
• a retinal detachment is an emergency, especiallyifthe maculais still attached (macula "on")
• prognosis for visual recoveryvaries inverselywith the amount oftime the retinais
detached and whether the maculais attached or not
Retinitis Plgmentosa
• worldwide incidence between 1/3500 and 1/7000 people
• many fonns ofinheritance, most commonlyautosomal recessive (60%)
• hereditarydegenerative disease ofthe retina manifested byrod >cone photoreceptor
degeneration and retinal atrophy
• symptoms: night blindness, decreased peripheralvision ("tunnel vision·), decreased central
vision (macular
changes), glare (from cataract)
• fundoscopy: areas of"bone-spicule· pigment clumpingin mid-periphery ofretina, narrowed
retinal arterioles, pale optic disc
• electrophysiologicaltests {ERG, EOG) assist in diagnosis
• management: no treatments available to reverse the condition; cataract extraction improves
visual function
Age-Related Macular Degeneration (ARMD)
• leading cause ofirreversible blindness in the western world, associated with increasing age,
usuallybilateral
• 10% ofpeople >65 years old have some degree ofARMD
• female >male
• degenerative changes are concentrated at the macula thus onlycentral vision is lost; peripheral
vision (importantfur navigation) is maintained so patients can usually maintain an independent
lifestyle
Classification
• Non-Exudativef"Dry,. (Non-Neovascular) ARMD
• most common type ofARMD {90% ofcases)
• slowly progressive loss ofvisualfunction
• drusen: pale, yellow-white deposits between the retinal pigment epithelium (RPE) and
Bruch's membrane (area separating inner choroidalvessels from RPE)
• RPE atrophy: coalescence ofdepigmented RPE, clumps offocal hyperpigmentation or
hypopigmentation
• may progress to neovascular ARMD
• l!xudativef'Wet'" {Neovascular) ARMD
• 10% ofARMD, but 80% ofARMD resulting in severe visual loss
• choroidal neovascularization: drusen predispose to breaks in Bruch's membrane causing
subsequent growth and proliferation ofchoroidal capillaries
• may getserous detachment ofoverlyingRPE and retina, hemorrhage and lipid precipitates
into subretinal space
• can also get an elevatedsubretinalmass due to :fibrous metaplasia ofhemorrhagic retinal
detachment
• leads to disciform scarring and severe central visual loss
Risk Factors
• female
• increased age
• family history
• smoking
• Caucasian race
• blue irides
Clinical Features
• variable degree ofprogressive central visual loss
• metamorphopsia {distortedvision characterized by straight parallellines appearing convergent
or wavy) due to macular edema
27. 'IbroDloNota2011 Retina/Glaucoma
Investigations
• Amslergrid:held atnormalreadmgdistancewith glasses on, assesses macularfunction
• ft.uorescein angiography(FA): asseli8 degreeofneOVB.IIcularization - pathologicnewvessel.Bleak
dye
Tnatment
• non-neovascular '"dry'"ARMD
• monl.tor,.Amslergridallows patientsto c:heck.for metamorphopaia
• lowvisionaids (e.g.magnifiers, closed-circuittelevision)
• anti-oxidants,greenleafyvegetables
• sunglasses/visors
• seeAREDSsidebar
• neOVB.IIc::ular"wei' ARMD
• see Common Medlcaticns
• laserphotocoagulationfor neovascularizati.on
• 5096 ofchoroidalneovasc::ularizationcannotbetreated iDitially
• no definitivetreatmentfor disciformscarring
• photodynamictherapy(PDT) withverteporfin(Visudyne•)
• IVinjectionofverteporfinfollowed bylowintensitylaserto area ofchoroidal
neovasclllarWrtion
• PhotodynamicTherapyStudyGroup showedthatfor patients with subfoveallesionsin
ARMDwith predominantlyclassicchoroidalneovascularlzation, verteportintreatment
c:an reduce theriskofmoderatevisionloss fur atleast2years; th18therapycannotstop or
revene vision loss
• intravitrealinjection ofanti-angiogenesisgrowthfactor (anti-VEGF)
• pegaptanib (Macugen•), raniblzumab (Luc:entis->, bevacizumab (Awstin•)
Glaucoma
Definition
• progressiveopticneuropathyinvolvingcharacteristic:structural changesto optic nervehead
withassodated visualfield changes
• c:ommonlyassociatedwithhighlOP, butnot requ.iredfor diagnosis
Background
• aqueousis producedbythe c.lliarybodyand flows from the posteriorchamberto the anterior
chamberthroughthe pupil. and drainsinto theepiscleralveinsviathetrabecularmeahworkand
CanalofSchlemm (Figure 18)
• an isolatedincreasein lOP is termedocularhypertension (orglaucomasuspect) andthese
patients shouldbe followed for increasedrisk ofdevelopingglaucoma(1096 iflOP=
20-30mmHg; 4096 iflOP = 30-40 mmHg; andmostiflOP >40mmHg)
• pressures >21 mmHgaremorelikelyto be associatedwithglaucoma;however,up to SO% of
patients withglauc:omado nothavelOP >21 mmHg
• besuspicious ofglaw:omaifC:Dmtio >0.6, C:D ratio difference betweeneyes >0.2, or cup
approaches discmargin
• loss ofperipheralvisionmostcommonlyprecedes centralloss
• sequenceofevents: gradualpressurerise -+ increasedC:D ratio -+ visualfield loss
• screeningtests shouldinclude
• medicalandfamilyhistory
• visual acuitytesting
• slitlampaamto assess anterior chamber depth
• ophthalmoscopyto assessthe discfeatures
• tonometrybyapplanation orindentationto measure the lOP
• visualfield testing
Ophthalmology OP27
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Primary Open Angle Glaucoma (POAG)
• most commonform, >9596 ofall glaucoma cases
• dueto obstruction ofaqueous drainagewithin thetrabecular meshwork and itsdrainageinto
the CanalofSchlemm
• insl.dl.ousand asymptomatic. so screening Is criticalfor earlydetection
Major Risk Factors
• elevatedintraocular (>21 mmHg)
• age:prevalencein40 y.o. is 1-296 andin80 y.o. 1096
• ethnidty: African descent
• familial (2-3xincreasedrisk); polygenic
Minor Risk Factors
• myopia
• hypertension
• diabetes
• hyperthyroidism (Graves' disease)
• chronictopical ophthalmic steroid useinsteroidresponders - yearlyeye eumsrecommended
If>4 weeksofsteroiduse
• previous oculartrauma
• anemia/hemodynamiccrisis (askabout bloodtransfusionsinpast)
Clinical Features
• asymptomatic initially
• lnsl.dl.ous,palnlt:sa, gradualrise in lOP due torestriction ofaqueousoutflow
• bilateral, butusuallyasymmetric
• earliestsignsareoptic discchanges
• increasedcup:discratio (verticalC:D >0.6)
• significantcup:disc asymmetrybetweeneyes (>0.2difference)
29. Toronto Notes 2011 Glaucoma
• thinning, notching ofthe neuroretinal rim
• flame shaped disc hemorrhage
• 360• ofperipapillary atrophy
• nerve fibre layer defect
• large vessels become nasally displaced
• visual field loss
• slow, progressive, irreversible loss ofperipheralvision
• paracentral defects, arcuate scotoma and nasal step are characteristic
• late loss ofcentral vision ifuntreated
Treatment
• medical treatment: decrease lOP byincreasing the drainage and/or decreasing the production of
aqueous (see Glaucoma Medications, Table 10, OP45)
• increase aqueous outflow
• topical cholinergics
• topical prostaglandin analogues
• topical alpha-adrenergics
• decrease aqueous production
• topical beta-blockers
• topical and oral carbonic anhydrase inhibitor
• topical alpha-adrenergics
• laser trabeculoplasty, cyclophotocoagulation = selective destruction ofciliary body (for
refractory cases)
• trabeculectomy (see Surgical Ophthalmology, OP43)
• optic nerve head examination, lOP measurement and visual field testing to monitor course of
disease
• pachymetry to measure corneal thickness
Normal Pressure Glaucoma
• POAG with lOP in normal range
• often found in women >60 but may occur earlier
• damage to optic nerve may be due to vascular insufficiency
Treatment
• treat any causative underlying medical condition and lower the lOP further
Secondary Open Angle Glaucoma
• increased lOP secondary to ocular/systemic disorders that clog the trabecular meshwork
• steroid-induced glaucoma
• traumatic glaucoma
• pigmentary dispersion syndrome
• pseudoexfoliation syndrome
Primary Angle Closure Glaucoma
• 5% ofall glaucoma cases
• peripheral iris bows forward in an already suscept:J.ole eye with a shallow anterior chamber
obstructing aqueous access to the trabecular meshwork
• sudden shifting forward ofthe lens-iris diaphragm= pupillary block, results in inability ofthe
aqueous to flow from the posterior chamber to the anterior chamber and a sudden rise in lOP
(Figure20)
Risk Factors
• hyperopia: small eye, big lens -large lens crowds the angle
• age >70
• female
• family history
• more common in people ofAsian and Inuit descent
• mature cataracts
• shallow anterior chamber
• pupil dilation (topical and systemic anticholinergics, stress, darkness)
Ophthalmology OP29
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31. Toronto Notes 2011 Pupils Ophthalmology OP31
Pupillary Light Reflex
• light shone directly into eye travels along optic nerve -+ optic tracts -+ both sides ofmidbrain
• impulses enterboth sides ofmidbrain via prc:tc:ctal area and Edinger-Westphal nuclei
• nerve impulses then travel down CN III bilaterallyto reach the ciliaryganglia, and finally to the
iris sphincter muscle, which results in direct and consensual light reflex
Pupil Abnormalities
Denervation Hypersensitivity
• when post-ganglionic fibres are damaged, the understimulated end-organ develops an excess of
receptor and becomes hypersensitive
• postganglionic parasympathetic lesions (ie. Adie's pupil)
• pupil will constrict with 0.12596 pilocarpine (cholinergic agonist), nonnal pupil willnot
• postganglionic sympathetic lesions (this test is used to differentiate between pre- and post-
ganglionic lesionsin Homer's syndrome)
• pupil will dilate with 0.12596 adrenaline, nonnal pupil will not
Local Disorders of Iris
• posterior synechiae (adhesions between iris andlens) due to iritis can present as an abnormally
shaped pupil
• ischemic damage [e.g. post-acute angle-closure glaucoma (ACG)]
• ischemic damage usually at 3 and 9 o'clock positions result in a vertically oval pupil that
reacts poorlyto light
• trauma (e.g. post intraocular surgery)
Anisocoria
• unequal pupil size
• idiopathic/physiologic anisocoria
• 2096 ofpopulation
• round, regular, <1 mm difference
• pupils reactive to light and accommodation
• responds normallyto mydiatrics/miotics
• see Table 6 for other causes ofanisocoria
Table 6. Summary of Conditions Causing Anisocoria
Futu1'81 Siteof!Mion Light ud Accommodation Anisocoria MwdrillictJMioticl EfftctofPilocarpine
ABNORMAL MIGnC PUPIL pmpairad pupiluy dilation)
Argyll-llobertsan Pupil negular, usuallybilateral
Ham•'• Syndrama Round. unilateral,
ptosis. amydrosis.
pseudoenophlhamos
Midbrain PoortD li;rt; bettErto
accommodation
Symplllheticsystem Bothbrisk
ABNORMAL MYDRIATIC PUPIL {impaired pupillaryconstriction)
Adie'a Tonic Pupil negular, la111er in bright light Ciliary Poorto betterto
accommodation
CN Ill Palsy Round CNIII ± fixed (acutely) at
7·9mm
Mwdrillic: Pupil Round, uni· arbilatural lri& !iphincllll' Fixsd at7·8 nm
Dilates/Constricts
Greaterin da!X Dilates/Constricts
Greaterin light Dilates/Constricts Constricts
(hypersensitivityto dilute
pilocarpins)
Greaterin light Dilate&IConstricts Constricts
Greaterin light No ulfsct Will not con&lrict
32. OP32 Ophthalmology
.... ,
..
In a CN Ul palsy, ifthe pupil is involved,
considartha possibility of apostarior
communiCIIIing army .,eurysm. The
pupillomotorfibenl run on the outside
ofthe nerve and an most susceptible
to compression. Ischemic changes are
men liUiy to ceun apalsywithout
pupillary involvement.
Pupils Toronto Notes 2011
Relevant hi.tory and llllllminalion with specific .ttention to:
• History of oculartrauma
• Checkold photiJvraphs (ptosis, ocular deviation, long st.-,ding anisocoria}
• Use of topical medications
• Exposn to toxins and drugs
• Associated ocularand neurologic symptDm.tsigns
Phpiolagic anilacoria
Figura 21. Approa.:h to Aniso.:oria
Mthpenrissillnfrom: Ked1rS. BiausseV, Newrr11n Ill!beprlienrwilllllliRM:olil. In:UpToDI!e.llose. BD ledl UpTolllte,Wlllthun,MA.
2008. Copyright2008 UpTolliiB,Inc. FG!mcn infarmlllionvisitwww.uptodllll.com.
Dilated Pupil (Mydriasis)
Sympathetic Stimulation
• fight or flight response
• mydriatic drugs: epinephrine. dipivefrin (Propine•), phenylephrine
Parasympathetic Understimulation
• cycloplegics/mydriatics: atropine. tropicamide, cyclopentolate (parasympatholytic)
• CN III palsy
• eye deviated down and out with ptosis present
• etiology includes stroke, neoplasm, aneurysm, acute rise in ICP, diabetes mellitus (may spare
pupil), trauma
• CN III palsywill respond to drugs (e.g. pilocarpine}, unlike a pupil dilated from medication
(rnydriatics)
Acute Angle Closure Glaucoma
• fixed, mid-dilated pupil
Adie's Tonic Pupil
• 80% unilateral, females > males
• pupil is tonic or reacts poorly to light (both direct and consensual) but constricts with
accommodation
• ifdecreased deep tendon reflexes = Adie's syndrome
• caused bybenign lesion in ciliary ganglion; results in denervation hypersensitivity of
parasympatheticallyinnervated constrictor muscle
• dilute (0.125%) solution ofpilocarpine will constrict tonic pupil but have no effect on
normal pupil
• pupil eventuallygets smaller than pupil ofunaffected eye
33. Toronto Notes 2011 Pupils
Trauma
• damage to iris sphincter from blunt orpenetrating trauma
• iris transillumination defects may be apparent using ophthalmoscope or slit lamp
• pupilmay be dilated (traumatic mydriasis) or irregularlyshaped from tinysphincterruptures
Constricted Pupil (Miosis)
Senile Miosis
• decreased sympathetic stimulation with age
Parasympathetic Stimulation
• localor systemic medications such as:
• cholinergic agents: pilocarpine, carbachol
• cholinesterase inhibitor: phospholine iodide
• opiates, barbiturates
Horner's Syndrome
• see Neurolog)'. N24
• lesion in sympathetic pathway
• difference in pupil size greater in dim light, due to decreased innervation ofadrenergicsto iris
dilator muscle
• associatedwith ptosis, anhydrosis ofipsilateral face/neck
• application ofcocaine 4% (blocks reuptake ofnoradrenaline) to eye does not resultin pupil
dilation (vs. physiologic anisocoria)
• hydroxyamphetamine 1% (stimulates noradrenalinerelease) will dilate pupil ifcentral or
preganglioniclesion, not postganglionic lesion
• postganglioniclesions result in denervation hypersensitivity, which will cause pupil to
dilate with 0.125% adrenaline, whereas nonnal pupilwill not
• causes: carotid or subclavian aneurysm, brainstem infarct, demyelinatingdisease, cervical
or mediastinal tumour, Pancoasttumour, goiter, cervicallymphadenopathy, surgical
sympathectomy, Lyme disease, cervicalribs, tabes dorsalis, cervicalvertebral fractures
Iritis
• miotic pupil initially
• later, may beirregularlyshapedpupil due to posterior synechiae
• later stages non-reactive to light
Argyll Robertson Pupil
• both pupils irregularand <3 mm in diameter, ± ptosis
• does not respond to light stimulation
• responds to accommodation (light-near dissociation)
• suggestive ofCNS syphilis orother conditions (DM, encephalitis, MS, chronicalcoholism,
CNS degenerative diseases)
Relative Afferent Pupillary Defect (RAPD)
• see N23
• also known as Marcus Gunn pupil
• lesion in visual afferent (sensory) pathway anterior to optic chiasm
• DDX: largeretinal detachment, BRAO, CRAO, CRVO, advanced glaucoma, opticnerve
compression, optic neuritis
• does not occur with mediaopacity (e.g. corneal edema, cataracts)
• test: swingingflashlight
• iflightis shone in the affectedeye, direct and consensualresponse to light is decreased
• iflightis shone in the unaffectedeye, direct andconsensualresponse to light is normal
• ifthe lightis moved quicklyfrom the unaffectedeye to the affected eye, ·paradOJticaln
dilation ofboth pupils occurs
• observe red reflex, especially in patients with dark iris
Ophthalmology OP33
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34. OP34 Ophthalmology Malignancl.es/OcuJar ManifestationaofSystemicDisease
Malignancies
• uncommon site for primarymalignancies
• eye usually affected secondarilybycancer or cancer treatments
• see Retinoblastoma section, OP41
Lid Carcinoma
Etiology
• basal cell carcinoma (90%)
• spread via local invasion, rarely metastasizes
• 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 oflesion
• sebaceous cell carcinoma {1-5%)
• often masquerades as chronic blepharitis or recurrent chalazion
• highly invasive, metastasize
Toronto Notes 2011
• Kaposi's sarcoma. malignant melanoma. Merkel cell tumour, metastatictumour
Treatment
• incisional or excisional biopsies
• may require cryotherapy, radiotherapy, chemotherapy, immunotherapy
• surgical reconstruction
Malignant Melanoma
• most commonprimaryintraocular malignancy in adults
• more prevalentin Caucasians
• arise from uveal tract
• hepatic metastases predominate
Treatment
• choice is dependent on the size ofthe tumour
• radiotherapy, enucleation (removal ofglobe from eye socket),limited surgery
Metastases
• most common intraocular malignancy in adults
• most commonlyfrom breast and lung in adults, neuroblastoma in children
• usuallyinfiltrate the choroid, but may also affect the optic nerve or extraocular muscles
• may present with decreased or distorted vision, irregularly shaped pupil, iritis, hyphema
Treatment
• local radiation, chemotherapy
• enucleation ifblind, painful eye
Ocular Manifestations of Systemic Disease
HIV/AIDS
• up to 75% ofpatients with AIDS have ocular manifestations
External ocular signs
• Kaposi's sarcoma
• affects conjunctiva oflid or globe
• numerous vascular skin malignancies
• DDx: subconjunctival hemorrhage (non-clearing), hemangioma
• multiple molluscum contagiosum
• herpes simplex keratitis
• herpes zoster keratitis
35. Toronto Notes 2011 Ocular Manifestations ofSyatemic Disease
Retina
• HIV retinopathy (most common}
• cotton wool spots in >50% ofHIV
• intraretinal hemorrhage
• cytomegalovirus (CMV} retinitis
• ocular opportunisticinfection that develops in late stages ofHIV when severely
immunocompromised (CD4 count
• a necrotizing retinitis, with retinal hemorrhage and vasculitis, "brushfiren or "pizzapien
appearance
• symptoms and signs: scotomas (macular involvement and retinal detachment}, blurred
vision and floaters
• untreated infection will progress to other eyein 4-6 weeks
• treatment: virostatic agents, e.g. gancyclovir orfoscarnet via IV or intravitreal injection
• necrotizing retinitis
• from herpes simplex virus, herpes zoster, toxoplasmosis
• disseminated choroiditis
• Pneumoc:ystis cwinii, Mycobacterium avium intracellulare, Candida
Other Systemic Infections
• herpes zoster
• see Herpes Zoster Keratitis section, OP19
• candidal endophthalmitis
• fluffy, white-yellow, superficial retinal infiltrate that may eventuallyresult in vitritis
• maypresent with inflammation ofthe anterior chamber
• treatment: systemic amphotericin B, oral fluconazole
• toxoplasmosis
• focal, grey-yellow-white, chorioretinallesions with surrounding vasculitis and vitreous
infiltration (vitreous cells}
• can be congenital (transplacental} or acquired (caused by Toxoplasma gondii protozoa
transmitted through raw meat and cat feces)
• congenitalform more often visual impairingas more likelyto involve macula
• treatment: pyrimethamine, sulfonamide, folinic add, or clindam.ydn. Consider steroids if
severe inflammation (vitritis, macular or optic nerve involvement)
Diabetes Mellitus (DM)
• see E6
• most common cause ofblindness in youngpeoplein North America
• consider DM ifunexplained retinopathy, cataract, EOM palsy, optic neuropathy, sudden change
in refractive error
• loss ofvision due to:
• progressive microangiopathy leading to macular edema
• progressive diabetic retinopathy -+ neovascularization -+ traction -+ retinal detachment and
vitreous hemorrhage
• rubeosis iridis (neovascularizationofthe iris) leadingto neovascularglaucoma (poorprognosis)
• macular ischemia
DIABETIC RETINOPATliY (DR)
Background
• altered vascular permeability (loss ofpericytes, breakdown ofblood-retinal barrier, thickening
ofbasement membrane)
• retinal vessel closure
Classification
• non-proliferative: increased vascular permeability and retinal ischemia
• dot and blot hemorrhages
• microaneurysms
• hard exudates (lipid deposits)
• macular edema
• advanced. non-proliferative (or pre-proliferative):
• non-proliferative findings plus:
• venous beading (in of4 retinal quadrants}
• intraretinal microvascular anomalies (IRMA) in 1of4 retinal quadrants
- IRMA: dilated, leaky vessels within the retina
• cotton wool spots (nerve fibre layer infarcts)
Ophthalmology OP35
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Macular edema thlil most common
cause of visual loss in patientswith
bBCkgllJUnd IJR.
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Type1 DM
60'1(i after 1Dyeers
>80'1(illfter 15 years
Type2DM
20'1(i Ill time ofdi111nosis
60'1(i after 20 yeers