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0P3 I Ophthalmology Toronto Notes 2023

Retina

• HIV retinopathy (most common)

cotton wool spots in >50% of HIV patients

• intraretinal hemorrhage

• CMV retinitis

a necrotizing retinitis, with retinal hemorrhages and vasculitis, “brushfire” or “pizza pie”

appearance

presents with scotoma (macular involvement and RD), blurred vision,and floaters

• untreated infection will progress to the other eye in 4-6 wk

treatment:virostatic agents(e.g.ganciclovir or foscarnet) via IV, intravitreal injection,or

sometimes PC)

• necrotizing retinitis

• from herpes simplex virus, herpes zoster, toxoplasmosis

Pneumocystis carinii and Mycobacterium avium intracellulare can present with choroiditis

• Candida can present as retinitis and vitritis

Other Systemic Infections

• herpes zoster

• sec Herpes Zoster Ophthalmicus, OPI 9

• candidal endophthalmitis

fluffy,white-yellow,superficial retinal infiltrates that may eventually result in vitritis

may present with inflammation of the anterior chamber

• treatment:systemic amphotericin B, oral fluconazole, and voriconazole

• toxoplasmosis

focal, grey-yellow-white,chorioretinal lesions with surrounding vasculitis and vitreous

inflammation (vitreous cells)

can be congenital (transplacental) or acquired (caused by Toxoplasma gondii protozoa

transmitted through raw meat and cat feces)

congenital form more often causes visual impairment (more likely to involve the macula)

treatment: pyrimethamine,sulfonamide,folinic acid, or clindamycin.Consider adding steroids

after if severe inflammation (vitritis, macular, or optic nerve involvement)

Diabetes Mellitus

•most common cause of blindness in working age adults in North America

•loss of vision due to:

• progressive microangiopathy leading to macular edema

progressive DR -> neovascularization -> traction -> RD and vitreous hemorrhage

rubeosis iridis (neovascularization of the iris) leading to neovascular glaucoma (poor prognosis)

macular ischemia

Macular edema is the most common

cause of visual loss in patients with

background DR

DIABETIC RETINOPATHY

Clinically significant macular edema is

defined asthickening of the retina at

or within 500 pm of the centre of the

macula

Background

•altered vascular permeability (loss of pericytes and thickening of basement membrane causing

breakdown of blood-retinal barrier)

•predisposition to retinal vessel obstruction (CRAO,CRVO, and BRVO)

Classification

•non-proliferative:increased vascular permeability and retinal ischemia

hard exudates (lipid deposits)

dot and blot hemorrhages

microaneurysms

retinal edema

Presence of DR in

T1DM

• 25% after 5 yr

• 60% after10 yr

. >80% after15 yr

T20M

• 20% at time of diagnosis

• 60% after 20 yr

•advanced non-proliferative (or pre-proliferative)

• non-proliferative findings plus:

intraretinal microvascular abnormalities(IRMA) in I of 4 retinal quadrants

- IRMA:dilated, non-leaky collateral vessels within the retina

retinal hemorrhages ± microvascular anomalies (MAs) (in all 4 retinal quadrants)

retinal nerve fibre layer ( NI:

L) infarcts (i.e. cotton-wool spots)

r1

•proliferative

• 5% of patients with DM will reach thisstage

neovascularization of iris,disc,and/or retina

« neovascularization of iris(rubeosis iridis) can lead to neovascular glaucoma

vitreous hemorrhage, bleeding front fragile new vessels,fibrous tissue can contract causing

tractional RD

may remain asymptomatic in early stage

high-risk ofsevere vision losssecondary to vitreous hemorrhage, R D

L

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OP35 Ophthalmology Toronto Notes 2023

Screening Guidelines for Diabetic Retinopathy

• TT DM

• screen for retinopathy annually beginning 5 yr after disease onset

annualscreening indicated for all patients over 12 yr and/or entering puberty

• T2DM

initial examination at time of diagnosis, then annually

• pregnancy

• ocular exam in I st trimester, close follow-up throughout, as pregnancy can exacerbate DR

patients with gestational diabetes are not at risk of having DR

Treatment

• 1‘ prevention: tight control ofblood glucose, blood pressure,serum lipid levels, kidney function, and

microvascular complications (Diabetic Control and Complications T rial (DCCT))

• 2‘ prevention: regular screening to monitor for progression

• 3

'

prevention:

pan-retinal laser photocoagulation (RRP) for PDR: reduces neovascularization, hence reducing

the angiogenic stimulusfrom ischemic retina by decreasing retinal metabolic demand > reduces

risk of blindness

intravitreal injection of corticosteroids or anti-VEGT for fovea-involved diabetic macular edema

• macular photocoagulation laser for clinically significant macular edema (when not involving

centre of macula)

vitrectomy for non-clearing vitreous hemorrhage + tractional RD in PDR

vitrectomy before vitreous hemorrhage does not improve the visual prognosis

Anti-Vascular Endothelial Growth Factor loi

Diabetic Macular Oedema:A Network Meta

Analysis

Cochrane DBSyst Rev 2018:10^

0007419

Purpose:la compare the effectiveness and safety

of the afferent anti-VEGF drugs using network metaanalysis methods.

Results: included 24 studies with 6007 patients with

delete macular edema (DM£|ard noderate vision

loss.Aftibercept. bevacejmab. hndianibiuimab were

all more effective than laser therapyfor improving

vision by 3or move lines after one yr.Aflibercept

may confer some advantage over ran buumab and

hevacuumab. there were nodifferences in adverse

events

Conclusions: Anti-VEGF drugsaie effective at

improving vision m people with 0ME with three

to four in every10 pe op le likely to evperience an

improvement of 3or more lines VAat one yr.More

evidence on the long-term (greater than two yr]

comparative effects of these anti-VEGF agents is

needed.

LENS CHANGES

• earlier onset of senile nuclear sclerotic and cortical cataracts

• may get hyperglycemic cataract due to sorbitol accumulation (rare)

• changes in blood glucose levels ( poor control) can suddenly cause refractive changes by 3-1 diopters

due to induced osmotic changes of the lens

EXTRAOCULAR MUSCLE PALSY

• usually CN 111 infarct

• pupil usually spared in diabetic CN 111 palsy, hut ptosis is observed

• may involveCN IV and VI

• usually recover within a few months

Aflibercept, Bevaciiumab, or Ranibiiumab for

Diabetic Macular Edema: 2 Vear Result Irom a

Comparative EffectivenessRandom iicd Clinical

trial

Ophthalmology 2016:123:1351-1359

All 3anti-VEGF agentsshowed improvement of VA and

decreased numbev of injections in yr 2.Among eyes

mtb worse baseline VA. aflibercept bad superior 2 yr

VA compared with hevacuumab, butsuperiority over

lambitumab in yr 1was no longer identified.

Effects of Medical therapies on Retinopathy

Progression in T2DM

REJM 2010;363:233-244

See tandmaik Ophthalmology Ihalstiblelor more

information on Effects of Med calIberapies on

Retinopathy Progression in I20M.which details

whether intensive glycemic control.combination

therapy for dyslipidenia. and intensive blond

pressure control can limit the progression of OR.

OPTIC NEUROPATHY

• VA loss due to infarction of optic disc/nerve

Inner limiting mumbrnno

Nerve fibre layer Flame shaped

hemorrhage

Ganglion cell layor

Inner ploxiform Inyor Cotton wool

spots

Hypertension retinopathy

Inner nuclear layer

Optic disc

Outor ploxiform layor

Outer nuclear layor

External limiting membrane

Dot and blot

hemorrhage

Rod and cono

outer sogmonts Hard oxudate

Diabetes mcllitus retinopathy Pigmontod epithelium l

L

Figure 24. DM vs. HTN retinopathy r 1

Hypertension

• retinopathy is the most common ocular manifestation

• acute HTN retinopathy: retinal arteriolarspasm,superficial retinal hemorrhage, cotton wool spots,

optic disc edema

• chronic HT N retinopathy: arteriovenous(AV) nicking, flame/dot/blot retinal hemorrhages, cotton

wool spots

• increases risk for many other ocular diseases (DR, BRVO, CRAO/BRAO)

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OP36 Ophthalmology Toronto Notes 2023

Table 10. Modified Scheie Classification

Classification

Grade 0

Grade1

Grade 2

Grade 3

Grade 4

No changes

Mild arterialnarrowing

Obvious arterial narrowing with local irregularities

Grade 2 ^retinal hemorrhagesandfor exudate

Grade 3 swollen optic nerve Imalignanl HIN|

Multiple Sclerosis

• see Neurology, N55 Corticosteroids lorlreatingOptic Neuritis

Cochrane OB Syst Dev 201S;8:CD001430

S ummary: No conclusve evidence of benefit in

terms ol recovery to normal VA. visual held.«

contrastsensitvitysm mo after Initiation of IV or oral

corticosteroids.

Results:After renew of 6RCIs evaluating systemic

corticosteroidsfor treatment of acuteoptic neuritis,

all meta-analysesshow sim ilar outcomesfor placebo

vs. corticosteroid grouplor VA, contrast sensitivity,

and visual held.

Clinical Features

• blurred vision and decreased colour vision secondary to optic neuritis

• central scotoma due to damage to papillomacular bundle of retinal nerve fibres

• diplopia secondary to1N0

• RAPD, ptosis, nystagmus, uveitis, optic atrophy, optic neuritis

• white matter demvelinating lesions of optic nerve on MR1

Treatment

• IV steroids with taper to oral form for optic neuritis

DO NOT treat with oralsteroids in isolation due to increased risk of developing MS

Transient Ischemic Attack/Amaurosis Fugax

• sudden, transient blindness from intermittent vascular compromise

• ipsilateral carotid most frequent embolic source

• typically monocular, lasting <5-10 min

• Hollenhorst plaques (glistening microemboliseen at branch points of retinal arterioles) sometimes

seen

Graves’ Disease

• ophthalmopathy occurs despite control of thyroid gland status

• ocular manifestations occur mainly due to increased fibroblast proliferation and accumulation of

hydrophilic glycosaminoglycans (mostly hyaluronic acid) in the extraocular muscles and orbital

tissues The most common cause of unilateral

or bilateral proptosis in adults is Graves'

disease

Clinical

• initial inflammatory phase is followed by a quiescent cicatricial phase

Treatment

• treat hyperthyroidism

• monitor for corneal exposure and maintain corneal hydration

• manage diplopia, proptosis, and compressive optic neuropathy with one or a combination of:

steroids (during acute phase)

• orbital bony decompression

• external beam radiation of the orbit

• considerstrabismus and/or eyelid surgical procedures once acute phase subsides

Progression

*

of Signs and Symptoms of

Graves' Ophthalmopathy

NO SPECS

No signs/symptoms

Only signs (lidretraction, lid lag)

Soft tissue swelling (periorbital edema)

Proptosis (exophthalmos)

Extraocular muscle weakness (causing

diplopia)

Corneal exposure

Sight loss

Connective Tissue Disorders

• RA, juvenile idiopathic arthritis, SIT, Sjogren'

s syndrome, ankylosing spondylitis, polyarteritis

nodosa

• most common ocular manifestation:dry eyes (keratoconjunctivitissicca)

Giant Cell Arteritis/Temporal Arteritis

rt

• see Rheumatology, RH 22 u

Clinical Features

• more common in women >60 yr

• sudden loss of vision, pain over the temporal artery, jaw claudication,scalp tenderness, constitutional

symptoms, and PMHx of polymyalgia rheumatica

• ischemic optic neuropathy or, less commonly,CRAO often preceded by transient monocular vision

loss

• very high risk of vision loss in contralateral eye if untreated

ESR in GCA/Temporal Arteritis +

Males >agc/2

Females >(age 10)/2

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Diagnosis

• CBC (thrombocytosis), elevated ESR and CRP

• temporal artery biopsy

Treatment

• high dose corticosteroids to prevent further ischemic complications and improve systemic symptoms

• if diagnosis of GCA is suspected clinically:start STAT treatment + perform temporal artery biopsy to

confirm diagnosis within 2 wk of initial presentation

Sarcoidosis

Clinical Features

• granulomatous uveitis with large “mutton fat” keratic precipitates and posteriorsynechiae

• complications include glaucoma, cataracts, retinal hemorrhages, peripheral retina neovascularization,

and dry eye

• neurosarcoidosis: optic neuropathy, oculomotor abnormalities, visual field loss

Treatment

• topical/systemic steroids and mydriatics

Paediatric Ophthalmology

Strabismus

Strabismus in children under 4 mo o<

age sometimes resolves, particularly if

the deviation is intermittent, variable, or

measures <40 prism diopters

•ocular misalignment in one or both eyes, can be found in up to 3% of children

•classification

manifest (constant) vs. latent (hidden) alignment

comitant (deviation equal in all positions of gaze, also known as non-paralytic or concomitant)

vs.incomitant (deviation worse in certain positions, also known as paralytic or restrictive)

described in direction of deviation relative to the fixating eye

•distinguish from pseudostrabismus (prominent epicanthal folds, hypertelorism)

•complications: amblyopia, cosmesis

Heterotropia

•manifest deviation

•deviation not corrected by the fusion mechanism (i.e.deviation is apparent when the patient is using

both eyes)

Heterophoria

•latent deviation

•deviation corrected in the binocular state by the fusion mechanism (i.e. deviation not seen when

patient is focusing with both eyes)

•very common - majority are asymptomatic

•may be exacerbated or become manifest with asthenopia (eye strain, fatigue)

Types

•exo- (lateral deviation), eso- (medial deviation)

•hyper- (upward deviation),hypo- (downward deviation)

•esotropia = “crossed-eyes”; exotropia = “wall-eyed"

All children with strabismus and/or

possible reduced vision require prompt

referral to an ophthalmologist

Tests

•Hirschberg test (corneal light reflex): positive if the light reflex on both corneas is asymmetrical

false positives occur if visual axis and anatomic pupillary axis of the eye are not aligned (angle K )

• positive in -tropias; negative in -phorias

•cover-uncover test allows to differentiate between -tropias and -phorias

any movement of the non-occluded eye in a single cover test indicates a -tropia, asthat eye picks

up fixation in the absence of visual input to the dominant eye

any movement of the occluded eye in a cover-uncover test indicates a -phoria

•alternate cover test

• alternating the cover between both eyes reveals the total deviation, both latent and manifest

• maintain cover over one eye for 2-3 s before rapidly shifting to other eye

deviation can be quantified using a prism over one eye (alternate prism cover test)

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Cover tests

Esotropia

»

>

Normal Right eye under the cover

moves in the seme direction

<• w- a>

Exotropia

Rgttt eye under the cover

moves in the some direction Lett Hypertropia

Cover-uncover tests

Esophoria

Lett Esotropia

—

Exophoria

Figure 25. Cover and cover-uncover tests for detection of tropia and phoria Left Pseudoesotropia

(POani Sayeau 2019

^

Table 11. Paralytic vs. Non-Paralytic Strabismus

Clinical Characteristics Paralytic Strabismus Non-Paralytic Strabismus Figure 26. Hirschberg test

Concomitant strabismus

Often sudden but may be gradual or congenital Usually gradual oi shortly alter birth; rarely

sudden

Usually during infancy

Develops early in childhood

No reslrictionin range of eye movements

Neural(CN III.IV,VI);Ischemia (e.g.DM).MS. Monocular,alternating,or intermittent

aneurysm,brain tumour,trauma

Muscular;myasthenia giavis (neuromuscular

junction pathology). Craves' disease

Structural: restriction oienlrapmenl

ol extraocular muscles due to orbital

inflammation,tumour, fracture of the orbital

Definition

Onset

Incomitant strabismus

Age of Onset

Etiology

Any age;most often acquired

Reduction or restriction inrange of eye

movements due to:

wall

Diplopia Common Uncommon;image from the misaligned eye is

suppressed

Usually unaffected inthe other eye.unless CN Deviated eye may become amblyopic if no)

treated when the childis young

Amblyopia frealment rarelysuccessful after

age 8-10 yr

Amblyopia usually doesnot develop if child

has alternating strabismus or intermiltency,

which allows neural pathways lot both eyes

to develop

Common

Usually absent

VisualAcuity in Other Eye

IIisinvolved

Possibility ol Amblyopia

Neurologic Findingsor Systemic Disease

Uncommon

May be present

Accommodative Esotropia

• normal response to approachingobject is the triad ofthe near reflex:convergence,accommodation,

and miosis

• hyperopes must constantly accommodate - excessive accommodation can lead to esotropia in young

children via over-activation of the near reflex

• average age of onset is 2.5 yr

• reversible with correction ofrefractive error

• called partially accommodative esotropia ifcorrection ofrefractive error only resolves part of the

esotropia

rT

L J

Non-Accommodative Esotropia

• accounts for 50% ofchildhood strabismus

• most are idiopathic

• congenital (or infantile) esotropia is a common and important subtype

• may be due to monocular visual impairment (e.g. cataract,corneal scarring, anisometropia,

retinoblastoma) or divergence insufficiency (ocular misalignment that is greater at distance fixation

than at near fixation)

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Exotropia

• accounts for 11-18% of childhood strabismus

• congenital:onset before 6 mo, may be associated with other conditions (e.g. neurologic,craniofacial

disorders)

• acquired

intermittent exotropia:typically apparent when patient is tired of looking in the distance

consecutive exotropia:develops afterstrabismussurgery

Amblyopia

Definition

• most common cause of vision loss in children; a neurodevelopmental visual disorder with unilateral

or bilateral (less common) reduction of BCVA that cannot be attributed only to the effect of an ocular

structural abnormality

• cannot be remedied immediately by prescription eyewear alone

Etiology

• progressive suppression of visual input from eye receiving suboptimal image (blurry,deviated)

• in approximately half of the cases, amblyopia issecondary to strabismus (mainly esotropia)

• other causes may include uncorrected refractive errors, anisometropia (asymmetric refractive

errors, usually in the more hyperopic eye), and deprivation due to structural ocular problems (ptosis,

cataract, corneal opacity/scarring, retinoblastoma)

Diagnosis

• “Holler Test": young child upset if good eye is covered

• quantitative VA by age 3-4 yr using picture charts and/or matching game (Sheridan-(iardiner), testing

each eye separately

Management

• strabismus

correct with glassesfor accommodative esotropia

occlusion therapy (see below)

surgery: recession (weakening) by moving muscle insertion further back on the globe or resection

(strengthening) by shortening the muscle

botulinum toxin for single muscle weakening

• after ocular alignment is restored (glasses,surgery, botulinum toxin), patching is frequently

necessary to maintain vision until ~8 yr of age

no proven value for vision therapy/training in the treatment of strabismus or amblyopia

• anisometropia

the eye with the lower refractive error receives a clear image, while the less emmetropic eye

receives a blurred image;input from the blurred eye is cortically suppressed and visual pathway

fails to develop normally

treat with glasses to correct refractive error

patching is required if VA difference persists after using glasses for 4-8 wk

• deprivation: treat underlying cause

• amblyopia treatment lesssuccessful after age 8-10 yr. but a trial should be given no matter what age

prognosis: 90% of strabismic/anisometropic amblyopia will have good vision restored and

maintained if treated before age 4 yr, but dcprivational has a worse prognosis

Amblyopia Therapy

• occlusion:full or part-time patching of the good eye to force the brain to use the non-dominant eye

and redevelop its vision with follow-up to prevent occlusion amblyopia

• cycloplegic drops (e.g.atropine) to impair accommodation and blur vision in the good eye

Risks

• permanent loss of vision in the affected eye

• possibility of injury to “remaining” good eye (e.g.occlusion amblyopia)

• safety glasses or polycarbonate lenses recommended if VA in worse eye is <20/50 to reduce risk of

traumatic injury to good eye

• lossofstereopsis

LJ

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Leukocoria

Definition

• white pupillary'reflex (red reflex is absent)

• the presence of leukocoria warrants urgent referral to an ophthalmologist

Differential Diagnosis

• retinoblastoma

• cataract

• Coats disease (exudative retinal telangiectasis)

• persistent hyperplastic primary vitreous or persistent fetal vasculature

• retinal coloboma (chorioretinal)

. KD

• congenital infections (e.q. toxoplasmosis and toxocariasis)

• ROP

Retinoblastoma

Definition

• intraocular malignancy that rapidly develops from immature cells of the retina

Retinal Zones

• Zone I: circle centred at the nerve

with radius twice the distance from

the disc to the macula (most difficult

to treat)

• Zone II: annulus from zone I to nasal

extent of retina (nasal ora serrata)

• Zone III:remaining retina

Epidemiology

• most common primary intraocular malignancy in children

• incidence: 1 /15000

• unilateral (2/3) or bilateral (1/3)

• malignant - direct or hematogenous spread

Etiology

• sporadic or genetic transmission;screening of siblings/children is essential

• inherited forms likely tohe bilateral

• often caused by mutations in RBI on chl 3ql4, the first tumour suppressor gene discovered, and less

commonly by amplifications of MYCN, an oncogene

Diagnosis

• often presents with leukocoria and/or strabismus

• other signs: red eye, eye enlargement if advanced disease

• fundus examination (nodular, white/cream-coloured masses with intralesional blood vessels)

• U/S (A & B-scan) or MRI may demonstrate RD and/or calcified mass (present in most cases)

Zone II

Lane, Tone I

Optic

nerve

Macula

Figure 27. Zones of the retina in ROP

Treatment

• local (laser, cryotherapy, chemotherapy), systemic chemotherapy, and/or enucleation + genetic

counseling

Retinopathy of Prematurity

Definition

• vasoproliferative retinopathy that is a major cause of childhood blindness in low- and middle-income

countries

Anti-VEGF Drugsfor Treatment of Retinopathy of

Prematurity (ROP)

Cochrane 06 Syst Set 2018:1 C 000S734

SummaryConclusions: Rene*

ol 6 RCK'Ouas ICIs

companng anti-VEGf agentsn.conventional therapy

for ROP|rr383).

• Insufficient data precludes strong conpuvonsfoe

routine use ol mlimlrMl anti-VEGf agentslor

treatment ol ROP

• Intravrtreal bevBCizumab,

'ran izumab as

monotherapy reducesrisk of refractory errors

during childiood

• htrar.treal pegaplenib •laser therapy reduces the

nsk of retinal detachment for type1ROP

. Effect on other critical outconnes and long-term

systemic adverse effectsare unknown

Risk Factors

• non-Black race (Black infants have lower risk of developing ROP)

• earlier gestational age, birth weight <1500 g, low caloric intake, postnatal hyperglycemia

• high oxygen exposure after birth (iatrogenic), i.e. assisted ventilation >1 wk

Classification (ROP Staging)

• stage 1 : Hat white demarcation line at the junction between the vascular and avascular retina

• stage 2: elevated ridge

• stage 3: extra-retinal fibrovascular tissue extending into vitreous

• stage 4: partial RD (4A: macula “

on", 4B: macula “

off”)

• stage 5: total RD

• plus ( +) disease: dilatation and tortuosity of retinal vessels

• threshold disease: stage 3+ in zones 1 or 2 with circumferential extent of ROP involvement in 5

continuous or 8 cumulative clock hours

r i

c

Treatment

• laser ablation is currently the treatment standard for stages 3+;intravitreal bevacizumab and

ranihizumab both showed significant benefits in zone I compared to laser ablation therapy in infants

with stage 31 ROP

• stage 4-5 is treated with vitrectomy/scleral buckle (goal is to release vitreous tractional forces on the

retina)

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Prognosis

• higher incidence of myopia among ROP infants, even if treated successfully (less refractive error

among anti-VEGP treated vs. laser treated)

• stage 4B and 5 have poor prognosis for visual outcome despite treatment

Nasolacrimal System Defects

Definition

• congenital obstruction of the nasolacrimal duct (failure of canalization ) at valve of Hasner,

-1-2 mo of

age

Signs and Symptoms

• epiphora (overflow of tears), periocular crusting, mucopurulent discharge, recurrent conjunctivitis

• can have reflux of mucopurulent material from lacrimal punctum when pressure is applied over

lacrimal sac

Treatment

• circular massage over lacrimal sac at medial canthus

• vast majority spontaneously resolve in 9-12 mo, otherwise consider referral for duct probing

Ophthalmia Neonatorum

Definition

• purulent conjunctivitis with profuse exudate in the first few days of life; can cause blindness

Etiology

• chemical/toxic;silver nitrate, erythromycin (secondary to prophylaxis,self-limiting)

• infectious; bacterial (e.g. N.goiwrrlioeac - most common, trachomatis),herpes simplex virus

Gonococcal Infection isthe mostserious

threat to sight asit can rapidly penetrate

corneal epithelium, causing corneal

ulceration

Treatment

• systemic antibiotics and saline irrigation with possible hospitalization if infectious etiology

Congenital Glaucoma

Epiphora in children -rule out

congenital glaucoma Definition

• elevated IOP within the first year of life

Etiology

• not entirely known - may be due to inadequate development of anterior chamber

• sporadic and hereditary (autosomal recessive); males more often affected

• secondary congenital glaucoma can be associated with ocular and systemic disorders

ocular: aniridia, microcornea, megalocornea, microphthalmos, persistent hyperplastic primary

vitreous,Sturge-Webersyndrome,Axenfeld-Riegersyndrome, neurofibromatosis

systemic: Prader-Willi,trisomies,fetal alcohol syndrome, mucopolysaccharidoses,and many

others

Clinical Features

• photophobia,epiphora, and blepharospasm

• cloudy cornea due to edema;Haab’sstriae due to breaks in Descemet’s membrane

• increased IOP, rapidly-progressive myopia

• buphthalmos (large cornea, "ox eye") and enlarged Q)R

Treatment

• immediate angle surgery after diagnosis

Ocular Trauma

Blunt Trauma

LJ

• caused by blunt object such as fist

• HPI:injury, ocular history,drug allergy, tetanusstatus

• PEx: VA first,

pupil size and reaction, hOM (diplopia), external and slit-lamp exam, ophthalmoscopy

if VA normal orslightly reduced:globe less likely to be perforated

if VA reduced: possible globe perforation, corneal abrasion,lens dislocation,retinal tear

• bone fractures

blow out fracture:restricted EOM, diplopia, enophthalmos(sunken eye)

ethmoid fracture:subcutaneous emphysema (air) of lid

lays test VA first- medicolegal

tection

61.7

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• lids:swelling,laceration, emphysema

• conjunctiva:subconjunctival hemorrhage

• cornea: abrasion (detect with fluorescein staining and cobalt blue filter using slit-lamp or

ophthalmoscope)

• anterior chamber: assess depth, hyphema, hypopyon

• iris: prolapse, iritis

• lens:cataract,dislocation

• vitreous:hemorrhage

• retina: tear, detachment

Refer if You Observe Any of These

Signs

• Decreased VA

• Shallow anterior chamber

• Hyphema

• Abnormal pupil

• Ocular misalignment

• Retinal damage

Penetrating Trauma (§)

Management of Suspected Globe

Rupture • includes: ruptured globe ± lid laceration, prolapsed iris, intraocular foreign body

• rule out intraocular foreign body with O'

orbit, especially if history of “metal striking metal ”

• OCULAR EMERGENCY: initial management - REFER IMMEDIATELY

• ABCs

• avoid pressing on eye globe

avoid checking IOP

• check vision, diplopia

• apply rigid eye shield to protect from further trauma

keep head elevated 30-45°to keep IOP down

• keep NPO

• check tetanus status

• give IV antibiotics

selecting appropriate agents depends on the mechanism of injury;Gram-positive bacteria are

more commonly involved than Gram-negative;retained intraocular foreign objects increase

the risk of infections with Bacillus species, whereas exposure to vegetable matter increase the

risk of a fungal etiology

CAN’T forget

CT orbits

Ancef (cefazolin) ± Aminoglycoside IV

NPO

Tetanusstatus

Pojl

-franmtk Infectious Endophthalmitis

Surv Ophthalmol 2011;56:214- 251

• Delayed primary repair (>24 h after

open globe injury) increases risk for

post-traumatic endophthalmitis in

the absence of an intraocular foreign

body (IOFB)

• If IOFB present, early vitrectomy and

IOFB removal must be performed

within 24 h of injury

• Extreme pain with hypopyon and

vitritisindicate endophthalmitis until

proven otherwise, and samples must

be obtained for culture

• Treat with empirical intravitreal and

intravenous antibiotic guided by

nature of trauma, and adjust based

on culture

Hyphema

Definition

• blood in anterior chamber, often due to damage to root of the iris

• may occur with blunt trauma

Treatment

• refer to ophthalmology

• shield and bedrest for 5 d or as determined by ophthalmologist

• sleep with head upright

• may need surgical drainage if hyphema persists or if re-bleed

Complications

• risk of re-bleed highest on day 2-5, and may result in secondary glaucoma, corneal staining, and iris

necrosis

• never prescribe Aspirin* (increases risk of re-bleed)

Shaken Baby Syndrome

Syndrome of findings characterized

by absence of external signs of abuse

with respiratory arrest seizures,

or coma.Ocular exam findings are

important diagnostically for Shaken

Baby Syndrome. These findings

include extensive retinal and vitreous

hemorrhagesthat occur during the

shaking process and are extremely

rare in accidental trauma. A detailed

fundoscopic exam or an ophthalmology

referralshould be conducted for all

infants in whom abuse issuspected.

Blow-Out Fracture

.see Plastic Surgery, PL34

Definition

•blunt trauma causing fracture of orbital floor and herniation of orbital contents into maxillary sinus

•orbital rim remains intact

•inferior rectus and/or inferior oblique muscles maybe incarcerated at fracture site

•infraorbital nerve courses along the floor of the orbit and may be damaged

Clinical Features

•pain and nausea at time of injury

•diplopia, restriction of EOM

•infraorbital and upper lip paresthesia or anesthesia (CN V 2)

•enophthalmos (sunken eye) and periorbital ecchymosis

Investigations

•CT: anteroposterior and coronal view of orbits

Treatment

•avoid coughing, blowing nose, and Valsalva maneuvers

•systemic antibiotics may be indicated

•surgery if fracture >50% orbital floor, diplopia not improving,or enophthalmos >2 mm

•may delay surgery if the diplopia improves

Classic Signs of Blow-Out Fracture

• Enophthalmos

• Decreased upgaze (inferior rectus

trapped)

• Cheek anesthetized (infraorbital

nerve trapped)

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OP-13Ophthalmology Toronto Notes 2023

Chemical Burns

•alkali burns have a worse prognosis than acid burns because acids coagulate tissue and inhibit further

corneal penetration

•poor prognosis if cornea opaque, likely irreversible stromal damage

•even with a clear cornea initially, alkali burns can progress for weeks - thus, very guarded prognosis

Treatment

•immediately irrigate with water or balanced saline solution ( BSS)

• irrigate with eyelids retracted in emergency department with IV drip to physiologic pH (test with

litmus paper)

• swab upper and lower fornices to remove possible particulate matter

•do not attempt to neutralize an acid with a base, or vice versa

•topical antibiotics and patching

•topical cycloplegics to decrease iris spasm (pain) and preventsecondary glaucoma (due to posterior

synechiae formation)

•topical steroids (prescribed by ophthalmologist) to decrease inflammation, use for <2 wk in the case of

a persistent epithelial defect

Ocular Drug Toxicity

Table 12. Drugs with Ocular Toxicity

Drugs

Amiodaronc Corneal microdeposits and superficial keratopathy (vortex keratopathy)

Rate:Ischemic optic neuropathy

Pupillary dilation (risk of angle-closure glaucoma)

Inflammatory eye disease (iritis,sderilis, episcleritis)

Bull's eye maculopathy

Vortex keratopathy

Anteriorsubcapsular cataract

Decreased tolerance to contact lenses

Migraine

Optic neuritis

Retinal vein occlusion

Benign increase in ICP

Yellow vision

Blurred vision

Optic neuropathy

Oculogyric crises

Blurred vision

Superficial keratopathy

Relinal hemorrhages and cotton woolspots

Optic neuropathy

Papilledema

Posterior subcapsular cataract

Glaucoma

Papilledema (systemic steroids)

Increased severity of NSV infections (geographic ulcers)

Predisposition to fungal infections

Stevons-Johnson syndrome

Intraoperative floppy irissyndrome (can complicate cataractsurgery)

Papilledema (associated with pseudotumour cerebri)

Pigmentary degeneration ol retina

Relinal deposition with macularsparing, peripheral visual field loss

Papilledema

Band keralopalhy

Atropine, benrtropine

Bisphosphonates (Fosamax .Actonol )

Chlotoqulno, hydroxychloroquine

Chlorpromazine

Contraceptive pills

Digitalis

Ethambutol

Halopcridol (Haldol )

Indomethacin

Interferon

Isoniaiid

Nalidixic acid

Steroids

Sulfonamides. NSAIDs

Tamsulosin (Flomax )

Tetracycline

Thioridazine

Vigabatrin

Vitamin Atoxicity

Vitamin D toxicity

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OP-11 Ophthalmology Toronto Notes 2023

Common Medications

TOPICAL OCULAR DIAGNOSTIC DRUGS

Fluorescein Dye

• water-soluble orange-yellow dye

• green under cobalt blue light (ophthalmoscope,slit-lamp ± applanation tonometry)

• absorbed in areas of epithelial loss (ulcer, abrasion, laceration)

• stains mucus, contact lenses,foreign bodies

Rose Bengal Stain

• stains devitalized epithelial cells and mucus to indicate tear film abnormalities (e.g. mucin deficiency)

Anesthetics

• e.g. proparacaine HC10.5%, tetracaine 0.5%

• indications: removal of foreign body and sutures, tonometry, and examination of painful cornea

• toxic to corneal epithelium (inhibit mitosis and migration) and can lead to corneal ulceration and

scarring with prolonged use,therefore NEVER prescribe

Mydriatics

• dilate pupils

• two classes

cholinergic blocking (e.g. tropicamide -Mvdriacyl*)

dilation plus cycloplegia (loss of accommodation) by paralysis of iris sphincter and the ciliary

body

indications: refraction,ophthalmoscopy, therapy for iritis

• adrenergic stimulating (e.g. phenylephrine HC) 2.5%)

stimulate pupillary dilator muscles, no effect on accommodation

usually used with tropicamide for additive effects

side effects:HTN, tachycardia, arrhythmias

Table 13. Mydriatic Cydoplegic Drugs and Duration of Action

Drugs Duration of Action

tropicamide (Mydriacyl -

) 0.5%,1%

Cydopentolate HCI 0.5%,1%

HomatropineHBr1%,2%

Atropine sulfateO.S%.1%

Scopolamine HBi 0 25%,5%

4 5 h

3-6 h

3-7 d

1-2 wk

1-2 wk

GLAUCOMA MEDICATIONS

Table 14. Glaucoma Medications

Drug Category Dose Effect Comment/Side Effects Ophthalmic Drop Cap Colours

Green Cholinergics

Anticholinergics

White Anesthetics,antibiotics.

artificial tears,steroids

Yellow (3-blockers

(3-blocker combinations

Purple a-agonists

Prostaglandins

Orange Carbonic anhydrase

inhibitors

Fluoroquinolones

NSAIDs

Anti-inflammatories,

steroids

o-Agonist

a2-selcctivc

• brimonidine 0.2% (Alphagan I

• apradonidine 0.5% (lopidine- )

1git 0S /0D BID/ tID Non selective:reduced aqueous

production *

increased TM outflow

Selective:reduced aqueous

production *increased

uveosderal outflow

Reduced aqueous production Bronchospasm (caution in

asthma/COPD)

Increased CNF

Bradycardia,hypotension,

depression,heart block,

impotence

Reduced aqueous production Must ask about sulfa allergy

Generally local side effects with

topical preparations

Oral: diuresis,laliguc.

paresthesia,Glupset

Miosis

Reduced night vision

Increased Gl motility,brow ache,

headache

Reduced heart rale

Increaseduveosderaloutflow Iris colour change

(uveosderal responsible for 20% Periorbital skin pigmentation

Lash growth

Conjunctival hyperemia

Non- selective: mydriasis,macular

edema,tachycardia

Selective: contact allergy,

hypotension/apnea in children

Red

Blue

P-Blockcr Non-sclcctive

• timolol (Ilmoptic '

l

• levobunolol (Bclagan |

p1-sclectivc

• belaxolol (Betoptic )

1gtt 0S/0D once dailyl8IO

Teal

Tan

Grey

Carbonic Anhydrase Inhibitor

• doreolamide (Trusopt )

• briniolamidc|Aiopl '

|

• oral:ucetaiolamide (Dianio

*

).

methacolamide (Neptaiane -

)

Parasympathomimetic

(cholinergic stimulating)

• pilocarpine (Pilopine -

)

• carbachol (Isopto Carbachol -

)

1gtt OS ,’0D 1ID

Diamo« :500 mgP0 BID

Pink

1-2 gits OS/OD TIDJOIO Increased TM outflow

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Prostaglandin Analogues

• latanoprost (Xalatan )

• travaprost(Travatan:

)

• bimatoprost (Lumigan1)

1gtt 0S /0D OHS

of drainage)

+

Cosopt = timolol douolamide;Xalacom = timolol lantanoprost:Combigan* = timolol brimonidine;DuoTrav = timolol travaprost:gtt =

drop, gtts drops

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OP-15Oplnhalmology Toronto Notes 2023

WET AGE-RELATED MACULAR DEGENERATION MEDICATIONS

VEGF Inhibitors (Anti-VEGF)

• anti-VEGF agents prevent ocular angiogenesis and development of choroidal neovascularization

• administered via intravitreal injections

• aflibercept (Eylea*) is a VEGF “trap"

agent that binds VEGF-A, B, and placental growth factor

• ranihizumab (Lucentis*) is a monoclonal l ab fragment and non-selective anti

-VEGF agent

• brolucizumab (Beovu*) is a humanized monoclonal single-chain variable fragment antibody directed

against human VEGF-A

• bevacizumab (Avastin*) is recombinant humanized monoclonal IgG antibody and non-selective antiVEGF agent

• FDA-approved only for treatment of metastatic breast cancer, colorectal cancer, and non-small

cell lung cancer; therefore, its widespread ophthalmologic use is off-label

Intravitreal Bevacizumab vs. Ranibizumab for

Treatment of NeovascnlarAge-Related Macular

Degeneration:findingsfrom a Cochrane

Systematic Review

Ophthalmology 2016; Q«1|:)0-W

Summary: In 6 RCIsmth 2009 participants, there

were no important differences in effectiveness or

safety between bevacirnmob and ranibirnmab.

despite a significant cost difference.

Antiplatelet and Anticoagulant Drugs Do Not

Affect Visual Outcome in Neovascular Age-Related

Macular Degeneration in the BRAMD Trial

AmJ Ophthalmol 2018:187:130137

Summary: In 330 MVAMO patients receiving edbev

bevacizumab or ranibtnunab treatment, use o!

anti-coagulantand anti-platelet agents was not

associated with visual decline or occurrence of ocular

hemorrhages.

TOPICAL OCULAR THERAPEUTIC DRUGS

NSAIDs

• used for less serious chronic inflammatory conditions

• e.g. ketorolac (Acular*),diclofenac ( Voltaren*), nepafenac (Nevanac*) drops

Anti-Histamines

• used to relieve red and itchy eyes, often in combination with decongestants

• sodium cromoglycate - stabilizes membranes

• olopatadine (Patanol*, Pataday*)

Decongestants

• weak adrenergic stimulating drugs (vasoconstrictor)

• e.g. naphazoline, phenylephrine (Isopto Frin*)

• rebound vasodilation with overuse; rarely can precipitate angle-closure glaucoma

Antibiotics

• indications:bacterial and hyperpurulent conjunctivitis, corneal abrasions and ulcers,

endophthalmitis, keratitis, blepharitis, globe rupture, cellulitis, lacrimal sac, and lacrimal gland

infections

• commonly as topical drops or ointments, may give systemically

• e.g.sulfonamide (sodium sulfacetamide,sultisoxazole), aminoglycosides (gentamicin (Garamycin*),

tobramycin (Tobrex*)), erythromycin, tetracycline,bacitracin,polymyxin B,fluoroquinolones

(ciprofloxacin (Ciloxan*), ofloxacin (Ocuflox*),moxifloxacin (Vigamox*),gatifloxacin (Zymar*))

Corticosteroids

• e.g. fluorometholone (FML*), betamethasone, dexamethasone (Maxidex*), prednisolone (Predsol*

0.5%, Pred Forte* 1%), rimexolone (Vexol*),loteprednol etabonate 0.5% (Lotamax*), and difluprednate

(Durezol*)

• primary care physicians should avoid prescribing topical corticosteroids due to risk of glaucoma,

cataracts, and reactivation of HSV keratitis

• complications

potentiates HSV keratitis and fungal keratitis as well as masking symptoms

increased 10P,more rapidly in steroid responders(within weeks)

• posteriorsubcapsular cataract (within months)

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OP16 Ophthalmology Toronto Notes 2023

Landmark Ophthalmology Trials

Trial Name Reference Clinical Trial Details

AGE-RELATED MACULAR DEGENERATION

AREDS2 JAMA 2013:3091191:2005-2015 Title:lutein Tcaxanlhin and Omega-3 fatly Adds lor AMO: The Age -Related Eye Disease Study 2 (AREDS2)

Randomired Clinical Trial

Purpose:to determine whether adding lutein *

zeaxanthin.OHA EPA.or both to the AREDS formulation (vitamins

C and E.3- carotene, zinc,and copper) decreases the risk of developing advanced AMD and lo evaluate the effect of

eliminating 3-carotene,lowering zinc doses,or both in the AREDS formulation.

Methods:Patients at risk for progression to advanced AMD were randomized to receive lutein *

zeaxanlhrn. DHA *

EPA.lutein •zeaxanthin and DHA EPA,or placebo,In addition lo taking the AREDS formula.

Results:Comparison with placebo (ARE0S formula alone)inthe primary analyses demonstrated no statistically

significant reduction inprogression to advanced AMD.There was no apparent effect of 3-carotene elimination or

lower-dose zinc on progression lo advanced AMD. More lungcancers werenoted in the 3- carotene,mostly in former

smokers.

Conclusions:Addition of lulein

'

zeaxanthin.OHA

’