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Toronto Notes 2011 Ophthalmology.pdf

This document provides an overview of common ophthalmological topics including: 1) Basic anatomy of the eye, differential diagnoses for common presentations like vision loss and red eye, and ocular emergencies. 2) How to perform an ocular examination including assessing visual acuity, optics of the eye, and examination of structures like the orbit, lids, conjunctiva, cornea and more. 3) Common ocular conditions organized by structure or system affected such as the lacrimal apparatus, uvea, lens, vitreous, retina, glaucoma and others. Pediatric ophthalmology topics and ocular manifestations of systemic diseases are also reviewed.

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OP Ophthalmology Faazil Kusam, Kay Lam and Jenna Tessolini, chapter editors Alaina Garbens and Modupe Oyewumi, associate editors Adam Gladwish, EBM editor Dr. Wai-ChingLam, statfeditor Basic Anatomy Review ................... 2 Differential Diagnoses of Common Presentations . . . . . . . . . . . . . . . . . . . . . . . . . . 3 Ocular Emergencies ..................... 5 The Ocular Examination .................. 5 Optics ................................. 8 The Orbit ............................. 10 Globe Displacement Preseptal Cellulitis Orbital Cellulitis Lacrimal Apparatus . • • •• • • . • • •• • • •• • •• . • 11 Dry Eye Syndrome Dacryocystitis Epiphora (Tearing) Dacryoadenitis Lids and Lashes ....................... 13 Lid Swelling Hordeolum (Stye) Ptosis Chalazion Trichiasis Blepharitis Entropion Xanthelasma Ectropion Conjunctiva ........................... 15 Pinguecula Pterygium Subconjunctival Hemorrhage Conjunctivitis Sclera ................................ 16 Episcleritis Scleritis Cornea ............................... 17 Foreign Body Herpes Zoster Corneal Abrasion Keratoconus Recurrent Erosions Arcus Senilis Corneal Ulcer Kayser-Fleischer Ring Herpes Simplex The Uveal Tract ........................ 20 Uveitis Anterior Uveitis (Iritis) Posterior Uveitis (Choroiditis) Lans ................................. 21 Cataracts Dislocated Lens (Ectopia Lentis) V"rtreous .............................. 22 Posterior Vitreous Detachment (PVD) Vitreous Hemorrhage Endophthalmitis and Vitritis Toronto Notes 2011 Retina ................................ 23 Central Retinal Artery Occlusion (CRAO) Branch Retinal Artery Occlusion (BRAO) CentraVBranch Retinal Vein Occlusion (CRVO/BRVO) Retinal Detachment (RD) Retinitis Pigmentosa Age-Related Macular Degeneration (ARMD) Glaucoma ............................. 27 Primary Open Angle Glaucoma (POAG) Normal Pressure Glaucoma Secondary Open Angle Glaucoma Primary Angle Closure Glaucoma (PACG) Secondary Angle Closure Glaucoma Pupils ................................ 30 Pupillary Light Reflex Pupil Abnormalities Dilated Pupil (Mydriasis) Constricted Pupil (Miosis) Relative Afferent Pupillary Defect (RAPD) Malignancies .......................... 34 Lid Carcinoma Malignant Melanoma Metastases Ocular Manifestations of Systemic Disease...34 HIV/AIDS Other Systemic Infections Diabetes Mellitus (DM) Hypertension Multiple Sclerosis (MS) TIA/Amaurosis Fugax Graves' Disease Connective Tissue Disorders Giant Cell/Temporal Arteritis (GCA) Sarcoidosis Pediatric Ophthalmology ................ 38 Strabismus Amblyopia Leuk.ocoria Retinoblastoma Retinopathy of Prematurity (ROP) Nasolacrimal System Defects Ophthalmia Neonatorum Congenital Glaucoma Ocular Trauma ......................... 42 Blunt Trauma Blow-Out Fracture Penetrating Trauma Chemical Burns Hyphema Surgical Ophthalmology ................. 43 Ocular Drug Toxicity ••••••••.••••••.•••• 44 Common Medications................... 44 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46 Ophthahnology OPI
OP2 Opblhalmology LltaniV"18W Basic Anatomy Review RETINAL LAYERS 11D) 1. lmll'limili'lg membnlne 2. Narvefin IIIYIIr 3. Ganglillll cell IIIYIIr 4. 1m•pladonn IIIYIIr 5. lm•ruclaer IIIYIIr 6. Out.-pltxifunn IIIYIIr 1. Out.-niii:IIIIU IIIYIIr 8. E'xllrmllimiting IIIYIIr 9. l'hoiDraceptor IIIY8r SuperiorView 1'oroDio 2011 CB!.TYPES Vllnlous hu11111ur Ganglillllcella Bipoia"calls Rod nuclei 'NI'MIrhl·- Coneruchi Rlld cei'- 106-H-fi- Conecells I0. Rllillll pigm..t apitllelilm Pigmllllll;ti" Bruch"s ChDrDid c s.at1A. Kim2005
'IbroDloNota2011 Figure 3. Tear from tlte Eye (Lacllmal Appai'BIUI) Differential Diagnoses of Common Presentations Loss ofVIsion l.olsDIV1111111 ildanic lllack(1IAl • Mi!Pine wilhl!ln -+ CGmlllr/AIQdor ....... • CCIIMII ed111111 • Al:uiiiii"Qkt- closlUI glaucoma body Figu111 4. Laa IfVilian Red Eye • llda/orbJ.tllacrlmalsystem • hordeolum/chalazion • blepharitis • foreign body/laceration Vlhaur/RIIIul GpticiiMvll • V"llnlous t.n.lrrlwgl • llll!illll delactment • Relilll nrd veinoccUiion • Acdii'IIIICU.. leeion • Opti: rJIIWitis • Tanporalal1aritis • AnbnJrischanic opticI1IIUtllll1hY tAlON) • dacryocystitis/dacryoadenitis • COD:lunctivalsclera • subconjunctivalhemorrhage • conjunctivitis • dryeyes • pterygium • episcleritisJscleritis • preseptallorbltal celluliti& • cornea • foreign body • keratitis • abrasion,laceration • ulcer I + CarllcaWiher • Occptal irfarctiorV' t.n.lrrlwgl • Cortieal bbtlaas • Flllc1ionlll (11011-IJIIIMie. di'IIJ!Diisaf IDWiln) -+ ....d • Cornell l11:811'ircVed111111 • llllfnlcliVIerrar • l:allnllt • Glaucoma Gplii:NIIrw • Aclt-l'llded .,... degenenilion • Diablltic • RJilal'IIISCU.. iraltliciency + CarllcaWiher • PiluilaJy ldanDma ntur:lld (lid.,. ll!liodarcne) • M.ltritional dalicimcy • l'aDilllldllml opliclllllrapathy (inlrlcllnialman, 01bi1111111111) naaplum • Rllililil pQr!'entola(RP) Ophthalmology OP3 ,,, Top lin DIJJItfAcull l.asaGfVIIItn 1. Tr..ruw'furaign bod'f 2. Ralillll.my/winIICCUion 3. Ralilllldlllllclrnent ,, , ,. 'lb'S11 DDxofC...,. l.asiGfVIIIIn lllvenillll I.Catnct 2.R!lilactive lrrGI 3. Comaal dystrophy lrraRni.la 1.Agt-ralalld macular 2. Glaucol'lll 3. Dilbatic rstiriiJIIIIIhy
OP4 Ophthalmology Differential Diagnose5 ofCommon Presentations Toronto Notes2011 • anterior chamber • uveitis (iritis, iridocyclitis) • acute angle-closureglaucoma • hyphema • hypopyon • endophthalmitis T1ble 1. Common Differenti1l Di1gnosis of Red Eye Conjunctivitis Acldllritis Ac.aAnale Keratitis Cl01111 Glaucoma Dildllrge Bacteria: purulent No No Profusetearing Virus: 5erous Allergy: mucous Pain No ++ (tender globs) +++ ++(on blinking) Plurtophobia No +++ + ++ Blurllld Vilian No ++ +++ Varies Pupil Normal Smaller Fixed in rnid-(jilation Same ar smaller ConjunctiVII with Ciliary Hush Dilluse Dilluse liltal pallor Com111 Normal aropacifiad KBratic precipitates StBIImy Infiltrate, adsma, epithelial defects Wraocular p...re Normal Varies lncraasad marlaKiy Normal ar increased Anteriorchamber Normal Cells+ flare Shallow Cels + flare ornormal Olher Large, lEnder Posteriorsynechiae Caloured haiDS (auricLJar] node vil'lll NIIISea and vomiting Ocular Pain • differentiate from ocular ache: eye fatigue (asthenopia) • herpes zoster prodrome • trauma/foreign body • keratitis • corneal abrasion, corneal ulcer • acute angle-closure glaucoma • acute uveitis • scleritis, episcleritis • opticneuritis • ocular migraine Floaters • vitreous syneresis (shrinkage and collapse ofvitreous gel) • posterior vitreous detachment (PVD) • vitreous hemorrhage • retinal tear/detachment • posterior uveitis Flashes of Light (Photopsia) • posterior vitreous detachment (PVD) • retinal tear/detachment • migraine with aura Photophobia (Severe Light Sensitivity) • corneal abrasion, corneal ulcer • keratitis • acute angle-closure glaucoma • iritis • meningitis, encephalitis • migraine Diplopia (Double Vision) • binocular diplopia: strabismus, CNpalsy(Ill, IV. VI) secondaryto ischemia, diabetes, tumour, trauma, myasthenia gravis, muscle restriction/entrapment, thyroid ophthalmopathy, internuclear ophthalmologia (INO) 2°to multiple sclerosis, brainstem infarct • monocular diplopia: refractive error, strands ofmucus intear film, keratoconus, cataracts, dislocated lens, peripheral iridotomy
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
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)
'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
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
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
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
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
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
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.
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
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
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
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.
OP18 OphthalmoloBf Topic;alanlllgelics1houldonly ba Ulld 11:1 n.ylllho"" NE"JEEI beUllld IStraa1mantfarany ocul•problem. fEVER plb:h lb111i1111patient- can1actlanaa{puna1lll"s8urromonu ilfllction). "' I fnJm orvanie malblr (e.g. twig. mg•nlllltl:..) h1V8 higher recurrence. even Yllllllata'. "' I C111118111 Allnni111: Ta ,_.11 Nit ta Patch PdchingforCDrlllllllbllliOIL CDcMine RIMsw2006 Pdching is not indiCit8dfarsmpla callllllllllllllsions, m•sumg lassthan 10mm. Thin il no impiUVIImant il hilling ra1111 on diiVI 1..3, no chlng• in reporllld pamand no difla'a1cainlhe Ule ofanlilicllic:s b81wean the prnx;h and non-jlllll:h ppa. NormaiCa!MII 1? . . ' F'IIJ•ra 14. Cornall Allraaion n. Ull* 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
TorontoNota2011 Cornea Table 5. Cumelll Abrasi1111 ws. Camellll Olear Almion Ulta' liMCalnll Acuta(instanllniM) tiac:ulaldavsl lisiDryofTmiiU Y8l NatUIUIIy Carnal !lear WhiiB, nacrtJtic araa lritDetlil !lear Obsclmd earn.1nicb- N1111111l Mayhava Exbnoflelian LimitadIDepilhiiiUII Exlalaian iniDstroma Herpes Simplex Keratitis • usuallyHSVtype 1(90% ofpopulation arecarriers) • maybetriggered bystress,fever, sun exposure.Immunosuppression Clinical Features • pain.tearing, foreign bodysensation, red eye,mayhave decreasedvision. eyelidedema • cornealhypocsthesia • dendritic (thin and branchlng) lesion inepitheliumthat stains with fluorescein Complications • cornealscarring (canleadtoloss ofvision) • chronicinterstitialkeratitis due to penetration ofvirus into stroma • secondaryiritis, secondaryglaucoma Treatment • topicalantiviral suchastrlfluridine,considerS}'5temic antiviralsuch as acyclovir • dendriticdebridement • NO STEROIDSinitially- mayaacerbete condition • ophthalmologistmuste.xerdse cautionifaddingtopicalsteroidsfor chronickeratitis oriritis Herpes Zoster • dermatitis ofthe forehead (the CNVl territory) mayinvolve theglobe (Figure 15) • Hutchinson's sign: iftipofnoseisinvolved (nasociliarybranchofVl) then eyewillbeinrolved inapproximately7596 ofcasa • ifno nasal involvement,theeyeisinvolvedin 1/3 ofpatienlll Clinical Features • pain.tearing, photophobia, redeye • cornealedema, paeudodendrite, superftdalpunctatekeratitis • cornealhypoesthesia Complications • cornealkeratitis, ulceration..perforation andscarring • secondaryiritis, secondaryglaucoma,cataract • musclepalsies (rare) dueto CNS involvement • occasionallyseverepost-herpeticneuralgia Treatment • oralantiviral (acyclovir, valcyclovirorfamc:iclovir) immediately • topical steroids,cycloplegiaas indk:atedforkeratitis, irltis • erythromycin ointmentifconjunctivalinvolvement Keratoconus • bilateralparacentralthinningandbulging (ectasia) ofthecorneatoform a.conicalshape • usuallyspora.dic, butassociatedwith Down's syndrome. atopy, contactlensuse (theorizedtobe relared to chronicvigorous eyerubbing) • a.ssociatedwith breab inDescemefs and Bowman's membrane • resultsinirregularastigmatism, scarring, stromal edema. Treatment • attempt:correctl.onwithspecta.clesorcontactlens • cross-linldnglasertrelltment ma.yhaltorslowdiseaseprogression • penetratingkeratoplasty(cornealtransplant) 9096 successful • post-operativecomplications: endopbthalmitis,graft rejection, graft:fiillure. graftdehiscence Opbtbalmololf OP19 _,, Abi'BIIan •· UICiro•lllt....., An •lnlian llppaii!W clllllrwhila.. ucar ilmen OINIQIII. Figu111 15. Trigarinll Distrib.tia• -, S1lnid lnliltmantfur DGUIIIrdilordars onlybepr8ICiiledand 11.1pii'Vill8d by..aphlhllrnalagilll, u thgycan in.-ircam•l h1111ing..d IIXIIcabn harpalil: al'lllitia. ' •.}---------------, Tadet8ct1!8nrtDcorw.laokfur bUging aftha IIIWIIr ll'fllid whentha patiant loakaclownwlnl (l'lobllan'l aign).
OP20 OphthalmoloBf 16. Canj11nctinl Hypar•i• vs. CiliaryRush CorneaflheUTeal.Tract 1'oroDio 2011 Arcus Sanilis • hazywhite ringinperipheralcornea, <2 mmwide, clearlyseparatedfrom limbus • common,bilateral, benign corneal degeneration dueto lipiddeposition, partofthe aging process • maybe associatedwithhypercholesterolemiaifage <40yean, check.lipidprofile • no assoclatedvisualsymptoms, no complications, no treatmentnecessary Kayser-Fleischer Ring • brown-yellow-green plgmented ringin peripheralcornea, startingInferiorly • dueto deposition ofcopperpigmentin Descemet's membrane • associatedwithWilson'sdisease (9596, b.epatolenticula.rdegeneration) • no associs.tedsymptoms or complications ofring • treat underlyingdisease The Uveal Tract • uvealtract= iris,ciliarybody. choroid • vascularized, pigmentedmiddle layer ofthe eye, between the scleraandtheretina Uveitis • mayinvolveone orallthree parts ofthetract • idlopathicor associatedwithautolmmune, infectious,granulomatcus, malignant causes • shouldbe managedbyanophthalmologist Anterior Uveitis (Iritis) • ln1lammation ofIris, usuallyaccompaniedbycyclitis (Inflammation ofciliarybody), whenboth = iridocyclitis • usuallyunilateral Etiology • usuallyidiopathic • connectivetissue diseases • HLA-B27: reactive arthritis, ankylosing spondylitis (AS), psoriatic arthritis, inflammatory boweldisease (IBD) • non-HLA-B27: juvenileidiopathicarthrit:is (JIA) • infectious: syphilis, Lymedisease, toxoplasmosis, TB, HSY, herpes zoster • other: sa.rooidosis,trauma, large abrasion,postocularsurgery Clinieel fHtures • photophobia(dueto reactivespasm ofinflamedirismuscle), ocularpain, tenderness ofthe globe,browache (ciliarymuscle spasm), decreasedvisualacuity,tearing • ciliaryflush (perilimbel conjunctivalinjection), miosis (spasm ofsphinctermuscle) (Figure 16) • anteriorchamber"cells"' (WBCin anteriorchamberdueto anteriorsegmentinflammation) and"ffare'" (protein predpltatesin anteriorchambersecondaryto in11ammation),hypopyon (collectionofneutrophilicexudatesinferiorlyin the anteriorchamber) • occaslonallykeratl.cprecipitates (clumps ofcells on corneal endothelium) • iritistyplcallyreduces intraocularpressurebecause dllarybodyinflammationcausesdecreased aqueousproduction;however. severeIritis, oriritisfrom herpes simplexandzostermaycause aninflammatoryglaucoma Compliartions • infl.amma.toryglaucoma • posteriorsynechiae • adhesions ofporterioriristo anteriorlens capsule • indicated byan irregularlyshapedpupil • ifoccurs 360m, entrapsaqueousinporteriorchamber, irisbomforward "irisbomb€ ' -+ angleclosureglaucoma • peripheralanteriorsynechiae (PAS) (rare): adhesionsofiristo cornea-+ glaucoma • cataracts • bandke:ratopathy(withchronic iritis) • superficialcornealcalcificationkeratopathy • macularedemawith chroniciritis
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
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
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. I'IIIOIIhthiDtit....,llully EndgpllthllmihVi1r81:1DmySludyliwp.ltealbrl 1lleElllgpllthllmitisl{rtmclomySUiy.ArdWe$ at 11311Z):147Hi Fortrlltmlnt alpost·calltlctlllliiiY endoplllhllmitis: • lllli'lvilalantibioticsprDrad IMirl)'lblmic l11tililltics • 1{11r8ctomy'indicalldonlrhilion LPonwrsa
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 BllnchYain StudyGnllp:Argon lll8r 101macularedeml inbmui•'lein accllsiaii.AmJOp/rlhllmD/19BUB: Zll-2112. BVOSsiD.wd!hit arganilllrlrlltrr.ntim!1M1 sijlt inpetian1switiiiiiiCUaredan. 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
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 9t-----------------, 8-1 0% risk afdaveloping CRVO orBRVO in other eyu. "". I •t-----------------, Superotemporal rvtina is the most common site fur horseshoetllllrs.
OP26 Ophthalmology Triad oflllltiniti1 PigrnllntDA APO ArteriDIIIr n11r0wing Perivascular bony-spicula pigmantation Opticdisc pallor ......Eye o-.StudriAIEDSI with iibrmilsCll!df. ll!d1incb'lfiHII*/IIIKIW degrlltllllion lllllllisilrltm.AREDS_,No.B. 118:1417-1438 AR!n'!lllJdildth11111i:tof hiQIHl1111 cantilltian rlvDmiiC,Wlmil E, meia patientswitll and witlloutARMD.'1'hDIIwho 111 an.dyllflectedbrARMD showed I"decne1e ilrilkallllthlrvUI loa,.._tllisll'llllrWit nobenelitin pitilrDl'lith llll1yII'no ARM!l ..._ , .. w.t ARMD U.iona on Flu••cein Classic: well-ilefined leakage Occult: mutllad or ill-dafinud luaklv& .... Dru•n vs. Exudate Drusen: h'filline materill secre1Bd by RPE 111811 fTvquunlly in ARMD typiclllly in pari·macular region Hard/Soft ExudllbJs: lipid duposi._ in 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
'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 11111 .... II!QriiiiiiiAnk.u.r .....&.-hclllrlllll..... ..._...AgfHIIIbll......... liu2 a..,:Coc:tn!elpllnicIBI'iawalRCrs ir.wlgati"Gthtlltalmi&(wlallu lllldolhalllllP'o1hflcllrJrnodllliMfar... m.tnartalwrtlgHIIInd IAflt.tl), 1'1111111:Cluli:Ill'occUI'MIItypeAIMl. . . . . IDJ1Ibadallillrodei:llddlu.tbill'otGFI. .. (ami't'EGI'fnQrrart nibadyjlrld 1hnJrf!I'D'n Ill*ThaMARNAtrillhr.wd1hlltht)IIIOIII ..._•(ll!tb'agailai15CJIIIIIIIIalln rlwUBCUIJWIII5.8'1frJrriii.IIBI- plabo,'llllil81hlFOCUS1rill!illoiwd111111111 paoladIllfarI Qlilllf15OIIIJII81111111U101"1 yea"W1114A4 rllWitiunlb + Wl1lpalfinPD!'Iftd'l'l18podilPDTIlona. lllrillilrnllllnalaiameutblllllfi1 b'1hl--ri'MIIAIMIMhIigman inJ1Mnat1sinJatarracWYiluilaculyIt IDyll!. I. CliarybodVJRC88886 l. P141IIIV block 3. Pra1ralwnu• 4. Trabecular S. PDit-lrlbiiCiilr Figure 18. Flow and litHof Pata.till Rllilblnca .... , i .B 4 0 . Ave1'11118 lOP =15 :t 3 mmHg Nannll :s:D.4
OP28 OphthalmoloBf a.....-....c........... .. PClAG PACB • CommDn (9ft) • Rlre • Qnnic ca.11e • Acute Ol'llet • I'Ull-&yll • l'li1fiJ red aya withoutra- • Exlmlaly1'lOP • MDderatllly1' lOP • HIIZV l*llBI • Nonnal cornea • Mid-dild8d and pupil pi4Ji ......:tiva • No fW tD light • No halouruund • ± HIV. lllldomilal pain • H11D11nmd light llllkFHIIIn fir POA& AFOO Age Frnily Hillury lOP Nric11 delclllll 11*1 Camaa ;b Collnll'lllcdiiW_, Dlldla • NelnlogiCIIIIbnormality pupl a111111111ant • ShallowIIIIWiorchlmber • lriwupporltciiiiiWiorchlmberiOL Glaucoma 1'oroDio 2011 o,tlc nern bHd dlmaga VIsual flllll chiiiD Small pll'aCan1niiiCO!oml Ara.llla dafact cenlnll island f"IG•ra 19. GlaucDJnllblua Damage 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)
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 bMiilnrllnnacdlr,_...-'GIIiuclml l'llglllliln 120:1268-1279 S1udy: RlndalrDd COOO'ollldclinicll1rill. l'llillb: 2.55 puticiiW, - ..clldllmlgh I piiiUitianICII.pniiDI:Oi.llgld!iG-81with rMydlllctJdopi!Hingil . .ilk! dlllaell, •dandian irmaMirpn11110 001'1 d20IIIdta- lillllrlllpicll IIIIHIIacka'!llltlmoQplaltgllll lulrtllbeculaPniYarno inililllr8llmlal,with - obsiMtionlorbothPIP'- Mldilli -6ym. ...lkllaaml:!illtJCOI!IIpmgrusian• dllfinlld byWulfieldIIIIIapti;dill: llbaarnJUtiel_ bnlll:l(f- Riducadby (1!1111115.1 T11ll'flg) illheIJealmenl Glu:on prgareaion-Mlilrt in62rJindio.UJ• il11-. The pruijntlllill-li(jllliclndv,..... inlhahltmeot VI.11-. alllinlls. Rule Ill' Furs 1/4 ol u-rlll population after u5ing 4weeks of topical steroid 4x/davwill develop 111 increase in lOP. lhlklllnlmlllilnalllrI'IIIIIIJa,..A191 Gllll:anlllldOc:U....... C/rJrnDIII!JisetiS)'III!mlti:llellilws21101, Issue 4. lludr.Cocmn IMiwrJ Z611M andme1Hnlf¥sis of10lrillsiMstilllliYJihe dlupicllplllrlmcologi;III111111PM far]Jii1wy111*11111111QiluCGII'IjPOAG) II OQIIIr hyperlinsiun(0111)_ I'IIIMII: 4919 PlfliciparaIWidomiz8dii261Ji._ l'ltiera llldOIITwlbm-ulupressure(KI') >21 IJidt.l orap1nqil(lllualml_ ..........:1opi131 eye n.tlc:aliani, ilduding blll-blackm.dormlllrida. brimulilila. andepiletlllrilevenuseldioilier 1111 pllaillo. llllil...-..: Re6JclionrJprogre..or ,.nond Glial afWulfilld dlllcts. ._..:MttHIII¥SiS on111111Uihll18118d cWilsllllitstIDcahoarIIIINaiJd Clllllds clernonslnlal11111bllerilgKf!educesinddence d;uamllilllviullilkldlflciJ.withIll oddsIIIia rJD-62 (M C1 0.47-0.811-llilwMr. 1MsRid is d mtadpractical 1118.me. --.lillnpieswere pooled.No dlmormiBd ignificllltwiullilkl pndlc:lion. llawM!,n1 clnl,11111-blackmshawld baldartnaliQMicenceinr8lb:ilg 1111111Ill (lllualmlil patilllllwillDlfTwt.n Cll11fiiii(IID pllcebo,Nih • OR of0.67!SClDA5-1.00). c:.t111ianl: lawlringlOP Cllll'llb:lprogrlllian ofllisuallil*ldefa:ls inpllierGwithOIIT.
OP30 OphthalmoloBf 1.Aq-ftgw 2.Ci.ybody 3.ComR 4.Ln 5. Bloc:bdIJibecljarmesbwork Flg1re zo.Nomaal OpenAntle varsuaAn1la Cl01ure Gl1ucam1 _...c.._.._.. IIAI:H Txwi1h mioticsIIIII leta-Biocbrs, Adrenqict. Cholinqiet ltyperuS'IIotiCllgllnbl ,, , ...--------------. liTarplalf RltNI Silnall • nuclu jpupillalyniiiiiVBYB movemlnbl) • l.81arll garicullda badycrf1h11lrn111 • Superiorcclicu IIYIImovemenll) • Suprachi11malic nucleusjaptokiaic) • Acca-.yoptic lci'l:adian rl1ylhm) Clinical Features • unilateral,butothereyeprecllsposed • red, painfuleye = RED FLAG • decreasedvisual acuity, vill:ion acutelyblurred from cornealedema • halosaroundlights • nauseaandvmnftlng, abdominalpain • fixed, mid-dllatedpupU • cornealedema withconjunctivalinjection • marked increueinlOP: maybenoticeable evento palpation (>40 mmHg) • shallowa.ntmorchamber± cellsinanterior chamber Complications • lrreverslbleloss ofvision withinhours to days ifuntreated • permanentperipheralanteriorsynechiae Treatment • referto ophthalmologist •laseriridotomy • aqueoussuppressants aruihyperosmoticagents • immediatetreatment importantto: • preservevision 1'oroDio 2011 • preventadhesions ofperipheraliristo trabecularmeshwork(peripheralanterior synechiae) resultinginpermanent closureofangle • medicaltreatment (see Glmu:oma Medications, Table 10,OP45) • mioticdrops (pilocarpine) to reversepupillaryblock • decreaselOP • topicalbeta-blockers • topical adrenergic& • topical cholinergics -pilocarpine 1-496 ql5min, upto q5min • systemiccarbonicanhydraseInhibitors - IVacetazolamide250-500mg • &ylil:emic byperosmotic agents - oralglycerine 1glkg - IV mannitnll glkg Secondary Angle Closure Glaucoma Uveitis • inflamediris adheres tolens (posteriorsynechiae) Neovascular Glaucoma • abnonnalbloodwssels developonsurfaceofiris (rubeosisiridis),intheangle, aruiwithin the trabecularmeshwork • dueto retinalischemiaassociatedwith proliferativ'ediabeticretinopathyand CRVO • treatment withlasertherapyto retina reduces neowscular lrtimulusto iris vessels Pupils • pupilsizeis determinedbythe balance between the sphincter muscle andthe dilator muscle • sphinctez muscle Isinnervatedbytheparasympatheticnervous system(PNS) • carriedbyCN m:pre- and post-ganglionicfibres synapseinciliaryganglion. anduse acetylchollneastheneurotransmitter • dilatormuscleis innervatedbythesympatheticnervous system {SNS) • first orderneuron = hypothalamus -+ brainstem -+ spinal cord • secondorder/preganglionicneuron= spinalcord -+ sympathetictrunkviainternalcarotid artery-+ superim cervicalganglioninneck • third order!postganglionicfibres originab:inthesuperim cervical ganglion, neurotransmitterIsnoradrenaline • asa dlagnostictest, 4% cocaine preventsthe re-uptakeofnoradrenaline, andwillcause dllatlonofnormalpupil, butnatonewithloss ofsympatheticinnervation {Homer's Syndrome)
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
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
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 "'' 11om•'•MAP Mia.ia Anhydrosis Ptotit Argyll Robermon Plpil (AlP) Accomodation lllfl&x Presant PupillllfY Rellex Absent ...... , ---, ..... , is poai!U to haw RAPD and nonnal viaion atthe siiiTietime. i.e. in damaged s...,arior coUiculus CIUsed by thalamic hemorrhage. ....,, .. When aii8Ssing for an RAPD, aslight dilatation lifter constriction is normal when from eye111 11'(8.
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
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 .... Macular edema thlil most common cause of visual loss in patientswith bBCkgllJUnd IJR. .... , 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
OP36 OphthalmoloBf ,, , ClinicaiiV llignifilad macularadlln. ill dsfinad ..tickiDlg ofItallllilllld orwillil5001111 ofthecentre Df1be IIIBQJia. lllll*tlllriiiiiii._....TIIII NE.JIII8t3211") OCCTtrilla-....,.gl,canl:llllllmwil ndlcl1111rista!dllblli:lllliDpldrf1Jt78IIIII lrf54l. fiiiJTIIIIIIIIIIIWIIicllliqrdr5lllr lirttTr8linlrtDilbe1i:RlinaplllrfSW{ hwiQDQ:Atpiril*"onnWilvITCI lllllbiityi1palildJwilldiiiiJailllTIIIul.EIJIIS /lrtDfIt.MM1!1!11;2111:12!1Z-13111.Andodw EIDBa..nlll • NGbnfitGlll!liini118didoniu•Ill ... iJmllldrii:rlilmM1hlgaIiiia" • Ealtthllllnrltlllilgpmtirll .. • Oiicltfllig16:utiiiiC'JI. .IItaJIIba 1NDI.Irtb:alillllr OcularMani&stalionsofSyatemlcDisease 1'oroDio 2011 • pmlifa'alive • 5%ofpatientswithdiabeteswill reachthis stage • neovasculuizationofiris, disc,retinato vitreous • neovascularization ofiris (rubeoaisirldis) canleadto neovascularglaucoma • vitreoushemorrhage from bleeding.fragile newvasels, fibrous tissuecan contract clm&lngtractional retinal deta.clunent • highrisk ofsevere visual loss 2°to vitreous hemorrhage. retinaldetachment Screening Guidelinesfor Dlabedc Retinopathy • Type! DM • saeenfor retinopathybeglnningannually5 yearsafterdisease onset • saeeningnotIndicated beforetheonsetofpuberty • Type2DM • Initial examination attime ofdiagnosis,then annually •pregnancy • ocu.larexam in 1sttrimester, closefollow-up throughout as pregnancycan exacerbate DR • gertat:ionaldiabetics not atrisk for retinopathy Treatment • Diabetic ControlandComplications Trial (DCCf) • tightcontrolofbloodsugardecreases frequencyandseverityofmkrovascularcomplications • bloodpressurecontrol • focal. laserfor clinicallysignificantm.acula.redema • panretinallaserphotocoagulation forproliferativediabeticretinopathy: reduces neovascularization, hencereducingtheangiogenicstimulusfrom ischemicretinabydecreasing retinal metabolicdemand-+ reducesrisk ofblindness • vitrectomyfur non-clearingvitreous hemorrhageandretinaldetachmentin proliferative diabeticretinopathy • vitrectomybeforevitreoushemorrhagedoesnotImprovethevisualprognosis Lens Changes • earlier onsetofsen.Uenuclearsclerosis andcorticalcataract • mayget hyperglyceml.ccataract.dueto sorbitolaccumulation (rare) • changesInbloodglucoselevels (poorcontrol) can suddenlycauserefractivechangesby 3-4 diopter& Extra Ocular Muscle (EOM) Palay • usuallyCN IIIinfarct • pupll usuallysparedIn diabetic CNIII palsy.butgetptosis • mayInvolveCN IV and VI • usuallyrecoverwithin few months Optic Neuropathy • visual acuiLyloss dueto Infarction ofopticdisc/nerve Ganglan eel layerI Innerpktxifurmlaywr Inner layer Oulllrplexiform laylr lllllr layer Exlemallmilinclme.,._,.e Rod and cone a !j "' Dilbatlllmallitul re&!o,..., j 0
Toronto Notes 2011 Ocular Manifestations ofSyatemic Disease Hypertension • retinopathyis the most common ocular manifestation • keyfeatures ofchronic HTN retinopathy: AV nicking. blot retinal hemorrhages, microaneurysms, cotton wool spots • keyfeatures ofacute HTN retinopathy: retinalarteriolar spasm, superficialretinal hemorrhage:, cotton wool spots. optic disc edema Tabla 7. Kaitii.Waganar-Barkar Classification Graup1 Mild arl!!rial narrowing Graup2 Graup3 Graup4 Obvious arterial narrowing with focal Group 2plus Cotton-wool spots Hemorrilllge and/or exudate Group3plus papilledema Multiple Sclerosis (MS) • see N49 Clinical Features • blurredvision and decreased colourvision: 2° to optic neuritis • central scotoma: due to damage to papillomacularbundle ofretinal nerve fibres • diplopia: 2° to internuclear ophthalmoplegia (INO) o RAPD, ptosis, nystagmus, uveitis, opticatrophy, opticneuritis o white matter demyc:linatinglesions ofoptic nerve on MRI Treatment o IV steroids with taper to oral form for optic neuritis • NOT oral steroids in isolation as this increases likelihoodofdeveloping MSlater TIA/Amaurosis Fugax • sudden, transient blindness from intermittentvascular compromise; ipsilateral carotid most frequent embolic source • typically monocular, lasting <5-10 minutes • Hollenhorst plaques (glisteningmicroemboli seen at branch points ofretinal arterioles) Graves' Disease • ophthalmopathy occurs despite control ofthyroid gland status • ocular manifestations occur secondaryto sympathetic overdrive and/or specificinflammatory infiltrate: ofthe: orbital tissue Clinical • initial inflammatoryphase is followed by a quiescentcicatricial phase Treatment • treat hyperthyroidism • monitor for corneal exposure and maintain cornealhydration • manage diplopia, proptosis and compressive optic neuropathy with one ora combination of. • steroids (duringacute phase) • orbital bony decompression • external beam radiation ofthe orbit • consider strabismus and/or eyelid surgical procedures once acute phase subsides Connective Tissue Disorders • RA, juvenile: idiopathic arthritis (JIA), SLE, Sjogren's syndrome:, ankylosingspondylitis, polyarteritis nodosa (PAN) • most common ocularmanifestation: dryeyes (keratoconjunctivitis sicca) Ophthalmology OP37 Optic N.m.11111111...TrilllDNTTJ Optic N.m.$WJG._.1htOpticNlllliil 113:136-137 ONTTIICIUilldPl!iantswilll&allll nawGIISII optic naurmllnllllbdad autcomaofthraatnlllmllnt +cnl Uoidx11d,andpllcebllx14d.Theyfaund 11111 cnlstaroidatUlaiiyin-riskofIICIIIIIICI, IV+0111 slliroidexpderecu;ety,1nd'"D.! trallmlnt'"I vilblltlmpaltic option.IV +1111 Uoidas r&: r1 recurence. Furtbannore,lnil Mil is wklabla in prediction lAonstt!AMS. ', , The most common cause of unilateral or bilateral proptosis in adults is Graves' di181118. ', , of Signs and Symplllms ofGr-' Ophtbalmopdly NO SPECS No siullf/sympiDms Only signs llid retraction, lid lag) Soft tiQue swelling lperiorbital edema) Proptosis{exophthalmos) Extraocular muscle weakness (causing diplopia) Comeal exposure Sightloss
OP38 Ophthalmology Ocular ManifestationsofSystemic:Diseaae/Pediatrlc:Ophthalmology Toronto Notes 2011 .....,' ESRin GCA Males> 11111112 F11111.ia > (av- + 1Dl/2 O.thill'llilni....CCA? .JAM42002; 287:92-101 ,.ill: jMcllulkldion11111 dip._ onhiltury, 11rnp1H1IIItlry'-ding,prani!IIICI althlllllry 111111endemess-the lll!!yanmm. ,.aut no11mpotlllltlryllllnormelities on exam.nDmlllESR. Giant Cell/Temporal Arteritis (GCA)- - - - - - - - • see Rheumatology; Rl7 Clinical • more common in women >60 y.o. • abrupt monocular loss ofvision, pain over the temporal artery, jawclaudication, scalp tenderness, polymyalgia rhc:umatica, and constitutional symptoms • ischemic optic atrophy • 50% lose vision in other eye ifuntreated Diagnosis • temporal arterial biopsy+ increased ESR (ESR can be normal, butlikely80-100 in firsthour), CRP • ifbiopsy ofone side is negative. biopsythe other side Treatment • high dose corticosteroid to relieve pain and prevent further ischemic episodes • ifdiagnosis ofGCA is suspected clinically: start treatment + perform temporal artery biopsyto confirm diagnosis within 2 weeks ofintial presentation (DO NOT WAIT TO TREAT) Sarcoidosis • granulomatous uveitis with large "mutton fat" keratitic precipitates and posterior synechiae • neurosarcoidosis: optic neuropathy, oculomotor abnormalities, visual field loss Treatment • steroids and mydriatics Pediatric Ophthalmology Strabismus • ocular misalignment, found in 3% ofchildren • object not visualized simultaneously byfovea ofeach eye • often presents with parental concern about a wandering eye, crossing eye, or poor vision • types: heterotropia (paralytic or non-paralytic), heterophoria • 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) Types • exo- (lateral deviation), eso- (medial deviation) • hyper- (upward deviation), hypo- (downward deviation) • esotropia= "crossed-eyes"; exotropia= • pseudoesotropia: epicanthal folds give appearance ofesotropia but Hirschberg test is normaL more common in Asians Tests • Hirschberg test (corneal light reflex): positive ifthe light reflex in the cornea ofthe two eyesis asymmetrical • light reflex lateral to central cornea indicates esodeviation; light reflex medial to central cornea indicates exodeviation • false positives occur ifvisual axis and anatomic pupillary axis ofthe eye are not aligned (angle kappa) • cover test (Figure 23) • ask patient to fixate on target • cover the fixating eye, the deviated eye will then move to fixate on the target • ifdeviated eye moves inward = exotropia • ifdeviated eye moves outward = esotropia • the deviation can be quantified using prisms
'IbroDloNota2011 HETEROPHORIA • latentdeviation PecllatricOphthalmology o deviation correctedinthe binocularstatebythe fusion mechanism (i.e. deviation not seenwhen patientis usingbotheyes) • Hirschbergtestwillbe normal (lightreflexes symmetrical) • verycommon - majorityareasymptomatic • maybeexacerbatedorbecomemanifestwith asthenopia (eye mam,fatigue) Teats • cover-uncovertest (Figure 23) • placinga cowrOft!' an eyewith a phoriacauses a breakdown offixation of which allows itto movetJJ a misalignedposition • uncoveringthe coveredeyewill allowitto return to a normalcentralposition • coveredeyemovesinwardonremovingcover= emphoria • coveredeyemoves outward onremovingcover= esophoria. o alternate covertest • alternatingthe coverbetweenboth eyesrevealsthe totaldeviation, bothlatent andmanifest • maintain cover over oneeyefor 2-3 secondsbeforerapidlyshiftingto other eye Canrtalla 0 ,...... .. Eautrapill D ... ·1.> Exlllrupil Cover-Uncover t8lll 0 e J .... l@ .. -@.' > Esophoria 0 .... Ext!phoria Figura Z3. Cower and Conr-UncDVBrTestsfur DetBCtion af Tropiasa.t Pharias PARALYTIC STRABISMUS o incomitantstrabJsmus (i.e. devla.tionvariesIn differentpositions ofgaze) • reductionor restrictioninrange ofeye movements Etiology o neural (CN III, IY, Vl): ischemia (e.g. DM), MS,aneurysm. braintumour, trauma j :§ g o m118CUlar: myastheniagravis (neuromuscularjunctionpathology), Gravei disease o structural: restriction/entrapmentofextraocularmuscles dW!to orbitalinflammation, tumour, fracture ofthe orbitalwall Clinical Features o mostlyin adults, acquired o presentmainlywith dJplopla • greatestdeviation infield ofaction ofthe weakenedmuscle • visual acuityis usuallyunaffectedin either eye. unless CN nis involved NON-PARALYTIC STRABISMUS • concomitantstnlbismus (ie. deviation equal inalldirections ofgaze) • no restrictioninrangeofeyemovements o monocular, alternating.orintermittent Clinical Features • usuallybeginsininfancy,upto age 8-10 • usuallyno diplopia (childsuppressestheimagefrom themisalignedeye) o deviatedeyemaybecome amblyopiclfnottreated whenthe childis young.Amblyopia treatment rarelysuccessfulafter age8-10 (seeAmblyopia, OP39) o amblyopiausuallydoes notdevelopifchildhasalternatiDgstrablamus orintermittency- allomneuralpathways furbotheyestJJ develop Ophthalmology 01'39 ..... , _._____________ All chikhn with mbi8I!UIIIIdlor poaibll llldueed vilion pron¢ nfllmlto an optdhlllmDklgist.
OP40 Ophthalmology Pediatric Ophthalmology Toronto Notes 2011 Accommodative Esotropia • normal response to approaching object is the triad ofthe near reflex: convergence, accommodation and miosis • hyperopes must constantlyaccommodate - excessive accommodation can leadto esotropia in young children via over-activation ofthe near reflex • average age ofonset is 2.5 years • usually reversible with correction ofrefractive error Non-accommodative Esotropia • accounts for 50% ofchildhood strabismus • most are idiopathic • maybe due to monocularvisual impairment (e.g. cataract, corneal scarring, anisometropia, retinoblastoma) or divergence insufficiency (ocular misalignment that is greaterat distance fixation than at nearfixation) Amblyopia Definition • reduction ofbest correctedvisual acuitydue to cortical suppression ofsensoryinput from an eyethat is receiving blurredor conflictingvisual information, leading to disruption ofthe normal development ofvisual pathways servingthat eye Detection • «Holler Test": young child upset ifgood eyeis covered • quantitative visual acuitybyage 3-4 years using picture charts and/or matching game (Sheridan- Gardiner), testingeach eye separately • amblyopia treatmentless successfulafter age 8-10 years, but a trial should be given no matter what age • prognosis: 90% will have good vision restored and maintained iftreated <4 years old Etiology and Management • strabismUJ • correct with glasses for accommodative esotropia (5096 ofchildren experience reliefoftheir esotropiawith glasses and will not require surgery) • occlusion ofunaffected eye forces brain to use previouslystrabismic eye; aims to bringvision in previouslysuppressedeye to normal before surgery • surgery: recession (weakening) = moving muscle insertion further back on the globe; or resection (strengthening) = 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 approximately age 8 • refractiveerrors • anisometropia (difference in refractive power between the eyes) • amblyopia usuallyin the more hyperopic eye • the less hyperopic eye receives a clear image while the more hyperopic eye receives a blurred image; input from the blurred eye is cortically suppressed and visual pathwayfails to develop normally • treat with glasses to correct refractive error • patching is required ifvisual acuity difference persists after 4-8 weeks ofusing glasses • deprintion amblyopia • occlusion due to ptosis, cataract, retinoblastoma, corneal opacity • occlusion amblyopia: prolonged patching ofgood eye maycauseit to become amblyopic General Treatment • correctthe underlying cause • occlusion therapy (patching) oratropine cycloplegia (opticaldegradation therapy) ofthe good eye Laukocoria • white pupil (red reflex is absent) Differential Diagnosis • cataract • retinoblastoma • retinal coloboma • retinopathyofprematurity(ROP) • persistent hyperplastic primaryvitreous (PHPV) • Coat's disease (exudative retinitis) • toxocariasis • retinal detachment
Toronto Notes 2011 Pediatric Ophtbahnology Retinoblastoma • most common primary intraocular malignancy in children • incidence: 1/1000; sporadic or genetic transmission; screening ofsiblings/offspring essential • unilateral or bilateral (in 1/3 of cases) • malignant - direct orhematogenous spread • diagnosis • maybe detected byleukocoria in infant • CT scan: dense radiopaque appearance (contains calcium) Treatment • radiotherapy, chemotherapycombined with laser, cryopexy, and/or enucleation Retinopathy of Prematurity (ROP) • vasoproliferative retinopathythat is a major cause ofblindness in the developed world Risk Factors • non-blackrace (black infants have lower risk ofdeveloping ROP) • low gestational age, birth weight (<1500 g) • high oxygen exposure after birth Classification • Stage 1: faint demarcation line at the junction between thevascularized and avascular retina • Stage 2: elevated ridge • Stage 3: extra-retinal fibrovascular tissue extending into utereous • Stage 4: partial retinal detachment (4A: macula 4B: macula • Stage 5: total retnal detachment • Plus (+) disease = dilatation and tortuosityifretinal vessels • threshold disease: stage 3+ in zones 1 or 2 with 5 continuous or8 cumulative clockhours of ROP involvement (Figure 24) Treatment • threshold disease is treated with cryotherapy or laser (laser is now the standard treatment, with better refractive outcome) • ROP beyond threshold level is either watched carefully (usually stage 4A) or treated with vitrectomy/scleral buckle Prognosis • higher incidence ofmyopia among ROP infants, eveniftreated successfully • stage 4B and 5 have poor prognosis for visual outcome despite treatment Nasolacrimal System Defects • congenital obstruction ofthe nasolacrimal duct (failure ofcanalization), usually occurs at 1-2 months of age • increased tearing, crusting, discharge, recurrent conjunctivitis • can have reflux ofmucopurulent material from lacrimal punctum when pressure is applied over lacrimal sac • treatment: massage over lacrimal sac at medial comer ofeyelid • consider referral for duct probingifno spontaneous resolution after 9-12 months Ophthalmia Neonatorum ------------------------------- • newborn conjunctivitis in first month oflife • causes: • toxic: silver nitrate, erythromycin • infectious: bacterial (e.g. N. gono"hoeae- most common, Chlamydia trachoma/is), herpes simplex virus (HSV) • gonococcal infection is the most serious threat to sight as it can rapidly penetrate corneal epithelium, causing corneal ulceration • diagnose using stains and cultures • treatment: systemic antibiotics with possible hospitalization ifinfectious etiology • topical prophylaxis, most commonly with erythromycin (or silver nitrate), is required bylaw at birth Ophtbahnology OP41 -.. nerw Macula Figura 24. Zonas of tha Retina in ROP
OP42 Ophthalmology .....,, Always test visual acuity (VA] first - mlldicoi8QIII pratBction. ..... ,, I!Rr if you•-any ofth- llipl • llec:relll8d VA • ShaDow antlrior chamber • Hyphema • Abnonnal pupil • Ocul11r misalignment • Retinal damage Manag11118111 of S.Piehld Glolle Rapture CAN'Tforget Clorbib Ancef IV NPO Tetanu..mtus Shabn Bally Syndnlme Syndrome of findings characterized by no external signs ofabuse and respimDry arrest, seizures, and corTIII. Ocular axam findings 11r11 important for Shaken Baby Syndrome. These findings include amnsiv1 rwtinal and vitreous hemorrhages 1hat occur during 1he lhakilg proce11 and n extramely rm in accidentll1nuna. Adetailed fundoscopic exam or an ophthalmology refemll should be conductEd for an infants in whom abuse il suspected. Pediatric Ophthalmology/OcularTrauma Toronto Notes 2011 Congenital Glaucoma • due to inadequate development ofthe filtering mechanism ofthe anterior chamber angle Clinical Features • cloudy cornea, increased IOP • photophobia. tearing • buphthalmos (large "ox eye"), blepharospasm Treatment • filtration surgery is required soon after birth to prevent blindness Ocular Trauma Blunt Trauma • caused byblunt object such as fist, squash ball • history: injury, ocular history, drug allergy, tetanus status • exam: VA first, pupil size and reaction, EOM (diplopia), external and slitlamp exam, ophthalmoscopy • ifVA normal or slightlyreduced, globe less likelyto be perforated • ifVA reduced maybe perforated globe, corneal abrasion, lens dislocation, retinal tear • bone fractures • blowout fracture: restricted EOM, diplopia, enophthalmos (sunken eye) • ethmoidfracture: subcutaneous emphysema oflid • lids: swelling, laceration, emphysema • conjunctiva: subconjunctival hemorrhage • cornea: abrasion - detect with fluorescein staining and cobalt blue filter using slitlamp or ophthalmoscope • anterior chamber: assess depth, hyphema, hypopyon • iris: prolapse, iritis • lens: cataract, dislocation • retinal tear/detachment Penetrating Trauma • include ruptured globe ± prolapsed iris, intraocularforeign body • rule out intraocular foreign body, especiallyifhistoryof"metal striking orbit cr • initialmanagement: refer immediately!! •ABCs • don't press on eyeball! • don't checklOP ifpossibility ofglobe rupture • checkvision, diplopia • apply rigid eye shieldto minimize further trauma • keep headelevated30-45° to keep IOP down • keepNPO • tetanus status • give IV antibiotics Hyphama • bloodin anteriorchamber often due to damage to root ofthe iris • may occur with blunttrauma Treatment • refer to ophthalmology • shieldand bedrestx 5 days or as determined by ophthalmologist • sleep with head upright • may need surgical drainage ifhyphema persists orifre-bleed Complications • risk ofre-bleed highest on days 2-5, resultingin secondary glaucoma. corneal staining, and iris necrosis • never prescribe aspirin, as itincreases the risk ofare-bleed
Toronto Notes 2011 Ocnlar Trauma/Surgical Ophthalmology Blow-Out Fracture • see PL30 • blunt trauma causing fracture oforbital floor and herniation oforbital contents into maxillary sinus • orbital rim remains intact • inferior rectus and/or inferior oblique muscles maybe incarceratedat fracture site • infraorbital nerve courses along the floor ofthe orbit and may be damaged Clinical Features • pain and nausea at time ofinjury • diplopia, restriction ofEOM • infraorbital and upper lip paresthesia (CN V2) • enophthalmos (sunken eye),perim:bital ecchymoses Investigations • plain films: Waters' view and lateral • CT: anteroposterior and coronal view oforbits Treatment • refrain from coughing, blowing nose • systemic antibiotics maybe indicated • surgery iffracture >50% orbital floor, diplopia not improving, or enophthalmos >2 mm • may delay surgeryifthe diplopia improves Chemical Burns • alkaliburns have a worse prognosis than acid bums because acids coagulate tissue and inhibit further corneal penetration • poor prognosis ifcornea opaque, likelyirreversible stromaldamage • even with a clear cornea initially, alkaliburns can progress for weeks (thus, veryguarded prognosis) Treatment • irrigate at site of accident immediately with water or buffered solution • IV drip for at least 20-30 minutes with eyelids retracted in emergency department • swab upper and lower fornices to remove possible particulate matter • do not attempt to neutralize because the heat produced bythe reaction will damage the cornea • cycloplegic drops to decrease iris spasm (pain) and prevent secondaryglaucoma (due to posterior synechiaeformation) • topical antibiotics and patching • topical steroids (byophthalmologist) to decrease inflammation, use for less than two weeks {in the case ofa persistent epithelial defect) Surgical Ophthalmology • daaoqstorhinostomy {DCR) - excision ofbone coveringthe nasolacrimal sac to restore tear drainage • LASIK {laser-usiatedin-situkeratomlleu.sia) - a microkeratome is used to create a corneal flap followed by laser remodeling ofthe stroma to correct refractive error • trabeculectomy- creation ofa new outflow tract from anterior chamber to under conjunctiva; fibrosis prevented with mitomycin Cor 5-FU injection during surgery • phacoem.ulsification {cataractextraction) - the use ofultrasonic waves to breakup and aspirate a cataract followed by replacement with an artificial lens implant • vitrectomy- the use ofsmall trochars to enter the posterior segmentand remove vitreous; commonly used to treat vitreous hemorrhage and retinal detachment • pneumatic retinopexy- intraocular injection ofair or an expandable gas in order to tamponade a retinal break • scleral buckle - a bandis secured on the outside ofthe globe that indents the eye walL thereby relieving tension on the retina around any tears/holes and allowing the tears/holes to remain sealed Ophthalmology OP43 ....' , Cluslc Signs ofBlow-Out Enophlhalmos O.cnaud UPQID (IR trapped) Cheek anesthetized (infniO!bital nerve lnlppad) ..... ' Fluomc1in lights up alkali so you can dutact itnlllHIIIIi whether it hH been removed.
OP44 Ophthalmology OcularDrugToxicity/Common Medications Toronto Notes 2011 Ocular Drug Toxicity Table B. Drugs with Ocular Tu:xicity Amiod11111e COITIBIII microdeposits andtupsrficial kenrtcpathy (vortex ksnrtopathy) Re: ischemicoptic neuropathy A1rupine. benztropine ActonaP) Chloroquine, Chlorpromazine Contracsptiwpill& Digitalis Ethlllrilutol Haloperidol (Haldoi®) Indomethacin lntelferon Isoniazid Nalidixic scid Steroids NSAIDS Tamsulosin (Aofllill(8 ) Tetracycline Thioridazine Vigabatm Vitamin Aintoxication Vitamin Dintoxicfllion Pupilla.y dilfllion (risk Dlangle closure glaucoma) lnflammfllory syu di888se (iritis. scleritis, episclsritis) Bull's syu rnaculopathy Vortexkerlllopathy Anterior subcapsularCllbnct Decreased tDiellllCeto contact lenses Migraine Optic neuritis Central vein occlusion Yellowvision Blurred vision Optic neuropathy Oculogyriccrises Blurred vision Retinal hemorrhages and clllton wool spots Optic neuropathy Papilledema Posterior subcapsularcalllracts Glaucoma Papilledema (systemic mroidsl lncf'lliiSed severity Dl HSV infections (gsographic ulcers) Predispositiontofungal infections Stevens.Johnson syndrome lntlliCJI)erative FloppyIris Syndrome (FIS), which can c01J1)1icate cataract surgery Papilledema (essociated pseudotumoLI' cerebri) Pigmenlllrydegeneration ri relila Retinal deposition with mscular sparing. visualfield loss Papilledema Bandkeratopathy Common Medications TOPICAL OCULAR DIAGNOSTIC DRUGS Fluorescein Dye • water soluble orange-yellow dye • green under cobalt blue light (ophthalmoscope or slit lamp) • absorbedin areas ofepithelial loss (ulcer or abrasion) • also stains mucus and contact lenses Rose Bengal Stain • stains devitalized epithelialcells and mucus Anesthetics • e.g. proparacaine HCl 0.5%, tetracaine 0.5% • indications: removal offoreign body and sutures, tonometry, examination ofpainful cornea • toxic to corneal epithelium (inhibit mitosis and migration) and can lead to corneal ulceration and scarring with prolonged use, therefore NEVER prescribe
Toronto Notes 2011 Common Medications Ophthalmology OP45 Mydriatics • dilate pupils • two classes • cholinergic blocking (e.g. tropicamide [Mydriacyl•]) • dilation plus cycloplegia (lose accommodation) byparalysis ofiris sphincter and the ciliary body • indications: refraction, ophthalmoscopy, therapy for iritis • adrenergic stimulating (e.g. phenylephrine HC12.5%) • stimulate pupillarydilator muscles, no effect on accommodation • usuallyused with tropicamide for additive effects • side effects: hypertension, tachycardia, arrhythmias Tabla 9. Mydriatic Cycloplegic Drugs and Duration uf Action Dnlgs Tropicamide (MydriacyP) 0.5%, 1% Cydopentolate HCL 0.5%, 1% Homatropine HBr1%, 2% Atropine sulfate 0.5%, 1% Scopolamine HBr 0.25%, 5% Duman afAl:tian 4-5 hours 3-6 hours 3-7 days 1-2weeks 1-2weeks GLAUCOMA MEDICATIONS Tabla 10. Glaucoma Medications Dnlg CAlgary Alphi-AQonilt No..lectin o epilephrine HCI1% o dipivalyl D.1% (Propine8 ) o brimonidine 0.2% (Aiphagan8 ) o apraclonidine 0.5%{Lopidine8 ) Beta-Blocker No..lectin o lirnolal (Timaptic•) o lewbunolol{Betaganil}) Bm.-celective o bstaxolol {Betoptic8 ) Carbonic AnhY*-Inhllilllr o dorzolamide {Trusopt®) o brinzolamide (Azopt®) o oral: acetamlamide {Diamax®) Pamymplthomimelic {cholinergic stimulating) o pilocarpine (Pilopine®l o carbachol (l&apto 1gtt OSIOD bid/tid 1 gtt DSIOD qd,.tid 1gtt DSIODtid Diamox8 : 500 mg PO bid 1.Nort-&Bisctiw - "- production + 1'1M outflow 2. Selecliva- "- aqueous pralllction + 1' UY808clnl outflow "- aqueous production "- aqueous production 1-2 gtts DSIOD lill/qid 1'1M outflow 1. Non-selective - mydriasis, macular edema,tachycarcia 2. Selective-contactale111v. hypotension in chillhn BrunchC11p81111 (cuelul in athiiii/COPD) 1' CHF Bnulycardia Hypotension Depression Heartblock Impotence ••Mustaskaboutsulllllllergrl Generally local side efh!cts with topical preparlllions Oral: diuresis, fatigue, paresthesia&, Gl upset etc. Miosis -.1- ni;rtvision 1' Gl motiity Brow ache Headache -.1-heartrate Prasllgllndin Analog1111 o lillirlopra&t(Xalatan8 ) 1gtt DSIOD qhs 1' uveoscleral outflow{uveoscleral responsible lri1 colour change 0 travaprast (JI'IIVllbll®) for 20% of drainage) Periorbital skin pigmentation Lash growth o bimatoprost (Lumigan•) timulol +doJZDimila; limciJI +h1Drlop!UII;Corrmig..• timobl+bri111111idine; lbl tinokll +1IMpust WET AGE-RELATED MACULAR DEGENERATION MEDICATIONS vascular Endothelial Growth Factors (VEGF) Inhibitors Conjunctival hyperemia • block vascular endothelial growth factor which prevents ocular angiogenesis and further development ofchoroidal neovascularization • administered via intravitreal injections • pegaptanib (Macugen•) is a selective anti-VEGF targeting VEGF isoform 165 o ranibizumab (Lucentis•) is a non-selective anti-VEGF agent o bevacizumab (Avastin•) is another non-selective anti-VEGF agent but is only FDA approved for metastatic breast cancer, colorectal cancer and non-small cell lung cancer. Therefore, its use in ophthalmologic is off-label
OP46 Ophthalmology Common Medications/References/Referen TOPICAL OCULAR THERAPEUTIC DRUGS NSAIDs • usedfor less serious chronic inflammatoryconditions Toronto Notes 2011 • e.g. ketorolac (Acular-), diclofenac (Voltaren•), nepafenac (Nevanac•) drops Anti-Histamines • used to relieve redanditchy eye. often in combination with decongestants • sodium cromoglycate - stabilizes membranes Decongestants • weak adrenergic stimulating drugs (vasoconstrictor) • e.g. naphazoline, phenylephrine (Isopto Frin•) • rebound vasodilation with overuse; rarelycanprecipitate angle closure glaucoma Antibiotics • indications: bacterial conjunctivitis, keratitis, or blepharitis • commonlyas topical drops or ointments, may give systemically • e.g. sulfonamide (sodium sulfacetamide, sulfisoxazole),gentamicin (Garamycin•), erythromycin. tetracycline,bacitracin, polymyxinB, fluoroquinolones (CiJ.oxan•, Ocuflmt"',VJg31Uax•, Zymar-) Corticosteroids • e.g. fluorometholone (FML•), betamethasone, dexamethasone (Maxidex•), prednisolone (Predsol• 0.5%, Pred Forte• 1%), rimexolone (Vexol•) • primary care ph)15icians should avoid prescribingtopical corticosteroids due to risk ofglaucoma, cataracts, and reactivationofHSV keratitis • complications • potentiates herpes simplex keratitis and fungal keratitis as well as masks symptoms • increased lOP, more rapidlyin steroid responders (within weeks) • posterior subcapsular cataract (within months) References Complicztions: Your8Y'15&dilbftic retinopllhy. Clnldiln lilbel81Aaoc:iltion Nov2003. lilbaticRatiiiiJFIIhy.Diabns Cara 1998;2111]:143·156. liabet81 in OntJrio: 1111 IC6 l'rll:tica June 2003. llloil llrllord C. Illsic Oi*tfwlmolowforMedicalS1udlnand PrimuyCare R111id8111s. 7th ed.San Fnl11l:ilco:AmericanAcademyrJOphthalmology, 1199. WIIDnFM.I'rlcti:alOphlllllmab.rl: AManuallor Begilninq llelidenbi. 41h ed. Americllll Academyrl Ophtlillmology,2005. Frimlul N, Plned1R, KliArP. TheM11111ChulatllEyu1ndElr ManuIIrJ OphthalrnDIDII'f.Tmnlll:W.B. Saunders 1988. KlnskiJJ.Clinical ASystamlticApproech. &1h lid.Oxhxd: llut18rwGrth·lllilem111ll, 2007. S18in R,Stein H. Mnqernent Oc:ularEine'V'"Cill5. 41h ed.Mgntr111l: Medico11cept. 2006. lllillilll HuxJ.et al. Dlabll8sinOntario: an ICES l'nlc1iceAtlls.TGI'On!o: hstiMIforCiii:alEvluativa Sciences, 2003. The CD!T1111itteefDIthe chmffiCitiDIIofretilopathyol premmrity.AnintemlliDnal cllssiliCitiDnolletinoPIIhYrJprar'llblrity.An:hOphlllai!DIDgy. 1984;102: 1130-34. IIIIIIQII Red Alln. www.radlllln.Grq LII:Cini/Cia llriYersi!y MicliiQIII KeiDgg EyeCentrewww.kltlgv.unicli.edWtheeyeslnrveMndu.html

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Toronto Notes 2011 Ophthalmology.pdf

  • 1.
    OP Ophthalmology Faazil Kusam,Kay Lam and Jenna Tessolini, chapter editors Alaina Garbens and Modupe Oyewumi, associate editors Adam Gladwish, EBM editor Dr. Wai-ChingLam, statfeditor Basic Anatomy Review ................... 2 Differential Diagnoses of Common Presentations . . . . . . . . . . . . . . . . . . . . . . . . . . 3 Ocular Emergencies ..................... 5 The Ocular Examination .................. 5 Optics ................................. 8 The Orbit ............................. 10 Globe Displacement Preseptal Cellulitis Orbital Cellulitis Lacrimal Apparatus . • • •• • • . • • •• • • •• • •• . • 11 Dry Eye Syndrome Dacryocystitis Epiphora (Tearing) Dacryoadenitis Lids and Lashes ....................... 13 Lid Swelling Hordeolum (Stye) Ptosis Chalazion Trichiasis Blepharitis Entropion Xanthelasma Ectropion Conjunctiva ........................... 15 Pinguecula Pterygium Subconjunctival Hemorrhage Conjunctivitis Sclera ................................ 16 Episcleritis Scleritis Cornea ............................... 17 Foreign Body Herpes Zoster Corneal Abrasion Keratoconus Recurrent Erosions Arcus Senilis Corneal Ulcer Kayser-Fleischer Ring Herpes Simplex The Uveal Tract ........................ 20 Uveitis Anterior Uveitis (Iritis) Posterior Uveitis (Choroiditis) Lans ................................. 21 Cataracts Dislocated Lens (Ectopia Lentis) V"rtreous .............................. 22 Posterior Vitreous Detachment (PVD) Vitreous Hemorrhage Endophthalmitis and Vitritis Toronto Notes 2011 Retina ................................ 23 Central Retinal Artery Occlusion (CRAO) Branch Retinal Artery Occlusion (BRAO) CentraVBranch Retinal Vein Occlusion (CRVO/BRVO) Retinal Detachment (RD) Retinitis Pigmentosa Age-Related Macular Degeneration (ARMD) Glaucoma ............................. 27 Primary Open Angle Glaucoma (POAG) Normal Pressure Glaucoma Secondary Open Angle Glaucoma Primary Angle Closure Glaucoma (PACG) Secondary Angle Closure Glaucoma Pupils ................................ 30 Pupillary Light Reflex Pupil Abnormalities Dilated Pupil (Mydriasis) Constricted Pupil (Miosis) Relative Afferent Pupillary Defect (RAPD) Malignancies .......................... 34 Lid Carcinoma Malignant Melanoma Metastases Ocular Manifestations of Systemic Disease...34 HIV/AIDS Other Systemic Infections Diabetes Mellitus (DM) Hypertension Multiple Sclerosis (MS) TIA/Amaurosis Fugax Graves' Disease Connective Tissue Disorders Giant Cell/Temporal Arteritis (GCA) Sarcoidosis Pediatric Ophthalmology ................ 38 Strabismus Amblyopia Leuk.ocoria Retinoblastoma Retinopathy of Prematurity (ROP) Nasolacrimal System Defects Ophthalmia Neonatorum Congenital Glaucoma Ocular Trauma ......................... 42 Blunt Trauma Blow-Out Fracture Penetrating Trauma Chemical Burns Hyphema Surgical Ophthalmology ................. 43 Ocular Drug Toxicity ••••••••.••••••.•••• 44 Common Medications................... 44 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46 Ophthahnology OPI
  • 2.
    OP2 Opblhalmology LltaniV"18W Basic AnatomyReview RETINAL LAYERS 11D) 1. lmll'limili'lg membnlne 2. Narvefin IIIYIIr 3. Ganglillll cell IIIYIIr 4. 1m•pladonn IIIYIIr 5. lm•ruclaer IIIYIIr 6. Out.-pltxifunn IIIYIIr 1. Out.-niii:IIIIU IIIYIIr 8. E'xllrmllimiting IIIYIIr 9. l'hoiDraceptor IIIY8r SuperiorView 1'oroDio 2011 CB!.TYPES Vllnlous hu11111ur Ganglillllcella Bipoia"calls Rod nuclei 'NI'MIrhl·- Coneruchi Rlld cei'- 106-H-fi- Conecells I0. Rllillll pigm..t apitllelilm Pigmllllll;ti" Bruch"s ChDrDid c s.at1A. Kim2005
  • 3.
    'IbroDloNota2011 Figure 3. Tearfrom tlte Eye (Lacllmal Appai'BIUI) Differential Diagnoses of Common Presentations Loss ofVIsion l.olsDIV1111111 ildanic lllack(1IAl • Mi!Pine wilhl!ln -+ CGmlllr/AIQdor ....... • CCIIMII ed111111 • Al:uiiiii"Qkt- closlUI glaucoma body Figu111 4. Laa IfVilian Red Eye • llda/orbJ.tllacrlmalsystem • hordeolum/chalazion • blepharitis • foreign body/laceration Vlhaur/RIIIul GpticiiMvll • V"llnlous t.n.lrrlwgl • llll!illll delactment • Relilll nrd veinoccUiion • Acdii'IIIICU.. leeion • Opti: rJIIWitis • Tanporalal1aritis • AnbnJrischanic opticI1IIUtllll1hY tAlON) • dacryocystitis/dacryoadenitis • COD:lunctivalsclera • subconjunctivalhemorrhage • conjunctivitis • dryeyes • pterygium • episcleritisJscleritis • preseptallorbltal celluliti& • cornea • foreign body • keratitis • abrasion,laceration • ulcer I + CarllcaWiher • Occptal irfarctiorV' t.n.lrrlwgl • Cortieal bbtlaas • Flllc1ionlll (11011-IJIIIMie. di'IIJ!Diisaf IDWiln) -+ ....d • Cornell l11:811'ircVed111111 • llllfnlcliVIerrar • l:allnllt • Glaucoma Gplii:NIIrw • Aclt-l'llded .,... degenenilion • Diablltic • RJilal'IIISCU.. iraltliciency + CarllcaWiher • PiluilaJy ldanDma ntur:lld (lid.,. ll!liodarcne) • M.ltritional dalicimcy • l'aDilllldllml opliclllllrapathy (inlrlcllnialman, 01bi1111111111) naaplum • Rllililil pQr!'entola(RP) Ophthalmology OP3 ,,, Top lin DIJJItfAcull l.asaGfVIIItn 1. Tr..ruw'furaign bod'f 2. Ralillll.my/winIICCUion 3. Ralilllldlllllclrnent ,, , ,. 'lb'S11 DDxofC...,. l.asiGfVIIIIn lllvenillll I.Catnct 2.R!lilactive lrrGI 3. Comaal dystrophy lrraRni.la 1.Agt-ralalld macular 2. Glaucol'lll 3. Dilbatic rstiriiJIIIIIhy
  • 4.
    OP4 Ophthalmology DifferentialDiagnose5 ofCommon Presentations Toronto Notes2011 • anterior chamber • uveitis (iritis, iridocyclitis) • acute angle-closureglaucoma • hyphema • hypopyon • endophthalmitis T1ble 1. Common Differenti1l Di1gnosis of Red Eye Conjunctivitis Acldllritis Ac.aAnale Keratitis Cl01111 Glaucoma Dildllrge Bacteria: purulent No No Profusetearing Virus: 5erous Allergy: mucous Pain No ++ (tender globs) +++ ++(on blinking) Plurtophobia No +++ + ++ Blurllld Vilian No ++ +++ Varies Pupil Normal Smaller Fixed in rnid-(jilation Same ar smaller ConjunctiVII with Ciliary Hush Dilluse Dilluse liltal pallor Com111 Normal aropacifiad KBratic precipitates StBIImy Infiltrate, adsma, epithelial defects Wraocular p...re Normal Varies lncraasad marlaKiy Normal ar increased Anteriorchamber Normal Cells+ flare Shallow Cels + flare ornormal Olher Large, lEnder Posteriorsynechiae Caloured haiDS (auricLJar] node vil'lll NIIISea and vomiting Ocular Pain • differentiate from ocular ache: eye fatigue (asthenopia) • herpes zoster prodrome • trauma/foreign body • keratitis • corneal abrasion, corneal ulcer • acute angle-closure glaucoma • acute uveitis • scleritis, episcleritis • opticneuritis • ocular migraine Floaters • vitreous syneresis (shrinkage and collapse ofvitreous gel) • posterior vitreous detachment (PVD) • vitreous hemorrhage • retinal tear/detachment • posterior uveitis Flashes of Light (Photopsia) • posterior vitreous detachment (PVD) • retinal tear/detachment • migraine with aura Photophobia (Severe Light Sensitivity) • corneal abrasion, corneal ulcer • keratitis • acute angle-closure glaucoma • iritis • meningitis, encephalitis • migraine Diplopia (Double Vision) • binocular diplopia: strabismus, CNpalsy(Ill, IV. VI) secondaryto ischemia, diabetes, tumour, trauma, myasthenia gravis, muscle restriction/entrapment, thyroid ophthalmopathy, internuclear ophthalmologia (INO) 2°to multiple sclerosis, brainstem infarct • monocular diplopia: refractive error, strands ofmucus intear film, keratoconus, cataracts, dislocated lens, peripheral iridotomy
  • 5.
    Toronto Notes 2011Dl1fermtialDlagnolesofCommon 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 .....', .. • ODoculusdut.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 movementofeyeball 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.: RIGHTEYE 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 2011Optics 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 cellulitisislif&-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 2011TheOrbit/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 tearingcan 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 2011Lida 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 Uclaand 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 2011Conjunctiva 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/ScleraToronto 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 2011Sclera/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 baUlld 11:1 n.ylllho"" NE"JEEI beUllld IStraa1mantfarany ocul•problem. fEVER plb:h lb111i1111patient- can1actlanaa{puna1lll"s8urromonu ilfllction). "' I fnJm orvanie malblr (e.g. twig. mg•nlllltl:..) h1V8 higher recurrence. even Yllllllata'. "' I C111118111 Allnni111: Ta ,_.11 Nit ta Patch PdchingforCDrlllllllbllliOIL CDcMine RIMsw2006 Pdching is not indiCit8dfarsmpla callllllllllllllsions, m•sumg lassthan 10mm. Thin il no impiUVIImant il hilling ra1111 on diiVI 1..3, no chlng• in reporllld pamand no difla'a1cainlhe Ule ofanlilicllic:s b81wean the prnx;h and non-jlllll:h ppa. NormaiCa!MII 1? . . ' F'IIJ•ra 14. Cornall Allraaion n. Ull* 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
  • 19.
    TorontoNota2011 Cornea Table 5.Cumelll Abrasi1111 ws. Camellll Olear Almion Ulta' liMCalnll Acuta(instanllniM) tiac:ulaldavsl lisiDryofTmiiU Y8l NatUIUIIy Carnal !lear WhiiB, nacrtJtic araa lritDetlil !lear Obsclmd earn.1nicb- N1111111l Mayhava Exbnoflelian LimitadIDepilhiiiUII Exlalaian iniDstroma Herpes Simplex Keratitis • usuallyHSVtype 1(90% ofpopulation arecarriers) • maybetriggered bystress,fever, sun exposure.Immunosuppression Clinical Features • pain.tearing, foreign bodysensation, red eye,mayhave decreasedvision. eyelidedema • cornealhypocsthesia • dendritic (thin and branchlng) lesion inepitheliumthat stains with fluorescein Complications • cornealscarring (canleadtoloss ofvision) • chronicinterstitialkeratitis due to penetration ofvirus into stroma • secondaryiritis, secondaryglaucoma Treatment • topicalantiviral suchastrlfluridine,considerS}'5temic antiviralsuch as acyclovir • dendriticdebridement • NO STEROIDSinitially- mayaacerbete condition • ophthalmologistmuste.xerdse cautionifaddingtopicalsteroidsfor chronickeratitis oriritis Herpes Zoster • dermatitis ofthe forehead (the CNVl territory) mayinvolve theglobe (Figure 15) • Hutchinson's sign: iftipofnoseisinvolved (nasociliarybranchofVl) then eyewillbeinrolved inapproximately7596 ofcasa • ifno nasal involvement,theeyeisinvolvedin 1/3 ofpatienlll Clinical Features • pain.tearing, photophobia, redeye • cornealedema, paeudodendrite, superftdalpunctatekeratitis • cornealhypoesthesia Complications • cornealkeratitis, ulceration..perforation andscarring • secondaryiritis, secondaryglaucoma,cataract • musclepalsies (rare) dueto CNS involvement • occasionallyseverepost-herpeticneuralgia Treatment • oralantiviral (acyclovir, valcyclovirorfamc:iclovir) immediately • topical steroids,cycloplegiaas indk:atedforkeratitis, irltis • erythromycin ointmentifconjunctivalinvolvement Keratoconus • bilateralparacentralthinningandbulging (ectasia) ofthecorneatoform a.conicalshape • usuallyspora.dic, butassociatedwith Down's syndrome. atopy, contactlensuse (theorizedtobe relared to chronicvigorous eyerubbing) • a.ssociatedwith breab inDescemefs and Bowman's membrane • resultsinirregularastigmatism, scarring, stromal edema. Treatment • attempt:correctl.onwithspecta.clesorcontactlens • cross-linldnglasertrelltment ma.yhaltorslowdiseaseprogression • penetratingkeratoplasty(cornealtransplant) 9096 successful • post-operativecomplications: endopbthalmitis,graft rejection, graft:fiillure. graftdehiscence Opbtbalmololf OP19 _,, Abi'BIIan •· UICiro•lllt....., An •lnlian llppaii!W clllllrwhila.. ucar ilmen OINIQIII. Figu111 15. Trigarinll Distrib.tia• -, S1lnid lnliltmantfur DGUIIIrdilordars onlybepr8ICiiledand 11.1pii'Vill8d by..aphlhllrnalagilll, u thgycan in.-ircam•l h1111ing..d IIXIIcabn harpalil: al'lllitia. ' •.}---------------, Tadet8ct1!8nrtDcorw.laokfur bUging aftha IIIWIIr ll'fllid whentha patiant loakaclownwlnl (l'lobllan'l aign).
  • 20.
    OP20 OphthalmoloBf 16. Canj11nctinlHypar•i• vs. CiliaryRush CorneaflheUTeal.Tract 1'oroDio 2011 Arcus Sanilis • hazywhite ringinperipheralcornea, <2 mmwide, clearlyseparatedfrom limbus • common,bilateral, benign corneal degeneration dueto lipiddeposition, partofthe aging process • maybe associatedwithhypercholesterolemiaifage <40yean, check.lipidprofile • no assoclatedvisualsymptoms, no complications, no treatmentnecessary Kayser-Fleischer Ring • brown-yellow-green plgmented ringin peripheralcornea, startingInferiorly • dueto deposition ofcopperpigmentin Descemet's membrane • associatedwithWilson'sdisease (9596, b.epatolenticula.rdegeneration) • no associs.tedsymptoms or complications ofring • treat underlyingdisease The Uveal Tract • uvealtract= iris,ciliarybody. choroid • vascularized, pigmentedmiddle layer ofthe eye, between the scleraandtheretina Uveitis • mayinvolveone orallthree parts ofthetract • idlopathicor associatedwithautolmmune, infectious,granulomatcus, malignant causes • shouldbe managedbyanophthalmologist Anterior Uveitis (Iritis) • ln1lammation ofIris, usuallyaccompaniedbycyclitis (Inflammation ofciliarybody), whenboth = iridocyclitis • usuallyunilateral Etiology • usuallyidiopathic • connectivetissue diseases • HLA-B27: reactive arthritis, ankylosing spondylitis (AS), psoriatic arthritis, inflammatory boweldisease (IBD) • non-HLA-B27: juvenileidiopathicarthrit:is (JIA) • infectious: syphilis, Lymedisease, toxoplasmosis, TB, HSY, herpes zoster • other: sa.rooidosis,trauma, large abrasion,postocularsurgery Clinieel fHtures • photophobia(dueto reactivespasm ofinflamedirismuscle), ocularpain, tenderness ofthe globe,browache (ciliarymuscle spasm), decreasedvisualacuity,tearing • ciliaryflush (perilimbel conjunctivalinjection), miosis (spasm ofsphinctermuscle) (Figure 16) • anteriorchamber"cells"' (WBCin anteriorchamberdueto anteriorsegmentinflammation) and"ffare'" (protein predpltatesin anteriorchambersecondaryto in11ammation),hypopyon (collectionofneutrophilicexudatesinferiorlyin the anteriorchamber) • occaslonallykeratl.cprecipitates (clumps ofcells on corneal endothelium) • iritistyplcallyreduces intraocularpressurebecause dllarybodyinflammationcausesdecreased aqueousproduction;however. severeIritis, oriritisfrom herpes simplexandzostermaycause aninflammatoryglaucoma Compliartions • infl.amma.toryglaucoma • posteriorsynechiae • adhesions ofporterioriristo anteriorlens capsule • indicated byan irregularlyshapedpupil • ifoccurs 360m, entrapsaqueousinporteriorchamber, irisbomforward "irisbomb€ ' -+ angleclosureglaucoma • peripheralanteriorsynechiae (PAS) (rare): adhesionsofiristo cornea-+ glaucoma • cataracts • bandke:ratopathy(withchronic iritis) • superficialcornealcalcificationkeratopathy • macularedemawith chroniciritis
  • 21.
    Toronto Notes 2011The 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 2011Vitreous/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. I'IIIOIIhthiDtit....,llully EndgpllthllmihVi1r81:1DmySludyliwp.ltealbrl 1lleElllgpllthllmitisl{rtmclomySUiy.ArdWe$ at 11311Z):147Hi Fortrlltmlnt alpost·calltlctlllliiiY endoplllhllmitis: • lllli'lvilalantibioticsprDrad IMirl)'lblmic l11tililltics • 1{11r8ctomy'indicalldonlrhilion LPonwrsa
  • 24.
    OP24 Ophthalmology Treatmentfor aCllntralratinal1118ry occlusion !CRAOI must be initiated within 2 hours of symptom onsatfor .,y hope ofres!Dring vision. llllldlVail Oa:luian Sludy IIIVDII BllnchYain StudyGnllp:Argon lll8r 101macularedeml inbmui•'lein accllsiaii.AmJOp/rlhllmD/19BUB: Zll-2112. BVOSsiD.wd!hit arganilllrlrlltrr.ntim!1M1 sijlt inpetian1switiiiiiiCUaredan. 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 2011Retina • 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 9t-----------------, 8-1 0% risk afdaveloping CRVO orBRVO in other eyu. "". I •t-----------------, Superotemporal rvtina is the most common site fur horseshoetllllrs.
  • 26.
    OP26 Ophthalmology Triad oflllltiniti1PigrnllntDA APO ArteriDIIIr n11r0wing Perivascular bony-spicula pigmantation Opticdisc pallor ......Eye o-.StudriAIEDSI with iibrmilsCll!df. ll!d1incb'lfiHII*/IIIKIW degrlltllllion lllllllisilrltm.AREDS_,No.B. 118:1417-1438 AR!n'!lllJdildth11111i:tof hiQIHl1111 cantilltian rlvDmiiC,Wlmil E, meia patientswitll and witlloutARMD.'1'hDIIwho 111 an.dyllflectedbrARMD showed I"decne1e ilrilkallllthlrvUI loa,.._tllisll'llllrWit nobenelitin pitilrDl'lith llll1yII'no ARM!l ..._ , .. w.t ARMD U.iona on Flu••cein Classic: well-ilefined leakage Occult: mutllad or ill-dafinud luaklv& .... Dru•n vs. Exudate Drusen: h'filline materill secre1Bd by RPE 111811 fTvquunlly in ARMD typiclllly in pari·macular region Hard/Soft ExudllbJs: lipid duposi._ in 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:heldatnormalreadmgdistancewith 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 11111 .... II!QriiiiiiiAnk.u.r .....&.-hclllrlllll..... ..._...AgfHIIIbll......... liu2 a..,:Coc:tn!elpllnicIBI'iawalRCrs ir.wlgati"Gthtlltalmi&(wlallu lllldolhalllllP'o1hflcllrJrnodllliMfar... m.tnartalwrtlgHIIInd IAflt.tl), 1'1111111:Cluli:Ill'occUI'MIItypeAIMl. . . . . IDJ1Ibadallillrodei:llddlu.tbill'otGFI. .. (ami't'EGI'fnQrrart nibadyjlrld 1hnJrf!I'D'n Ill*ThaMARNAtrillhr.wd1hlltht)IIIOIII ..._•(ll!tb'agailai15CJIIIIIIIIalln rlwUBCUIJWIII5.8'1frJrriii.IIBI- plabo,'llllil81hlFOCUS1rill!illoiwd111111111 paoladIllfarI Qlilllf15OIIIJII81111111U101"1 yea"W1114A4 rllWitiunlb + Wl1lpalfinPD!'Iftd'l'l18podilPDTIlona. lllrillilrnllllnalaiameutblllllfi1 b'1hl--ri'MIIAIMIMhIigman inJ1Mnat1sinJatarracWYiluilaculyIt IDyll!. I. CliarybodVJRC88886 l. P141IIIV block 3. Pra1ralwnu• 4. Trabecular S. PDit-lrlbiiCiilr Figure 18. Flow and litHof Pata.till Rllilblnca .... , i .B 4 0 . Ave1'11118 lOP =15 :t 3 mmHg Nannll :s:D.4
  • 28.
    OP28 OphthalmoloBf a.....-....c........... .. PClAGPACB • CommDn (9ft) • Rlre • Qnnic ca.11e • Acute Ol'llet • I'Ull-&yll • l'li1fiJ red aya withoutra- • Exlmlaly1'lOP • MDderatllly1' lOP • HIIZV l*llBI • Nonnal cornea • Mid-dild8d and pupil pi4Ji ......:tiva • No fW tD light • No halouruund • ± HIV. lllldomilal pain • H11D11nmd light llllkFHIIIn fir POA& AFOO Age Frnily Hillury lOP Nric11 delclllll 11*1 Camaa ;b Collnll'lllcdiiW_, Dlldla • NelnlogiCIIIIbnormality pupl a111111111ant • ShallowIIIIWiorchlmber • lriwupporltciiiiiWiorchlmberiOL Glaucoma 1'oroDio 2011 o,tlc nern bHd dlmaga VIsual flllll chiiiD Small pll'aCan1niiiCO!oml Ara.llla dafact cenlnll island f"IG•ra 19. GlaucDJnllblua Damage 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 2011Glaucoma • 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 bMiilnrllnnacdlr,_...-'GIIiuclml l'llglllliln 120:1268-1279 S1udy: RlndalrDd COOO'ollldclinicll1rill. l'llillb: 2.55 puticiiW, - ..clldllmlgh I piiiUitianICII.pniiDI:Oi.llgld!iG-81with rMydlllctJdopi!Hingil . .ilk! dlllaell, •dandian irmaMirpn11110 001'1 d20IIIdta- lillllrlllpicll IIIIHIIacka'!llltlmoQplaltgllll lulrtllbeculaPniYarno inililllr8llmlal,with - obsiMtionlorbothPIP'- Mldilli -6ym. ...lkllaaml:!illtJCOI!IIpmgrusian• dllfinlld byWulfieldIIIIIapti;dill: llbaarnJUtiel_ bnlll:l(f- Riducadby (1!1111115.1 T11ll'flg) illheIJealmenl Glu:on prgareaion-Mlilrt in62rJindio.UJ• il11-. The pruijntlllill-li(jllliclndv,..... inlhahltmeot VI.11-. alllinlls. Rule Ill' Furs 1/4 ol u-rlll population after u5ing 4weeks of topical steroid 4x/davwill develop 111 increase in lOP. lhlklllnlmlllilnalllrI'IIIIIIJa,..A191 Gllll:anlllldOc:U....... C/rJrnDIII!JisetiS)'III!mlti:llellilws21101, Issue 4. lludr.Cocmn IMiwrJ Z611M andme1Hnlf¥sis of10lrillsiMstilllliYJihe dlupicllplllrlmcologi;III111111PM far]Jii1wy111*11111111QiluCGII'IjPOAG) II OQIIIr hyperlinsiun(0111)_ I'IIIMII: 4919 PlfliciparaIWidomiz8dii261Ji._ l'ltiera llldOIITwlbm-ulupressure(KI') >21 IJidt.l orap1nqil(lllualml_ ..........:1opi131 eye n.tlc:aliani, ilduding blll-blackm.dormlllrida. brimulilila. andepiletlllrilevenuseldioilier 1111 pllaillo. llllil...-..: Re6JclionrJprogre..or ,.nond Glial afWulfilld dlllcts. ._..:MttHIII¥SiS on111111Uihll18118d cWilsllllitstIDcahoarIIIINaiJd Clllllds clernonslnlal11111bllerilgKf!educesinddence d;uamllilllviullilkldlflciJ.withIll oddsIIIia rJD-62 (M C1 0.47-0.811-llilwMr. 1MsRid is d mtadpractical 1118.me. --.lillnpieswere pooled.No dlmormiBd ignificllltwiullilkl pndlc:lion. llawM!,n1 clnl,11111-blackmshawld baldartnaliQMicenceinr8lb:ilg 1111111Ill (lllualmlil patilllllwillDlfTwt.n Cll11fiiii(IID pllcebo,Nih • OR of0.67!SClDA5-1.00). c:.t111ianl: lawlringlOP Cllll'llb:lprogrlllian ofllisuallil*ldefa:ls inpllierGwithOIIT.
  • 30.
    OP30 OphthalmoloBf 1.Aq-ftgw 2.Ci.ybody 3.ComR 4.Ln 5. Bloc:bdIJibecljarmesbwork Flg1rezo.Nomaal OpenAntle varsuaAn1la Cl01ure Gl1ucam1 _...c.._.._.. IIAI:H Txwi1h mioticsIIIII leta-Biocbrs, Adrenqict. Cholinqiet ltyperuS'IIotiCllgllnbl ,, , ...--------------. liTarplalf RltNI Silnall • nuclu jpupillalyniiiiiVBYB movemlnbl) • l.81arll garicullda badycrf1h11lrn111 • Superiorcclicu IIYIImovemenll) • Suprachi11malic nucleusjaptokiaic) • Acca-.yoptic lci'l:adian rl1ylhm) Clinical Features • unilateral,butothereyeprecllsposed • red, painfuleye = RED FLAG • decreasedvisual acuity, vill:ion acutelyblurred from cornealedema • halosaroundlights • nauseaandvmnftlng, abdominalpain • fixed, mid-dllatedpupU • cornealedema withconjunctivalinjection • marked increueinlOP: maybenoticeable evento palpation (>40 mmHg) • shallowa.ntmorchamber± cellsinanterior chamber Complications • lrreverslbleloss ofvision withinhours to days ifuntreated • permanentperipheralanteriorsynechiae Treatment • referto ophthalmologist •laseriridotomy • aqueoussuppressants aruihyperosmoticagents • immediatetreatment importantto: • preservevision 1'oroDio 2011 • preventadhesions ofperipheraliristo trabecularmeshwork(peripheralanterior synechiae) resultinginpermanent closureofangle • medicaltreatment (see Glmu:oma Medications, Table 10,OP45) • mioticdrops (pilocarpine) to reversepupillaryblock • decreaselOP • topicalbeta-blockers • topical adrenergic& • topical cholinergics -pilocarpine 1-496 ql5min, upto q5min • systemiccarbonicanhydraseInhibitors - IVacetazolamide250-500mg • &ylil:emic byperosmotic agents - oralglycerine 1glkg - IV mannitnll glkg Secondary Angle Closure Glaucoma Uveitis • inflamediris adheres tolens (posteriorsynechiae) Neovascular Glaucoma • abnonnalbloodwssels developonsurfaceofiris (rubeosisiridis),intheangle, aruiwithin the trabecularmeshwork • dueto retinalischemiaassociatedwith proliferativ'ediabeticretinopathyand CRVO • treatment withlasertherapyto retina reduces neowscular lrtimulusto iris vessels Pupils • pupilsizeis determinedbythe balance between the sphincter muscle andthe dilator muscle • sphinctez muscle Isinnervatedbytheparasympatheticnervous system(PNS) • carriedbyCN m:pre- and post-ganglionicfibres synapseinciliaryganglion. anduse acetylchollneastheneurotransmitter • dilatormuscleis innervatedbythesympatheticnervous system {SNS) • first orderneuron = hypothalamus -+ brainstem -+ spinal cord • secondorder/preganglionicneuron= spinalcord -+ sympathetictrunkviainternalcarotid artery-+ superim cervicalganglioninneck • third order!postganglionicfibres originab:inthesuperim cervical ganglion, neurotransmitterIsnoradrenaline • asa dlagnostictest, 4% cocaine preventsthe re-uptakeofnoradrenaline, andwillcause dllatlonofnormalpupil, butnatonewithloss ofsympatheticinnervation {Homer's Syndrome)
  • 31.
    Toronto Notes 2011Pupils 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 .... , .. Ina 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 2011Pupils 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 "'' 11om•'•MAP Mia.ia Anhydrosis Ptotit Argyll Robermon Plpil (AlP) Accomodation lllfl&x Presant PupillllfY Rellex Absent ...... , ---, ..... , is poai!U to haw RAPD and nonnal viaion atthe siiiTietime. i.e. in damaged s...,arior coUiculus CIUsed by thalamic hemorrhage. ....,, .. When aii8Ssing for an RAPD, aslight dilatation lifter constriction is normal when from eye111 11'(8.
  • 34.
    OP34 Ophthalmology Malignancl.es/OcuJarManifestationaofSystemicDisease 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 2011Ocular 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 .... Macular edema thlil most common cause of visual loss in patientswith bBCkgllJUnd IJR. .... , 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
  • 36.
    OP36 OphthalmoloBf ,, , ClinicaiiVllignifilad macularadlln. ill dsfinad ..tickiDlg ofItallllilllld orwillil5001111 ofthecentre Df1be IIIBQJia. lllll*tlllriiiiiii._....TIIII NE.JIII8t3211") OCCTtrilla-....,.gl,canl:llllllmwil ndlcl1111rista!dllblli:lllliDpldrf1Jt78IIIII lrf54l. fiiiJTIIIIIIIIIIIWIIicllliqrdr5lllr lirttTr8linlrtDilbe1i:RlinaplllrfSW{ hwiQDQ:Atpiril*"onnWilvITCI lllllbiityi1palildJwilldiiiiJailllTIIIul.EIJIIS /lrtDfIt.MM1!1!11;2111:12!1Z-13111.Andodw EIDBa..nlll • NGbnfitGlll!liini118didoniu•Ill ... iJmllldrii:rlilmM1hlgaIiiia" • Ealtthllllnrltlllilgpmtirll .. • Oiicltfllig16:utiiiiC'JI. .IItaJIIba 1NDI.Irtb:alillllr OcularMani&stalionsofSyatemlcDisease 1'oroDio 2011 • pmlifa'alive • 5%ofpatientswithdiabeteswill reachthis stage • neovasculuizationofiris, disc,retinato vitreous • neovascularization ofiris (rubeoaisirldis) canleadto neovascularglaucoma • vitreoushemorrhage from bleeding.fragile newvasels, fibrous tissuecan contract clm&lngtractional retinal deta.clunent • highrisk ofsevere visual loss 2°to vitreous hemorrhage. retinaldetachment Screening Guidelinesfor Dlabedc Retinopathy • Type! DM • saeenfor retinopathybeglnningannually5 yearsafterdisease onset • saeeningnotIndicated beforetheonsetofpuberty • Type2DM • Initial examination attime ofdiagnosis,then annually •pregnancy • ocu.larexam in 1sttrimester, closefollow-up throughout as pregnancycan exacerbate DR • gertat:ionaldiabetics not atrisk for retinopathy Treatment • Diabetic ControlandComplications Trial (DCCf) • tightcontrolofbloodsugardecreases frequencyandseverityofmkrovascularcomplications • bloodpressurecontrol • focal. laserfor clinicallysignificantm.acula.redema • panretinallaserphotocoagulation forproliferativediabeticretinopathy: reduces neovascularization, hencereducingtheangiogenicstimulusfrom ischemicretinabydecreasing retinal metabolicdemand-+ reducesrisk ofblindness • vitrectomyfur non-clearingvitreous hemorrhageandretinaldetachmentin proliferative diabeticretinopathy • vitrectomybeforevitreoushemorrhagedoesnotImprovethevisualprognosis Lens Changes • earlier onsetofsen.Uenuclearsclerosis andcorticalcataract • mayget hyperglyceml.ccataract.dueto sorbitolaccumulation (rare) • changesInbloodglucoselevels (poorcontrol) can suddenlycauserefractivechangesby 3-4 diopter& Extra Ocular Muscle (EOM) Palay • usuallyCN IIIinfarct • pupll usuallysparedIn diabetic CNIII palsy.butgetptosis • mayInvolveCN IV and VI • usuallyrecoverwithin few months Optic Neuropathy • visual acuiLyloss dueto Infarction ofopticdisc/nerve Ganglan eel layerI Innerpktxifurmlaywr Inner layer Oulllrplexiform laylr lllllr layer Exlemallmilinclme.,._,.e Rod and cone a !j "' Dilbatlllmallitul re&!o,..., j 0
  • 37.
    Toronto Notes 2011Ocular Manifestations ofSyatemic Disease Hypertension • retinopathyis the most common ocular manifestation • keyfeatures ofchronic HTN retinopathy: AV nicking. blot retinal hemorrhages, microaneurysms, cotton wool spots • keyfeatures ofacute HTN retinopathy: retinalarteriolar spasm, superficialretinal hemorrhage:, cotton wool spots. optic disc edema Tabla 7. Kaitii.Waganar-Barkar Classification Graup1 Mild arl!!rial narrowing Graup2 Graup3 Graup4 Obvious arterial narrowing with focal Group 2plus Cotton-wool spots Hemorrilllge and/or exudate Group3plus papilledema Multiple Sclerosis (MS) • see N49 Clinical Features • blurredvision and decreased colourvision: 2° to optic neuritis • central scotoma: due to damage to papillomacularbundle ofretinal nerve fibres • diplopia: 2° to internuclear ophthalmoplegia (INO) o RAPD, ptosis, nystagmus, uveitis, opticatrophy, opticneuritis o white matter demyc:linatinglesions ofoptic nerve on MRI Treatment o IV steroids with taper to oral form for optic neuritis • NOT oral steroids in isolation as this increases likelihoodofdeveloping MSlater TIA/Amaurosis Fugax • sudden, transient blindness from intermittentvascular compromise; ipsilateral carotid most frequent embolic source • typically monocular, lasting <5-10 minutes • Hollenhorst plaques (glisteningmicroemboli seen at branch points ofretinal arterioles) Graves' Disease • ophthalmopathy occurs despite control ofthyroid gland status • ocular manifestations occur secondaryto sympathetic overdrive and/or specificinflammatory infiltrate: ofthe: orbital tissue Clinical • initial inflammatoryphase is followed by a quiescentcicatricial phase Treatment • treat hyperthyroidism • monitor for corneal exposure and maintain cornealhydration • manage diplopia, proptosis and compressive optic neuropathy with one ora combination of. • steroids (duringacute phase) • orbital bony decompression • external beam radiation ofthe orbit • consider strabismus and/or eyelid surgical procedures once acute phase subsides Connective Tissue Disorders • RA, juvenile: idiopathic arthritis (JIA), SLE, Sjogren's syndrome:, ankylosingspondylitis, polyarteritis nodosa (PAN) • most common ocularmanifestation: dryeyes (keratoconjunctivitis sicca) Ophthalmology OP37 Optic N.m.11111111...TrilllDNTTJ Optic N.m.$WJG._.1htOpticNlllliil 113:136-137 ONTTIICIUilldPl!iantswilll&allll nawGIISII optic naurmllnllllbdad autcomaofthraatnlllmllnt +cnl Uoidx11d,andpllcebllx14d.Theyfaund 11111 cnlstaroidatUlaiiyin-riskofIICIIIIIICI, IV+0111 slliroidexpderecu;ety,1nd'"D.! trallmlnt'"I vilblltlmpaltic option.IV +1111 Uoidas r&: r1 recurence. Furtbannore,lnil Mil is wklabla in prediction lAonstt!AMS. ', , The most common cause of unilateral or bilateral proptosis in adults is Graves' di181118. ', , of Signs and Symplllms ofGr-' Ophtbalmopdly NO SPECS No siullf/sympiDms Only signs llid retraction, lid lag) Soft tiQue swelling lperiorbital edema) Proptosis{exophthalmos) Extraocular muscle weakness (causing diplopia) Comeal exposure Sightloss
  • 38.
    OP38 Ophthalmology OcularManifestationsofSystemic:Diseaae/Pediatrlc:Ophthalmology Toronto Notes 2011 .....,' ESRin GCA Males> 11111112 F11111.ia > (av- + 1Dl/2 O.thill'llilni....CCA? .JAM42002; 287:92-101 ,.ill: jMcllulkldion11111 dip._ onhiltury, 11rnp1H1IIItlry'-ding,prani!IIICI althlllllry 111111endemess-the lll!!yanmm. ,.aut no11mpotlllltlryllllnormelities on exam.nDmlllESR. Giant Cell/Temporal Arteritis (GCA)- - - - - - - - • see Rheumatology; Rl7 Clinical • more common in women >60 y.o. • abrupt monocular loss ofvision, pain over the temporal artery, jawclaudication, scalp tenderness, polymyalgia rhc:umatica, and constitutional symptoms • ischemic optic atrophy • 50% lose vision in other eye ifuntreated Diagnosis • temporal arterial biopsy+ increased ESR (ESR can be normal, butlikely80-100 in firsthour), CRP • ifbiopsy ofone side is negative. biopsythe other side Treatment • high dose corticosteroid to relieve pain and prevent further ischemic episodes • ifdiagnosis ofGCA is suspected clinically: start treatment + perform temporal artery biopsyto confirm diagnosis within 2 weeks ofintial presentation (DO NOT WAIT TO TREAT) Sarcoidosis • granulomatous uveitis with large "mutton fat" keratitic precipitates and posterior synechiae • neurosarcoidosis: optic neuropathy, oculomotor abnormalities, visual field loss Treatment • steroids and mydriatics Pediatric Ophthalmology Strabismus • ocular misalignment, found in 3% ofchildren • object not visualized simultaneously byfovea ofeach eye • often presents with parental concern about a wandering eye, crossing eye, or poor vision • types: heterotropia (paralytic or non-paralytic), heterophoria • 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) Types • exo- (lateral deviation), eso- (medial deviation) • hyper- (upward deviation), hypo- (downward deviation) • esotropia= "crossed-eyes"; exotropia= • pseudoesotropia: epicanthal folds give appearance ofesotropia but Hirschberg test is normaL more common in Asians Tests • Hirschberg test (corneal light reflex): positive ifthe light reflex in the cornea ofthe two eyesis asymmetrical • light reflex lateral to central cornea indicates esodeviation; light reflex medial to central cornea indicates exodeviation • false positives occur ifvisual axis and anatomic pupillary axis ofthe eye are not aligned (angle kappa) • cover test (Figure 23) • ask patient to fixate on target • cover the fixating eye, the deviated eye will then move to fixate on the target • ifdeviated eye moves inward = exotropia • ifdeviated eye moves outward = esotropia • the deviation can be quantified using prisms
  • 39.
    'IbroDloNota2011 HETEROPHORIA • latentdeviation PecllatricOphthalmology o deviationcorrectedinthe binocularstatebythe fusion mechanism (i.e. deviation not seenwhen patientis usingbotheyes) • Hirschbergtestwillbe normal (lightreflexes symmetrical) • verycommon - majorityareasymptomatic • maybeexacerbatedorbecomemanifestwith asthenopia (eye mam,fatigue) Teats • cover-uncovertest (Figure 23) • placinga cowrOft!' an eyewith a phoriacauses a breakdown offixation of which allows itto movetJJ a misalignedposition • uncoveringthe coveredeyewill allowitto return to a normalcentralposition • coveredeyemovesinwardonremovingcover= emphoria • coveredeyemoves outward onremovingcover= esophoria. o alternate covertest • alternatingthe coverbetweenboth eyesrevealsthe totaldeviation, bothlatent andmanifest • maintain cover over oneeyefor 2-3 secondsbeforerapidlyshiftingto other eye Canrtalla 0 ,...... .. Eautrapill D ... ·1.> Exlllrupil Cover-Uncover t8lll 0 e J .... l@ .. -@.' > Esophoria 0 .... Ext!phoria Figura Z3. Cower and Conr-UncDVBrTestsfur DetBCtion af Tropiasa.t Pharias PARALYTIC STRABISMUS o incomitantstrabJsmus (i.e. devla.tionvariesIn differentpositions ofgaze) • reductionor restrictioninrange ofeye movements Etiology o neural (CN III, IY, Vl): ischemia (e.g. DM), MS,aneurysm. braintumour, trauma j :§ g o m118CUlar: myastheniagravis (neuromuscularjunctionpathology), Gravei disease o structural: restriction/entrapmentofextraocularmuscles dW!to orbitalinflammation, tumour, fracture ofthe orbitalwall Clinical Features o mostlyin adults, acquired o presentmainlywith dJplopla • greatestdeviation infield ofaction ofthe weakenedmuscle • visual acuityis usuallyunaffectedin either eye. unless CN nis involved NON-PARALYTIC STRABISMUS • concomitantstnlbismus (ie. deviation equal inalldirections ofgaze) • no restrictioninrangeofeyemovements o monocular, alternating.orintermittent Clinical Features • usuallybeginsininfancy,upto age 8-10 • usuallyno diplopia (childsuppressestheimagefrom themisalignedeye) o deviatedeyemaybecome amblyopiclfnottreated whenthe childis young.Amblyopia treatment rarelysuccessfulafter age8-10 (seeAmblyopia, OP39) o amblyopiausuallydoes notdevelopifchildhasalternatiDgstrablamus orintermittency- allomneuralpathways furbotheyestJJ develop Ophthalmology 01'39 ..... , _._____________ All chikhn with mbi8I!UIIIIdlor poaibll llldueed vilion pron¢ nfllmlto an optdhlllmDklgist.
  • 40.
    OP40 Ophthalmology PediatricOphthalmology Toronto Notes 2011 Accommodative Esotropia • normal response to approaching object is the triad ofthe near reflex: convergence, accommodation and miosis • hyperopes must constantlyaccommodate - excessive accommodation can leadto esotropia in young children via over-activation ofthe near reflex • average age ofonset is 2.5 years • usually reversible with correction ofrefractive error Non-accommodative Esotropia • accounts for 50% ofchildhood strabismus • most are idiopathic • maybe due to monocularvisual impairment (e.g. cataract, corneal scarring, anisometropia, retinoblastoma) or divergence insufficiency (ocular misalignment that is greaterat distance fixation than at nearfixation) Amblyopia Definition • reduction ofbest correctedvisual acuitydue to cortical suppression ofsensoryinput from an eyethat is receiving blurredor conflictingvisual information, leading to disruption ofthe normal development ofvisual pathways servingthat eye Detection • «Holler Test": young child upset ifgood eyeis covered • quantitative visual acuitybyage 3-4 years using picture charts and/or matching game (Sheridan- Gardiner), testingeach eye separately • amblyopia treatmentless successfulafter age 8-10 years, but a trial should be given no matter what age • prognosis: 90% will have good vision restored and maintained iftreated <4 years old Etiology and Management • strabismUJ • correct with glasses for accommodative esotropia (5096 ofchildren experience reliefoftheir esotropiawith glasses and will not require surgery) • occlusion ofunaffected eye forces brain to use previouslystrabismic eye; aims to bringvision in previouslysuppressedeye to normal before surgery • surgery: recession (weakening) = moving muscle insertion further back on the globe; or resection (strengthening) = 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 approximately age 8 • refractiveerrors • anisometropia (difference in refractive power between the eyes) • amblyopia usuallyin the more hyperopic eye • the less hyperopic eye receives a clear image while the more hyperopic eye receives a blurred image; input from the blurred eye is cortically suppressed and visual pathwayfails to develop normally • treat with glasses to correct refractive error • patching is required ifvisual acuity difference persists after 4-8 weeks ofusing glasses • deprintion amblyopia • occlusion due to ptosis, cataract, retinoblastoma, corneal opacity • occlusion amblyopia: prolonged patching ofgood eye maycauseit to become amblyopic General Treatment • correctthe underlying cause • occlusion therapy (patching) oratropine cycloplegia (opticaldegradation therapy) ofthe good eye Laukocoria • white pupil (red reflex is absent) Differential Diagnosis • cataract • retinoblastoma • retinal coloboma • retinopathyofprematurity(ROP) • persistent hyperplastic primaryvitreous (PHPV) • Coat's disease (exudative retinitis) • toxocariasis • retinal detachment
  • 41.
    Toronto Notes 2011Pediatric Ophtbahnology Retinoblastoma • most common primary intraocular malignancy in children • incidence: 1/1000; sporadic or genetic transmission; screening ofsiblings/offspring essential • unilateral or bilateral (in 1/3 of cases) • malignant - direct orhematogenous spread • diagnosis • maybe detected byleukocoria in infant • CT scan: dense radiopaque appearance (contains calcium) Treatment • radiotherapy, chemotherapycombined with laser, cryopexy, and/or enucleation Retinopathy of Prematurity (ROP) • vasoproliferative retinopathythat is a major cause ofblindness in the developed world Risk Factors • non-blackrace (black infants have lower risk ofdeveloping ROP) • low gestational age, birth weight (<1500 g) • high oxygen exposure after birth Classification • Stage 1: faint demarcation line at the junction between thevascularized and avascular retina • Stage 2: elevated ridge • Stage 3: extra-retinal fibrovascular tissue extending into utereous • Stage 4: partial retinal detachment (4A: macula 4B: macula • Stage 5: total retnal detachment • Plus (+) disease = dilatation and tortuosityifretinal vessels • threshold disease: stage 3+ in zones 1 or 2 with 5 continuous or8 cumulative clockhours of ROP involvement (Figure 24) Treatment • threshold disease is treated with cryotherapy or laser (laser is now the standard treatment, with better refractive outcome) • ROP beyond threshold level is either watched carefully (usually stage 4A) or treated with vitrectomy/scleral buckle Prognosis • higher incidence ofmyopia among ROP infants, eveniftreated successfully • stage 4B and 5 have poor prognosis for visual outcome despite treatment Nasolacrimal System Defects • congenital obstruction ofthe nasolacrimal duct (failure ofcanalization), usually occurs at 1-2 months of age • increased tearing, crusting, discharge, recurrent conjunctivitis • can have reflux ofmucopurulent material from lacrimal punctum when pressure is applied over lacrimal sac • treatment: massage over lacrimal sac at medial comer ofeyelid • consider referral for duct probingifno spontaneous resolution after 9-12 months Ophthalmia Neonatorum ------------------------------- • newborn conjunctivitis in first month oflife • causes: • toxic: silver nitrate, erythromycin • infectious: bacterial (e.g. N. gono"hoeae- most common, Chlamydia trachoma/is), herpes simplex virus (HSV) • gonococcal infection is the most serious threat to sight as it can rapidly penetrate corneal epithelium, causing corneal ulceration • diagnose using stains and cultures • treatment: systemic antibiotics with possible hospitalization ifinfectious etiology • topical prophylaxis, most commonly with erythromycin (or silver nitrate), is required bylaw at birth Ophtbahnology OP41 -.. nerw Macula Figura 24. Zonas of tha Retina in ROP
  • 42.
    OP42 Ophthalmology .....,, Always testvisual acuity (VA] first - mlldicoi8QIII pratBction. ..... ,, I!Rr if you•-any ofth- llipl • llec:relll8d VA • ShaDow antlrior chamber • Hyphema • Abnonnal pupil • Ocul11r misalignment • Retinal damage Manag11118111 of S.Piehld Glolle Rapture CAN'Tforget Clorbib Ancef IV NPO Tetanu..mtus Shabn Bally Syndnlme Syndrome of findings characterized by no external signs ofabuse and respimDry arrest, seizures, and corTIII. Ocular axam findings 11r11 important for Shaken Baby Syndrome. These findings include amnsiv1 rwtinal and vitreous hemorrhages 1hat occur during 1he lhakilg proce11 and n extramely rm in accidentll1nuna. Adetailed fundoscopic exam or an ophthalmology refemll should be conductEd for an infants in whom abuse il suspected. Pediatric Ophthalmology/OcularTrauma Toronto Notes 2011 Congenital Glaucoma • due to inadequate development ofthe filtering mechanism ofthe anterior chamber angle Clinical Features • cloudy cornea, increased IOP • photophobia. tearing • buphthalmos (large "ox eye"), blepharospasm Treatment • filtration surgery is required soon after birth to prevent blindness Ocular Trauma Blunt Trauma • caused byblunt object such as fist, squash ball • history: injury, ocular history, drug allergy, tetanus status • exam: VA first, pupil size and reaction, EOM (diplopia), external and slitlamp exam, ophthalmoscopy • ifVA normal or slightlyreduced, globe less likelyto be perforated • ifVA reduced maybe perforated globe, corneal abrasion, lens dislocation, retinal tear • bone fractures • blowout fracture: restricted EOM, diplopia, enophthalmos (sunken eye) • ethmoidfracture: subcutaneous emphysema oflid • lids: swelling, laceration, emphysema • conjunctiva: subconjunctival hemorrhage • cornea: abrasion - detect with fluorescein staining and cobalt blue filter using slitlamp or ophthalmoscope • anterior chamber: assess depth, hyphema, hypopyon • iris: prolapse, iritis • lens: cataract, dislocation • retinal tear/detachment Penetrating Trauma • include ruptured globe ± prolapsed iris, intraocularforeign body • rule out intraocular foreign body, especiallyifhistoryof"metal striking orbit cr • initialmanagement: refer immediately!! •ABCs • don't press on eyeball! • don't checklOP ifpossibility ofglobe rupture • checkvision, diplopia • apply rigid eye shieldto minimize further trauma • keep headelevated30-45° to keep IOP down • keepNPO • tetanus status • give IV antibiotics Hyphama • bloodin anteriorchamber often due to damage to root ofthe iris • may occur with blunttrauma Treatment • refer to ophthalmology • shieldand bedrestx 5 days or as determined by ophthalmologist • sleep with head upright • may need surgical drainage ifhyphema persists orifre-bleed Complications • risk ofre-bleed highest on days 2-5, resultingin secondary glaucoma. corneal staining, and iris necrosis • never prescribe aspirin, as itincreases the risk ofare-bleed
  • 43.
    Toronto Notes 2011Ocnlar Trauma/Surgical Ophthalmology Blow-Out Fracture • see PL30 • blunt trauma causing fracture oforbital floor and herniation oforbital contents into maxillary sinus • orbital rim remains intact • inferior rectus and/or inferior oblique muscles maybe incarceratedat fracture site • infraorbital nerve courses along the floor ofthe orbit and may be damaged Clinical Features • pain and nausea at time ofinjury • diplopia, restriction ofEOM • infraorbital and upper lip paresthesia (CN V2) • enophthalmos (sunken eye),perim:bital ecchymoses Investigations • plain films: Waters' view and lateral • CT: anteroposterior and coronal view oforbits Treatment • refrain from coughing, blowing nose • systemic antibiotics maybe indicated • surgery iffracture >50% orbital floor, diplopia not improving, or enophthalmos >2 mm • may delay surgeryifthe diplopia improves Chemical Burns • alkaliburns have a worse prognosis than acid bums because acids coagulate tissue and inhibit further corneal penetration • poor prognosis ifcornea opaque, likelyirreversible stromaldamage • even with a clear cornea initially, alkaliburns can progress for weeks (thus, veryguarded prognosis) Treatment • irrigate at site of accident immediately with water or buffered solution • IV drip for at least 20-30 minutes with eyelids retracted in emergency department • swab upper and lower fornices to remove possible particulate matter • do not attempt to neutralize because the heat produced bythe reaction will damage the cornea • cycloplegic drops to decrease iris spasm (pain) and prevent secondaryglaucoma (due to posterior synechiaeformation) • topical antibiotics and patching • topical steroids (byophthalmologist) to decrease inflammation, use for less than two weeks {in the case ofa persistent epithelial defect) Surgical Ophthalmology • daaoqstorhinostomy {DCR) - excision ofbone coveringthe nasolacrimal sac to restore tear drainage • LASIK {laser-usiatedin-situkeratomlleu.sia) - a microkeratome is used to create a corneal flap followed by laser remodeling ofthe stroma to correct refractive error • trabeculectomy- creation ofa new outflow tract from anterior chamber to under conjunctiva; fibrosis prevented with mitomycin Cor 5-FU injection during surgery • phacoem.ulsification {cataractextraction) - the use ofultrasonic waves to breakup and aspirate a cataract followed by replacement with an artificial lens implant • vitrectomy- the use ofsmall trochars to enter the posterior segmentand remove vitreous; commonly used to treat vitreous hemorrhage and retinal detachment • pneumatic retinopexy- intraocular injection ofair or an expandable gas in order to tamponade a retinal break • scleral buckle - a bandis secured on the outside ofthe globe that indents the eye walL thereby relieving tension on the retina around any tears/holes and allowing the tears/holes to remain sealed Ophthalmology OP43 ....' , Cluslc Signs ofBlow-Out Enophlhalmos O.cnaud UPQID (IR trapped) Cheek anesthetized (infniO!bital nerve lnlppad) ..... ' Fluomc1in lights up alkali so you can dutact itnlllHIIIIi whether it hH been removed.
  • 44.
    OP44 Ophthalmology OcularDrugToxicity/CommonMedications Toronto Notes 2011 Ocular Drug Toxicity Table B. Drugs with Ocular Tu:xicity Amiod11111e COITIBIII microdeposits andtupsrficial kenrtcpathy (vortex ksnrtopathy) Re: ischemicoptic neuropathy A1rupine. benztropine ActonaP) Chloroquine, Chlorpromazine Contracsptiwpill& Digitalis Ethlllrilutol Haloperidol (Haldoi®) Indomethacin lntelferon Isoniazid Nalidixic scid Steroids NSAIDS Tamsulosin (Aofllill(8 ) Tetracycline Thioridazine Vigabatm Vitamin Aintoxication Vitamin Dintoxicfllion Pupilla.y dilfllion (risk Dlangle closure glaucoma) lnflammfllory syu di888se (iritis. scleritis, episclsritis) Bull's syu rnaculopathy Vortexkerlllopathy Anterior subcapsularCllbnct Decreased tDiellllCeto contact lenses Migraine Optic neuritis Central vein occlusion Yellowvision Blurred vision Optic neuropathy Oculogyriccrises Blurred vision Retinal hemorrhages and clllton wool spots Optic neuropathy Papilledema Posterior subcapsularcalllracts Glaucoma Papilledema (systemic mroidsl lncf'lliiSed severity Dl HSV infections (gsographic ulcers) Predispositiontofungal infections Stevens.Johnson syndrome lntlliCJI)erative FloppyIris Syndrome (FIS), which can c01J1)1icate cataract surgery Papilledema (essociated pseudotumoLI' cerebri) Pigmenlllrydegeneration ri relila Retinal deposition with mscular sparing. visualfield loss Papilledema Bandkeratopathy Common Medications TOPICAL OCULAR DIAGNOSTIC DRUGS Fluorescein Dye • water soluble orange-yellow dye • green under cobalt blue light (ophthalmoscope or slit lamp) • absorbedin areas ofepithelial loss (ulcer or abrasion) • also stains mucus and contact lenses Rose Bengal Stain • stains devitalized epithelialcells and mucus Anesthetics • e.g. proparacaine HCl 0.5%, tetracaine 0.5% • indications: removal offoreign body and sutures, tonometry, examination ofpainful cornea • toxic to corneal epithelium (inhibit mitosis and migration) and can lead to corneal ulceration and scarring with prolonged use, therefore NEVER prescribe
  • 45.
    Toronto Notes 2011Common Medications Ophthalmology OP45 Mydriatics • dilate pupils • two classes • cholinergic blocking (e.g. tropicamide [Mydriacyl•]) • dilation plus cycloplegia (lose accommodation) byparalysis ofiris sphincter and the ciliary body • indications: refraction, ophthalmoscopy, therapy for iritis • adrenergic stimulating (e.g. phenylephrine HC12.5%) • stimulate pupillarydilator muscles, no effect on accommodation • usuallyused with tropicamide for additive effects • side effects: hypertension, tachycardia, arrhythmias Tabla 9. Mydriatic Cycloplegic Drugs and Duration uf Action Dnlgs Tropicamide (MydriacyP) 0.5%, 1% Cydopentolate HCL 0.5%, 1% Homatropine HBr1%, 2% Atropine sulfate 0.5%, 1% Scopolamine HBr 0.25%, 5% Duman afAl:tian 4-5 hours 3-6 hours 3-7 days 1-2weeks 1-2weeks GLAUCOMA MEDICATIONS Tabla 10. Glaucoma Medications Dnlg CAlgary Alphi-AQonilt No..lectin o epilephrine HCI1% o dipivalyl D.1% (Propine8 ) o brimonidine 0.2% (Aiphagan8 ) o apraclonidine 0.5%{Lopidine8 ) Beta-Blocker No..lectin o lirnolal (Timaptic•) o lewbunolol{Betaganil}) Bm.-celective o bstaxolol {Betoptic8 ) Carbonic AnhY*-Inhllilllr o dorzolamide {Trusopt®) o brinzolamide (Azopt®) o oral: acetamlamide {Diamax®) Pamymplthomimelic {cholinergic stimulating) o pilocarpine (Pilopine®l o carbachol (l&apto 1gtt OSIOD bid/tid 1 gtt DSIOD qd,.tid 1gtt DSIODtid Diamox8 : 500 mg PO bid 1.Nort-&Bisctiw - "- production + 1'1M outflow 2. Selecliva- "- aqueous pralllction + 1' UY808clnl outflow "- aqueous production "- aqueous production 1-2 gtts DSIOD lill/qid 1'1M outflow 1. Non-selective - mydriasis, macular edema,tachycarcia 2. Selective-contactale111v. hypotension in chillhn BrunchC11p81111 (cuelul in athiiii/COPD) 1' CHF Bnulycardia Hypotension Depression Heartblock Impotence ••Mustaskaboutsulllllllergrl Generally local side efh!cts with topical preparlllions Oral: diuresis, fatigue, paresthesia&, Gl upset etc. Miosis -.1- ni;rtvision 1' Gl motiity Brow ache Headache -.1-heartrate Prasllgllndin Analog1111 o lillirlopra&t(Xalatan8 ) 1gtt DSIOD qhs 1' uveoscleral outflow{uveoscleral responsible lri1 colour change 0 travaprast (JI'IIVllbll®) for 20% of drainage) Periorbital skin pigmentation Lash growth o bimatoprost (Lumigan•) timulol +doJZDimila; limciJI +h1Drlop!UII;Corrmig..• timobl+bri111111idine; lbl tinokll +1IMpust WET AGE-RELATED MACULAR DEGENERATION MEDICATIONS vascular Endothelial Growth Factors (VEGF) Inhibitors Conjunctival hyperemia • block vascular endothelial growth factor which prevents ocular angiogenesis and further development ofchoroidal neovascularization • administered via intravitreal injections • pegaptanib (Macugen•) is a selective anti-VEGF targeting VEGF isoform 165 o ranibizumab (Lucentis•) is a non-selective anti-VEGF agent o bevacizumab (Avastin•) is another non-selective anti-VEGF agent but is only FDA approved for metastatic breast cancer, colorectal cancer and non-small cell lung cancer. Therefore, its use in ophthalmologic is off-label
  • 46.
    OP46 Ophthalmology CommonMedications/References/Referen TOPICAL OCULAR THERAPEUTIC DRUGS NSAIDs • usedfor less serious chronic inflammatoryconditions Toronto Notes 2011 • e.g. ketorolac (Acular-), diclofenac (Voltaren•), nepafenac (Nevanac•) drops Anti-Histamines • used to relieve redanditchy eye. often in combination with decongestants • sodium cromoglycate - stabilizes membranes Decongestants • weak adrenergic stimulating drugs (vasoconstrictor) • e.g. naphazoline, phenylephrine (Isopto Frin•) • rebound vasodilation with overuse; rarelycanprecipitate angle closure glaucoma Antibiotics • indications: bacterial conjunctivitis, keratitis, or blepharitis • commonlyas topical drops or ointments, may give systemically • e.g. sulfonamide (sodium sulfacetamide, sulfisoxazole),gentamicin (Garamycin•), erythromycin. tetracycline,bacitracin, polymyxinB, fluoroquinolones (CiJ.oxan•, Ocuflmt"',VJg31Uax•, Zymar-) Corticosteroids • e.g. fluorometholone (FML•), betamethasone, dexamethasone (Maxidex•), prednisolone (Predsol• 0.5%, Pred Forte• 1%), rimexolone (Vexol•) • primary care ph)15icians should avoid prescribingtopical corticosteroids due to risk ofglaucoma, cataracts, and reactivationofHSV keratitis • complications • potentiates herpes simplex keratitis and fungal keratitis as well as masks symptoms • increased lOP, more rapidlyin steroid responders (within weeks) • posterior subcapsular cataract (within months) References Complicztions: Your8Y'15&dilbftic retinopllhy. Clnldiln lilbel81Aaoc:iltion Nov2003. lilbaticRatiiiiJFIIhy.Diabns Cara 1998;2111]:143·156. liabet81 in OntJrio: 1111 IC6 l'rll:tica June 2003. llloil llrllord C. Illsic Oi*tfwlmolowforMedicalS1udlnand PrimuyCare R111id8111s. 7th ed.San Fnl11l:ilco:AmericanAcademyrJOphthalmology, 1199. WIIDnFM.I'rlcti:alOphlllllmab.rl: AManuallor Begilninq llelidenbi. 41h ed. Americllll Academyrl Ophtlillmology,2005. Frimlul N, Plned1R, KliArP. TheM11111ChulatllEyu1ndElr ManuIIrJ OphthalrnDIDII'f.Tmnlll:W.B. Saunders 1988. KlnskiJJ.Clinical ASystamlticApproech. &1h lid.Oxhxd: llut18rwGrth·lllilem111ll, 2007. S18in R,Stein H. Mnqernent Oc:ularEine'V'"Cill5. 41h ed.Mgntr111l: Medico11cept. 2006. lllillilll HuxJ.et al. Dlabll8sinOntario: an ICES l'nlc1iceAtlls.TGI'On!o: hstiMIforCiii:alEvluativa Sciences, 2003. The CD!T1111itteefDIthe chmffiCitiDIIofretilopathyol premmrity.AnintemlliDnal cllssiliCitiDnolletinoPIIhYrJprar'llblrity.An:hOphlllai!DIDgy. 1984;102: 1130-34. IIIIIIQII Red Alln. www.radlllln.Grq LII:Cini/Cia llriYersi!y MicliiQIII KeiDgg EyeCentrewww.kltlgv.unicli.edWtheeyeslnrveMndu.html