8/18/2019 Ophthalmology PDA http://slidepdf.com/reader/full/ophthalmology-pda 1/35 Ophthalmology – Toronto Notes Abridged for the PDA To be used only in conjunction with the printed Toronto Notes Ishtiaq Ahmed, Edmund Chen and Xiaoxing Catherine Tong, chapter editors Cagla Eskicioglu and Nadra Ginting, associate editors Maja Segedi, EBM editor Dr. Lawrence Weisbrod, staff editor Common ComplaintsOcular Emergencies The Ocular Examination OpticsThe Orbit Lacrimal Apparatus Lids and Lashes ConjunctivaCornea The Uveal Tract LensVitreousRetina GlaucomaPupils Neuro-Ophthalmology Malignancies Ocular Manifestations of Systemic Diseases Strabismus Pediatric Ophthalmology Trauma Ocular Medications
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• Cranial Nerve III – superior rectus, medial rectus, inferior rectus, inferior oblique
• Cranial Nerve IV – superior oblique
• Cranial Nerve VI – lateral rectus
External Examination
• the four L’s
lymph nodes (preauricular, submandibular)
lids
lashes
acrimal system
Slit-Lamp Examination
• systematically examine all structures of the anterior segment + anterior vitreouslids (including upper lid eversion if necessary), lashes, and lacrimal system
• “nearsightedness”• prevalence of 30-40% in U.S. population
Clinical Features• usually presents in 1st or 2nd decade, stabilizes in 2nd and 3rd decade; rarely
begins after 25 years except in diabetes or cataracts• blurring of distance vision; near vision usually unaffected
Complications • retinal tear/detachment• macular hole• open angle glaucoma
• complications not prevented with refractive correction
Treatment • correct with negative diopter/concave/”negative” lenses to diverge light rays
Hyperopia
• “farsightedness”• may be developmental or due to any etiology that shortens the eyeball• to quantify hyperopia, cycloplegic drops are used to prevent accommodation
Clinical Features • youth: usually do not require glasses (still have sufficient accommodative ability to
focus image on retina), but may develop accommodative esotropia• 30s-40s: blurring of near vision due to decreased accommodation, may need
reading glasses• > 50s: blurring of distance vision due to severely decreased accommodation
Complications • angle-closure glaucoma, particularly later in life as lens enlarges
Treatment • when symptomatic, correct with positive Diopter/convex/”plus” lenses to
converge light rays
Presbyopia
• normal aging process (especially over 40 years)• experienced by emmetropes, myopes, hyperopes, and astigmatics
Pathophysiology • hardening/reduced deformability of the lens results in decreased accommodativeability
• near images cannot be focused onto retina (focus is behind retina as in hyperopia)
Clinical Features• if initially emmetropic, person begins to hold reading material further away, but
distance vision remains unaffected• if initially myopic, person begins removing distance glasses to read• if initially hyperopic, symptoms of presbyopia occur earlier
Treatment • correct vision with positive diopter/convex/”plus” lenses for reading• reading glasses will blur distance vision (avoided by using bifocal or progressive
• light rays not refracted uniformly in all meridians• due to non-spherical surface of cornea or non-spherical lens (eg. football-shaped)• two types of astigmatism
regular - curvature uniformly different in meridians right angles to eachotherirregular - distorted cornea, caused by injury or keratoconus (cone-shapedcornea)
Treatment • correct with cylindrical lens (if regular)
Anisometropia
• difference in refractive error between eyes• second most common cause of amblyopia in children
• infection of soft tissue anterior to orbital septum
Etiology • usually follows periorbital trauma or dermal infection
Clinical Features• tender, swollen and erythematous lids• may have low-grade fever• normal visual acuity, pupils, extraocular movements (EOM)• no exophthalmos or RAPD
Treatment• systemic antibiotics (Suspect H. influenza in children; S. aureus or Streptococci in adults)• warm compresses
Orbital Cellulitis• inflammation of orbital contents posterior to orbital septum• common in children, but also in the aged and immunocompromised
Etiology • usually secondary to sinus/facial/tooth infections or trauma
Clinical Features• decreased visual acuity, pain, red eye, headache, fever• lid erythema, tenderness, and edema with difficulty opening• conjunctival injection and chemosis (conjunctival edema)• proptosis, limitation of ocular movements (ophthalmoplegia) and pain with
movement• RAPD, optic disc swelling
Treatment • admit, IV antibiotics, blood cultures, orbital CT• surgical drainage of abscess• follow closely
Complications• orbital apex syndrome, cavernous sinus thrombosis, meningitis, blindness
Finding Preseptal Cellulitis Orbital Cellulitis Fever May be present Present Lid edema Moderate to severe Severe Chemosis Absent or mild Moderate or marked Proptosis Absent Present Pain on eye movement Absent Present Ocular mobility Normal Decreased
Vision Normal Diminished ± diplopia RAPD Absent May be seen Leukocytosis Minimal or moderate Marked ESR Normal or elevated Elevated Additional findings Skin infection Sinusitis, dental abscess
Table 2. Differentiating Between Preseptal and Orbital Cellulitis
Etiology • physiologic - tear production normally decreases with aging• ectropion - downward and outward turning of lower eyelid• decreased blinking (CN VII palsy)• blepharitis• diminished corneal sensitivity (eg. neurotrophic keratitis)• systemic diseases: rheumatoid arthritis, Sjögren’s syndrome, sarcoidosis,
amyloidosis, leukemia, lymphoma• vitamin A deficiency• medications: anticholinergics, diuretics, antihistamines
Clinical Features• dry eyes, red eyes, foreign body sensation, blurred vision, tearing• slit-lamp exam: decreased tear meniscus, decreased tear break up time (TBUT),
superficial punctate keratitis (SPK)• stains with fluorescein/Rose Bengal• Schirmer’s test: measures tear quantity on surface of eye in 5 minute time period
(< 10 mm of paper strip wetting in 5 minutes is considered a dry eye)
Complications• erosions and scarring of cornea
Treatment • nonpreserved artificial tears up to q1h and ointment at bedtime• punctal occlusion, lid taping, tarsorrhaphy (sew lids together) if severe• treat underlying cause
• fibrovascular triangular encroachment of epithelial tissue onto the cornea, usually nasal• may induce astigmatism, decrease vision• excision for chronic inflammation, threat to visual axis, cosmesis
• one-third recur after excision• much decreased 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 if no other ocular findings, resolves in 2-3 weeks• if recurrent, consider medical/hematology work-up
• non-infectiousallergy: atopic, seasonal, giant papillary conjunctivitis (in contact-lens wearers)toxic: irritants, dust, smoke, irradiationsecondary to another disorder such as dacryocystitis, dacryoadenitis, cellulitis,Kawasaki’s disease
Clinical Features• red eye, itching, foreign body sensation, tearing, discharge, crusting of lashes in the
morning• lid edema, conjunctival injection often with limbal pallor, preauricular node,
subepithelial infiltrates• follicles
pale lymphoid elevations of the conjunctivafound in viral and chlamydial conjunctivitis
• papillaefibrovascular elevations of the conjunctiva with central network of finely branching vesselsnonspecific; found in giant papillary conjunctivitis (GPC) and vernalconjunctivitis
BACTERIAL CONJUNCTIVITIS• purulent discharge, lid swelling, conjunctival injection, chemosis• common agents include S. aureus, S. pneumoniae, H. influenzae and M. catarrhalis • in neonates and sexually active people must consider N. gonorrhea
(invades cornea to cause keratitis)• Chlamydia trachomatis is the most common cause in neonates
Treatment
• topical broad-spectrum antibiotic• systemic antibiotics if indicated, especially in children• usually a self-limited course of 10-14 days if no treatment, 1-3 days with treatment
VIRAL CONJUNCTIVITIS• serous discharge, lid edema, follicles, subepithelial corneal infiltrates• may be associated with rhinorrhea• preauricular node often palpable and tender• initially unilateral, often progresses to the other eye• mainly due to adenovirus – highly contagious for up to 12 days
Treatment • cool compresses, topical lubrication• usually self-limiting (7-12 days)
Trachoma (serotypes A-C)• leading cause of blindness in the world• severe keratoconjunctivitis• follicles on superior palpebral conjunctiva• conjunctival scarring leads to entropion with trichiasis, corneal abrasions ± ulceration
and scarring• keratitis leads to superior vascularization (pannus) and corneal scarring• treatment: topical and systemic tetracycline
Inclusion Conjunctivitis (serotypes D-K)• chronic conjunctivitis with follicles and subepithelial infiltrates• most common cause of conjunctivitis in newborns• prevention: topical erythromycin at birth• treatment: topical and systemic tetracycline, doxycycline or erythromycin
Seasonal• associated with hay fever• treatment: cool compresses, antihistamine, mast cell stabilizer
Giant Papillary Conjunctivitis (GPC)• immune reaction to mucous debris on lenses in contact lens wearers• large papillae form on superior palpebral conjunctiva• specific treatment: clean, change or discontinue use of contact lens
Vernal Conjunctivitis• large papillae (cobblestones) on superior palpebral conjunctiva with corneal ulcers,
keratitis• seasonal (warm weather)• occurs in children, lasts for 5-10 years and then resolves• specific treatment: consider topical steroid, cyclosporine (not in primary care)
• may have associated rust ring if metallic that may be toxic to the cornea• patients may note tearing, photophobia, foreign body sensation, redness• signs include foreign body, conjunctival injection, epithelial defect that stains
with fluorescein, corneal edema, anterior chamber cell/flare
Complications • abrasion, infection, scarring, rust ring, secondary iritisTreatment• remove under magnification using local anesthetic and sterile needle or refer to
ophthalmology (depending on depth and location)• treat as per corneal abrasion (below)
Corneal Abrasion
• epithelial defect usually due to trauma (e.g. fingernails, paper, twigs), contact lens
Clinical Features• pain, redness, tearing, photophobia, foreign body sensation• de-epithelialized area stains with fluorescein dye• pain relieved with topical anesthetic
Treatment • topical antibiotic (drops or ointment)• consider topical NSAID, cycloplegic (relieves pain and photophobia by paralyzing
ciliary muscle), light patch• pressure patch is not effective
• most abrasions clear spontaneously within 24-48 hours
Herpes Simplex Keratitis
• usually HSV type 1 (90% of population are carriers)• may be triggered by stress, fever, sun exposure, immunosuppression
Clinical Features• pain, tearing, foreign body sensation, redness, may have decreased vision, eyelid
edema• corneal hypoesthesia• dendritic (thin and branching) lesion in epithelium that stains with fluorescein
Complications• corneal scarring (can lead to loss of vision)• chronic interstitial keratitis due to penetration of virus into stroma• secondary iritis
Treatment • topical antiviral such as trifluridine, consider systemic antiviral such as acyclovir• dendritic debridement• NO STEROIDS initially – may exacerbate condition• ophthalmologist must exercise caution if adding topical steroids for chronic
Complications • corneal keratitis, ulceration, perforation and scarring• iritis, secondary glaucoma, cataract• muscle palsies (rare) due to CNS involvement• occasionally severe post-herpetic neuralgia
Treatment • oral antiviral (acyclovir, valcyclovir or famciclovir)• topical steroids as indicated for keratitis, iritis (prescribed by an ophthalmologist)
• cycloplegic, antibiotic if indicated
Keratoconus
• bilateral central thinning and bulging (ectasia) of the cornea to form a conical shape• familial occurrence; associated with Down’s syndrome and atopy• associated with breaks in Descemet's and Bowman's membrane• results in irregular astigmatism, corneal striae, scarring, stromal edema• blurring of visual acuity is the only symptom
Clinical Features• photophobia (from reactive spasm of inflamed iris muscle), ocular pain, tenderness of
the globe, brow ache (ciliary muscle spasm), decreased visual acuity, tearing• ciliary flush (perilimbal conjunctival injection), miosis (spasm of sphincter muscle)• anterior chamber “cells” (WBC in anterior chamber due to anterior segment
inflammation) and “flare” (protein precipitates in anterior chamber secondaryto inflammation), hypopyon (collection of neutrophilic exudates inferiorly in the
anterior chamber)• occasionally keratitic precipitates (clumps of cells on corneal endothelium)• iritis typically reduces intraocular pressure though severe iritis may cause an
• emboli from carotid arteries or heart (e.g. arrhythmia, endocarditis, valvulardisease)
• thrombus• temporal arteritis
Clinical Features• sudden, painless (except in temporal arteritis), severe monocular loss of vision• relative afferent pupillary defect (RAPD)• patient will often have experienced transient episodes in the past (amaurosis fugax)• fundoscopy
“cherry-red spot” at centre of macula (visualization of unaffected highlyvascular choroid through the thin fovea)retinal pallornarrowed arterioles, boxcarring (segmentation of blood in arteries)cotton-wool spots (retinal infarcts)cholesterol emboli (Hollenhorst plaques) - usually located at arteriole bifurcationsafter ~ 6 weeks: cherry-red spot recedes and optic disc pallor becomesevident
Treatment • OCULAR EMERGENCY: attempt to restore blood flow within 2 hours• Sooner the treatment = better prognosis (irreversible retinal damage if >90 min. of complete CRAO)
massage the globe (compress eye with heel of hand for 10 sec, releasefor 10 sec, repeat for 5 minutes) to dislodge embolusdecrease intraocular pressure
IV mannitol (draws fluid from eye)drain aqueous fluid- anterior chamber paracentesis (carries risk of endophthalmitis)treat underlying cause to prevent CRAO in fellow eye
• f/u 1 month to r/o neovascularization
Central/Branch Retinal Vein Occlusion (CRVO/BRVO)
• an uncommon cause of blindness in the elderly, usually a manifestation of asystemic disease
• thrombus occurs within the lumen of the blood vessel
• two fairly distinct groupsvenous stasis/non-ischemic retinopathy
no RAPD ,VA approximately 20/80mild hemorrhage, few cotton wool spotsresolves spontaneously over weeks to monthsmay regain normal vision if macula intact
hemorrhagic/ischemic retinopathy
usually older patient with deficient arterial supplyRAPD, VA approximately 20/200, reduced peripheral visionmore hemorrhages, cotton wool spots, congestion poor visual prognosis
Complications • degeneration of retinal pigment epithelium• liquefaction of vitreous• neovascularization of retina and iris (secondary rubeosis), leading to secondary
glaucoma
Treatment • no treatment available to restore vision• treat underlying cause/ contributing factor• fluorescein angiography to determine extent of retinal non-perfusion = risk of neovascularization• retinal laser photocoagulation to reduce neovascularization and prevent
neovascular glaucoma
Retinal Detachment (RD)
• cleavage in the plane between the neurosensory retina and the retinal pigment epithelium (RPE)• three types
rhegmatogenousmost common type of RDcaused by a tear or hole in the neurosensory retina, allowingfluid from the vitreous to pass into the subretinal spacetears may be caused by posterior vitreous detachment (PVD),degenerative retinal changes, trauma or iatrogenically
incidence increases with advancing age, and more likely to occurspontaneously in high myopes, or after ocular surgery/traumatractional
caused by traction (due to vitreal, epiretinal or subretinal membrane) pulling the neurosensory retina away from the underlying RPEfound in conditions such as diabetic retinopathy, CRVO, sickle celldisease, retinopathy of prematurity (ROP), and ocular trauma
exudativecaused by damage to the RPE resulting in fluid accumulation in thesubretinal spacemain causes are intraocular tumours, posterior uveitis, central serousretinopathy
Clinical Features• sudden onset
• flashes of lightdue to mechanical stimulation of the retinal photoreceptors
• floatershazy spots in the line of vision which move with eye position, due to dropsof blood in the vitreous (blood vessels tear as the retina tears)
• curtain of blackness/peripheral field lossdarkness in one field of vision when the retina detaches in that area
• loss of central visionvisual acuity dramatically drops if the macula becomes detached
• decreased IOP (usually 4-5 mmHg lower than other, normal eye)• ophthalmoscopy: detached retina is grey with surface blood vessels, loss of red
Treatment • prophylactic: a symptomatic tear (flashes or floaters) can be sealed off with laser or
cryotherapy, with the goal of preventing progression to detachment• therapeutic
rhegmatogenous retinal detachmentscleral buckle (a band is secured on the outside of the globe that
indents the wall, thereby relieving tension on the retina around anytears/holes, allowing the tears/holes to remain sealed) pneumatic retinopexy (intraocular injection of air or an expandablegas in order to tamponade the retinal break) both above treatments are used in combination with localization ofretinal tears/holes and subsequent treatment with diathermy,cryotherapy or laser to create adhesions between the RPE and theneurosensory retinavitrectomy plus injection of silicone oil in cases of recurrentdetachments
tractional retinal detachment:vitrectomy +/- membrane removal/scleral buckling/injection ofintraocular gas as necessary
exudativetreatment of underlying cause
Complications • loss of vision, vitreous hemorrhage, recurrent retinal detachments• a retinal detachment should be considered an emergency, especially if the macula is
still attached• prognosis for visual recovery varies inversely with the amount of time the retina is
detached and whether the macula is attached or not
Age-Related Macular Degeneration (ARMD)
• leading cause of blindness in the western world, associated with increasing age,usually bilateral
• 10% of people > 65 years old have some degree of ARMD, female > male
• degenerative changes are concentrated at the macula thus only central vision is lost• peripheral vision (important for navigation) is maintained so sufferers can usuallymaintain an independant lifestyle
Classification • “Dry”/Non-Exudative ARMD
most common type of ARMD (90% of cases)slowly progressive loss of visual functiondrusen: pale, yellow-white deposits of membranous vesicles and collagendeposited between the retinal pigment epithelium (RPE) and Bruch’smembrane (area separating inner choroidal vessels from RPE)RPE atrophy: coalescence of depigmented RPE, clumps of focalhyperpigmentationmay progress to neovascular ARMD
• Neovascular (Exudative/”Wet”) ARMD10% of ARMD, but 80% of ARMD resulting in severe visual losschoroidal neovascularization: drusen predispose to breaks in Bruch’smembrane which cause subsequent growth and proliferation of choroidalcapillariesmay get serous detachment of overlying RPE and retina, hemorrhage andlipid precipitates into subretinal spacecan also get an elevated subretinal mass due to fibrous metaplasia ofhemorrhagic retinal detachmentleads to disciform scarring and severe central visual loss
Clinical Features• variable amount of progressive central visual loss• metamorphopsia (distorted vision characterized by straight parallel lines appearing
convergent or wavy) due to macular edema
Investigations• Amsler Grid: held at normal reading distance with glasses on, assesses macular function• Fluorescein angiography (FA): assess degree of neovascularization - pathologic new
vessels leak dye
Treatment • non-neovascular ARMD
monitor, Amsler grid allows patients to check for metamorphopsialow vision aids e.g. magnifiers, closed-circuit television
anti-oxidants, green leafy vegetables• neovascular ARMD
laser photocoagulation for neovascularization50% of choroidal neovascularization cannot be treated initiallyno definitive treatment for disciform scarringfocal laser for macular edema
photodynamic therapy (PDT) with verteporfino
IV injection of verteporfin followed by low intensity laser to area of choroidalneovascularization
• Treatment of Age Related Macular Degeneration with Photodynamic Therapy(TAP) Study Group indicated that for selected patients with subfoveal lesions inARMD with predominantly classic choroidal neovascularization, verteporfintreatment can reduce the risk of moderate vision loss for at least 1 year; thistherapy cannot stop or reverse vision loss in all patients with ARMD
• due to obstruction to aqueous drainage within the trabecular meshwork and itsdrainage into the canal of Schlemm
• insidious and asymptomatic, so screening is critical for early detection
Major Risk Factors• elevated intraocular pressure (> 21 mm Hg)• age: prevalence in 40yo is 1-2% and in 80yo 10%• black race• familial; polygenic (10x increased risk)
Minor Risk Factors• myopia• hypertension• diabetes• hypothyroidism• chronic topical ophthalmic steroid use on eyes in steroid responders – yearly eye
exams recommended if > 4 weeks steroid use• previous ocular trauma• anemia/hemodynamic crisis (ask about blood transfusions in past)
Clinical Features• asymptomatic initially• insidious, painless, gradual rise in IOP due to restriction of aqueous outflow• bilateral, but usually asymmetric• earliest signs are optic disc changes (safe to dilate pupil)
increased cup to disc ratio (vertical C/D > 0.6) orsignificant C/D asymmetry between eyes (> 0.2 difference)thinning, notching of the neuroretinal rimflame shaped disc hemorrhage
360 degrees of peripapillary atrophynerve fibre layer defectlarge vessels become nasally displaced
• visual field lossslow, progressive, irreversible loss of peripheral vision paracentral defects, arcuate scotoma and nasal step are characteristiclate loss of central vision if untreated
Treatment • principles: decrease IOP by increasing the drainage and/or decreasing the production
• 12% of all glaucoma cases• peripheral iris bows forward in an already susceptible eye with a shallow anterior
chamber obstructing aqueous access to the trabecular meshwork• sudden shifting forward of the lens-iris diaphragm = pupillary block, results in
inability of the aqueous to flow from the posterior chamber to the anterior chamber
and a sudden rise in IOP
Risk Factors• hyperopia: small eye, big lens – large lens crowds the angle• age > 70• female• family history• more common in Asians and Inuits• mature cataracts• shallow anterior chamber• pupil dilation (topical and systemic anticholinergics, stress, darkness)
Clinical Features • unilateral, but other eye predisposed• red, painful eye = RED FLAG• decreased visual acuity, vision acutely blurred from corneal edema• halo around lights• nausea and vomiting, abdominal pain• fixed mid-dilated pupil• corneal edema with conjunctival injection• marked increase in IOP even to palpation (> 40 mm Hg)• shallow anterior chamber, ± cells in anterior chamber
Complications • irreversible loss of vision if untreated, within hours to days• permanent peripheral anterior synechiae
Treatment • refer to ophthalmologist
topical steroids (not in primary care)laser iridectomy
• immediate treatment important to preserve vision prevent adhesions of peripheral iris to trabecular meshwork (peripheral anteriorsynechiae) resulting in permanent closure of angle
• medical treatment: see Ocular Medications miotic drops (pilocarpine) to reverse pupilary block§ IOP
topical beta-blockers
topical adrenergics topical cholinergics
o
pilocarpine 1-4% q15min, up to q5min
systemic carbonic anhydrase inhibitorso
IV acetazolamide 250-500mg systemic hyperosmotic agents
• pupil size is determined by the balance between the sphincter muscle and the dilatormuscle
• sphincter muscle is innervated by the parasympathetic nervous system (PNS)carried by CN III: pre- and post-ganglionic fibres synapse in ciliary ganglion,and use acetylcholine as the neurotransmitter
• dilator muscle is innervated by the sympathetic NSfirst order neuron = hypothalamus ’ brainstem ’ spinal cordsecond order/preganglionic neuron = spinal cord ’ sympathetic trunk viainternal carotid artery ’ superior cervical ganglion in neckthird order/postganglionic fibres originate in the superior cervical ganglion,neurotransmitter is noradrenaline
as a diagnostic test, 4% cocaine which prevents the re-uptake ofnoradrenaline, will cause dilatation of normal pupil, but not one withloss of sympathetic innervation (Horner’s Syndrome)
• denervation hypersensitivitywhen post-ganglionic fibres are damaged, understimulated end-organ developsan excess of receptor and becomes hypersensitive
• postganglionic parasympathetic lesions (Adie’s pupil) pupil will constrict with 0. 125% pilocarpine (cholinergic agonist), whereas
normal pupil will not• postganglionic sympathetic lesions (i.e. Horner’s Syndrome)
pupil will dilate with 0.125% adrenaline, whereas normal pupil will not. Thistest is used to differentiate between pre- and post-ganglionic lesions in Horner’ssyndrome
Local Disorders of Iris• posterior synechiae (adhesions between iris and lens) due to iritis and presents as an
abnormally shaped pupil margin• ischemic damage
i.e. post acute glaucomaischemic damage usually at 3 and 9 o’clock positions results in verticallyoval pupil that reacts poorly to light
Relative Afferent Pupillary Defect (RAPD)
• defect in visual afferent pathway anterior to optic chiasm• differential diagnosis: optic nerve compression, optic neuritis, large retinal detachment,
BRAO, CRAO, CRVO, advanced glaucoma• does not occur with media opacity e.g. corneal edema, cataracts• test: swinging flashlight
if light is shone in the affected eye, direct and consensual response tolight is decreased
if light is shone in the unaffected eye, direct and consensual response tolight is normalif the light is moved quickly from the unaffected eye to the affected eye,“paradoxical” dilation of both pupils occursuse ophthalmoscope with “+4” setting, using red reflex especially in patientswith dark iris
Etiology • In children: craniopharyngioma• In middle aged: pituitary mass• In elderly: meningioma
Homonymous Hemianopsia• a retrochiasmal lesion• the more congruent, the more posterior the lesion• check all hemiplegic patients for ipsilateral homonymous hemianopsia• e.g. left hemisphere ’ right visual field (VF) defect in both eyes
Internuclear Ophthalmoplegia
• lesion of medial longitudinal fasciculus (MLF)• damage to MLF ^ disrupts coordination between CN VI nucleus in pons and CN III
nucleus in mid brain ^ disrupts conjugate horizontal gaze• commonly seen in multiple sclerosis (MS)• loss of ipsilateral eye adduction• monocular nystagmus in contralateral abducting eye• other causes of INOP: brain stem infarction, tumours, AV malformations, Wernicke’s
encephalopathy and encephalitis
Nystagmus
• definition: rapid, involuntary, small amplitude movements of the eyes that arerhythmic in nature
• direction of nystagmus is defined by the rapid component of the eye movement• can be categorized by movement type (pendular, jerking, rotatory, coarse) or as
cular Manifestations of Systemic DiseaseO Diabetes Mellitus (DM)
• most common cause of blindness in young people in North America• blurring of distance vision with rise of blood sugar• consider DM if unexplained retinopathy, cataract, EOM palsy, optic neuropathy,
sudden change in refractive error• loss of vision due to
progressive microangiopathy, leading to macular edema progressive diabetic retinopathy ’ neovascularization ’ traction ’ retinaldetachment and vitreous hemorrhagerubeosis iridis (neovascularization of the iris) leading to neovascular glaucoma(poor prognosis)
Classification• non-proliferative: increased vascular permeability and retinal ischemia
dot and blot hemorrhagesmicroaneurysmshard exudates (lipid deposits)macular edema
• advanced non-proliferative (or pre-proliferative): non-proliferative findings plusvenous beading (in 2 of 4 retinal quadrants)intraretinal microvascular anomalies-IRMA (in 1 of 4 retinal quadrants)
IRMA: dilated, leaky vessels within the retinacotton wool spots (nerve fibre layer infarcts)
• proliferative 5% of patients with diabetes will reach this stageneovascularization: iris, disc, retina to vitreous
neovascularization of iris (rubeosis iridis) leading to neovascular glaucomavitreous hemorrhage from bleeding fragile new vessels, fibrous tissue cancontract causing tractional retinal detachmentincreased risk of severe visual loss
Screening Guidelines for Diabetic Retinopathy• Type I DM
screen for retinopathy beginning annually 5 years after disease onsetscreening not indicated before the onset of puberty
• Type II DMinitial examination shortly after diagnosis, then repeat annuallyif initial exam negative, repeat in 4 years, then annual exams
• pregnancyocular exam in 1st trimester, close follow-up throughout as pregnancy canexacerbate DR
gestational diabetics not at risk for retinopathy
Treatment • Diabetic Control and Complications Trial (DCCT)
tight control of blood sugar decreases frequency and severity of microvascularcomplications
• blood pressure control• focal laser for clinically significant macular edema• panretinal laser photocoagulation, for proliferative diabetic retinopathy, reduces
neovascularization, hence reducing the angiogenic stimulus from ischemic retina by decreasing retinal metabolic demand ^ reduces risk of blindness
• vitrectomy for vitreous hemorrhage and retinal detachment in proliferative diabeticretinopathy which is complicated by non-clearing vitreous hemorrhage or retinal
detachment• the diabetic retinopathy vitrectomy study indicated that early vitrectomy (before
hemorrhage) does not improve the visual prognosis
Lens • earlier onset of senile nuclear sclerosis and cortical cataract• may get hyperglycemic cataract, due to sorbitol accumulation (rare)
• sudden changes in refraction of lens: changes in blood glucose levels (poor control)may cause refractive changes by 3-4 diopters
Extra Ocular Muscle (EOM) Palsy• usually CN III infarct• pupil usually spared in diabetic CN III palsy, but get ptosis• may involve CN IV and VI• usually recover within few months
Optic Neuropathy• visual acuity loss due to infarction of optic disc/nerve
Multiple Sclerosis (MS)
• relapsing, progressive CNS disease characterized by disseminated patches ofdemyelination in the brain and spinal cord resulting in varied symptoms and signs
• many ocular manifestations
Clinical Features • 40% of patients with MS develop optic neuritis which results in blurred vision and
§ colour vision• central scotoma: because of damage to papillomacular bundle of retinal nerve fibres• diplopia: secondary to internuclear ophthalmoplegia (INO)• RAPD, ptosis, nystagmus, uveitis, optic atrophy, optic neuritis• white matter demyelinating lesions of optic nerve on MRI
Treatment • with optic neuritis, treatment with oral steroids leads to greater likelihood of getting
MS later on than treatment with IV steroids
Hypertension
• retinopathy is the most common ocular manifestation of hypertension• key features of chronic HTN retinopathy: AV nicking, blot retinal hemorrhages,
microaneurysms, cotton wool spots• key features of acute HTN retinopathy: retinal arteriolar spasm, superficial retinal
• typically monocular, lasting < 5-10 minutes• may be associated with paresthesia/weakness in contralateral limbs• Hollenhorst plaques (glistening microemboli seen at branch points of retinal arterioles)
Graves’ Disease
Clinical • dry eye• lid retractions• exophthalmos• retinal and optic nerve changes 2º to intraorbital pressure• exposure keratitis
Treatment • treat hyperthyroidism• maintain corneal hydration• manage diplopia, proptosis and compressive optic neuropathy by eyelid surgery
(lateral tarsorrhaphy), steroids (during acute phase), orbital radiation and surgicaldecompression of the orbit
Giant Cell (Temporal) Arteritis
• common in women > 60• clinical findings: abrupt monocular loss of vision; pain over the temporal artery• ischemic optic atrophy
50% lose vision in other eye if untreated
Diagnosis • temporal arterial biopsy + 6ESR (ESR can be normal, but likely 80-100 in first hour)
Treatment • high dose corticosteroid to relieve pain and prevent further ischemic episodes
Definition • reduction of best-corrected visual acuity not directly due to structural pathology
• cortical suppression of sensory input from an eye that is receiving blurred orconflicting visual information ^ disruption of the normal development of visual pathways in that eye ^ amblyopia
Detection • "Holler Test": young child upset if good eye is covered• quantitative visual acuity by age 3-4 years using picture charts and/or matching game
(Sheridan-Gardiner), testing each eye separately• not commonly treatable after age 8-10 years since the neural pathways for vision are
now formed• prognosis: 90% will have good vision restored and maintained if treated < 4 years old
Etiology and Management• strabismus
correct with glasses for accommodative esotropia (50% of children experience
relief of their esotropia with glasses and will not require surgery)occlusion of unaffected eye forces brain to use previously strabismic eye, to bring vision in previously suppressed eye to normal before surgerysurgery: recession (weakening) = moving muscle insertion further back on theglobe; or resection (strengthening) = shortening the muscle botulinum toxin for single muscle weakeningafter ocular alignment is restored (glasses, surgery, botulinum toxin), patching isfrequently necessary to maintain vision until approximately age 8
• refractive errorsanisometropia (amblyopia usually in the more hyperopic eye)causes the less hyperopic eye to receive a clear image while the more hyperopiceye receives a blurred image so that its optic pathway does not developnormallytreat with glasses to correct refractive errors patching is required if visual acuity difference persists after 4-8 weeks ofusing glasses
• deprivation amblyopiaocclusion due to ptosis, cataract, retinoblastoma, corneal opacityocclusion amblyopia: prolonged patching of good eye may cause it to becomeamblyopic
General Treatment• correct the underlying cause• occlusion therapy (patching) or optical degradation therapy (atropine) of the good eye
• caused by blunt 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 slit lamp exam,ophthalmoscopy
• if VA normal or slightly reduced, globe less likely to be perforated• if VA reduced, may be perforated globe, corneal abrasion, lens dislocation, retinal tear• bone fractures
blow out fracture: restricted EOM, diplopia, enopthalmos (sunken eye)ethmoid fracture: subcutaneous emphysema of lid
• lids: swelling, laceration, emphysema• conjunctiva: subconjunctival hemorrhage• cornea: abrasions - detect with fluorescein staining and cobalt blue filter in
• include ruptured globe ± prolapsed iris, intraocular foreign body (FB)• r/o intraocular FB; especially if history of “metal striking metal” Orbit CT• initial management: refer immediately!!
ABCsdon’t press on eyeball!check vision, diplopiaapply rigid eye shield to minimize further traumakeep head elevated 30-45 degrees to keep IOP downkeep NPO
hemical BurnsC • alkali burns have a worse prognosis vs. acid burns because acids coagulate tissue and
inhibit further corneal penetration• poor prognosis if cornea opaque, likely irreversible stromal damage• even with a clear cornea initially, alkali burns can progress for weeks (thus, very
guarded prognosis)
Treatment • irrigate at site of accident immediately, with water or buffered solution
IV drip for at least 20-30 minutes with eyelids retracted in emergencydepartment
• do not attempt to neutralize because the heat produced by the reaction will damagethe cornea
• cycloplegic drops to decrease iris spasm (pain) and prevent secondary glaucoma (due
to posterior synechiae formation)• topical antibiotics and patching• topical steroids (not in primary care) to decrease inflammation, use for less than
two weeks (in the case of a persistent epithelial defect)
low-Out FractureB • blunt trauma causing fracture of orbital floor and orbital contents to herniate
into maxillary sinus• orbital rim remains intact• inferior rectus and/or inferior oblique muscles may be incarcerated at fracture site• infraorbital nerve courses along the floor of the orbit and may be damaged
Clinical Features• pain and nausea at time of injury• diplopia, restriction of EOM• infraorbital and upper lip paresthesia (CN V2)• enophthalmos (sunken eye), periorbital ecchymoses
Investigations
• plain films: Waters view and lateral• CT: anteroposterior and coronal view of orbits
Treatment • refrain from coughing, blowing nose• systemic antibiotics may be indicated• surgery if fracture > 50% orbital floor, diplopia not improving, or enophthalmos
> 2 mm• may delay surgery if the diplopia improves
Fluorescein Dye• water soluble orange-yellow dye• green under cobalt blue light - ophthalmoscope or slit lamp• absorbed in areas of epithelial loss (ulcer or abrasion) ; note also stains mucus and
contact lenses
Anesthetics • e.g. proparacaine HCl 0.5%, tetracaine 0.5%• indications: removal of foreign body and sutures, tonometry, examination of painful
cornea• toxic to corneal epithelium (inhibit mitosis and migration) and can lead to corneal
ulceration and scarring with prolonged use, therefore NEVER prescribe
Mydriatics• dilate pupils
• two classescholinergic blockingdilation plus cycloplegia (lose accommodation) by paralysis of irissphincter and the ciliary bodye.g. mydriacyl (Tropicamide)indications: refraction, ophthalmoscopy, therapy for iritis
adrenergic stimulatingstimulate pupillary dilator muscles, no effect on accommodatione.g. phenylephrine HCl 2.5% (duration: 30-40 minutes)usually used with tropicamide for additive effectsside effects: hypertension, tachycardia, arrhythmias
Table 6. Mydriatic Cycloplegic Drugs and Duration of Action