ophthalmology pda

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 editorsMaja Segedi, EBM editor

Dr. Lawrence Weisbrod, staff editor

Common Complaints

Ocular Emergencies

The Ocular Examination

Optics

The Orbit

Lacrimal Apparatus

Lids and Lashes

Conjunctiva

Cornea

The Uveal Tract

Lens Vitreous

Retina

Glaucoma

Pupils

Neuro-Ophthalmology

Malignancies

Ocular Manifestations of Systemic Diseases

Strabismus

Pediatric Ophthalmology

Trauma

Ocular Medications



Common Complaints

Acute Loss of Vision (occurring in seconds to days)

• trauma/foreign body

• corneal edema

• hyphema• acute angle-closure glaucoma

• vitreous hemorrhage

• retinal detachment

• acute macular lesion

• retinal artery/vein occlusion

• optic neuritis

• temporal arteritis

• anterior ischemic optic neuropathy (AION)

• occipital infarction/hemorrhage

• cortical blindness

• functional

Chronic Loss of Vision (occurring over weeks to months)

• refractive error• corneal dystrophy, scarring, edema

• cataract

• glaucoma

• age-related macular degeneration (ARMD)

• diabetic retinopathy

• retinal vascular insufficiency

• compressive optic neuropathy (intracranial mass, orbital mass)

• intraocular neoplasm

• retinitis pigmentosa (RP)

• medication-induced

Transient Loss of Vision (lasting seconds to hours)

• transient ischemic attack (TIA)

• migraine• papilledema

Red Eye

• lids/orbit/lacrimal system

hordeolum/chalazion

blepharitis

foreign body/laceration

dacryocystitis/dacryoadenitis

preseptal/orbital cellulitis

• conjunctiva/sclera

subconjunctival hemorrhage

conjunctivitis

dry eyes

pterygium/pinguecula

episcleritis/scleritis

• cornea

foreign body/laceration

ßeratitis

abrasion

ulcer

• anterior chamber

iritis

acute angle-closure glaucoma

hyphema

• endophthalmitis



Ocular Pain

• trauma/foreign body

• keratitis

• corneal abrasion, corneal ulcer

• acute angle-closure glaucoma

• acute uveitis

• scleritis, episcleritis

• optic neuritis• ocular migraine

• herpes zoster prodrome

• differentiate from ocular ache: eye fatigue (asthenopia)

Floaters

• vitreous syneresis

• posterior vitreous detachment (PVD)

• vitreous hemorrhage

• retinal tear/detachment

Flashes of Light (Photopsia)

• posterior vitreous detachment (PVD)

• retinal tear/detachment

• migraine

Photophobia (Severe Light Sensitivity)

• keratitis

• corneal abrasion, corneal ulcer


• iritis

• migraine

• meningitis, encephalitis

Diplopia (Double Vision)

• binocular diplopia: strabismus, CN palsy (III,IV,VI), myasthenia gravis, muscle

restriction/entrapment, thyroid ophthalmopathy

• monocular diplopia: refractive error, strands of mucous in tear film, keratoconus,

cataract, dislocated lens

Ocular Problems in the Elderly

• presbyopia

• dry eyes

• epiphora

• ptosis

• cataracts

• age-related macular degeneration

• retinal artery/vein occlusion

• temporal arteritis (Arteritic Ischemic Optic Neuropathy)

Ocular Problems in Contact Lens Wearer

• superficial punctate keratitis (SPK)/dry eyes

(solution hypersensitivity, tight lens syndrome)

• corneal abrasion• giant papillary conjunctivitis

• sterile corneal infiltrates (immunologic)

• infected ulcers (Pseudomonas, Acanthamoeba)



Ocular Emergencies

These Require Urgent Consultation to an Ophthalmologist for Management

• intraocular foreign body

• lid/globe lacerations

• corneal ulcer

• gonococcal conjunctivitis• orbital cellulitis

• chemical burns

• acute iritis


• central retinal artery occlusion (CRAO)

• retinal detachment (especially macula threatening)

• endophthalmitis

• temporal arteritis



The Ocular Examination

Visual Acuity - Distance

Colour Vision

Visual Fields

Pupils

Anterior Chamber DepthExtraocular Muscles

Alignment

Movement

• 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

conjunctiva and sclera

cornea

iris

anterior chamber (for depth, cells, and flare)

lens

anterior vitreous

Tonometry

Ophthalmoscopy/Fundoscopy

• contraindications to pupillary dilatation:

shallow anterior chamber

iris-supported anterior chamber lens implant

potential neurologic abnormality requiring pupil evaluation

use caution with cardiovascular disease - mydriatics may cause tachycardia



Optics

Emmetropia

• no refractive error

Myopia

• “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



lenses)

Astigmatism

• 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



The Orbit

Preseptal Cellulitis

• 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



Lacrimal ApparatusDry Eye Syndrome (Keratoconjunctivitis Sicca)

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



Lids and LashesPtosis

•

drooping of upper eyelid

Etiology• aponeurotic: disinsertion or dehiscence of levator aponeurosis

most common causeassociated with advancing age, trauma, surgery, pregnancy, chronic lidswelling

• mechanicaleyelid prevented from opening completely by mass or scarring

• myogenic poor levator function associated with myasthenia gravis, myotonicdystrophy

• neurogenicCN III palsyHorner’s syndrome

• congenital•

pseudoptosis (e.g. dermatochalasis, enophthalmos, contralateral exophthalmos)

Treatment • treat underlying cause• surgery

Ectropion

• lid margin turns outward from globe causing tearing and possibly exposurekeratitis

Etiology • involutional (weak orbicularis oculi)• paralytic (CN VII palsy)• cicatricial (burns, trauma, surgery)• mechanical (lid edema, tumour, herniated fat)• congenital

Treatment • topical lubrication, surgery

Blepharitis

• inflammation of lid margins

Etiology • staphylococcal (S. aureus): ulcerative, dry scales• seborrheic: no ulcers, greasy scales

Clinical Features• itching, tearing, foreign body sensation• thickened, red lid margins, crusting, discharge with pressure on lids

(“toothpaste sign”)

Complications • recurrent chalazia• conjunctivitis• keratitis (from poor tear film)• corneal ulceration and neovascularization

Treatment • warm compresses and lid scrubs with diluted “baby shampoo” (diluted to 25%)• topical or systemic antibiotics as needed



ConjunctivaPterygium

• 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

Conjunctivitis

Etiology• infectious bacterial, viral, chlamydial, fungal, parasitic

• 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)



• proper hygiene is very important• may develop corneal epithelial defects and subepithelial infiltrates requiring specific

treatment

CHLAMYDIAL CONJUNCTIVITIS• caused by Chlamydia trachomatis (various serotypes)• affects neonates on day 3-5, sexually active people, etc.

• causes trachoma, inclusion conjunctivitis, lymphogranuloma venereum

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

Lymphogranuloma Venereum (serotype L)• conjunctival granulomas, interstitial keratitis, lymphadenopathy, fever, malaise• treatment: systemic tetracycline

ALLERGIC CONJUNCTIVITIS

Atopic • associated with rhinitis, asthma, dermatitis• small papillae, chemosis, thickened, erythematous lids, corneal neovascularization• treatment: cool compresses, antihistamine, mast cell stabilizer

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)



Cornea

Foreign Body

• foreign material in or on cornea

• 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

Complications • infection, ulceration, recurrent erosion, secondary iritis

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

keratitis or iritis



Herpes Zoster Keratitis

• dermatitis of the forehead (the CN V1 territory) involves the globe in 1/2 to 3/4 ofcases

• Hutchinson’s sign: if tip of nose is involved (nasociliary branch of V1) then eye will beinvolved in 1/2 of cases

• if no nasal involvement, the eye is involved in 1/3 of patients

Clinical Features• pain, tearing, photophobia, red eye• corneal edema, pseudodendrite, superficial punctate keratitis• corneal hypoesthesia

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

Treatment • attempt correction with spectacles or contact lens• penetrating keratoplasty (corneal transplant) 90% successful• post-operative complications: endophthalmitis, graft rejection, graft dehiscence



The Uveal Tract• uveal tract = iris, ciliary body, and choroid• vascularized, pigmented middle layer of the eye, between the sclera and the retina

Uveitis• may involve one or all three parts of the tract• idiopathic or associated with autoimmune, infectious, granulomatous,

malignant causes• should be managed by an ophthalmologist

Anterior Uveitis/Iritis

• inflammation of iris, usually with cyclitis (inflammation of ciliary body),when both = iridocyclitis

• usually unilateral

Etiology

• usually idiopathic• connective tissue diseases:HLA-B27 (usually anterior uveitis): Reiter’s syndrome, ankylosing spondylitis

(AS), psoriasis, inflammatory bowel disease (IBD) Non-HLA-B27: Juvenile rheumatoid arthritis (JRA)

• infectious: syphilis, Lyme disease, toxoplasmosis, TB, HSV, herpes zoster• other: sarcoidosis, trauma, large abrasion

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

inflammatory glaucoma

Complications • inflammatory glaucoma• posterior synechiae

adhesions of posterior iris to anterior lens capsuleindicated by an irregularly shaped pupilif occur 360º, entraps aqueous in posterior chamber, iris bows forward “iris bombe” ^ angle closure glaucoma

• peripheral anterior synechiae (PAS) (rare): adhesions of iris to cornea ’ glaucoma• cataracts• band keratopathy (with chronic iritis)

superficial corneal calcification keratopathy• macular edema with chronic iritis

Treatment (by Ophthalmologists)• mydriatics: dilate pupil to prevent formation of posterior synechiae and to decrease

pain from ciliary spasm• steroids: topical, subconjunctival or systemic• systemic analgesia• medical workup may be indicated to determine etiology



LensCataracts

• any opacity of the lens• most common cause of reversible blindness

Etiology• aquired (acquired)

age-related (over 90% of all 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 promptly to prevent amblyopia

Clinical Features• gradual, painless, progressive decrease in visual acuity

• glare, dimness, haloes around lights at night, monocular diplopia

• “second sight” phenomenon – patient is more myopic than previously noted,due to increased refractive power of the lens (in nuclear sclerosis only)

cataract increases power of lens causing artificial myopia – patient may readwithout previously needed reading glasses

• diagnose by slit-lamp exam, and by noting changes in red reflex using

ophthalmoscope

• may impair view of retina during fundoscopy

Treatment • medical: attempt correction of refractive error

• surgical: definitive treatment is via surgical removal of cataractindications for surgery

to improve visual function in patients whose visual loss leads to

functional impairment (patients may be inclined to postpone surgery

as long as one eye has sufficient vision)

to aid management of other ocular disease (e.g. cataract that prevents

adequate retinal exam or laser treatment of diabetic retinopathy)

congenital or traumatic cataracts

phacoemulsification

most commonly used surgical technique

ultrasonic needle is used to emulsify and aspirate nucleus and cortex

synthetic intraocular lens (IOL) is placed in bag formed by empty

capsule

post-operative complications

retinal detachment, endophthalmitis, dislocated IOLup to 50% of patients get posterior capsular opacification, which is

treated with YAG laser

Prognosis • excellent if not complicated by other ocular disease



itreousV

Posterior Vitreous Detachment (PVD)

Etiology • normal ageing process of vitreous liquification (syneresis)

• liquid vitreous moves between posterior vitreous gel and retina• vitreous is peeled away and separates from the retina

Clinical Features• floaters, flashes of light

Complications• traction to areas of abnormal vitreoretinal adhesions may cause retinal

tears/detachment• retinal tears/detachment may cause vitreous hemorrhage if tear bridges blood

vessel• complications more common in high myopes and following ocular trauma (blunt

or perforating)

Treatment • acute onset of PVD requires a dilated fundus exam to rule out retinal tears/

detachment• no specific treatment available for floaters/flashes of light symptoms



Retina

Central Retinal Artery Occlusion (CRAO)

Etiology

• 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

topical -blockersinhaled oxygen – carbon dioxide mixtureIV Diamox(tm) (carbonic anhydrase inhibitor)

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

Predisposing Factors• arteriosclerotic vascular disease

• hypertension• diabetes mellitus• glaucoma• hyperviscosity (e.g. polycythemia rubra vera, sickle-cell disease, lymphoma,

leukemia)• drugs (OCP, duretics)

Clinical Features• painless, monocular, gradual or sudden visual loss• +/- relative afferent pupillary defect (RAPD)• fundoscopy

“blood and thunder” appearancediffuse retinal hemorrhages, cotton-wool spots, venous engorgement,swollen optic disc, macular edema



• 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

reflex• +/- relative afferent pupillary defect (RAPD)



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

Risk Factors• female



• increased age• family history• smoking

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



GlaucomaPrimary Open Angle Glaucoma (POAG)

• most common form, > 55% of all glaucoma cases

• 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

of aqueous• medical treatment:

increases aqueous outflowtopical cholinergicstopical prostaglandin agonist

topical alpha-adrenergicsdecreases aqueous production

topical beta-blockerstopical and oral carbonic anhydrase inhibitortopical alpha-adrenergics

• laser trabeculoplasty, cyclophotocoagulation = selective destruction of ciliary body (forrefractory cases)

• microsurgery: trabeculectomy (filtering bleb), tube shunt placement (shunts fluid toreservoir under conjunctiva)

• optic nerve head examination, IOP measurement and visual field testing to monitorcourse of disease



Primary Angle Closure Glaucoma

• 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

o

oral glycerine, 1.0g/kgo

mannitol IV 1.0g/kg



upilsP

Pupil Abnormalities

Innervation

• 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



Neuro-Ophthalmology

Visual Field Defects

• lesions in the visual system have characteristic pattern losses• several tests used: confrontation (screening), tangent screen, Humphrey fields

(computerized automated perimetry), Goldman perimetry

Bitemporal Hemianopsia

• a chiasmal lesion

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

normal vs. pathological



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)

DIABETIC RETINOPATHY (DR)• background:

altered vascular permeabilityretinal vessel closure

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

hemorrhage, cotton-wool spots, optic disc edema Table 5. Keith-Wagener-Barker Classification

Group 1 Mild to moderate narrowing or sclerosis of the arteioles

Group 2 Moderate to marked narrowing of the aterioles

Local and/or generalized narrowing of arterioles

Exaggeration of the light reflexAnteriovenous crossing changes

Group 3 Retinal arteriolar narrowing and focal constriction

Retinal edema

Cotton-wool patches

Hemorrhage

Group 4 As for Group 3, plus papilledema

TIA/Amaurosis Fugax

• sudden, transient blindness from intermittent vascular compromise; ipsilateral carotidmost frequent embolic source



• 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



Pediatric OphthalmologyAmblyopia

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



Ocular TraumaBlunt Trauma

• 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

ophthalmoscope or slit lamp• anterior chamber: assess depth, hyphema, hypopyon• iris: prolapse, iritis• lens: cataract, dislocation• retinal tear/detachment

Penetrating Trauma

• 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



Ocular Medications

Topical Ocular Diagnostic Drugs

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

Drugs Duration of action

Tropicamide (Mydriacyl) 0.5%, 1% 4-5 hours

Cyclopentolate HCL 0.5%, 1% 3-6 hours

Homatropine HBr 1%, 2% 3-7 days

Atropine sulfate 0.5%, 1% 1-2 weeks

Scopolamine HBr 0.25%, 5% 1-2 weeks



Glaucoma Medications

Beta-Adrenergic Blockers• decrease aqueous humour production

• beta-blockers e.g. timolol (Timoptic), levobunolol (Betagan), metapranolol (Apotex),

betaxolol (Betoptic), carteolol (Teoptic)• systemic side effects: bronchospasm, exacerbation of congestive heart failure,

bradycardia, heart block, hypotension, impotence, depression

Cholinergic Stimulating• increases aqueous outflow• e.g. pilocarpine (Pilopine), carbachol (Isopto Carbachol)

• side effects: miosis, brow ache, decreased night vision, headache, increased GI motility,decreased heart rate

Adrenergic Stimulating• decrease aqueous production and increase outflow

• e.g. epinephrine HCl, dipivifrin, brimonidine (Alphagan), apraclonidine (Lopidine)• side effects: contact allergy, hypotension in children

Carbonic Anhydrase Inhibitor• decrease aqueous production

• e.g. oral acetazolamide (Diamox), topical dorzolamide (Trusopt), topical brinzolamide

(Azopt)• side effects: renal calculi, nausea, vomiting, diarrhea, weight loss, aplastic anemia, bone

marrow suppression, systemic acidosis• side effects generally absent with topical preparations

Prostaglandin Agonists• improves uveoscleral outflow

• e.g. latanoprost (Xalatan), travaprost (Travatan), bimatoprost (Lumigun)• side effects: iris colour change, lash growth, trichiasis



Topical Ocular Therapeutic Drugs

NSAIDs• used for less serious chronic inflammatory conditions

• decreased risk of complications

• e.g. Ketorolac (Acular) drops, Diclofenac (Voltaren) drops

Anti-Histamines• used to relieve red and itchy eye, often in combination with decongestants

• sodium cromoglycate (stabilizes most all membranes)

Corticosteroids• never prescribed by primary care physician unless emergency indications

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

prednisolone (Predsol 0.5%, Pred Forte 1%), rimexolone (Velox)

• complications:

potentiates herpes simplex keratitis and fungal keratitis as well as masking

symptoms (within days)

posterior subcapsular cataract (within months)

increased IOP, more rapidly in steroid responders (within weeks)

Decongestants• weak adrenergic stimulating drugs (vasoconstrictor)

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

• rebound vasodilation with over use; rarely can precipitate angle closure glaucoma

Antibiotics

• indications: bacterial conjuntivitis, keratitis, or blepharitis

• commonly as topical drops or ointments, may give systemically

• e.g. sulfonamide (sodium sulfacetamide, sulfisoxazole), gentamicin (Garamycin),

erythromycin, tetracycline, bacitracin, polymyxin B



Ocular Drug ToxicityAmiodarone Corneal microdeposits and superficial keratopathy

Atropine, Benztropine, Benzhexol Pupillary dilation (risk of angle closure glaucoma)

Chloroquine, hydroxychloroquine Bull’s eye lesion at macula, vortex keratopathy

Chlorpromazine Anterior subcapsular cataract

Contraceptive Pills Decreased tolerance to contact lenses, Migraine, Optic

neuritis, Central vein occlusion

Digitalis Yellow vision, Blurred vision

Ethambutol Optic neuropathy

Haloperidol (Haldol) Oculogyric crises, Blurred vision

Indomethacin Superficial keratopathy

Isoniazid Optic neuropathy

Nalidixic Acid Papilloedema

Steroids Posterior subcapsular cataracts, Glaucoma, Papilloedema

(systemic steroids), Increased severity of HSV infections

(geographic ulcers), Predisposition to fungal infections

Sulphonamides, NSAIDS Stevens-Johnson syndrome

Tetracycline Papilloedema

Thioridazine Pigmentary degeneration of retina

Vitamin A Intoxication Papilloedema Vitamin D Intoxication Band keratopathy

Table 7. Drugs with Ocular Toxicity

ophthalmology pda

Documents