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 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 eratitis 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 acute angle-closure glaucoma 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, keratoconu s, 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 acute angle-closure glaucoma 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 Depth Extraocular Muscles Alignment Movement Cranial Nerve III que Cranial Nerve IV Cranial Nerve VI 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 vitreou s lids (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 superior rectus, medial rectus, inferior rectus, inferior obli superior oblique lateral rectus

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 abili

ty 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 accommodative ability near images cannot be focused onto retina (focus is behind retina as in hyperopi a)

Clinical Features if initially emmetropic, person begins to hold reading material further away, bu t 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 ve

lenses for reading

reading glasses will blur distance vision (avoided by using bifocal or progressi

lenses) Astigmatism

light rays not refracted uniformly in all meridians due to non-spherical surface of cornea or non-spherical lens (eg. football-shape d) two types of astigmatism regular - curvature uniformly different in meridians right angles to each other irregular - distorted cornea, caused by injury or keratoconus (cone-shaped cornea)

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 Streptococc i 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 Apparatus Dry 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, Sjgren 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 Lashes Ptosis

drooping of upper eyelid

Etiology aponeurotic: disinsertion or dehiscence of levator aponeurosis most common cause associated with advancing age, trauma, surgery, pregnancy, chronic lid swelling mechanical eyelid prevented from opening completely by mass or scarring myogenic poor levator function associated with myasthenia gravis, myotonic dystrophy neurogenic CN III palsy Horner 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 exposure keratitis

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 topical or systemic antibiotics as needed

(diluted to 25%)

Conjunctiva Pterygium

fibrovascular triangular encroachment of epithelial tissue onto the cornea, usua lly 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-infectious allergy: atopic, seasonal, giant papillary conjunctivitis (in contact-lens wear ers) toxic: irritants, dust, smoke, irradiation secondary to another disorder such as dacryocystitis, dacryoadenitis, celluliti s, 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 conjunctiva found in viral and chlamydial conjunctivitis papillae fibrovascular elevations of the conjunctiva with central network of finely branching vessels nonspecific; found in giant papillary conjunctivitis (GPC) and vernal conjunctivitis

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 treat ment

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 s pecific 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 ulce ration 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 neovascularizati on 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 ulc ers, 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 stain s with fluorescein, corneal edema, anterior chamber cell/flare

Complications abrasion, infection, scarring, rust ring, secondary iritis Treatment 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), contac t 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, eyeli d 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 acyc lovir 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 of cases Hutchinson s sign: if tip of nose is involved (nasociliary branch of V1) then eye will be involved 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 ophthalmol ogist) 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 reti na 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, tenderne ss of

the globe, brow ache (ciliary muscle spasm), decreased visual acuity, tearing ciliary flush (perilimbal conjunctival injection), miosis (spasm of sphincter mu scle) anterior chamber cells (WBC in anterior chamber due to anterior segment (protein precipitates in anterior chamber secondary

inflammation) and flare

to inflammation), hypopyon (collection of neutrophilic exudates inferiorly in t he 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 capsule indicated by an irregularly shaped pupil if occur 360, entraps aqueous in posterior chamber, iris bows forward bombe ^ angle closure glaucoma peripheral anterior synechiae (PAS) (rare): adhesions of iris to cornea cataracts band keratopathy (with chronic iritis) superficial corneal calcification keratopathy macular edema with chronic iritis glaucoma iris

Treatment (by Ophthalmologists) mydriatics: dilate pupil to prevent formation of posterior synechiae and to decr ease pain from ciliary spasm steroids: topical, subconjunctival or systemic systemic analgesia

medical workup may be indicated to determine etiology

Lens Cataracts

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 without previously needed reading glasses diagnose by slit-lamp exam, and by noting changes in red reflex using ophthalmoscope patient may read

may impair view of retina during fundoscopy

Treatment medical: attempt correction of refractive error surgical: definitive treatment is via surgical removal of cataract indications 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 IOL up to 50% of patients get posterior capsular opacification, which is treated with YAG laser

Prognosis excellent if not complicated by other ocular disease

itreous V 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, valvular disease) 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 fu gax) fundoscopy cherry-red spot at centre of macula (visualization of unaffected highly vascular choroid through the thin fovea) retinal pallor narrowed arterioles, boxcarring (segmentation of blood in arteries) cotton-wool spots (retinal infarcts) cholesterol emboli (Hollenhorst plaques) - usually located at arteriole bifurcations after ~ 6 weeks: cherry-red spot recedes and optic disc pallor becomes evident

Treatment OCULAR EMERGENCY: attempt to restore blood flow within 2 hours 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, release for 10 sec, repeat for 5 minutes) to dislodge embolus decrease intraocular pressure topical -blockers inhaled oxygen carbon dioxide mixture

IV Diamox(tm) (carbonic anhydrase inhibitor) IV mannitol (draws fluid from eye) drain aqueous fluid- anterior chamber paracentesis (carries risk of endophthalm itis) 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 a systemic 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 appearance

diffuse retinal hemorrhages, cotton-wool spots, venous engorgement, swollen optic disc, macular edema

two fairly distinct groups venous stasis/non-ischemic retinopathy no RAPD ,VA approximately 20/80 mild hemorrhage, few cotton wool spots resolves spontaneously over weeks to months may regain normal vision if macula intact hemorrhagic/ischemic retinopathy usually older patient with deficient arterial supply RAPD, VA approximately 20/200, reduced peripheral vision more 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 n eovascularization 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 ep ithelium (RPE)

three types rhegmatogenous most common type of RD caused by a tear or hole in the neurosensory retina, allowing fluid from the vitreous to pass into the subretinal space tears may be caused by posterior vitreous detachment (PVD), degenerative retinal changes, trauma or iatrogenically incidence increases with advancing age, and more likely to occur spontaneously in high myopes, or after ocular surgery/trauma tractional caused by traction (due to vitreal, epiretinal or subretinal membrane) pulling the neurosensory retina away from the underlying RPE found in conditions such as diabetic retinopathy, CRVO, sickle cell disease, retinopathy of prematurity (ROP), and ocular trauma exudative caused by damage to the RPE resulting in fluid accumulation in the subretinal space main causes are intraocular tumours, posterior uveitis, central serous retinopathy

Clinical Features sudden onset flashes of light due to mechanical stimulation of the retinal photoreceptors floaters hazy spots in the line of vision which move with eye position, due to drops of blood in the vitreous (blood vessels tear as the retina tears) curtain of blackness/peripheral field loss darkness in one field of vision when the retina detaches in that area loss of central vision

visual 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 la ser or cryotherapy, with the goal of preventing progression to detachment therapeutic rhegmatogenous retinal detachment scleral buckle (a band is secured on the outside of the globe that indents the wall, thereby relieving tension on the retina around any tears/holes, allowing the tears/holes to remain sealed) pneumatic retinopexy (intraocular injection of air or an expandable gas in order to tamponade the retinal break) both above treatments are used in combination with localization of retinal tears/holes and subsequent treatment with diathermy, cryotherapy or laser to create adhesions between the RPE and the neurosensory retina vitrectomy plus injection of silicone oil in cases of recurrent detachments tractional retinal detachment: vitrectomy +/- membrane removal/scleral buckling/injection of intraocular gas as necessary exudative treatment 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 retin a 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 usua lly maintain an independant lifestyle

Classification Dry /Non-Exudative ARMD most common type of ARMD (90% of cases) slowly progressive loss of visual function drusen: pale, yellow-white deposits of membranous vesicles and collagen deposited between the retinal pigment epithelium (RPE) and Bruch s membrane (area separating inner choroidal vessels from RPE) RPE atrophy: coalescence of depigmented RPE, clumps of focal hyperpigmentation may progress to neovascular ARMD

Neovascular (Exudative/ Wet ) ARMD 10% of ARMD, but 80% of ARMD resulting in severe visual loss choroidal neovascularization: drusen predispose to breaks in Bruch s membrane which cause subsequent growth and proliferation of choroidal capillaries may get serous detachment of overlying RPE and retina, hemorrhage and lipid precipitates into subretinal space

can also get an elevated subretinal mass due to fibrous metaplasia of hemorrhagic retinal detachment leads 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 appear ing convergent or wavy) due to macular edema

Investigations Amsler Grid: held at normal reading distance with glasses on, assesses macular f unction Fluorescein angiography (FA): assess degree of neovascularization - pathologic n ew vessels leak dye

Treatment non-neovascular ARMD monitor, Amsler grid allows patients to check for metamorphopsia low vision aids e.g. magnifiers, closed-circuit television .. anti-oxidants, green leafy vegetables neovascular ARMD laser photocoagulation for neovascularization 50% of choroidal neovascularization cannot be treated initially no definitive treatment for disciform scarring focal laser for macular edema .. photodynamic therapy (PDT) with verteporfin o IV injection of verteporfin followed by low intensity laser to area of choroid al neovascularization

Treatment of Age Related Macular Degeneration with Photodynamic Therapy (TAP) Study Group indicated that for selected patients with subfoveal lesions i n ARMD with predominantly classic choroidal neovascularization, verteporfin treatment can reduce the risk of moderate vision loss for at least 1 year; this therapy cannot stop or reverse vision loss in all patients with ARMD

Glaucoma Primary Open Angle Glaucoma (POAG)

most common form, > 55% of all glaucoma cases due to obstruction to aqueous drainage within the trabecular meshwork and its drainage 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 exams recommended if > 4 weeks steroid use previous ocular trauma anemia/hemodynamic crisis (ask about blood transfusions in past) yearly eye

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) or significant C/D asymmetry between eyes (> 0.2 difference) thinning, notching of the neuroretinal rim flame shaped disc hemorrhage 360 degrees of peripapillary atrophy nerve fibre layer defect large vessels become nasally displaced visual field loss slow, progressive, irreversible loss of peripheral vision paracentral defects, arcuate scotoma and nasal step are characteristic late loss of central vision if untreated

Treatment principles: decrease IOP by increasing the drainage and/or decreasing the produc tion of aqueous medical treatment: increases aqueous outflow topical cholinergics topical prostaglandin agonist topical alpha-adrenergics decreases aqueous production topical beta-blockers topical and oral carbonic anhydrase inhibitor topical alpha-adrenergics laser trabeculoplasty, cyclophotocoagulation = selective destruction of ciliary body (for refractory cases) microsurgery: trabeculectomy (filtering bleb), tube shunt placement (shunts flui d to reservoir under conjunctiva)

optic nerve head examination, IOP measurement and visual field testing to monito r course of disease

Primary Angle Closure Glaucoma

12% of all glaucoma cases peripheral iris bows forward in an already susceptible eye with a shallow anteri or 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 cha mber and a sudden rise in IOP

Risk Factors hyperopia: small eye, big lens age > 70 female family history more common in Asians and Inuits mature cataracts shallow anterior chamber pupil dilation (topical and systemic anticholinergics, stress, darkness) large lens crowds the angle

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 anterio r synechiae) 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 inhibitors o IV acetazolamide 250-500mg .. systemic hyperosmotic agents o oral glycerine, 1.0g/kg o mannitol IV 1.0g/kg

upils P Pupil Abnormalities

Innervation pupil size is determined by the balance between the sphincter muscle and the dil ator muscle 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 NS first order neuron = hypothalamus brainstem spinal cord sympathetic trunk via

second order/preganglionic neuron = spinal cord internal carotid artery

superior cervical ganglion in neck

third order/postganglionic fibres originate in the superior cervical ganglion, neurotransmitter is noradrenaline as a diagnostic test, 4% cocaine which prevents the re-uptake of noradrenaline, will cause dilatation of normal pupil, but not one with loss of sympathetic innervation (Horner s Syndrome) denervation hypersensitivity when post-ganglionic fibres are damaged, understimulated end-organ develops an 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. This test is used to differentiate between pre- and post-ganglionic lesions in Horne r s

syndrome

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 glaucoma ischemic damage usually at 3 and 9 o clock positions results in vertically oval 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 d etachment, 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 to light is decreased if light is shone in the unaffected eye, direct and consensual response to light is normal if the light is moved quickly from the unaffected eye to the affected eye, paradoxical dilation of both pupils occurs setting, using red reflex especially in patients

use ophthalmoscope with +4 with 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 are rhythmic 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 Disease O 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 detachment and vitreous hemorrhage rubeosis iridis (neovascularization of the iris) leading to neovascular glaucom a (poor prognosis) neovascularization traction retinal

DIABETIC RETINOPATHY (DR) background: altered vascular permeability retinal vessel closure

Classification non-proliferative: increased vascular permeability and retinal ischemia dot and blot hemorrhages microaneurysms hard exudates (lipid deposits) macular edema advanced non-proliferative (or pre-proliferative): non-proliferative findings plus

venous beading (in 2 of 4 retinal quadrants) intraretinal microvascular anomalies-IRMA (in 1 of 4 retinal quadrants) IRMA: dilated, leaky vessels within the retina cotton wool spots (nerve fibre layer infarcts) proliferative 5% of patients with diabetes will reach this stage neovascularization: iris, disc, retina to vitreous neovascularization of iris (rubeosis iridis) leading to neovascular glaucoma vitreous hemorrhage from bleeding fragile new vessels, fibrous tissue can contract causing tractional retinal detachment increased risk of severe visual loss

Screening Guidelines for Diabetic Retinopathy Type I DM screen for retinopathy beginning annually 5 years after disease onset screening not indicated before the onset of puberty Type II DM initial examination shortly after diagnosis, then repeat annually if initial exam negative, repeat in 4 years, then annual exams pregnancy ocular exam in 1st trimester, close follow-up throughout as pregnancy can exacerbate 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 microvascular complications blood pressure control focal laser for clinically significant macular edema

panretinal laser photocoagulation, for proliferative diabetic retinopathy, reduc es 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 diabe tic retinopathy which is complicated by non-clearing vitreous hemorrhage or retinal

detachment the diabetic retinopathy vitrectomy study indicated that early vitrectomy (befor e 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 cont rol) 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 of demyelination in the brain and spinal cord resulting in varied symptoms and sig ns many ocular manifestations

Clinical Features 40% of patients with MS develop optic neuritis which results in blurred vision a nd colour vision

central scotoma: because of damage to papillomacular bundle of retinal nerve fib res 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 ret inal 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 reflex Anteriovenous 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 c arotid most 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 art erioles)

Graves

Disease

Clinical dry eye lid retractions exophthalmos retinal and optic nerve changes 2 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 su rgical decompression of the orbit Giant Cell (Temporal) Arteritis

common in women > 60 clinical findings: abrupt monocular loss of vision; pain over the temporal arter y 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 h our)

Treatment high dose corticosteroid to relieve pain and prevent further ischemic episodes

Pediatric Ophthalmology Amblyopia

Definition reduction of best-corrected visual acuity not directly due to structural patholo gy cortical suppression of sensory input from an eye that is receiving blurred or conflicting 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 year s 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 surgery surgery: recession (weakening) = moving muscle insertion further back on the globe; or resection (strengthening) = shortening the muscle botulinum toxin for single muscle weakening after ocular alignment is restored (glasses, surgery, botulinum toxin), patchin g is

frequently necessary to maintain vision until approximately age 8 refractive errors anisometropia (amblyopia usually in the more hyperopic eye) causes the less hyperopic eye to receive a clear image while the more hyperopic eye receives a blurred image so that its optic pathway does not develop normally treat with glasses to correct refractive errors patching is required if visual acuity difference persists after 4-8 weeks of using glasses deprivation amblyopia occlusion due to ptosis, cataract, retinoblastoma, corneal opacity occlusion amblyopia: prolonged patching of good eye may cause it to become amblyopic

General Treatment correct the underlying cause occlusion therapy (patching) or optical degradation therapy (atropine) of the go od eye

Ocular Trauma Blunt 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, reti nal 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 initial management: refer immediately!! ABCs don t press on eyeball! check vision, diplopia metal striking metal .. Orbit CT

apply rigid eye shield to minimize further trauma keep head elevated 30-45 degrees to keep IOP down keep NPO

hemical Burns C alkali burns have a worse prognosis vs. acid burns because acids coagulate tissu e 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, v ery 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 emergency department do not attempt to neutralize because the heat produced by the reaction will dama ge the 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 th an two weeks (in the case of a persistent epithelial defect) low-Out Fracture B 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 mucu s and contact lenses

Anesthetics e.g. proparacaine HCl 0.5%, tetracaine 0.5% indications: removal of foreign body and sutures, tonometry, examination of pain ful cornea toxic to corneal epithelium (inhibit mitosis and migration) and can lead to corn eal ulceration and scarring with prolonged use, therefore NEVER prescribe

Mydriatics dilate pupils two classes cholinergic blocking dilation plus cycloplegia (lose accommodation) by paralysis of iris sphincter and the ciliary body e.g. mydriacyl (Tropicamide) indications: refraction, ophthalmoscopy, therapy for iritis adrenergic stimulating stimulate pupillary dilator muscles, no effect on accommodation

e.g. phenylephrine HCl 2.5% (duration: 30-40 minutes) usually used with tropicamide for additive effects side 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 (Apot ex), 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 (Lopidin e) side effects: contact allergy, hypotension in children

Carbonic Anhydrase Inhibitor decrease aqueous production e.g. oral acetazolamide (Diamox), topical dorzolamide (Trusopt), topical brinzol amide (Azopt) side effects: renal calculi, nausea, vomiting, diarrhea, weight loss, aplastic a nemia, 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 glaucom a

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 Toxicity

Amiodarone 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