Ophthalmology

Toronto Notes
Abridged for the PDA To be used only in conjunction with the printed Toronto Not
es
Ishtiaq Ahmed, Edmund Chen and Xiaoxing Catherine Tong, chapter editors Cagla Es
kicioglu and Nadra Ginting, associate editors Maja Segedi, EBM editor Dr. Lawren
ce Weisbrod, staff editor
Common Complaints Ocular Emergencies The Ocular Examination Optics The Orbit Lac
rimal Apparatus Lids and Lashes Conjunctiva Cornea The Uveal Tract Lens Vitreous
Retina Glaucoma Pupils Neuro-Ophthalmology Malignancies Ocular Manifestations o
f 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 detachmen
t acute macular lesion retinal artery/vein occlusion optic neuritis temporal art
eritis 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 neur
opathy (intracranial mass, orbital mass) intraocular neoplasm retinitis pigmento
sa (RP)

medication-induced
Transient Loss of Vision (lasting seconds to hours) transient ischemic attack (T
IA) migraine papilledema
Red Eye lids/orbit/lacrimal system hordeolum/chalazion blepharitis foreign body/
laceration dacryocystitis/dacryoadenitis preseptal/orbital cellulitis conjunctiv
a/sclera subconjunctival hemorrhage conjunctivitis dry eyes pterygium/pinguecula
episcleritis/scleritis cornea foreign body/laceration eratitis abrasion ulcer ant
erior 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 ocul
ar migraine herpes zoster prodrome differentiate from ocular ache: eye fatigue (
asthenopia)
Floaters vitreous syneresis posterior vitreous detachment (PVD) vitreous hemorrh
age retinal tear/detachment Flashes of Light (Photopsia) posterior vitreous deta
chment (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), m

yasthenia gravis, muscle restriction/entrapment, thyroid ophthalmopathy monocula
r diplopia: refractive error, strands of mucous in tear film, keratoconu s, cata
ract, 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 pap
illary conjunctivitis sterile corneal infiltrates (immunologic) infected ulcers
(Pseudomonas, Acanthamoeba)

Ocular Emergencies
These Require Urgent Consultation to an Ophthalmologist for Management intraocul
ar foreign body lid/globe lacerations corneal ulcer gonococcal conjunctivitis or
bital cellulitis chemical burns acute iritis acute angle-closure glaucoma centra
l retinal artery occlusion (CRAO) retinal detachment (especially macula threaten
ing) endophthalmitis temporal arteritis

The Ocular Examination

Visual Acuity - Distance Colour Vision Visual Fields Pupils Anterior Chamber Dep
th Extraocular Muscles Alignment Movement Cranial Nerve III que Cranial Nerve IV
Cranial Nerve VI External Examination the four L s lymph nodes (preauricular, s
ubmandibular) lids lashes acrimal system Slit-Lamp Examination systematically ex
amine all structures of the anterior segment + anterior vitreou s lids (includin
g 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 obl
i superior oblique lateral rectus

Ophthalmoscopy/Fundoscopy contraindications to pupillary dilatation: shallow ant

erior 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 3
rd 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 complicat
ions not prevented with refractive correction
Treatment correct with negative diopter/concave/ negative lenses to diverge ligh
t rays Hyperopia farsightedness may be developmental or due to any etiology that
shortens the eyeball to quantify hyperopia, cycloplegic drops are used to preve
nt accommodation
Clinical Features youth: usually do not require glasses (still have sufficient a
ccommodative abili

ty to focus image on retina), but may develop accommodative esotropia 30s-40s: b

lurring 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 enlarge
s
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, myope
s, hyperopes, and astigmatics
Pathophysiology hardening/reduced deformability of the lens results in decreased
accommodative ability near images cannot be focused onto retina (focus is behin
d retina as in hyperopi a)
Clinical Features if initially emmetropic, person begins to hold reading materia
l further away, bu t distance vision remains unaffected if initially myopic, per
son 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
of cornea
regular irregular
ea)

not refracted uniformly in all meridians due to non-spherical surface

or non-spherical lens (eg. football-shape d) two types of astigmatism
curvature uniformly different in meridians right angles to each other
- distorted cornea, caused by injury or keratoconus (cone-shaped corn

Treatment correct with cylindrical lens (if regular) Anisometropia

difference in refractive error between eyes second most common cause of amblyopi
a 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 RA
PD
Treatment systemic antibiotics (Suspect H. influenza in children; S. aureus or S
treptococc 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 injecti
on 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, bli
ndness
Finding Preseptal Cellulitis Orbital Cellulitis Fever May be present Present Lid
edema Moderate to severe Severe Chemosis Absent or mild Moderate or marked Prop
tosis 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 e
levated 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, leuk
emia, lymphoma vitamin A deficiency medications: anticholinergics, diuretics, an
tihistamines
Clinical Features dry eyes, red eyes, foreign body sensation, blurred vision, te
aring slit-lamp exam: decreased tear meniscus, decreased tear break up time (TBU
T), superficial punctate keratitis (SPK) stains with fluorescein/Rose Bengal Sch
irmer 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 puncta
l 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 com
mon cause associated with advancing age, trauma, surgery, pregnancy, chronic lid
swelling mechanical eyelid prevented from opening completely by mass or scarrin
g myogenic poor levator function associated with myasthenia gravis, myotonic dys
trophy neurogenic CN III palsy Horner s syndrome congenital pseudoptosis (e.g. d
ermatochalasis, enophthalmos, contralateral exophthalmos)
Treatment treat underlying cause surgery Ectropion
lid margin turns outward from globe causing tearing and possibly exposure kerati
tis

Etiology involutional (weak orbicularis oculi) paralytic (CN VII palsy) cicatric
ial (burns, trauma, surgery) mechanical (lid edema, tumour, herniated fat) conge
nital
Treatment topical lubrication, surgery Blepharitis
inflammation of lid margins
Etiology staphylococcal (S. aureus): ulcerative, dry scales seborrheic: no ulcer
s, greasy scales
Clinical Features itching, tearing, foreign body sensation thickened, red lid ma
rgins, 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 ant
ibiotics 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 inflamma
tion, threat to visual axis, cosmesis one-third recur after excision much decrea
sed recurrence with conjunctival autograft (5%)
Subconjunctival Hemorrhage
blood beneath the conjunctiva, otherwise asymptomatic idiopathic or associated w
ith trauma, Valsalva maneuver, bleeding disorders, hypertension give reassurance
if no other ocular findings, resolves in 2-3 weeks if recurrent, consider medic
al/hematology work-up
Conjunctivitis
Etiology infectious bacterial, viral, chlamydial, fungal, parasitic non-infectio
us allergy: atopic, seasonal, giant papillary conjunctivitis (in contact-lens we
ar ers) toxic: irritants, dust, smoke, irradiation secondary to another disorder
such as dacryocystitis, dacryoadenitis, celluliti s, Kawasaki s disease Clinica
l Features

red eye, itching, foreign body sensation, tearing, discharge, crusting of lashes
in the morning lid edema, conjunctival injection often with limbal pallor, prea
uricular node, subepithelial infiltrates follicles pale lymphoid elevations of t
he conjunctiva found in viral and chlamydial conjunctivitis papillae fibrovascul
ar elevations of the conjunctiva with central network of finely branching vessel
s nonspecific; found in giant papillary conjunctivitis (GPC) and vernal conjunct
ivitis
BACTERIAL CONJUNCTIVITIS purulent discharge,
n, chemosis common agents include S. aureus,
catarrhalis in neonates and sexually active
invades cornea to cause keratitis) Chlamydia
e in neonates

lid swelling, conjunctival injectio

S. pneumoniae, H. influenzae and M.
people must consider N. gonorrhea (
trachomatis is the most common caus

Treatment topical broad-spectrum antibiotic systemic antibiotics if indicated, e

specially in children usually a self-limited course of 10-14 days if no treatmen
t, 1-3 days with treat ment
VIRAL CONJUNCTIVITIS serous discharge, lid edema, follicles, subepithelial corne
al infiltrates may be associated with rhinorrhea preauricular node often palpabl
e 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 sube
pithelial infiltrates requiring s pecific treatment
CHLAMYDIAL CONJUNCTIVITIS caused by Chlamydia trachomatis (various serotypes) af
fects neonates on day 3-5, sexually active people, etc. causes trachoma, inclusi
on conjunctivitis, lymphogranuloma venereum
Trachoma (serotypes A-C) leading cause of blindness in the world severe keratoco
njunctivitis follicles on superior palpebral conjunctiva conjunctival scarring l
eads to entropion with trichiasis, corneal abrasions ulce ration and scarring ker
atitis leads to superior vascularization (pannus) and corneal scarring treatment
: topical and systemic tetracycline
Inclusion Conjunctivitis (serotypes D-K) chronic conjunctivitis with follicles a
nd subepithelial infiltrates most common cause of conjunctivitis in newborns pre
vention: topical erythromycin at birth treatment: topical and systemic tetracycl
ine, doxycycline or erythromycin
Lymphogranuloma Venereum (serotype L) conjunctival granulomas, interstitial kera
titis, lymphadenopathy, fever, malaise treatment: systemic tetracycline

ALLERGIC CONJUNCTIVITIS
Atopic associated with rhinitis, asthma, dermatitis small papillae, chemosis, th
ickened, erythematous lids, corneal neovascularizati on treatment: cool compress
es, antihistamine, mast cell stabilizer
Seasonal associated with hay fever treatment: cool compresses, antihistamine, ma
st cell stabilizer
Giant Papillary Conjunctivitis (GPC) immune reaction to mucous debris on lenses
in contact lens wearers large papillae form on superior palpebral conjunctiva sp
ecific treatment: clean, change or discontinue use of contact lens
Vernal Conjunctivitis large papillae (cobblestones) on superior palpebral conjun
ctiva with corneal ulc ers, keratitis seasonal (warm weather) occurs in children
, lasts for 5-10 years and then resolves specific treatment: consider topical st
eroid, 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, epithelia
l defect that stain s with fluorescein, corneal edema, anterior chamber cell/fla
re
Complications abrasion, infection, scarring, rust ring, secondary iritis Treatme
nt remove under magnification using local anesthetic and sterile needle or refer
to ophthalmology (depending on depth and location) treat as per corneal abrasio
n (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 anes
thetic
Complications infection, ulceration, recurrent erosion, secondary iritis

Treatment topical antibiotic (drops or ointment) consider topical NSAID, cyclopl

egic (relieves pain and photophobia by paralyzing ciliary muscle), light patch p
ressure patch is not effective most abrasions clear spontaneously within 24-48 h
ours
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 decre
ased vision, eyeli d edema corneal hypoesthesia dendritic (thin and branching) l
esion 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 su
ch as acyc lovir dendritic debridement NO STEROIDS initially may exacerbate cond
ition

ophthalmologist must exercise caution if adding topical steroids for chronic ker
atitis 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, pseudodendr
ite, superficial punctate keratitis corneal hypoesthesia
Complications corneal keratitis, ulceration, perforation and scarring iritis, se
condary glaucoma, cataract muscle palsies (rare) due to CNS involvement occasion
ally severe post-herpetic neuralgia
Treatment oral antiviral (acyclovir, valcyclovir or famciclovir) topical steroid
s as indicated for keratitis, iritis (prescribed by an ophthalmol ogist) cyclopl
egic, 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 i
s the only symptom
Treatment attempt correction with spectacles or contact lens penetrating keratop
lasty (corneal transplant) 90% successful post-operative complications: endophth
almitis, graft rejection, graft dehiscence

The Uveal Tract

uveal tract = iris, ciliary body, and choroid vascularized, pigmented middle lay
er 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 au
toimmune, infectious, granulomatous, malignant causes should be managed by an op
hthalmologist
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 anterio
r uveitis): Reiter s syndrome, ankylosing spondylitis (AS), psoriasis, inflammat
ory bowel disease (IBD) Non-HLA-B27: Juvenile rheumatoid arthritis (JRA) infecti
ous: syphilis, Lyme disease, toxoplasmosis, TB, HSV, herpes zoster other: sarcoi
dosis, trauma, large abrasion
Clinical Features photophobia (from reactive spasm of inflamed iris muscle), ocu
lar pain, tenderne ss of

the globe, brow ache (ciliary muscle spasm), decreased visual acuity, tearing ci
liary flush (perilimbal conjunctival injection), miosis (spasm of sphincter mu s
cle) anterior chamber cells (WBC in anterior chamber due to anterior segment (pr
otein 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 cor
neal endothelium) iritis typically reduces intraocular pressure though severe ir
itis may cause an inflammatory glaucoma
Complications inflammatory glaucoma posterior synechiae adhesions of posterior i
ris to anterior lens capsule indicated by an irregularly shaped pupil if occur 3
60, 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 calcificat
ion 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 ass
ociated with systemic disease (may have juvenile onset) diabetes mellitus metabo
lic 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 phenom
enon patient is more myopic than previously noted,
due to increased refractive power of the lens (in nuclear sclerosis only) catara
ct increases power of lens causing artificial myopia without previously needed r
eading glasses diagnose by slit-lamp exam, and by noting changes in red reflex u
sing ophthalmoscope patient may read

may impair view of retina during fundoscopy

Treatment medical: attempt correction of refractive error surgical: definitive t
reatment is via surgical removal of cataract indications for surgery to improve
visual function in patients whose visual loss leads to functional impairment (pa
tients may be inclined to postpone surgery as long as one eye has sufficient vis
ion) to aid management of other ocular disease (e.g. cataract that prevents adeq
uate retinal exam or laser treatment of diabetic retinopathy) congenital or trau
matic cataracts phacoemulsification most commonly used surgical technique ultras
onic needle is used to emulsify and aspirate nucleus and cortex synthetic intrao
cular lens (IOL) is placed in bag formed by empty capsule post-operative complic
ations 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 vitr
eous 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 re
tinal tears/detachment retinal tears/detachment may cause vitreous hemorrhage if
tear bridges blood vessel complications more common in high myopes and followin
g 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, v
alvular disease) thrombus temporal arteritis
Clinical Features sudden, painless (except in temporal arteritis), severe monocu
lar loss of vision relative afferent pupillary defect (RAPD) patient will often
have experienced transient episodes in the past (amaurosis fu gax) fundoscopy ch
erry-red spot at centre of macula (visualization of unaffected highly vascular c
horoid through the thin fovea) retinal pallor narrowed arterioles, boxcarring (s
egmentation of blood in arteries) cotton-wool spots (retinal infarcts) cholester
ol emboli (Hollenhorst plaques) - usually located at arteriole bifurcations afte
r ~ 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 com
plete 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 topica
l -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 ne
ovascularization
Central/Branch Retinal Vein Occlusion (CRVO/BRVO)
an uncommon cause of blindness in the elderly, usually a manifestation of a syst
emic disease thrombus occurs within the lumen of the blood vessel
Predisposing Factors arteriosclerotic vascular disease hypertension diabetes mel
litus glaucoma hyperviscosity (e.g. polycythemia rubra vera, sickle-cell disease
, lymphoma, leukemia) drugs (OCP, duretics)
Clinical Features painless, monocular, gradual or sudden visual loss +/- relativ
e afferent pupillary defect (RAPD)

fundoscopy blood and thunder appearance

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

two fairly distinct groups venous stasis/non-ischemic retinopathy no RAPD ,VA ap

proximately 20/80 mild hemorrhage, few cotton wool spots resolves spontaneously
over weeks to months may regain normal vision if macula intact hemorrhagic/ische
mic retinopathy usually older patient with deficient arterial supply RAPD, VA ap
proximately 20/200, reduced peripheral vision more hemorrhages, cotton wool spot
s, congestion poor visual prognosis
Complications degeneration of retinal pigment epithelium liquefaction of vitreou
s neovascularization of retina and iris (secondary rubeosis), leading to seconda
ry glaucoma
Treatment no treatment available to restore vision treat underlying cause/ contr
ibuting factor fluorescein angiography to determine extent of retinal non-perfus
ion = risk of n eovascularization retinal laser photocoagulation to reduce neova
scularization 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 th

e neurosensory retina, allowing fluid from the vitreous to pass into the subreti
nal space tears may be caused by posterior vitreous detachment (PVD), degenerati
ve retinal changes, trauma or iatrogenically incidence increases with advancing
age, and more likely to occur spontaneously in high myopes, or after ocular surg
ery/trauma tractional caused by traction (due to vitreal, epiretinal or subretin
al membrane) pulling the neurosensory retina away from the underlying RPE found
in conditions such as diabetic retinopathy, CRVO, sickle cell disease, retinopat
hy of prematurity (ROP), and ocular trauma exudative caused by damage to the RPE
resulting in fluid accumulation in the subretinal space main causes are intraoc
ular 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 fi
eld of vision when the retina detaches in that area loss of central vision

visual acuity dramatically drops if the macula becomes detached decreased IOP (u
sually 4-5 mmHg lower than other, normal eye) ophthalmoscopy: detached retina is
grey with surface blood vessels, loss of red reflex +/- relative afferent pupil
lary defect (RAPD)

Treatment prophylactic: a symptomatic tear (flashes or floaters) can be sealed o

ff with la ser or cryotherapy, with the goal of preventing progression to detach
ment therapeutic rhegmatogenous retinal detachment scleral buckle (a band is sec
ured on the outside of the globe that indents the wall, thereby relieving tensio
n on the retina around any tears/holes, allowing the tears/holes to remain seale
d) pneumatic retinopexy (intraocular injection of air or an expandable gas in or
der to tamponade the retinal break) both above treatments are used in combinatio
n with localization of retinal tears/holes and subsequent treatment with diather
my, cryotherapy or laser to create adhesions between the RPE and the neurosensor
y retina vitrectomy plus injection of silicone oil in cases of recurrent detachm
ents tractional retinal detachment: vitrectomy +/- membrane removal/scleral buck
ling/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 macul
a is still attached prognosis for visual recovery varies inversely with the amou
nt 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 vi
sion is lost peripheral vision (important for navigation) is maintained so suffe
rers can usua lly maintain an independant lifestyle
Classification Dry /Non-Exudative ARMD most common type of ARMD (90% of cases) s
lowly progressive loss of visual function drusen: pale, yellow-white deposits of
membranous vesicles and collagen deposited between the retinal pigment epitheli
um (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 sev
ere visual loss choroidal neovascularization: drusen predispose to breaks in Bru
ch s membrane which cause subsequent growth and proliferation of choroidal capil
laries may get serous detachment of overlying RPE and retina, hemorrhage and lip
id precipitates into subretinal space

can also get an elevated subretinal mass due to fibrous metaplasia of hemorrhagi
c 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 metamorphop
sia (distorted vision characterized by straight parallel lines appear ing conver
gent or wavy) due to macular edema
Investigations Amsler Grid: held at normal reading distance with glasses on, ass
esses macular f unction Fluorescein angiography (FA): assess degree of neovascul
arization - 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 .. an
ti-oxidants, green leafy vegetables neovascular ARMD laser photocoagulation for
neovascularization 50% of choroidal neovascularization cannot be treated initial
ly no definitive treatment for disciform scarring focal laser for macular edema
.. photodynamic therapy (PDT) with verteporfin o IV injection of verteporfin fol
lowed by low intensity laser to area of choroid al neovascularization

Treatment of Age Related Macular Degeneration with Photodynamic Therapy (TAP) St

udy Group indicated that for selected patients with subfoveal lesions i n ARMD w
ith predominantly classic choroidal neovascularization, verteporfin treatment ca
n reduce the risk of moderate vision loss for at least 1 year; this therapy cann
ot 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 drai
nage within the trabecular meshwork and its drainage into the canal of Schlemm i
nsidious 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 o
phthalmic steroid use on eyes in steroid responders exams recommended if > 4 wee
ks 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 IO
P due to restriction of aqueous outflow bilateral, but usually asymmetric earlie
st signs are optic disc changes (safe to dilate pupil)

increased cup to disc ratio (vertical C/D > 0.6) or significant C/D asymmetry be
tween eyes (> 0.2 difference) thinning, notching of the neuroretinal rim flame s
haped disc hemorrhage 360 degrees of peripapillary atrophy nerve fibre layer def
ect 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 a
queous production topical beta-blockers topical and oral carbonic anhydrase inhi
bitor topical alpha-adrenergics laser trabeculoplasty, cyclophotocoagulation = s
elective destruction of ciliary body (for refractory cases) microsurgery: trabec
ulectomy (filtering bleb), tube shunt placement (shunts flui d to reservoir unde
r 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 trabecul
ar 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 dila
tion (topical and systemic anticholinergics, stress, darkness) large lens crowds
the angle
Clinical Features unilateral, but other eye predisposed red, painful eye = RED F
LAG decreased visual acuity, vision acutely blurred from corneal edema halo arou
nd lights nausea and vomiting, abdominal pain fixed mid-dilated pupil corneal ed
ema with conjunctival injection marked increase in IOP even to palpation (> 40 m
m Hg)

shallow anterior chamber, cells in anterior chamber

Complications irreversible loss of vision if untreated, within hours to days per
manent 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) resulti
ng in permanent closure of angle medical treatment: see Ocular Medications mioti
c drops (pilocarpine) to reverse pupilary block IOP topical beta-blockers .. topi
cal adrenergics .. topical cholinergics o pilocarpine 1-4% q15min, up to q5min .
. systemic carbonic anhydrase inhibitors o IV acetazolamide 250-500mg .. systemi
c 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 n
ervous system (PNS) carried by CN III: pre- and post-ganglionic fibres synapse i
n 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, n
eurotransmitter 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 hyperse
nsitivity when post-ganglionic fibres are damaged, understimulated end-organ dev
elops an excess of receptor and becomes hypersensitive postganglionic parasympat
hetic lesions (Adie s pupil) pupil will constrict with 0. 125% pilocarpine (chol
inergic agonist), whereas normal pupil will not postganglionic sympathetic lesio
ns (i.e. Horner s Syndrome) pupil will dilate with 0.125% adrenaline, whereas no
rmal pupil will not. This test is used to differentiate between pre- and post-ga
nglionic lesions in Horne r s

syndrome
Local Disorders of Iris posterior synechiae (adhesions between iris and lens) du
e 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 resu
lts in vertically oval pupil that reacts poorly to light
Relative Afferent Pupillary Defect (RAPD)
defect in visual afferent pathway anterior to optic chiasm differential diagnosi
s: optic nerve compression, optic neuritis, large retinal d etachment, BRAO, CRA
O, 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, dire
ct and consensual response to light is decreased if light is shone in the unaffe
cted eye, direct and consensual response to light is normal if the light is move
d quickly from the unaffected eye to the affected eye, paradoxical dilation of b
oth 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 us
ed: confrontation (screening), tangent screen, Humphrey fields (computerized aut
omated perimetry), Goldman perimetry
Bitemporal Hemianopsia
a chiasmal lesion
Etiology In children: craniopharyngioma In middle aged: pituitary mass In elderl
y: meningioma
Homonymous Hemianopsia
a retrochiasmal lesion the more congruent, the more posterior the lesion check a
ll hemiplegic patients for ipsilateral homonymous hemianopsia e.g. left hemisphe
re right visual field (VF) defect in both eyes
Internuclear Ophthalmoplegia
lesion of medial longitudinal fasciculus (MLF) damage to MLF ^ disrupts coordina
tion between CN VI nucleus in pons and CN III nucleus in mid brain ^ disrupts co
njugate horizontal gaze

commonly seen in multiple sclerosis (MS) loss of ipsilateral eye adduction monoc
ular nystagmus in contralateral abducting eye other causes of INOP: brain stem i
nfarction, tumours, AV malformations, Wernicke s encephalopathy and encephalitis
Nystagmus
definition: rapid, involuntary, small amplitude movements of the eyes that are r
hythmic in nature direction of nystagmus is defined by the rapid component of th
e 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 dist
ance vision with rise of blood sugar consider DM if unexplained retinopathy, cat
aract, EOM palsy, optic neuropathy, sudden change in refractive error loss of vi
sion due to progressive microangiopathy, leading to macular edema progressive di
abetic retinopathy detachment and vitreous hemorrhage rubeosis iridis (neovascul
arization of the iris) leading to neovascular glaucom a (poor prognosis) neovasc
ularization traction retinal
DIABETIC RETINOPATHY (DR) background: altered vascular permeability retinal vess
el closure
Classification non-proliferative: increased vascular permeability and retinal is
chemia dot and blot hemorrhages microaneurysms hard exudates (lipid deposits) ma
cular edema advanced non-proliferative (or pre-proliferative): non-proliferative
findings plus

venous beading (in 2 of 4 retinal quadrants) intraretinal microvascular anomalie

s-IRMA (in 1 of 4 retinal quadrants) IRMA: dilated, leaky vessels within the ret
ina cotton wool spots (nerve fibre layer infarcts) proliferative 5% of patients
with diabetes will reach this stage neovascularization: iris, disc, retina to vi
treous neovascularization of iris (rubeosis iridis) leading to neovascular glauc
oma vitreous hemorrhage from bleeding fragile new vessels, fibrous tissue can co
ntract causing tractional retinal detachment increased risk of severe visual los
s
Screening Guidelines for Diabetic Retinopathy Type I DM screen for retinopathy b
eginning annually 5 years after disease onset screening not indicated before the
onset of puberty Type II DM initial examination shortly after diagnosis, then r
epeat annually if initial exam negative, repeat in 4 years, then annual exams pr
egnancy ocular exam in 1st trimester, close follow-up throughout as pregnancy ca
n 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 pre
ssure 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 ret
ina by decreasing retinal metabolic demand ^ reduces risk of blindness vitrectom
y for vitreous hemorrhage and retinal detachment in proliferative diabe tic reti
nopathy which is complicated by non-clearing vitreous hemorrhage or retinal

detachment the diabetic retinopathy vitrectomy study indicated that early vitrec
tomy (befor e hemorrhage) does not improve the visual prognosis
Lens earlier onset of senile nuclear sclerosis and cortical cataract may get hyp
erglycemic cataract, due to sorbitol accumulation (rare) sudden changes in refra
ction of lens: changes in blood glucose levels (poor cont rol) may cause refract
ive changes by 3-4 diopters
Extra Ocular Muscle (EOM) Palsy usually CN III infarct pupil usually spared in d
iabetic CN III palsy, but get ptosis may involve CN IV and VI usually recover wi
thin 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 demy
elination in the brain and spinal cord resulting in varied symptoms and sig ns m
any ocular manifestations
Clinical Features 40% of patients with MS develop optic neuritis which results i
n 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, nys
tagmus, uveitis, optic atrophy, optic neuritis white matter demyelinating lesion
s of optic nerve on MRI
Treatment with optic neuritis, treatment with oral steroids leads to greater lik
elihood 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, microaneurysm
s, cotton wool spots key features of acute HTN retinopathy: retinal arteriolar s
pasm, 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 n
arrowing of arterioles Exaggeration of the light reflex Anteriovenous crossing c
hanges
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/w
eakness 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, prop
tosis 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 ov
er the temporal arter y ischemic optic atrophy 50% lose vision in other eye if u
ntreated
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 structu
ral patholo gy cortical suppression of sensory input from an eye that is receivi
ng blurred or conflicting visual information ^ disruption of the normal developm
ent of visual pathways in that eye ^ amblyopia
Detection "Holler Test": young child upset if good eye is covered quantitative v
isual acuity by age 3-4 years using picture charts and/or matching game (Sherida
n-Gardiner), testing each eye separately not commonly treatable after age 8-10 y
ears since the neural pathways for vision are now formed prognosis: 90% will hav
e good vision restored and maintained if treated < 4 year s old
Etiology and Management strabismus correct with glasses for accommodative esotro
pia (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 su
rgery surgery: recession (weakening) = moving muscle insertion further back on t
he globe; or resection (strengthening) = shortening the muscle botulinum toxin f
or 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 err

ors 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 b
lurred image so that its optic pathway does not develop normally treat with glas
ses to correct refractive errors patching is required if visual acuity differenc
e persists after 4-8 weeks of using glasses deprivation amblyopia occlusion due
to ptosis, cataract, retinoblastoma, corneal opacity occlusion amblyopia: prolon
ged patching of good eye may cause it to become amblyopic
General Treatment correct the underlying cause occlusion therapy (patching) or o
ptical 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 (dip
lopia), external and slit lamp exam, ophthalmoscopy if VA normal or slightly red
uced, globe less likely to be perforated if VA reduced, may be perforated globe,
corneal abrasion, lens dislocation, reti nal tear bone fractures blow out fract
ure: restricted EOM, diplopia, enopthalmos (sunken eye) ethmoid fracture: subcut
aneous emphysema of lid lids: swelling, laceration, emphysema conjunctiva: subco
njunctival hemorrhage cornea: abrasions - detect with fluorescein staining and c
obalt blue filter in ophthalmoscope or slit lamp anterior chamber: assess depth,
hyphema, hypopyon iris: prolapse, iritis lens: cataract, dislocation retinal te
ar/detachment
Penetrating Trauma
include ruptured globe prolapsed iris, intraocular foreign body (FB) r/o intraocu
lar FB; especially if history of initial management: refer immediately!! ABCs do
n 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 degre
es 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 cor
nea opaque, likely irreversible stromal damage even with a clear cornea initiall
y, alkali burns can progress for weeks (thus, v ery guarded prognosis)
Treatment irrigate at site of accident immediately, with water or buffered solut
ion IV drip for at least 20-30 minutes with eyelids retracted in emergency depar
tment do not attempt to neutralize because the heat produced by the reaction wil
l 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, us
e for less th an two weeks (in the case of a persistent epithelial defect) low-O
ut Fracture B blunt trauma causing fracture of orbital floor and orbital content
s to herniate into maxillary sinus

orbital rim remains intact inferior rectus and/or inferior oblique muscles may b
e incarcerated at fracture site infraorbital nerve courses along the floor of th
e 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), perio
rbital ecchymoses
Investigations plain films: Waters view and lateral CT: anteroposterior and coro
nal view of orbits
Treatment refrain from coughing, blowing nose systemic antibiotics may be indica
ted surgery if fracture > 50% orbital floor, diplopia not improving, or enophtha
lmos > 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 abras
ion) ; 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 cor
neal epithelium (inhibit mitosis and migration) and can lead to corn eal ulcerat
ion and scarring with prolonged use, therefore NEVER prescribe
Mydriatics dilate pupils two classes cholinergic blocking dilation plus cyclople
gia (lose accommodation) by paralysis of iris sphincter and the ciliary body e.g
. mydriacyl (Tropicamide) indications: refraction, ophthalmoscopy, therapy for i
ritis adrenergic stimulating stimulate pupillary dilator muscles, no effect on a
ccommodation

e.g. phenylephrine HCl 2.5% (duration: 30-40 minutes) usually used with tropicam
ide for additive effects side effects: hypertension, tachycardia, arrhythmias
Table 6. Mydriatic Cycloplegic Drugs and Duration of Action Drugs Duration of ac
tion 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 Scopol
amine HBr 0.25%, 5% 1-2 weeks

Glaucoma Medications
Beta-Adrenergic Blockers decrease aqueous humour production beta-blockers e.g. t
imolol (Timoptic), levobunolol (Betagan), metapranolol (Apot ex), betaxolol (Bet
optic), carteolol (Teoptic) systemic side effects: bronchospasm, exacerbation of
congestive heart failure, bradycardia, heart block, hypotension, impotence, dep
ression
Cholinergic Stimulating increases aqueous outflow e.g. pilocarpine (Pilopine), c
arbachol (Isopto Carbachol) side effects: miosis, brow ache, decreased night vis
ion, headache, increased GI motility, decreased heart rate
Adrenergic Stimulating decrease aqueous production and increase outflow e.g. epi
nephrine 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 eff
ects: 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, l
ash growth, trichiasis

Topical Ocular Therapeutic Drugs

NSAIDs used for less serious chronic inflammatory conditions decreased risk of c
omplications e.g. Ketorolac (Acular) drops, Diclofenac (Voltaren) drops
Anti-Histamines used to relieve red and itchy eye, often in combination with dec
ongestants sodium cromoglycate (stabilizes most all membranes)
Corticosteroids never prescribed by primary care physician unless emergency indi
cations e.g. fluorometholone (FML), betamethasone, dexamethasone (Maxidex), pred
nisolone (Predsol 0.5%, Pred Forte 1%), rimexolone (Velox) complications: potent
iates 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. naphazoli
ne, phenylephrine (Isopto Frin) rebound vasodilation with over use; rarely can p
recipitate 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, tetr
acycline, bacitracin, polymyxin B

Ocular Drug Toxicity

Amiodarone Corneal microdeposits and superficial keratopathy Atropine, Benztropi
ne, Benzhexol Pupillary dilation (risk of angle closure glaucoma) Chloroquine, h
ydroxychloroquine Bull s eye lesion at macula, vortex keratopathy Chlorpromazine
Anterior subcapsular cataract Contraceptive Pills Decreased tolerance to contac
t lenses, Migraine, Optic neuritis, Central vein occlusion Digitalis Yellow visi
on, Blurred vision Ethambutol Optic neuropathy Haloperidol (Haldol) Oculogyric c
rises, Blurred vision Indomethacin Superficial keratopathy Isoniazid Optic neuro
pathy Nalidixic Acid Papilloedema Steroids Posterior subcapsular cataracts, Glau
coma, Papilloedema (systemic steroids), Increased severity of HSV infections (ge
ographic ulcers), Predisposition to fungal infections Sulphonamides, NSAIDS Stev
ens-Johnson syndrome

Tetracycline Papilloedema Thioridazine Pigmentary degeneration of retina Vitamin

A Intoxication Papilloedema Vitamin D Intoxication Band keratopathy
Table 7. Drugs with Ocular Toxicity