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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, keratoconus,


cataract, dislocated lens
Ocular Problems in the Elderly

presbyopia

dry eyes

epiphora

ptosis

cataracts

age-related macular degeneration

retinal artery/vein occlusion

temporal arteritis (Arteritic Ischemic Optic Neuropathy)


Ocular Problems in Contact Lens Wearer

superficial punctate keratitis (SPK)/dry eyes


(solution hypersensitivity, tight lens syndrome)

corneal abrasion

giant papillary conjunctivitis

sterile corneal infiltrates (immunologic)

infected ulcers (Pseudomonas, Acanthamoeba)

Ocular Emergencies
These Require Urgent Consultation to an Ophthalmologist for Management

intraocular foreign body

lid/globe lacerations

corneal ulcer

gonococcal conjunctivitis

orbital cellulitis

chemical burns

acute iritis

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 superior rectus, medial rectus, inferior rectus, inferior oblique

Cranial Nerve IV superior oblique

Cranial Nerve VI lateral rectus


External Examination

the four Ls
lymph nodes (preauricular, submandibular)
lids
lashes
acrimal system
Slit-Lamp Examination

systematically examine all structures of the anterior segment + anterior vitreous


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
Ophthalmoscopy/Fundoscopy

contraindications to pupillary dilatation:


shallow anterior chamber
iris-supported anterior chamber lens implant
potential neurologic abnormality requiring pupil evaluation
use caution with cardiovascular disease - mydriatics may cause tachycardia

Optics
Emmetropia
no refractive error

Myopia
nearsightedness
prevalence of 30-40% in U.S. population

Clinical Features
usually presents in 1st or 2nd decade, stabilizes in 2nd and 3rd decade; rarely
begins after 25 years except in diabetes or cataracts
blurring of distance vision; near vision usually unaffected

Complications

retinal tear/detachment
macular hole
open angle glaucoma
complications not prevented with refractive correction

Treatment
correct with negative diopter/concave/negative lenses to diverge light rays

Hyperopia
farsightedness
may be developmental or due to any etiology that shortens the eyeball
to quantify hyperopia, cycloplegic drops are used to prevent accommodation

Clinical Features
youth: usually do not require glasses (still have sufficient accommodative ability to
focus image on retina), but may develop accommodative esotropia
30s-40s: blurring of near vision due to decreased accommodation, may need
reading glasses
> 50s: blurring of distance vision due to severely decreased accommodation

Complications
angle-closure glaucoma, particularly later in life as lens enlarges

Treatment
when symptomatic, correct with positive Diopter/convex/plus lenses to
converge light rays

Presbyopia
normal aging process (especially over 40 years)
experienced by emmetropes, myopes, hyperopes, and astigmatics

Pathophysiology
hardening/reduced deformability of the lens results in decreased accommodative
ability
near images cannot be focused onto retina (focus is behind retina as in hyperopia)

Clinical Features
if initially emmetropic, person begins to hold reading material further away, but
distance vision remains unaffected
if initially myopic, person begins removing distance glasses to read
if initially hyperopic, symptoms of presbyopia occur earlier

Treatment
correct vision with positive diopter/convex/plus lenses for reading
reading glasses will blur distance vision (avoided by using bifocal or progressive

lenses)

Astigmatism
light rays not refracted uniformly in all meridians
due to non-spherical surface of cornea or non-spherical lens (eg. football-shaped)
two types of astigmatism
regular - curvature uniformly different in meridians right angles to 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 Streptococci in adults)
warm compresses

Orbital Cellulitis
inflammation of orbital contents posterior to orbital septum
common in children, but also in the aged and immunocompromised

Etiology
usually secondary to sinus/facial/tooth infections or trauma

Clinical Features

decreased visual acuity, pain, red eye, headache, fever


lid erythema, tenderness, and edema with difficulty opening
conjunctival injection and chemosis (conjunctival edema)
proptosis, limitation of ocular movements (ophthalmoplegia) and pain with
movement
RAPD, optic disc swelling

Treatment
admit, IV antibiotics, blood cultures, orbital CT
surgical drainage of abscess
follow closely

Complications
orbital apex syndrome, cavernous sinus thrombosis, meningitis, blindness
Finding
Fever
Lid edema
Chemosis
Proptosis
Pain on eye movement
Ocular mobility
Vision
RAPD
Leukocytosis
ESR
Additional findings

Preseptal Cellulitis
May be present
Moderate to severe
Absent or mild
Absent
Absent
Normal
Normal
Absent
Minimal or moderate
Normal or elevated
Skin infection

Table 2. Differentiating Between Preseptal and Orbital Cellulitis

Orbital Cellulitis
Present
Severe
Moderate or marked
Present
Present
Decreased
Diminished diplopia
May be seen
Marked
Elevated
Sinusitis, dental abscess

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, Sjgrens 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
Schirmers 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
Horners 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 (diluted to 25%)
topical or systemic antibiotics as needed

Conjunctiva
Pterygium

fibrovascular triangular encroachment of epithelial tissue onto the cornea, usually nasal
may induce astigmatism, decrease vision
excision for chronic inflammation, threat to visual axis, cosmesis
one-third recur after excision
much decreased recurrence with conjunctival autograft (5%)

Subconjunctival Hemorrhage
blood beneath the conjunctiva, otherwise asymptomatic
idiopathic or associated with trauma, Valsalva maneuver, bleeding disorders,
hypertension
give reassurance if no other ocular findings, resolves in 2-3 weeks
if recurrent, consider medical/hematology work-up

Conjunctivitis
Etiology
infectious
bacterial, viral, chlamydial, fungal, parasitic
non-infectious
allergy: atopic, seasonal, giant papillary conjunctivitis (in contact-lens wearers)
toxic: irritants, dust, smoke, irradiation
secondary to another disorder such as dacryocystitis, dacryoadenitis, cellulitis,
Kawasakis 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 treatment

VIRAL CONJUNCTIVITIS

serous discharge, lid edema, follicles, subepithelial corneal infiltrates


may be associated with rhinorrhea
preauricular node often palpable and tender
initially unilateral, often progresses to the other eye
mainly due to adenovirus highly contagious for up to 12 days

Treatment
cool compresses, topical lubrication
usually self-limiting (7-12 days)

proper hygiene is very important


may develop corneal epithelial defects and subepithelial infiltrates requiring specific
treatment

CHLAMYDIAL CONJUNCTIVITIS
caused by Chlamydia trachomatis (various serotypes)
affects neonates on day 3-5, sexually active people, etc.
causes trachoma, inclusion conjunctivitis, lymphogranuloma venereum

Trachoma (serotypes A-C)

leading cause of blindness in the world


severe keratoconjunctivitis
follicles on superior palpebral conjunctiva
conjunctival scarring leads to entropion with trichiasis, corneal abrasions ulceration
and scarring
keratitis leads to superior vascularization (pannus) and corneal scarring
treatment: topical and systemic tetracycline

Inclusion Conjunctivitis (serotypes D-K)

chronic conjunctivitis with follicles and subepithelial infiltrates


most common cause of conjunctivitis in newborns
prevention: topical erythromycin at birth
treatment: topical and systemic tetracycline, doxycycline or erythromycin

Lymphogranuloma Venereum (serotype L)


conjunctival granulomas, interstitial keratitis, lymphadenopathy, fever, malaise
treatment: systemic tetracycline

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

Seasonal
associated with hay fever
treatment: cool compresses, antihistamine, mast cell stabilizer

Giant Papillary Conjunctivitis (GPC)


immune reaction to mucous debris on lenses in contact lens wearers
large papillae form on superior palpebral conjunctiva
specific treatment: clean, change or discontinue use of contact lens

Vernal Conjunctivitis
large papillae (cobblestones) on superior palpebral conjunctiva with corneal ulcers,
keratitis
seasonal (warm weather)
occurs in children, lasts for 5-10 years and then resolves
specific treatment: consider topical steroid, cyclosporine (not in primary care)

Cornea
Foreign Body

foreign material in or on cornea


may have associated rust ring if metallic that may be toxic to the cornea
patients may note tearing, photophobia, foreign body sensation, redness
signs include foreign body, conjunctival injection, epithelial defect that stains
with fluorescein, corneal edema, anterior chamber cell/flare

Complications
abrasion, infection, scarring, rust ring, secondary 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), contact lens

Clinical Features
pain, redness, tearing, photophobia, foreign body sensation
de-epithelialized area stains with fluorescein dye
pain relieved with topical anesthetic

Complications
infection, ulceration, recurrent erosion, secondary iritis

Treatment
topical antibiotic (drops or ointment)
consider topical NSAID, cycloplegic (relieves pain and photophobia by paralyzing
ciliary muscle), light patch
pressure patch is not effective
most abrasions clear spontaneously within 24-48 hours

Herpes Simplex Keratitis


usually HSV type 1 (90% of population are carriers)
may be triggered by stress, fever, sun exposure, immunosuppression

Clinical Features
pain, tearing, foreign body sensation, redness, may have decreased vision, eyelid
edema
corneal hypoesthesia
dendritic (thin and branching) lesion in epithelium that stains with fluorescein

Complications
corneal scarring (can lead to loss of vision)
chronic interstitial keratitis due to penetration of virus into stroma
secondary iritis

Treatment

topical antiviral such as trifluridine, consider systemic antiviral such as acyclovir


dendritic debridement
NO STEROIDS initially may exacerbate condition
ophthalmologist must exercise caution if adding topical steroids for chronic
keratitis or iritis

Herpes Zoster Keratitis


dermatitis of the forehead (the CN V1 territory) involves the globe in 1/2 to 3/4 of
cases
Hutchinsons 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 ophthalmologist)
cycloplegic, antibiotic if indicated

Keratoconus

bilateral central thinning and bulging (ectasia) of the cornea to form a conical shape
familial occurrence; associated with Downs syndrome and atopy
associated with breaks in Descemet's and Bowman's membrane
results in irregular astigmatism, corneal striae, scarring, stromal edema
blurring of visual acuity is the only symptom

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

The Uveal Tract


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

Uveitis
may involve one or all three parts of the tract
idiopathic or associated with autoimmune, infectious, granulomatous,
malignant causes
should be managed by an ophthalmologist

Anterior Uveitis/Iritis
inflammation of iris, usually with cyclitis (inflammation of ciliary body),
when both = iridocyclitis
usually unilateral

Etiology
usually idiopathic
connective tissue diseases:
HLA-B27 (usually anterior uveitis): Reiters syndrome, ankylosing spondylitis
(AS), psoriasis, inflammatory bowel disease (IBD)
Non-HLA-B27: Juvenile rheumatoid arthritis (JRA)
infectious: syphilis, Lyme disease, toxoplasmosis, TB, HSV, herpes zoster
other: sarcoidosis, trauma, large abrasion

Clinical Features
photophobia (from reactive spasm of inflamed iris muscle), ocular pain, tenderness of
the globe, brow ache (ciliary muscle spasm), decreased visual acuity, tearing
ciliary flush (perilimbal conjunctival injection), miosis (spasm of sphincter muscle)
anterior chamber cells (WBC in anterior chamber due to anterior segment
inflammation) and flare (protein precipitates in anterior chamber secondary
to inflammation), hypopyon (collection of neutrophilic exudates inferiorly in the
anterior chamber)
occasionally keratitic precipitates (clumps of cells on corneal endothelium)
iritis typically reduces intraocular pressure though severe iritis may cause an
inflammatory glaucoma

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

Treatment (by Ophthalmologists)


mydriatics: dilate pupil to prevent formation of posterior synechiae and to decrease
pain from ciliary spasm
steroids: topical, subconjunctival or systemic
systemic analgesia
medical workup may be indicated to determine etiology

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. Wilsons disease, galactosemia, homocystinuria)
hypocalcemia
traumatic (may be rosette shaped)
intraocular inflammation (e.g. uveitis)
toxic (steroids, phenothiazines)
radiation
congenital
present with altered red reflex or leukocoria
treat promptly to prevent amblyopia

Clinical Features
gradual, painless, progressive decrease in visual acuity
glare, dimness, haloes around lights at night, monocular diplopia
second sight phenomenon patient is more myopic than previously noted,
due to increased refractive power of the lens (in nuclear sclerosis only)
cataract increases power of lens causing artificial myopia patient may read
without previously needed reading glasses
diagnose by slit-lamp exam, and by noting changes in red reflex using
ophthalmoscope
may impair view of retina during fundoscopy

Treatment
medical: attempt correction of refractive error
surgical: definitive treatment is via surgical removal of 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

Vitreous
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 fugax)
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 endophthalmitis)
treat underlying cause to prevent CRAO in fellow eye
f/u 1 month to r/o neovascularization

Central/Branch Retinal Vein Occlusion (CRVO/BRVO)


an uncommon cause of blindness in the elderly, usually a manifestation of 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 neovascularization
retinal laser photocoagulation to reduce neovascularization and prevent
neovascular glaucoma

Retinal Detachment (RD)


cleavage in the plane between the neurosensory retina and the retinal pigment epithelium (RPE)
three types
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 laser 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 retina is
detached and whether the macula is attached or not

Age-Related Macular Degeneration (ARMD)


leading cause of blindness in the western world, associated with increasing age,
usually bilateral
10% of people > 65 years old have some degree of ARMD, female > male
degenerative changes are concentrated at the macula thus only central vision is lost
peripheral vision (important for navigation) is maintained so sufferers can usually
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 Bruchs
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 Bruchs
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 appearing
convergent or wavy) due to macular edema

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

Treatment
non-neovascular ARMD
monitor, Amsler grid allows patients to check for 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 choroidal
neovascularization
Treatment of Age Related Macular Degeneration with Photodynamic Therapy
(TAP) Study Group indicated that for selected patients with subfoveal lesions in
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 yearly eye
exams recommended if > 4 weeks steroid use
previous ocular trauma
anemia/hemodynamic crisis (ask about blood transfusions in past)

Clinical Features

asymptomatic initially
insidious, painless, gradual rise in IOP due to restriction of aqueous outflow
bilateral, but usually asymmetric
earliest signs are optic disc changes (safe to dilate pupil)
increased cup to disc ratio (vertical C/D > 0.6) 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 production
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 fluid to
reservoir under conjunctiva)
optic nerve head examination, IOP measurement and visual field testing to monitor
course of disease

Primary Angle Closure Glaucoma


12% of all glaucoma cases
peripheral iris bows forward in an already susceptible eye with a shallow anterior
chamber obstructing aqueous access to the trabecular meshwork
sudden shifting forward of the lens-iris diaphragm = pupillary block, results in
inability of the aqueous to flow from the posterior chamber to the anterior chamber
and a sudden rise in IOP

Risk Factors

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

Clinical Features

unilateral, but other eye predisposed


red, painful eye = RED FLAG
decreased visual acuity, vision acutely blurred from corneal edema
halo around lights
nausea and vomiting, abdominal pain
fixed mid-dilated pupil
corneal edema with conjunctival injection
marked increase in IOP even to palpation (> 40 mm Hg)
shallow anterior chamber, cells in anterior chamber

Complications
irreversible loss of vision if untreated, within hours to days
permanent peripheral anterior synechiae

Treatment
refer to ophthalmologist
topical steroids (not in primary care)
laser iridectomy
immediate treatment important to
preserve vision
prevent adhesions of peripheral iris to trabecular meshwork (peripheral anterior
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

Pupils
Pupil Abnormalities
Innervation
pupil size is determined by the balance between the sphincter muscle and the dilator
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
second order/preganglionic neuron = spinal cord sympathetic trunk via
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 (Horners Syndrome)
denervation hypersensitivity
when post-ganglionic fibres are damaged, understimulated end-organ develops
an excess of receptor and becomes hypersensitive
postganglionic parasympathetic lesions (Adies pupil)
pupil will constrict with 0. 125% pilocarpine (cholinergic agonist), whereas
normal pupil will not
postganglionic sympathetic lesions (i.e. Horners 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 Horners
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 oclock 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 detachment,
BRAO, CRAO, CRVO, advanced glaucoma
does not occur with media opacity e.g. corneal edema, cataracts
test: swinging flashlight
if light is shone in the affected eye, direct and consensual response 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
use ophthalmoscope with +4 setting, using red reflex especially in patients
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, Wernickes
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

Ocular Manifestations of Systemic Disease


Diabetes Mellitus (DM)
most common cause of blindness in young people in North America
blurring of distance vision with rise of blood sugar
consider DM if unexplained retinopathy, cataract, EOM palsy, optic neuropathy,
sudden change in refractive error
loss of vision due to
progressive microangiopathy, leading to macular edema
progressive diabetic retinopathy neovascularization traction retinal
detachment and vitreous hemorrhage
rubeosis iridis (neovascularization of the iris) leading to neovascular glaucoma
(poor prognosis)

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, reduces
neovascularization, hence reducing the angiogenic stimulus from ischemic retina
by decreasing retinal metabolic demand ^ reduces risk of blindness
vitrectomy for vitreous hemorrhage and retinal detachment in proliferative diabetic
retinopathy which is complicated by non-clearing vitreous hemorrhage or retinal

detachment
the diabetic retinopathy vitrectomy study indicated that early vitrectomy (before
hemorrhage) does not improve the visual prognosis

Lens
earlier onset of senile nuclear sclerosis and cortical cataract
may get hyperglycemic cataract, due to sorbitol accumulation (rare)
sudden changes in refraction of lens: changes in blood glucose levels (poor control)
may cause refractive changes by 3-4 diopters

Extra Ocular Muscle (EOM) Palsy

usually CN III infarct


pupil usually spared in diabetic CN III palsy, but get ptosis
may involve CN IV and VI
usually recover within few months

Optic Neuropathy
visual acuity loss due to infarction of optic disc/nerve

Multiple Sclerosis (MS)


relapsing, progressive CNS disease characterized by disseminated patches of
demyelination in the brain and spinal cord resulting in varied symptoms and signs
many ocular manifestations

Clinical Features
40% of patients with MS develop optic neuritis which results in blurred vision and
colour vision
central scotoma: because of damage to papillomacular bundle of retinal nerve fibres
diplopia: secondary to internuclear ophthalmoplegia (INO)
RAPD, ptosis, nystagmus, uveitis, optic atrophy, optic neuritis
white matter demyelinating lesions of optic nerve on MRI

Treatment
with optic neuritis, treatment with oral steroids leads to greater likelihood of getting
MS later on than treatment with IV steroids

Hypertension
retinopathy is the most common ocular manifestation of hypertension
key features of chronic HTN retinopathy: AV nicking, blot retinal hemorrhages,
microaneurysms, cotton wool spots
key features of acute HTN retinopathy: retinal arteriolar spasm, superficial retinal
hemorrhage, cotton-wool spots, optic disc edema
Table 5. Keith-Wagener-Barker Classification
Group 1 Mild to moderate narrowing or sclerosis of the arteioles
Group 2 Moderate to marked narrowing of the aterioles
Local and/or generalized narrowing of arterioles
Exaggeration of the light 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 carotid
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 arterioles)

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 surgical
decompression of the orbit

Giant Cell (Temporal) Arteritis


common in women > 60
clinical findings: abrupt monocular loss of vision; pain over the temporal artery
ischemic optic atrophy
50% lose vision in other eye if untreated

Diagnosis
temporal arterial biopsy + 6ESR (ESR can be normal, but likely 80-100 in first hour)

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

Pediatric Ophthalmology
Amblyopia
Definition
reduction of best-corrected visual acuity not directly due to structural pathology
cortical suppression of sensory input from an eye that is receiving blurred 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 years old

Etiology and Management


strabismus
correct with glasses for accommodative esotropia (50% of children experience
relief of their esotropia with glasses and will not require surgery)
occlusion of unaffected eye forces brain to use previously strabismic eye, to
bring vision in previously suppressed eye to normal before surgery
surgery: recession (weakening) = moving muscle insertion further back on the
globe; or resection (strengthening) = shortening the muscle
botulinum toxin for single muscle weakening
after ocular alignment is restored (glasses, surgery, botulinum toxin), patching is
frequently necessary to maintain vision until approximately age 8
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 good 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, retinal tear
bone fractures
blow out fracture: restricted EOM, diplopia, enopthalmos (sunken eye)
ethmoid fracture: subcutaneous emphysema of lid
lids: swelling, laceration, emphysema
conjunctiva: subconjunctival hemorrhage
cornea: abrasions - detect with fluorescein staining and cobalt blue filter in
ophthalmoscope or slit lamp
anterior chamber: assess depth, hyphema, hypopyon
iris: prolapse, iritis
lens: cataract, dislocation
retinal tear/detachment

Penetrating Trauma
include ruptured globe prolapsed iris, intraocular foreign body (FB)
r/o intraocular FB; especially if history of metal striking metal Orbit CT
initial management: refer immediately!!
ABCs
dont press on eyeball!
check vision, diplopia
apply rigid eye shield to minimize further trauma
keep head elevated 30-45 degrees to keep IOP down
keep NPO

Chemical Burns
alkali burns have a worse prognosis vs. acid burns because acids coagulate tissue and
inhibit further corneal penetration
poor prognosis if cornea opaque, likely irreversible stromal damage
even with a clear cornea initially, alkali burns can progress for weeks (thus, very
guarded prognosis)

Treatment
irrigate at site of accident immediately, with water or buffered solution
IV drip for at least 20-30 minutes with eyelids retracted in emergency
department
do not attempt to neutralize because the heat produced by the reaction will damage
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 than
two weeks (in the case of a persistent epithelial defect)

Blow-Out Fracture
blunt trauma causing fracture of orbital floor and orbital contents to herniate
into maxillary sinus
orbital rim remains intact
inferior rectus and/or inferior oblique muscles may be incarcerated at fracture site
infraorbital nerve courses along the floor of the orbit and may be damaged

Clinical Features

pain and nausea at time of injury


diplopia, restriction of EOM
infraorbital and upper lip paresthesia (CN V2)
enophthalmos (sunken eye), periorbital ecchymoses

Investigations
plain films: Waters view and lateral
CT: anteroposterior and coronal view of orbits

Treatment
refrain from coughing, blowing nose
systemic antibiotics may be indicated
surgery if fracture > 50% orbital floor, diplopia not improving, or enophthalmos
> 2 mm
may delay surgery if the diplopia improves

Ocular Medications
Topical Ocular Diagnostic Drugs
Fluorescein Dye
water soluble orange-yellow dye
green under cobalt blue light - ophthalmoscope or slit lamp
absorbed in areas of epithelial loss (ulcer or abrasion) ; note also stains mucus and
contact lenses

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

Mydriatics
dilate pupils
two 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 (Apotex),
betaxolol (Betoptic), carteolol (Teoptic)
systemic side effects: bronchospasm, exacerbation of congestive heart failure,
bradycardia, heart block, hypotension, impotence, depression

Cholinergic Stimulating
increases aqueous outflow
e.g. pilocarpine (Pilopine), carbachol (Isopto Carbachol)
side effects: miosis, brow ache, decreased night vision, headache, increased GI motility,
decreased heart rate

Adrenergic Stimulating
decrease aqueous production and increase outflow
e.g. epinephrine HCl, dipivifrin, brimonidine (Alphagan), apraclonidine (Lopidine)
side effects: contact allergy, hypotension in children

Carbonic Anhydrase Inhibitor


decrease aqueous production
e.g. oral acetazolamide (Diamox), topical dorzolamide (Trusopt), topical brinzolamide
(Azopt)
side effects: renal calculi, nausea, vomiting, diarrhea, weight loss, aplastic anemia, bone
marrow suppression, systemic acidosis
side effects generally absent with topical preparations

Prostaglandin Agonists
improves uveoscleral outflow
e.g. latanoprost (Xalatan), travaprost (Travatan), bimatoprost (Lumigun)
side effects: iris colour change, lash growth, trichiasis

Topical Ocular Therapeutic Drugs


NSAIDs
used for less serious chronic inflammatory conditions
decreased risk of complications
e.g. Ketorolac (Acular) drops, Diclofenac (Voltaren) drops

Anti-Histamines
used to relieve red and itchy eye, often in combination with decongestants
sodium cromoglycate (stabilizes most all membranes)

Corticosteroids
never prescribed by primary care physician unless emergency indications
e.g. fluorometholone (FML), betamethasone, dexamethasone (Maxidex),
prednisolone (Predsol 0.5%, Pred Forte 1%), rimexolone (Velox)
complications:
potentiates herpes simplex keratitis and fungal keratitis as well as masking
symptoms (within days)
posterior subcapsular cataract (within months)
increased IOP, more rapidly in steroid responders (within weeks)

Decongestants
weak adrenergic stimulating drugs (vasoconstrictor)
e.g. naphazoline, phenylephrine (Isopto Frin)
rebound vasodilation with over use; rarely can precipitate angle closure glaucoma

Antibiotics
indications: bacterial conjuntivitis, keratitis, or blepharitis
commonly as topical drops or ointments, may give systemically
e.g. sulfonamide (sodium sulfacetamide, sulfisoxazole), gentamicin (Garamycin),
erythromycin, tetracycline, bacitracin, polymyxin B

Ocular Drug Toxicity


Amiodarone
Atropine, Benztropine, Benzhexol
Chloroquine, hydroxychloroquine
Chlorpromazine
Contraceptive Pills
Digitalis
Ethambutol
Haloperidol (Haldol)
Indomethacin
Isoniazid
Nalidixic Acid
Steroids

Sulphonamides, NSAIDS
Tetracycline
Thioridazine
Vitamin A Intoxication
Vitamin D Intoxication

Table 7. Drugs with Ocular Toxicity

Corneal microdeposits and superficial keratopathy


Pupillary dilation (risk of angle closure glaucoma)
Bulls eye lesion at macula, vortex keratopathy
Anterior subcapsular cataract
Decreased tolerance to contact lenses, Migraine, Optic
neuritis, Central vein occlusion
Yellow vision, Blurred vision
Optic neuropathy
Oculogyric crises, Blurred vision
Superficial keratopathy
Optic neuropathy
Papilloedema
Posterior subcapsular cataracts, Glaucoma, Papilloedema
(systemic steroids), Increased severity of HSV infections
(geographic ulcers), Predisposition to fungal infections
Stevens-Johnson syndrome
Papilloedema
Pigmentary degeneration of retina
Papilloedema
Band keratopathy