OPHTHALMOLOGY

Dr. J.H. Fowler

Philip Dopp and Asif Salyani, chapter editors

Anna Kulidjian, associate editor

COMMON COMPLAINTS

CONJUNCTIVA

Common Ocular Problems in the Elderly

Pinguecula

Common Ocular Problems in Contact Lens Wearer

Pterygium

Subconjuctival Hemorrhage

THE OCULAR EXAMINATION

Conjunctivitis

Vision Assessment

Bacterial Conjunctivitis

Visual Fields

Viral Conjunctivitis

Pupils

Chlamydia Conjunctivitis

Anterior Chamber Depth

Allergic Conjuctivitis

Extraocular Muscles

Giant Papillary Conjunctivitis (GPC)

External Examination

Vernal Conjunctivitis

Slit-Lamp Examination

Tonometry

SCLERA

Ophthalmoscopy/Fundoscopy

Episcleritis

Scleritis

OPTICS

Scleromalacia Perforans

Emmetropia

Blue Sclerae

Refractive Errors

Staphyloma

Myopia

Hyperopia

CORNEA

Astigmatism

Foreign Bodies

Presbyopia

Corneal Abrasion

Anisometropia

Recurrent Erosions

Refraction

Corneal Ulcers

Refractive Eye Surgery

Herpes Simplex Keratitis

Herpes Zoster

THE ORBIT

Keratoconus

Exophthalmos (Proptosis)

Arcus Senilis

Enophthalmos

Kayser-Fleischer Rings

Preseptal Cellulitis

Orbital Cellulitis

THE UVEAL TRACT

Uveitis

LACRIMAL APPARATUS & LYMPH NODES

. .10

Anterior Uveitis

Lymph Nodes

Posterior Uveitis

Lacrimal Apparatus

Keratoconjunctivitis Sicca (Dry Eyes)

GLOBE

Epiphora (Tearing)

Endophthalmitis

Dacryocystitis

Dacryoadenitis

LENS

Cataracts

LIDS AND LASHES

Dislocated Lens

Lid Swelling

Ptosis

Trichiasis

Entropion

Ectropion

Hordeolum

Chalazion

Blepharitis

Xanthelasma

Lid Carcinoma

MCCQE 2006 Review Notes

Ophthalmology - OP1

. . . CONT.

OPHTHALMOLOGY

RETINA AND VITREOUS

OCULAR MANIFESTATIONS OF

Vitreous

SYSTEMIC DISEASE

Vitreous Hemorrhage

HIV

Retina

Other Systemic Infections

Central Retinal Artery Occlusion (CRAO)

Diabetes Mellitus (DM)

Branch Retinal Artery Occlusion

Multiple Sclerosis (MS)

Central Retinal Vein Occlusion (CRVO)

Hypertension

Retinal Detachment (RD)

Amaurosis Fugax

Retinitis Pigmentosa

Hyperthyroidism/Graves' Disease

Roth Spots

Connective Tissue Disorder

Age-Related Macular Degeneration (ARMD)

Giant Cell Arteritis

Sarcoidosis

BLURRED OPTIC DISC MARGINS

Drusen

STRABISMUS

Myelinated Nerve Fibres

Tropia

Phoria

GLAUCOMA

Paralytic Strabismus

Primary Open Angle Glaucoma

Non-Paralytic Strabismus

Primary Angle Closure Glaucoma

Secondary Open Angle Glaucoma

PEDIATRIC OPHTHALMOLOGY

Secondary Angle Closure Glaucoma

Amblyopia

Normal Pressure Glaucoma

Leukocoria

Congenital Glaucoma

Nasolacrimal System Defects

Ophthalmia Neonatorum

PUPILS

Rubella

Pupillary Light Reflex

Dilated Pupil: Differential Diagnosis

OCULAR TRAUMA

Constricted Pupil: Differential Diagnosis

Blunt Trauma

Relative Afferent Pupillary Defect (RAPD)

Penetrating Trauma

Chemical Burns

NEURO-OPHTHALMOLOGY

Hyphema

Visual Field Defects

Blow Out Fractures

Bitemporal Hemianopsia

Sympathetic Ophthalmia

Homonymous Hemianopsia

Internuclear Ophthalmoplegia (INO)

OCULAR EMERGENCIES

Nystagmus

DRUGS WITH OCULAR TOXICITY

INTRAOCULAR MALIGNANCIES

Topical Ocular Diagnostic Drugs

Malignant Melanoma

Glaucoma Medications

Retinoblastoma

Topcial Ocular Therapeutic Drugs

Metastases

OCULAR DRUG TOXICITY

REFERENCES

OP2 - Ophthalmology

MCCQE 2006 Review Notes

COMMON COMPLAINTS

Persistent Loss of Vision

gradual (weeks to months)

• refractive error

• cataracts

• diabetes

• macular degeneration

• glaucoma (chronic)

• intracranial compressive lesion

• tumour infiltration

• toxic degeneration

acute (minutes to days)

• vascular/ischemia

• cortical blindness

• central retinal vein/artery occlusion (CRVO/CRAO)

• vitreous hemorrhage

• optic neuropathy

• giant cell (temporal) arteritis

• anterior ischemic optic neuropathy (AION)

• optic neuritis

• multiple sclerosis (MS)

• papillitis or retrobulbar neuritis

• retinal detachment

• acute glaucoma

• acute iritis

Transient Loss of Vision (Amaurosis Fugax)

transient ischemic attack (TIA), microemboli

migrainous spasm of artery

hypertension

Floaters

physiologic; vitreous syneresis

vitreous hemorrhage

retinal detachment

Flashing Lights

vitreous traction

retinal tear/detachment

migraine

Ocular Pain

corneal abrasion, corneal ulcer, foreign body

acute angle closure glaucoma

acute uveitis

scleritis, episcleritis

optic neuritis

differentiate from ocular ache: eye fatigue/asthenopia

Photophobia (Light Sensitivity)

iritis

meningitis, encephalitis

light dispersion by mucus, lens, corneal opacities

retinal degeneration

acute glaucoma

Diplopia (Double Vision)

binocular diplopia: strabismus, CN paresis (III,IV,VI), muscle entrapment

monocular diplopia: dislocated lens, cataract, corneal scar

MCCQE 2006 Review Notes

Ophthalmology - OP3

COMMON COMPLAINTS

. . CONT.

Red Eye

Table 1. Differential Diagnosis of Red Eye

Conjunctivitis

Acute Iritis

Acute Glaucoma

Angle Closure Keratitis

Discharge

Bacteria: pus

Profuse tearing

Virus: serous

Allergy: mucous

Pain

++++

+++

(tender globe)

With nausea

With blinking

Photophobia

++++

Vision

Normal

Reduced

Varies with

(cloudy

(corneal edema)

site of lesion

aqueous)

Pupil

Normal

Smaller

Fixed

Same or smaller

in mid dilation

Clinical Pearl

All red eyes are not necessarily conjunctivitis.

Table 2. Additional Features of Red Eye

Conjunctivitis

Acute Iritis

Acute Angle Closure Glaucoma

Injection

Palpebral+bulbar

Ciliary flush

Diffuse

(limbal palor)

Intraocular Pressure (IOP)

Normal

Lower

Increased

Ant.chamber

Normal

Cells/flare

Shallow

Cornea

Normal

Keratic

Steamy

precipitates

Other

Preauricular node

Synechiae

Nausea/vomiting

(if viral)

other causes of red eye

• adnexal and lacrimal system

• hordeolum/stye

• chalazion

• blepharitis

• dacryocystitis

• canaliculitis

• dacryoadenitis

• preseptal cellulitis

• orbital cellulitis

• conjunctiva

• subconjunctival hemorrhage

• pterygium, pinguecula

• sclera

• episcleritis

• scleritis

• cornea

• abrasion

• ulcer

• foreign body

• endophthalmitis

OP4 - Ophthalmology

MCCQE 2006 Review Notes

COMMON COMPLAINTS

. . CONT.

COMMON OCULAR PROBLEMS

IN THE ELDERLY

cataracts

age-related macular degeneration (ARMD)

epiphora

• overflow of tears

• due to dry eyes, entropion, ectropion, trichiasis

neoplasia

vascular disease: CRVO, CRAO, giant cell arteritis

dry eyes

ptosis

COMMON OCULAR PROBLEMS

IN CONTACT LENS WEARER

corneal abrasion

superficial punctate keratitis

giant papillary conjunctivitis

sterile infiltrates (immunologic)

infected ulcers ( Pseudomonas, S. aureu)

THE OCULAR EXAMINATION

suprachoroidal space

sinus venosus sclerae

choroid

(canal of schlemm)

sclera

vitreous body

visual part of retina

lens

fovea centralis

aqueous outflow

hyaloid canal

sheath of optic nerve

anterior chamber

cornea

posterior chamber

central artery and vein of retina

iris

suspensory ligament

optic nerve

anterior chamber angle

of lens

lamina cribrosa of sclera

ciliary part of retina

ciliary body and

conjunctiva

ciliary muscle

intervaginal space

ora serrata

bulbar fascia (tendon’s capsule)

tendon of medial rectus muscle

Figure 1. Diagram of the Eye

Drawing by Luke Itani

VISION ASSESSMENT

always note best corrected vision first (e.g. with glasses if possible), especially in emergency room

test both near and distance vision

pinhole test will improve vision with most refractive errors

Visual Acuity (VA) Far

Snellen Fraction = testing distance (usually 6 metres or 20 feet)

smallest line patient can read on the chart

e.g. 20/40 -2 (missed two letters of 20/40 line)

OD = RIGHT EYE, OS = LEFT EYE, OU = BOTH EYES

Heirarchy for low vision - Snellen acuity - count fingers - hand motion - light perception - no light perception

Legal blindness is 20/200 or < 10 degress of visual field in better eye

Minimum visual acuity to operate an automobile is 20/40 in the better eye

Visual Acuity (VA) Near

use pocket vision chart (e.g. Rosenbaum)

record number and testing distance (usually 30 cm)

e.g. J2 @ 30cm

MCCQE 2006 Review Notes

Ophthalmology - OP5

THE OCULAR EXAMINATION . . . CONT.

Visual Acuity for Children,Illiterate Adults or Dysphasics with CVA

Sheridan-Gardiner matching test (most 4 year olds able to do it)

illiterate "E" chart (patient states direction of “E”)

Infant Visual Acuity

6-12 months - 20/120

1-2 years - 20/80

2-4 years - 20/20

VISUAL FIELDS

test visual field quadrants grossly by confrontation

automated field testing (e.g. Humphrey, Goldmann), or Tangent Screen

PUPILS

examine pupils with respect to

• equality, size, shape

• reactivity to light (both direct and consensual)

test for relative afferent pupillary defect (RAPD)

• use "swinging flashlight test" (use ophthalmoscope with “+4” setting especially with dark brown iris)

test pupillary constriction portion of near reflex

• bringing object from far to near results in

• lens accommodation

• eye convergence

• pupil constriction

• must use reduced illumination or pupillary constriction will be produced

ANTERIOR CHAMBER DEPTH

shine light tangentially from temporal side

shallow = > 2/3 of nasal iris in shadow

EXTRAOCULAR MUSCLES

Alignment

examine in primary position of gaze (e.g. straight ahead)

Hirschberg test (shine light into patient's eyes from 30 cm away)

• corneal light reflex should be symmetric and near centre of each cornea

strabismus testing as indicated - see Strabismus section

Movement

examine movement of eyeball through the nine diagnostic positions of gaze

(with six muscles responsible for extra-ocular movement (EOM))

determine if diplopia is present in any position of gaze

observe for nystagmus (horizontal and vertical)

EXTERNAL EXAMINATION

the four L’s

• lymph nodes

• lacrimal apparatus

• lids

• lashes

SLIT-LAMP EXAMINATION

systematically examine all structures of the anterior segment

• lids and lashes, including upper lid eversion if necessary

• conjunctiva and sclera

• cornea

• anterior chamber

• iris

• lens

also examine with

• fluorescein staining: (water-soluble dye stains de-epithelialized cornea green),

with cobalt blue filter

• Rose Bengal dye (stains devitalized corneal epithelium)

can examine structures in the posterior segment with special lenses (78D, 90D)

OP6 - Ophthalmology

MCCQE 2006 Review Notes

THE OCULAR EXAMINATION . . . CONT.

TONOMETRY

measurement of intraocular pressure

normal range is 8-21 mm Hg

commonly measured by

• indentation (Schiotz or Tonopen)

• applanation (Goldmann) - gold standard

• non-contact (air puff)

use topical anesthetic for Schiotz, Goldmann, Tonopen

OPHTHALMOSCOPY/FUNDOSCOPY

examination of the anterior segment

• fluorescein and colbat blue filter and +20 lens

• corneal opacity

• cataract

• the red reflex

examination of the posterior segment of the eye

• vitreous

• optic disc (colour, cup, margins, cup/disc ratio)

• nasal retinal vessels

• retina, macula (temporal)

best with pupillary dilatation (e.g. tropicamide) (see Table 6)

contraindications to dilatation

• narrow anterior chamber angles

• neurologic abnormality requiring pupillary evaluation

• iris supported anterior chamber lens implant (square pupil)

OPTICS

main refractive mechanisms are: cornea (2/3), lens (1/3)

EMMETROPIA

no refractive error

image of distant objects focused on the retina without accommodation

REFRACTIVE ERRORS(see Figure 2 and Figure 3)

distant light is not focused on retina, without accommodation

three types: myopia, hyperopia, and astigmatism

MYOPIA

"nearsightedness"

to remember: LMN (Long eyeball is Myopic, requiring negative/concave lens, and is Nearsighted)

Pathophysiology

globe too long relative to refractive mechanisms or refractive mechanisms too strong

image of distant object falls in front of retina without accommodation --> blurring of distant vision

Presentation

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 degeneration and detachment

chronic open angle glaucoma

complications not prevented with refractive correction

Management

correct with concave negative (-) spectacles or contact lenses, which diverge light rays

refractive eye surgery - see below

HYPEROPIA

"farsightedness"

hyperopia may be developmental, or may be due to any cause which shortens the eyeball

to quantitate hyperopia, cycloplegic drops are used to prevent accommodation

Pathophysiology

globe too short or refractive mechanisms too weak

image of distant object falls behind retina without accommodation

person will accommodate to try to bring image onto retina

MCCQE 2006 Review Notes

Ophthalmology - OP7

OPTICS . . . CONT.

Presentation

youth: usually do not require glasses (still have sufficient accommodative ability to focus image on retina),

+/- accommodative esotropia (see Strabismus section)

30s: 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 in later life as lens enlarges

Management

when symptomatic, correct with convex positive (+) lenses, which converge light rays

refractive eye surgery - see below

ASTIGMATISM

light rays not refracted uniformly in all meridians

due to non-spherical surface of cornea or non-spherical lens (e.g. football shaped)

regular astigmatism: curvature is uniformly different in meridians at right angles to each other

irregular astigmatism: distorted cornea, due to injury or keratoconus (cone-shaped cornea)

Management

correct with cylindrical lens, toric contact lens, arcuate keratotomy or refractive eye surgery (see below)

PRESBYOPIA

decreased ability of eye to accommodate with aging (decrease in lens elasticity, NOT a refractive error)

experienced by emmetropes as well as patients with refractive errors

normal decline in near vision with age (> 40 years) with distance spectacles in place

Presentation

if initially emmetropic, starts holding things further away to read, but distance vision unaffected

if initially myopic, remove distance glasses to read

if initially hyperopic, symptoms of presbyopia occurs earlier;

the hyperope needs distance glasses in later decades

Management

correct vision with convex positive (+) lens for reading

reading lens will blur distance vision; options are half-glasses or bifocals

ANISOMETROPIA

difference in refractive error between eyes

• second most common cause of amblyopia in children

Emmetropia

Converges

Hyperopia corrected with positive lens

Myopia

Hyperopia

Diverges

Figure 2. Refractive Errors and Emmetropia

Myopia corrected with negative lens

Figure 3. Correction of

Refractory Errors

OP8 - Ophthalmology

MCCQE 2006 Review Notes

OPTICS . . . CONT.

REFRACTION

technique of determining the lenses needed to correct the optical defects of the eye (ametropia)

two techniques used

1) Flash/Streak Retinoscopy

• refractive error determined objectively by use of retinoscope and lenses

2) Manifest (Acceptance)

• subjective trial of lenses used to refine retinoscopy findings

• a typical lens prescription would contain

• sphere power in D (diopters)

• cylinder power in D to correct astigmatism

• axis of cylinder (in degrees)

• add (reading lens) for presbyopes

• e.g. -1.50 + 1.00 x 120 degrees, add +2.00

REFRACTIVE EYE SURGERY

permanently altering the refractive properties of the cornea

used for correction of myopia, hyperopia, and astigmatism

most commonly using excimer laser system

ablation of the corneal surface - photorefractive keratectomy (PRK)

ablation of the stroma below a flap of corneal tissue (LASIK)

THE ORBIT

EXOPHTHALMOS (PROPTOSIS)

eyeball protrusion

Etiology

hyperthyroidism: Graves' disease (unilateral or bilateral, the most common cause in adults)

orbital cellulitis (unilateral, most common cause in children)

primary or secondary orbital tumours

orbital/retrobulbar hemorrhage

cavernous sinus thrombosis or fistula

sinus mucoceles

Diagnosis

exophthalmometer (Hertel): measure at lateral canthi

CT head

ENOPHTHALMOS

retracted globe

often due to "blow-out" fracture (see Ocular Trauma section)

PRESEPTAL CELLULITIS

infection of soft tissue anterior to orbital septum

Etiology

stye, chalazion, acute meibomitis

insect bite

secondary to lid laceration or lacrimal system inflammation

Symptoms and Signs

tender and erythematous lids

may have adenopathy and fever

normal VA, pupil, EOMs

no exophthalmos or RAPD

Management

topical and systemic antibiotics

warm compress

ORBITAL CELLULITIS

inflammation of orbital contents posterior to orbital septum

common in children, but also in the aged and immunocomprimised

Etiology

secondary to sinusitis, facial and/or tooth infections and trauma

MCCQE 2006 Review Notes

Ophthalmology - OP9

THE ORBIT . . . CONT.

Symptoms and Signs

RED FLAG - opthalmoplegia (because of pain on ocular movement)

lids swollen shut, chemosis (conjunctival swelling)

exophthalmos

decreased VA

RAPD due to optic disc edema may occur

adenopathy and fever

Management

admit, IV antibiotics, blood cultures and orbital CT

serious complications exist e.g. cavernous sinus thrombosis, meningitis and blindness

surgical evacuation of abscess if it develops

Table 3. Differences Between Preseptal and Orbital Cellulitis

Finding

Preseptal Cellulitis

Orbital Cellulitis

Fever

Present

Lid edema

Moderate to severe

Severe

Chemosis

Absent or mild

Moderate or marked

Proptosis

Unusual

Present

Pain on eye movement

Absent

Present

Ocular mobility

Normal

Decreased

Vision

Normal

Diminished vision +/- diplopia

RAPD

Absent

May be seen

Leukocytosis

Minimal or moderate

Marked

Adenopathy

Absent

May be seen

ESR

Normal or elevated

Very elevated

Additional findings

Skin infection

Sinusitis; dental abscess

LACRIMAL APPARATUS AND LYMPH NODES

LYMPH NODES

temporal conjunctival lymphatics drain to preauricular and parotid nodes

nasal conjunctival lymphatics drain to submandibular nodes

enlarged nodes significant for infectious etiology, especially viral or chlamydial conjunctivitis

LACRIMAL APPARATUS

tear film made up of three layers

• an outer oily layer, secreted by the meibomian glands

• a middle watery layer, constant secretion from conjunctival glands and

reflex secretion by lacrimal gland with ocular irritation or emotion

• an inner mucous layer, secreted by conjunctival goblet cells

KERATOCONJUNCTIVITIS SICCA (DRY EYES)

Etiology

with aging, tear production normally decreases

lid abnormality (ectropion), decreased blinking e.g. CN VII palsy

systemic diseases: rheumatoid arthritis, Sjögren's syndrome, sarcoidosis, amyloidosis, leukemia, lymphoma

vitamin A deficiency, especially in malnourished areas

post-cataract surgery

medications: anticholinergics, diuretics, antihistamines

Symptoms and Signs

dry eyes, red eyes, blurred vision, overflow tearing

Diagnosis

slit-lamp exam: decreased tear meniscus, decreased tear break up time (BUT),

superficial punctate keratitis (SPK)

revealed by fluorescein staining, rose bengal staining

Schirmer test: measures tear quantity on surface of eye in 5 minute time period

(< 10 mm of strip wetting in 5 minutes is considered a dry eye)

Complications

erosions and scarring of cornea

OP10 - Ophthalmology

MCCQE 2006 Review Notes

LACRIMAL APPARATUS AND LYMPH NODES.. . CONT.

Management

artificial tears and ointments

punctal occlusion

tarsorrhaphy (sew lids together)

treat underlying cause

EPIPHORA (TEARING)

Etiology

emotions

ocular irritation/inflammation (including entropion, trichiasis)

blocked tear outflow (ectropion; punctal, canalicular or nasolacrimal duct (NLD) obstruction)

• aging

• infection (dacryocystitis)

• rhinitis

• in infants: failure of NLD opening

paradoxical lacrimation (crocodile tears)

• excessive tearing while eating

• sequelae to Bell's palsy, due to aberrant regeneration of CN VII

• nerve fibres that formerly went to the salivary glands regrow to the lacrimal gland

Diagnosis

history and observation of lids

fluorescein dye put in eye, examine for punctal reflux by pressing on canaliculi

irrigate through punctum into nose, noting resistance/reflux

Management

lid repair for ectropion/entropion

punctal irrigation

NLD probe (infants)

tube placement: temporary (Crawford) or permanent (Jones)

surgical: dacryocystorhinostomy (DCR) = joining the lacrimal sac to the nasal mucosa,

thus restoring lacrimal drainage

DACRYOCYSTITIS

infection of the lacrimal sac

usually due to obstruction of the nasolacrimal duct

usually very young children (due to failure of NLD opening) or in persons > 40 years old

commonly associated with S. aureus or rarely ß-hemolytic streptococcus infection in acute setting;

S. pneumoniaein chronic infections

Symptoms and Signs (see Colour Atlas OP1)

tearing and discharge

inflammation, pain, swelling over lacrimal sac at inner canthus

pressure on the lacrimal sac may extrude pus through the punctum

in the chronic form, tearing may be the only symptom

Management

warm compresses, nasal decongestants

in newborns - gentle massage over sac, +/- probing

in adults - local or systemic antibiotics +/- irrigation (refer to ophthalmologist)

if chronic, treatment is surgical: dacryocystorhinostomy (DCR)

DACRYOADENITIS

very rare, usually children

inflammation of the lacrimal gland (outer third of upper eyelid)

acute causes: (infectious etiology) mumps, measles, influenza in children, gonorrhea in adults

chronic causes: lymphoma, leukemia, sarcoidosis, tuberculosis

Symptoms and Signs (see Colour Atlas OP9)

pain, swelling, redness of the outer region of the upper eyelid

Management

+/- systemic antibiotics

incision and drainage if required

MCCQE 2006 Review Notes

Ophthalmology - OP11

LIDS AND LASHES

LID SWELLING

Etiology

commonly due to allergy, with shrivelling of skin between episodes

dependent edema on awakening (e.g. CHF, renal or hepatic failure)

orbital venous congestion due to mass or cavernous sinus fistula

dermatochalasis: loose skin due to aging

lid cellulitis, hypothyroidism (e.g. myxedema), trauma (e.g. bruising), chemosis

adenoviral conjunctivitis

PTOSIS

drooping of upper lid > 2 mm below the superior corneal margin

Etiology

congenital: very rare

CN III palsy

• complete: eye is down and out, mydriasis (pupil dilation) (e.g. external compression)

• incomplete: pupil-sparing (e.g. diabetes mellitus)

Horner's syndrome

• ptosis, miosis, anhidrosis

• loss of sympathetic innervation causing Muller muscle paralysis

• see Pupils section for causes

myasthenia gravis (see Neurology Chapter)

• easy fatiguability, with ptosis and diplopia

• diagnose with Tensilon test

myogenic: disinsertion or dehiscence of levator aponeurosis

• most common cause of acquired ptosis in geriatrics

pseudoptosis (e.g. dermatochalasia, enophthalmos, contralateral endocrine exophthalmos)

trauma, infection (e.g. cellulitis)

mechanical

• eyelid prevented from opening completely by mass or scarring

Management

treat underlying cause

diabetic CN III palsy may resolve spontaneously

surgical correction if interferes with vision or for cosmesis

TRICHIASIS

eyelashes turn inward causing corneal irritation +/- ulceration

patient complains of irritation, tearing, mucous discharge

Management

pluck eyelash, electrolysis, surgery to remove eyelash +/- destroy hair follicles

ENTROPION

lid margin turns in towards globe

most commonly affects lower lid

symptoms: tearing, dry eye, cosmetic

may cause abrasions with secondary corneal scarring

Etiology

involutional (aging)

scar contraction (burns, surgery)

orbicularis oculi muscle spasm

congenital

Management

lubricants, evert lid with tape, surgery

ECTROPION

eversion of lower lid

often bilateral

symptoms: dry eye, tearing, cosmetic

may cause exposure keratitis

Etiology

weak orbicularis oculi (aging)

CN VII palsy

scarring (burns, surgery)

mechanical (tumour, herniated fat)

Management

upward massage with ointment or surgery

lubricants

OP12 - Ophthalmology

MCCQE 2006 Review Notes

LIDS AND LASHES . . . CONT.

HORDEOLUM ‘STYE’

infection of the glands of the eyelid, usually with S. aureus

painful, red swelling of lid

internal

• acute infection of meibomian gland (Meibomitis)

• chalazion in chronic stage

external

• stye, pimple

• acute infection of hair follicle or of glands of Zeis or Moll

Management

warm compresses, lid care

topical antibiotics

cellulitis may develop (necessitates systemic antibiotics)

usually resolves in 2-5 days

CHALAZION(see Colour Atlas OP10)

due to chronic sterile granuloma of a meibomian gland (following acute meibomitis),

usually pointing towards the conjunctiva

painless, often subsides

differential diagnosis: basal cell carcinoma, sebaceous cell adenoma, meibomian gland carcinoma

differentiate from hordeolum by absence of acute inflammatory signs

Management

warm compresses

surgical incision and curettage if needed

BLEPHARITIS (see Colour Atlas OP11)

chronic inflammation of lid margins

symptoms: redness of lid margins, scaling and discharge with misdirection or loss of lashes,

burning and/or itching of lids

most common types

• S. aureus

• ulcerative, with dry scales

• seborrheic

• no ulcers, with greasy scales

association with allergy, acne rosacea, seborrheic dermatitis

Complications

recurrent chalazia

conjunctivitis

keratitis

corneal ulceration and neovascularization (late sequelae from trichiasis)

Management (S. aureus )

warm compresses and lid hygiene

cleansing with dilute baby shampoo

topical or systemic antibiotics as needed

XANTHELASMA

lipid deposits in histiocytes in dermis of lids

frequently near inner canthus, may be bilateral

appears as pale, slightly raised yellowish patches or streaks

sometimes associated with increased serum cholesterol

of more concern in young; common in elderly

Management

surgical removal for cosmesis only, recurrences common

LID CARCINOMA

Etiology

basal cell carcinoma (95%)

• spread via local invasion

• rodent ulcer, indurated base with pearly rolled edges

squamous cell carcinoma (5%)

• spread via local invasion, may also spread to nodes and metastasize

• ulceration, keratosis of lesion

sebaceous cell carcinoma (rare)

• can present as non-resolving blepharitis (unilateral)

• highly invasive, metastasize

Management

(see Dermatology/Plastic Surgery Chapter)

surgical excision

irradiation optional for basal cell, sebaceous cell

biopsy to confirm diagnosis

MCCQE 2006 Review Notes

Ophthalmology - OP13

CONJUNCTIVA

a mucous membrane/epithelium

bulbar conjunctiva: covers sclera to the corneal limbus

palpebral conjunctiva: covers inside of lids

PINGUECULA

yellow nodule of hyaline and elastic tissue

commonly deep to conjunctiva adjacent to the limbus

associated with sun and wind exposure

common, benign, usually nasal

Management

does not require treatment, surgical excision rarely indicated

if ulcerated, topical antibiotics may be required

PTERYGIUM(see Colour Atlas OP8)

fleshy triangular encroachment of epithelial tissue onto the cornea (extension of pinguecula)

usually nasal and bilateral

associated with wind, ultraviolet light exposure

Management

surgery if threatens visual axis, causes irritation, or for cosmesis

may recur (10% with conjunctival grafts) and require repeated surgery

may decrease recurrence with conjunctival autograft or mitomycin C (anti-neoplastic) drops

SUBCONJUNCTIVAL HEMORRHAGE

blood beneath the conjunctiva

painless, normal vision

causes: idiopathic, valsalva, trauma, bleeding disorders

if bilateral and recurrent, rule out blood dyscrasias, hypertension, HIV, Kaposi sarcoma

Management

reassurance as it resorbs in 2-3 weeks, discourage rubbing

CONJUNCTIVITIS

Etiology

(see Table 4)

tired or dry eyes

allergy: pollutants, wind dust

infection: bacterial, viral, chlamydial, fungal, rickettsial, parasitic

chemical

irradiation associated with systemic disease

immune reaction e.g. giant papillary conjunctivitis especially in contact lens wearer

secondary to dacryocystitis or canaliculitis

Symptoms and Signs

gritty sensation, purulent discharge, crusts on lids upon awakening

inflamed and injected conjunctiva usually with limbal pallor

follicles (common)

• pale lymphoid elevations of the conjunctiva

• found in viral and chlamydial conjunctivitis

papillae

• vascularized elevations of the palpebral conjunctiva (contain PMNs)

• found in giant papillary conjunctivitis (GPC) and vernal conjunctivitis

(see Colour Atlas OP13)

often has a purulent white-yellow discharge, and less commonly papillae

causes: S. aureus , S. pneumoniae, and H. influenzae

may also be due to N. gonorrhea (in neonates and sexually active people),

Chlamydia is the most common cause in neonates

classification

1.Hyperacute: N. gonorrhea, N. meningitis

2.Acute: H.egyptius, S. pneumoniae

3.Subacute: H. influenzae

Management

topical antibiotics

systemic antibiotics if indicated

course - self-limited - 10-14 days if no treatment, 1-3 days with treatment

OP14 - Ophthalmology

MCCQE 2006 Review Notes

CONJUNCTIVA.. . CONT.

(see Colour Atlas OP14)

watery discharge (mucopurulent common), follicles, subepithelial corneal infiltrates may occur at 10-14 days

associated with cold symptoms, (recent upper respiratory tract infection (URTI) history)

preauricular node often palpable and tender

initially unilateral, often progresses to the other eye

cause: adenovirus

Management

self-limiting - (7 - 10 days or longer)

adenovirus is highly contagious therefore proper hygiene is very important

CHLAMYDIAL CONJUNCTIVITIS

caused by Chlamydia trachomatis

(various serotypes)

affects neonates on day 3-5, sexually active people

causes trachoma, inclusion conjunctivitis, lymphogranuloma venereum (L1, L2, L3)

Trachoma

severe keratoconjunctivitis

leading cause of blindness in the world

papillae and follicles on superior palpebral conjunctiva

conjunctival scarring leads to entropion, causing trichiasis, corneal abrasions +/- ulceration and scarring

keratitis leads to superior vascularization (pannus) and corneal scarring

treatment: systemic tetracycline

Inclusion Conjunctivitis

follicles with occasional keratitis

most common cause of conjunctivitis in newborns

prevention: topical erythromycin at birth

treatment: topical tetracycline and systemic erythromycin

(see Colour Atlas OP15)

intermittent

chemosis/injection with itching and burning

mucous discharge, lid edema, palpebral conjunctival papillae

Management

avoid irritants

cold compresses

topical medications: decongestant/antihistamines (e.g. Albalon-A), mast cell stabilizer (e.g. Opticrom)

combinations (e.g. Patanol), NSAIDs (e.g. Acular), steroids (not used in primary care)

GIANT PAPILLARY CONJUNCTIVITIS (GPC)

immune reaction to mucous debris on lenses in contact lens wearers

large papillae form on superior palpebral conjunctiva

Management

decrease wearing time, clean lenses thoroughly

switch to disposable lenses or hard lenses

topical mast cell stabilizer

if refractory to treatment stop using contacts

VERNAL CONJUNCTIVITIS

allergic condition, seasonal (warm weather)

large papillae on superior palpebral conjunctiva may cause corneal abrasions

occurs in first decade, may last for many years

Management

topical and/or systemic antihistamines

topical NSAIDs, mast cell stabilizer, steroids (not in primary care)

MCCQE 2006 Review Notes

Ophthalmology - OP15

SCLERA

sclera is the white fibrous outer protective coat of the eye

continuous with the cornea anteriorly and the dura of the optic nerve posteriorly

made of avascular collagen, biochemically similar to joint cartilage,

thus rheumatoid conditions may affect sclera and episclera

episclera is a thin layer of vascularized tissue covering the sclera anteriorly

EPISCLERITIS

usually unilateral; simple or nodular

non-specific immune response to irritants

Etiology

mostly idiopathic

associated with rheumatoid arthritis (RA), gout, Sjögren's syndrome, SLE,

herpes zoster, tuberculosis, syphilis or coccidioidomycosis in one third of cases

more frequent in women than men (3:1)

Symptoms and Signs (see Colour Atlas OP16)

localized, elevated, segmental hyperemia, pink/purple-coloured globe

pain, swelling, tenderness, photophobia, lacrimation

topical vasoconstrictor reduces redness

lasts for weeks, typically recurs

Management

generally self limited

chilled artificial tears

topical corticosteroids for 3-5 days if painful (prescribed and monitored by ophthalmologist)

SCLERITIS

uni- or bilateral; sectoral, diffuse, nodular or necrotizing

anterior scleritis: engorgement of vessels deep to conjunctiva

may cause scleral melt, corneal ulceration, secondary glaucoma

posterior scleritis: may cause exudative retinal detachment

usually with episcleral involvement

Etiology

over half are a manifestation of systemic disease

• autoimmune e.g. SLE, RA

• granulomatous e.g. TB, sarcoidosis, syphilis

• metabolic e.g. gout, thyrotoxicosis

• infectious e.g. S. aureus, S. pneumoniae, P. aeurginosa

, HSV, herpes zoster

chemical or physical agents e.g. thermal, alkali or acid burns

idiopathic

Symptoms and Signs (see Colour Atlas OP17)

severe pain and tenderness, more severe than in episcleritis

pain is best indicator of disease progression

conjunctival injection/scleral engorgement

bluish-red hue (in contrast to brighter red of episcleritis)

• topical vasoconstrictors will decrease redness of episcleritis, facilitating examination of scleritis

+/- decrease in visual acuity

Management

topical steroids, not used in primary care (may thin sclera)

systemic NSAIDs or steroids

SCLEROMALACIA PERFORANS

associated with severe rheumatoid arthritis (rare)

thinning of the sclera may lead to uveal dehiscence and globe rupture with minor trauma

prognosis poor, avoid steroids

very gentle examination of eye (Schiotz tonometry contraindicated)

BLUE SCLERAE

rare, uveal pigment seen through thin sclera

associated with: collagen vascular diseases (CVD) (e.g. osteogenesis imperfecta,

Ehlers-Danlos syndrome, Marfan's syndrome), prolonged use of corticosteroids

may occur in normal newborns

STAPHYLOMA

localized ballooning of thinned sclera - anteriorly, equatorially or posteriorly

seen in rheumatoid arthritis, high myopia, glaucoma, trauma

OP16 - Ophthalmology

MCCQE 2006 Review Notes

CORNEA

function

• transmission of light

• refraction of light (2/3 of total refractive power)

• barrier against infection, foreign bodies

transparency due to avascularity, uniform structure and deturgescence

5 layers: epithelium, Bowman's membrane, stroma, Descemet's membrane, endothelium

extensive sensory fibre network (V1 distribution); therefore abrasions and inflammation

(keratitis) are very painful

two most common corneal lesions: abrasions and foreign bodies

FOREIGN BODIES (see Colour Atlas I5)

RED FLAG -foreign body behind lid may cause multiple vertical epithelial abrasion due to blinking

tearing, photophobia, foreign body sensation

detected with fluorescein staining viewed under cobalt blue light of ophthalmoscope or slitlamp

Complications

scarring, infection, rust ring, secondary iritis

Management

remove under magnification using local anesthetic and sterile needle

or refer to ophthalmologist (depending on depth and location)

topical antibiotics

cycloplegia (paralysis of ciliary body = loss of accommodation) if iritis already present

no pressure patch if from contact lens wear

must see the next day and check for secondary iritis and infection

CORNEAL ABRASION

Etiology

trauma (e.g. fingernails, paper, twigs), contact lens

Symptoms and Signs (see Colour Atlas OP2)

pain on blinking, conjunctival injection, tearing, photophobia (after 24-48 hours)

de-epithelialized area stains green with fluorescein dye

pain relieved with topical anesthetic

Complications

infection, ulceration, recurrent erosion, secondary iritis

Management

topical antibiotics

+/- short acting topical cycloplegics (rest iris for comfort - prevents secondary iritis and posterior synechiae)

patch affected eye for comfort only if abrasion is large

NEVER patch abrasion secondary to contact lens wear (prone to Pseudomonas infection)

NEVER give topical analgesics (except to facilitate examination) - impedes epithelial healing

(unless needed to facilitate examination)

systemic analgesics as needed

most abrasions clear within 24-48 hours

bilateral occlusion gives fastest healing

RECURRENT EROSIONS

localized area of superficial corneal edema +/- de-epithelialization where the epithelium fails to

properly adhere to the underlying Bowman's membrane, therefore epithelial cells detach easily

Etiology

previous injury with incomplete healing

corneal dystrophy

spontaneous, idiopathic

Symptoms and Signs

patient usually awakes with pain in morning when poorly adherent epithelium

is dislodged during first eye opening of the day

examination reveals localized epithelial irregularity

Management

as for corneal abrasion

bandage contact lens (to protect corneal epithelium), bed rest

topical hypertonic 2% or 5% sodium chloride solution to dehydrate epithelial edema

anterior stromal needle puncture or YAG laser for chronic recurrence

excimer laser superficial keratectomy

MCCQE 2006 Review Notes

Ophthalmology - OP17

CORNEA . . . CONT.

Table 4. Corneal Abrasion vs. Corneal Ulcer

Abrasion

Ulcer

Time course

Acute (hours)

Subacute (days)

History of trauma

Yes

Cornea

Clear

White, necrotic

Iris detail

Clear

Obscured

Corneal thickness

Normal

May have crater effect

Extent of lesion

Limited to epithelium

Extension into stroma

CORNEAL ULCERS

Etiology

secondary to corneal abrasions, conjunctivitis, blepharitis, usually bacterial, rarely viral or fungal

contact lens use (50% of ulcers)

marginal ulcers are mostly due to staphylococcal toxins from associated blepharitis

and various autoimmune disorders

central ulcers are most serious because they can perforate or scar

Symptoms and Signs

RED FLAG - pain NOT relieved with topical anesthetic

pain, photophobia, tearing, decreased visual acuity (if central ulcer)

area of thinning with infiltrative base

surrounding corneal edema, conjunctivitis

+/- hypopyon (pus in anterior chamber)

Complications

corneal perforation

infection of globe - endopthalmitis

Management

OCULAR EMERGENCY - refer to Ophthalmology service

culture first

topical antibiotics every hour

must treat vigorously to avoid complications

HERPES SIMPLEX KERATITIS

usually HSV type I

may be triggered by stress, fever, UV light, immunosuppression

Symptoms and Signs (see Colour Atlas OP3)

pain, tearing, foreign body sensation, redness,

may have visual acuity loss

corneal hypoesthesia

occasional cold sore on lip, vesicles on skin

dendritic lesion seen in corneal epithelium with fluorescein staining + cobalt blue illumination

Complications

geographic ulcer (delicate denritic lesions) may often arise

corneal scarring (can lead to loss of vision)

chronic interstitial keratitis due to penetration of virus into stroma

secondary iritis

Management

epithelial debridement

NO STEROIDS initially - may exacerbate condition

antivirals such as topical trifluridine (Viroptic), or oral acyclovir (Zovirax)

ophthalmologist must exercise caution if adding topical steroids for chronic keratitis or iritis

OP18 - Ophthalmology

MCCQE 2006 Review Notes

CORNEA . . . CONT.

HERPES ZOSTER KERATITIS

CN V1 territory

Symptoms and Signs (see Colour Atlas OP18)

neuralgia-type pain (vesicular skin eruption ~ 2 weeks)

ocular tearing, pain and photophobia

corneal hypoesthesia

Hutchinson's sign: if tip of nose involved (nasociliary branch of V1), eye involvement likely (75% chance)

Complications

corneal keratitis, ulceration, perforation and scarring

uveititis

glaucoma secondary to trabeculitis

muscle palsies (rare) due to CNS involvement

occasionally severe post-herpetic neuralgia

Management

oral acyclovir, valcyclovir or famcyclovir +/- cycloplegic agent

topical steroids as indicated for keratitis, iritis (prescribed by an Ophthalmologist)

KERATOCONUS

bilateral central thinning and bulging (ectasia) of the cornea to form a conical shape

associated with Descemet's and Bowman's membrane folds

onset between 1st and 3rd decade

results in irregular astigmatism, corrects poorly with glasses

apical scarring

blurring of visual acuity is the only symptom

Management

contact lens initially if spectacle correction unsatisfactory

penetrating keratoplasty (corneal transplant) 90% successful

post-operative complications: endophthalmitis, graft rejection, graft dehiscence

ARCUS SENILIS

hazy white ring in peripheral cornea, < 2 mm wide, clearly separated from limbus

common, bilateral, benign corneal degeneration due to lipid deposition, part of the aging process

may be associated with hypercholesterolemia if age < 50 years

no associated visual symptoms, no complications

no treatment necessary

KAYSER-FLEISCHER RINGS

rare

pigmented ring 1-3 mm wide, located in the peripheral cornea

due to copper pigment deposition in Descemet's membrane

associated with Wilson's disease (hepatolenticular degeneration)

Management

penicillamine to chelate copper

THE UVEAL TRACT

uveal tract = iris, ciliary body, and choroid

vascularized, pigmented middle layer of the eye

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

IRITIS

inflammation of iris

usually unilateral

Etiology

usually idiopathic

connective tissue diseases: juvenile rheumatoid arthritis (JRA), ankylosing spondylitis (AS), Reiter's syndrome,

inflammatory bowel disease (IBD)

infectious: syphilis, Lyme disease, toxoplasmosis, TB, HSV, herpes zoster

other: sarcoidosis, trauma

MCCQE 2006 Review Notes

Ophthalmology - OP19

THE UVEAL TRACT. . . CONT.

Symptoms and Signs (see Colour Atlas OP4)

ocular pain,tenderness of the globe, PHOTOPHOBIA, decreased visual acuity,

brow ache (ciliary muscle spasm)

ciliary flush (perilimbal conjunctival injection), miosis

anterior chamber cells (WBC in anterior chamber due to anterior segment inflammation)

and flare (protein precipitates in anterior chamber secondary to inflammation)

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

• iritis leading to iris bombe (posterior iris adheres to anterior lens capsule entrapping aqueous

in posterior chamber) - angle closure glaucoma

• indicated by an irregularly shaped pupil

anterior synechiae (rare): adhesions of iris to cornea --> glaucoma

cataracts

band keratopathy (with chronic iritis)

• superficial corneal calcification keratopathy

macular edema with chronic iritis

Management

dilate pupil to prevent formation of posterior synechiae and to decrease pain from ciliary spasm

topical, subconjunctival, or systemic steroids

systemic analgesia

medical workup may be indicated to determine etiology

POSTERIOR UVEITIS

inflammation of the choroid

Etiology

bacterial: syphilis, tuberculosis

viral: herpes simplex virus, cytomegalovirus in AIDS

fungal: histoplasmosis, candidiasis

parasitic: toxoplasma, toxocara

immunosuppression may predispose to any of the above infections

autoimmune: Behcet's disease

malignancies: metastatic lesions, malignant melanoma

Symptoms and Signs

decreased visual acuity

floaters

frequently there is no conjunctival or scleral injection

vitreous cells and opacities

hypopion formation

Management

retrobulbar, or systemic steroids if indicated (e.g. threat of vision loss)

GLOBE

ENDOPHTHALMITIS

most commonly a postoperative complication of cataract surgery, or due to post-penetrating injury to eye,

but also bloodstream dissemination from elsewhere

Symptoms and Signs (see Colour Atlas OP6)

very painful, red eye with circumlimbal flush

anterior chamber cells, hypopyon

reduced vision, extreme photophobia

Management

OCULAR EMERGENCY: immediate admission to prevent loss of eye

vitreous tap and/or vitrectomy

intravitreal, topical, IV antibiotics

OP20 - Ophthalmology

MCCQE 2006 Review Notes

LENS

consists of an outer capsule surrounding a soft cortex and a firm inner nucleus

CATARACTS

lens opacity

most common cause of reversible blindness

Etiology

increased age is the most common cause

• includes nuclear sclerosis, cuneiform (spoke-like), cortical and posterior subcapsular cataracts

congenital

• presents with leukocoria

• treat promptly to prevent amblyopia

juvenile onset: diabetes mellitus, metabolic abnormalities

(e.g. Wilson's disease, galactosemia, homocystinuria)

medication toxicity

• steroids: posterior subcapsular cataracts

• phenothiazines: anterior subcapsular cataracts

• hypocalcemia: zonular cataracts (rare)

inflammatory: uveitis

radiation, UV light

traumatic: typically leaf-shaped or rosette cataracts, may see subcapsular cataracts

Symptoms and Signs (see Colour Atlas OP7)

gradual, progressive, painless decrease in visual acuity

• “second sight” phenomenon: only in cataracts due to nuclear sclerosis

• cataract increases power of lens causing artificial myopia - patient may read without reading glasses

halos around lights at night, double and triple images

diagnose by slit-lamp exam and by eliciting red reflex with direct ophthalmoscope

if severe enough may not be able to see fundus on ophthalmic exam

Management

surgical extraction of the cataract

phacoemulsification

• more common

• remove cataract nucleus and cortex, leaving the posterior capsule and a

peripheral rim of anterior capsule

• less commonly by extracapsular nuclear expression and leaving the

posterior capsule behind

• leaving an intact posterior capsule confines the vitreous to the posterior

segment, thereby reducing the incidence of retinal detachments and macular edema

• allows for posterior chamber intraocular lens, lowering risk of hyphema,

glaucoma and corneal endothelial damage

• approximately 5-30% get an "after-cataract" (opacification of posterior capsule)

which is treated with YAG laser capsulotomy

intracapsular: (now rarely used)

• remove whole lens with the cataract still in the capsule

• use with anterior chamber intraocular lens, glasses, or contact lenses

post-operative complications: retinal detachment, endophthalmitis, opacified

posterior capsule, corneal edema secondary to endothelial damage, macular edema

Indication for Surgery

absolute indications: trauma, congenital cataracts

relative indications: age related (elective surgery when cataract interferes with daily living)

DISLOCATED LENS ‘ECTOPIA LENTIS’

Etiology

associated with Marfan's Syndrome, Ehlers-Danlos type VI, homocystinuria, syphilis,

lens coloboma (congenital cleft due to failure of ocular adnexa to complete growth)

traumatic

Symptoms and Signs

decreased visual acuity

may get unilateral diplopia

iridodenesis (quivering of iris with movement)

direct ophthalmoscopy may elicit abnormal red reflex

Complications

cataract, glaucoma, uveitis

Management

surgical correction +/- lens replacement

MCCQE 2006 Review Notes

Ophthalmology - OP21

RETINA AND VITREOUS

VITREOUS

clear collagen-containing gel that fills the posterior segment of eye

normally firmly attached to optic disc and pars plana and apposed to the retina

commonly liquefies with age (syneresis)

when syneresis occurs, remaining vitreous gel can collapse on itself and lift

away from retinal surface (posterior vitreous detachment)

posterior vitreous detachment can cause vitreous hemorrhage, retinal tears and retinal detachment

if abnormal vitreoretinal adhesions are present (see Retinal Detachment and Vitreous Hemorrhage sections)

vitreous floaters

• shadow of a mobile vitreous opacity cast upon the retina

• must rule out retinal tears or hemorrhagic diseases

• harmless if no serious pathology

VITREOUS HEMORRHAGE

Etiology

diabetic retinopathy (most common cause)

retinal detachment/tear

retinal vein occlusion

posterior vitreous detachment

trauma

Symptoms and Signs

sudden loss of visual acuity

may be preceded by many floaters and/or flashes of light

ophthalmoscopy: retina not visible due to blood in vitreous

Management

ultrasound to rule out retinal detachment

expectant: in non-urgent cases (e.g. no retinal detachment) blood resorbs in 3-6 months

surgical: vitrectomy, retinal detachment repair

retinal endolaser to possible bleeding sites/vessels

RETINA

sensory component of eye

made up of photoreceptor, nerve cells and pigment epithelial layer

macula: area rich in cones, most sensitive area of retina and is darker

due to lack of retinal vessels and thinning of retina in this region

fovea: centre of macula, responsible for the most acute, fine vision

optic disc: normally reddish-orange, with central yellow cup (normal cup/disc (C:D) ratio is < 0.5),

retinal artery and vein pass through cup

CENTRAL RETINAL ARTERY OCCLUSION (CRAO)

Etiology

emboli from carotid arteries or heart (e.g. arrhythmia, endocarditis, valvular disease)

thrombus

temporal arteritis

Symptoms and Signs (see Colour Atlas OP19)

sudden, painless (except in temporal arteritis), unilateral loss of vision

relative afferent pupillary defect (RAPD)

fundoscopy

• cherry red spot (macula), retinal pallor

• boxcars (segmentation of blood in arteries), narrowed arteries

• non-pulsatile empty veins

• Hollenhorst plaques (small glistening cholesterol emboli, located commonly

at bifurcation of retinal arteries, originating from the carotid arteries or the aortic arch)

Management

OCULAR EMERGENCY: attempt to restore blood flow within 2 hours

if < 2 hours

• massage the globe

• decrease intraocular pressure

• topical ß-blockers

• inhaled oxygen - carbon dioxide mixture

• IV Diamox (carbonic anhydrase inhibitor)

• IV Mannitol (draws fluid from eye)

• anterior chamber paracentesis (carries risk of endophthalmitis)

BRANCH RETINAL ARTERY OCCLUSION (BRAO)

only part of the retina becomes ischemic resulting in loss of a visual field

more likely than a CRAO to be embolic; search for source

management: if < 2 hrs since onset of symptoms, ocular massage to dislodge embolus if VA is affected

OP22 - Ophthalmology

MCCQE 2006 Review Notes

RETINA AND VITREOUS . . . CONT.

CENTRAL RETINAL VEIN OCCLUSION (CRVO)

an uncommon cause of blindness in the elderly

choriocapillaris protects retina from ischemia

Predisposing Factors

hypertension

arteriosclerotic vascular disease

diabetes mellitus

glaucoma

hyperviscosity e.g. polycythemia rubra vera, sickle-cell disease, lymphoma, leukemia, macroglobulinemia

any condition that slows venous blood flow

Symptoms and Signs (see Colour Atlas OP20)

painless, unilateral, gradual or sudden visual loss

relative afferent pupillary defect (RAPD)

retina engorged with blood, "ketchup retina", "blood and thunder"

swollen disc, dilated veins, marked flamed-shaped hemorrhages

cotton wool spots in resolving phase

two fairly distinct groups

• venous stasis/non-ischemic retinopathy

• VA approximately 20/80, no RAPD

• 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

• VA approximately 20/200, reduced peripheral vision, RAPD

• more hemorrhages, cotton wool spots, congestion

• poor visual prognosis

Complications

occurs in 33% of cases

degeneration of retinal pigment epithelium

liquefaction of vitreous

neovascularization of retina and especially iris (secondary rubeosis),

which can lead to secondary glaucoma

iritis

Management

retinal laser photocoagulation to reduce neovascularization

RETINAL DETACHMENT (RD)

fluid collects between the neurosensory retina and the underlying retinal pigment epithelium

three types

rhegmatogenous

• most common type of RD

• indicates that the detachment originally started with a hole or tear in the retina

• tears may be caused by posterior vitreous detachment, trauma or iatrogenically

• fluid goes through the hole and lifts the neuroretina off the pigment layer and choroid

• more likely to occur spontaneously in high myopes, or after ocular surgery/trauma

tractional

• found in proliferative retinopathies such as diabetes, CRVO, sickle cell disease,

retinopathy of prematurity (ROP) and ocular trauma

• results from vitreal preretinal traction (due to vitreal, epiretinal or subretinal membrane)

pulling the sensory retina away from the underlying pigment epithelium

exudative

• may be due to choroidal tumour, metastatic tumour, uveitis

• caused by local or systemic conditions that damage the retinal pigment epithelium

which allows passage of the choroidal fluid into the subretinal space

Symptoms and Signs (see Colour Atlas OP24)

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 torn as the retina tears)

curtain of blackness (late)

• darkness in one field of vision when the retina detaches in that area and function is reduced

decreased vision

• visual acuity dramatically drops if the macula becomes detached

relative afferent pupillary defect (RAPD) may be seen

MCCQE 2006 Review Notes

Ophthalmology - OP23

RETINA AND VITREOUS . . . CONT.

Management

prophylactic: if a symptomatic tear (flashes or floaters) is detected, it can be sealed

off with laser therapy or cryotherapy, thereby preventing progression to detachment

therapeutic

• rhegmatogenous retinal detachment:

• scleral buckling (retinal break is mounted on sclera indented by an explant)

• pneumatic retinopexy (intraocular injection of air or an expandable gas

in order to tamponade the retinal break while the chorioretinal adhesion forms)

• both treatments used in combination with localization of the retinal break and treatment

with diathermy, cryotherapy or laser to create adhesion between the pigment epithelium

and the sensory retina

• intraocular injection of silicone oil in cases of recurrent retinal detachments

• tractional retinal detachment:

• vitreoretinal surgery (may involve vitrectomy, membrane removal,

scleral buckling and injection of intraocular gas)

• exudative

• treatment of underlying cause

complications: loss of vision, vitreous hemorrhage, recurrent retinal detachment

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

RETINITIS PIGMENTOSA

hereditary degenerative disease of the retina

degeneration of rod cells and retinal atrophy

areas of peppery/"bone-spicule" pigmentary degeneration scattered through mid- and peripheral retina

symptoms: night blindness, often beginning in adolescence, with expanding ring scotoma

(abnormal blind spot) leading to blindness

no satisfactory treatment

ROTH SPOTS

flame-shaped hemorrhages with central white fibrin thrombosis

seen in

• subacute bacterial endocarditis (SBE)

• leukemia (hemorrhage and extravasation of leukocytes)

• severe anemia

AGE-RELATED MACULAR DEGENERATION (ARMD)

leading cause of blindness in people > 65 years old

10% of people > 65 years old have some degree of ARMD

female > male

Non-Neovascular (Non-Exudative/"Dry") ARMD

most common type of ARMD - 90% of cases

drusen: pale, yellow-white deposits of membranous vesicles and collagen deposited between the

retinal pigment epithelium (RPE) and Bruch’s membrane (area separating inner choroidal vessels from RPE)

• no visual loss unless atrophy of overlying RPE and photoreceptors

RPE atrophy: coalescence of depigmented RPE, clumps of focal hyperpigmentation

Neovascular (Exudative/"Wet") ARMD

10% of ARMD, yet 80% results in severe visual loss

choroidal neovascularization: drusen predispose to breaks in Bruch’s membrane,

subsequent growth and proliferation of choroidal capillaries

• may get serous detachment of overlying RPE and retina, hemorrhage

and lipid precipitates into subretinal space

disciform scarring

• an elevated subretinal mass due to fibrous metaplasia of hemorrhagic retinal detachment

• causes severe central visual loss

Risk Factors

female

increased age

family history

smoking

Symptoms and Signs

variable amount of progressive visual loss

metamorphopsia (distorted vision characterized by straight parallel lines appearing convergent or wavy)

OP24 - Ophthalmology

MCCQE 2006 Review Notes

RETINA AND VITREOUS . . . CONT.

Investigations

Amsler Grid: commonly held at normal reading distance with glasses on, assesses macular function

fluorescein angiography: see neovascularization, leaks

Management

non-neovascular ARMD

• monitor

• low vision aids e.g. magnifiers, closed-circuit television

• query - anti-oxidants

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 with verteporfin: 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 indicate 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;

investigations are ongoing

BLURRED OPTIC DISC MARGINS

DRUSEN

German, plural for "granules"

"giant drusen": hyaline deposits at disc margin and in disc itself, commonly producing field defects

more common form is deposited in Bruch's membrane

(area separating inner choroidal vessels from retinal pigment epithelium)

seen with increasing age, retinal and choroidal degeneration and as a primary dystrophy

with drusen alone, vision is normal or near normal

MYELINATED NERVE FIBRES

a variant of normal in which the retinal nerve fibres are myelinated anterior to the cribriform plate

appear as white streaks extending from the cup and occasionally in retina remote from disc

Table 5. Differential Diagnosis of Blurred Optic Disc Margins

Papilledema

Optic

Ischemic

Central Retinal

(see Colour Atlas OP11)

Neuritis

Neuropathy

Vein Occlusion (CRVO)

Age

Any

< 50

> 50

Etiology

Increased intracranial

Idiopathic,

Idiopathic, vascular,

Idiopathic

pressure (ICP)

associated with MS

Giant Cell Arteritis (GCA)

Normal

Reduced

Other

Bilateral, enlarged

Unilateral, pain on

Altitudinal field loss,

Unilateral, hypertension,

sign or

blind spot,

eye movement,

+/- GCA findings

diabetes, increased

symptom

neurologic findings

RAPD, reduced

(e.g.jaw claudication,

viscosity, arteriosclerotic

(e.g. headache)

color vision,

headache, tender

vascular disease

+/- MS findings

scalp)

Fundoscopic

Swollen disc,

Hyperemic

Pale, swollen

“Blood and thunder”,

findings

hemorrhage,

swollen disc,

disc, flame

swollen disc,

dilated

normal if

hemorrhage

venous engorgement,

retinal veins

retrobulbar

retinal hemmorhage

neuritis

Investigation

CT head

Visual field (VF),

ESR

Fluorescein angiography,

CT (if atypical VF

medial evaluation

or if no improvement

in 6 weeks)

Treatment

Neurosurgy consult,

Steroids

High dose steroids

Panretinal laser

treat underlying

(for GCA)

photocoagulation

cause

steroids

MCCQE 2006 Review Notes

Ophthalmology - OP25

GLAUCOMA

Definition

progressive optic neuropathy involving characteristic structural changes to

optic nerve head with associated visual field changes

commonly associated with high intraocular pressure (IOP)

Background

aqueous is produced by the ciliary body and flows from the posterior chamber to the anterior chamber

through the pupil, and drains into the episcleral veins via the trabecular meshwork and the

canal of Schlemm (see Figure 1)

an isolated increase in IOP is termed ocular hypertension (or glaucoma suspect) and these patients

should be followed because ~10% if 20-30 mmHg; 40% if 30-40 mmHg; most if > 40 mm Hg (or more)

will develop glaucoma

normal, average IOP is 16 +/- 2 mm Hg (diurnal variation, higher in a.m.)

pressures > 21 more likely to be associated with glaucoma

normal C/D (cup/disc) ratio < 0.4

suspect if glaucoma if C/D ratio > 0.6, difference between eyes > 0.2 or cup approaches disc margin

loss of peripheral vision most commonly precedes central loss

sequence of events: gradual pressure rise, followed by increased in C/D ratio, followed by visual field loss

as cup approaches disc margin (usually asymptomatic)

screening tests should include

• medical and family history

• visual acuity testing

• slit lamp exam: to assess anterior chamber depth

• ophthalmoscopy: to assess the disc features

• tonometry by applanation or indentation: to measure the IOP

• Humphrey visual field testing

PRIMARY OPEN ANGLE GLAUCOMA

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

screening is critical for early detection

Risk Factors

elevated intraocular pressure (> 21 mm Hg)

age > 40

higher incidence in blacks

myopes

familial, polygenic (10x increased risk)

diabetes

chronic topical steroid use on eyes in steroid responders

previous ocular trauma

anemia/hemodynamic crisis (ask about blood transfusions in past)

hypertension

Symptoms and Signs (see Colour Atlas OP26)

asymptomatic initially

insidious, painless, gradual rise in IOP due to restriction of aqueous outflow

bilateral, but usually asymmetric

visual field loss

• slow, progressive, irreversible loss of peripheral vision

• arcuate scotoma and nasal step are characteristic

late loss of central vision if untreated

earliest signs are optic disc changes

• increased cupping of disc with a cup/disc ratio > 0.4 (the cup is usually enlarged asymmetrically

(i.e. eye more affected initially) and cup approaches disc margin)

• large vessels become nasally displaced

may have hemorrhage at disc margin

safe to dilate pupil

Management

principles: increase the drainage of aqueous and/or decrease the production of aqueous

medical treatment: see Ocular Medications section

• increases aqueous outflow

• topical cholinergics

• topical adrenergics

• topical prostaglandin agonist

• decreases aqueous outflow

• topical beta-blockers

• topical and oral carbonic anhydrase inhibitor

• topical adrenergics

surgical treatment

• laser: trabeculoplasty, selective destruction of ciliary body

• microsurgery: trabeculectomy, tube shunt placement

visual field testing to monitor course of disease

OP26 - Ophthalmology

MCCQE 2006 Review Notes

GLAUCOMA. . . CONT.

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

Risk Factors

hyperopia: small eye, big lens - large lens crowds the angle

age > 70, female

family history, more common in Asians and Inuit

mature cataracts

shallow anterior chamber

pupil dilation (topical and systemic anticholinergics, stress, darkness)

Symptoms

unilateral, but other eye predisposed

RED FLAG: red, painful eye

decreased visual acuity, vision acutely blurred from corneal edema

halo around lights

nausea and vomiting

abdominal pain

Signs

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

Management

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 section

• miotic drops (pilocarpine)

• topical beta-blockers

• systemic carbonic anhydrase inhibitors

• systemic hyperosmotic agents (oral glycerine; IV hypertonic mannitol)

• topical steroids (not in primary care)

surgical treatment (for acute angle closure glaucoma)

• laser iridotomy or surgical iridectomy

SECONDARY OPEN ANGLE GLAUCOMA

increased IOP secondary to ocular/systemic disorders which clog the trabecular meshwork

steroid-induced glaucoma

• due to topical/systemic corticosteroid use

• develop in 25% (higher in extended use) of general population (responders) after 4 weeks (or less)

of QID topical steroid use

• 5% of population are super-responders

traumatic glaucoma

• hyphema-induced increase in IOP

• angle recession glaucoma occurs with blunt, non-penetrating trauma to globe and orbit,

causing tears in trabecular meshwork and ciliary body with secondary scarring

pigmentary dispersion syndrome

• iris pigment clogs trabecular meshwork

• typically seen in younger myopes

pseudoexfoliation syndrome

• abnormal basement membrane-like material clogs trabecular meshwork

• seen mostly in the elderly

neovascular glaucoma

• abnormal blood vessels develop on surface of iris (rubeosis iridis)

• due to retinal ischemia associated with proliferative diabetic retinopathy and CRVO

• treatment with laser therapy to retina, to reduce neovascular stimulus to iris vessels

MCCQE 2006 Review Notes

Ophthalmology - OP27

GLAUCOMA. . . CONT.

SECONDARY ANGLE CLOSURE GLAUCOMA

uveitis

• inflamed iris adheres to lens (posterior synechiae)

NORMAL PRESSURE GLAUCOMA

IOP in normal range but cupping and field loss typical of glaucoma are present

often found in women > 60 but may occur earlier

may see splinter hemorrhages of disc margin

damage to optic nerve may be due to vascular insufficiency

Management

treat any underlying medical condition and lower the IOP still further

CONGENITAL GLAUCOMA

due to inadequate development of the filtering mechanism of the anterior chamber angle

Symptoms and Signs

cloudy cornea, increased IOP

photophobia, tearing

buphthalmos (large eye), blepharospasm

Management

filtration surgery is required soon after birth to prevent blindness

PUPILS

PUPILLARY LIGHT REFLEX(see Figure 4)

light shone directly into eye travels along optic nerve (1) to optic tracts (2) to both sides of midbrain

impulses enter both sides of midbrain via pretectal area (3) and Edinger-Westphal nuclei (4)

nerve impulses then travel down both CNs III (5) to reach the ciliary ganglia (6),

and finally to the iris sphincter muscle, which results in direct and consensual light reflex

1. optic nerve

2. optic tracts

3. pretectal area

4. Edinger-Wesphal nuclei

5. cranial nerve III

6. ciliary ganglia

LGB = lateral geniculate body

LGB

Figure 4. Pathway of direct light reflex from left eye and

consensual light reflex from right eye

Illustration by Aimée Worrell

OP28 - Ophthalmology

MCCQE 2006 Review Notes

PUPILS . . . CONT.

DILATED PUPIL (MYDRIASIS) DIFFERENTIAL DIAGNOSIS

Physiologic Anisocoria (unequal pupil size)

occurs in 20% of population

difference < 1-2 mm, most pronounced in dark

normal light reactivity, may vary from day to day

Sympathetic Stimulation

fight or flight response

drugs: epinephrine, dipivefrin (Propine), phenylephrine

Parasympathetic Understimulation

cycloplegics/mydriatics: atropine, tropicamide, cyclopentolate (parasympatholytic)

CN III palsy

• eye deviated down and out with ptosis present

• etiology includes cerebrovascular accident (CVA), neoplasm, aneurysm, diabetes mellitus (DM)

(may spare pupil)

dilated pupil from medication does not respond to constricting drugs (e.g. pilocarpine), unlike a CN III palsy

Acute Angle Closure Glaucoma

fixed, mid-dilated pupil

Adie's Tonic Pupil

80% unilateral, females > males

pupil reacts poorly to light (both direct and consensual) constricts with accomodation

hyporeflexic (Adie's syndrome)

defect at ciliary ganglion: results in denervation hypersensitivity of constrictor muscle

• 0.125% solution of pilocarpine will constrict tonic pupil

• no effect on normal pupil

pupil eventually gets smaller than the unaffected eye

Trauma

damage to iris sphincter from blunt or penetrating trauma

iris transillumination defects may be apparent using ophthalmoscope or slit lamp

pupil may be dilated (traumatic mydriasis) or irregularly shaped

CONSTRICTED PUPIL (MIOSIS) DIFFERENTIAL DIAGNOSIS

Physiologic Anisocoria (unequal pupil size)

as for Dilated Pupil section above

Senile Miosis

decreased sympathetic stimulation with age

Parasympathetic Stimulation

local or systemic medications

cholinergic agents: pilocarpine, carbachol

cholinesterase inhibitor: phospholine iodide

opiates, barbiturates

Horner's Syndrome

lesion in sympathetic pathway

difference in pupil size greater in dim light, due to decreased innervation of adrenergics to iris dilator muscle

associated with anhidrosis, ptosis of ipsilateral face/neck

application of cocaine to eye does not result in pupil dilation (vs. normal pupil)

causes: brainstem infarct, demyelinating disease, cervical or mediastinal tumour,

aneurysm of carotid or subclavians, goiter, cervical lymphadenopathy, surgical sympathectomy

Iritis

miotic initially

later, may be irregularly shaped pupil due to posterior synechiae

does not react to light in later stages

Argyll Robertson Pupil

pupils irregular and < 3 mm diameter, may have ptosis

does not respond to light stimulation

does respond to accommodation

suggestive of CNS syphilis or other conditions (DM, encephalitis, MS)

MCCQE 2006 Review Notes

Ophthalmology - OP29

PUPILS . . . CONT.

RELATIVE AFFERENT PUPILLARY DEFECT (RAPD)(see Neurology Chapter)

defect in visual afferent pathway anterior to optic chiasm

differential diagnosis: optic nerve compression, optic neuritis, large retinal detachment,

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 ophtalmoscope with “+4” setting, using red reflex especially in patients with dark irides

Clinical Pearl

Even dense cataracts do not produce a relative afferent pupillary defect.

NEURO-OPHTHALMOLOGY

VISUAL FIELD DEFECTS(see Neurology Chapter)

lesions in the visual system have characteristic pattern losses

several tests used: confrontation (screening), tangent screen, Humphrey fields, 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

commonly seen in multiple sclerosis (MS)

lesion of medial longitudinal fasciculus (MLF) (see Figure 5)

delayed movement in ipsilateral adducting eye

monocular nystagmus in contralateral abducting eye

The MLF connects the Pontine Paramedian

Reticular Formation (PPRF) to the nucleus of

CN III contralaterally. When looking left, nerve

impulses originate in the right frontal cortex

Lateral Rectus

Medial Rectus

“Look left”

(not shown) and travel to the left PPRF. The

Muscle

impulses then travel to the ipsilateral CN VI

nucleus and to the contralateral CN III nucleus

CN III

via the MLF. In INO, an MLF lesion inhibits

CN VI

transmission from the PPRF to the

PPRF

contralateral medial rectus muscle.

MLF

Figure 5. Pathway for left lateral gaze, in patient with

right internuclear ophthalmoplegia (INO)

NYSTAGMUS(see Otolaryngology Chapter)

definition: rapid, involuntary, small amplitude movements of the eyes that are rhythmic in nature

direction of nystagmus is defined by the rapid eye component of motion

can be categorized by movement type (pendular, jerking, rotatory, coarse) or as normal vs. pathological

Pendular Nystagmus

due to poor macular function or cerebellar lesion

eye oscillates equally about a fixation point

may be present in people who become blind early in life

OP30 - Ophthalmology

MCCQE 2006 Review Notes

NEURO-OPHTHALMOLOGY. . . CONT.

Jerking Nystagmus

due to brainstem, labyrinthine, cerebellar disease

rapid movement in one direction, slow movement in opposite direction

Coarse Nystagmus

due to weakness of ocular muscles or lower motor neuron disease

coarse jerking in the direction of the weakened muscle

Normal Nystagmus

endpoint

• at extremes of gaze, subsides after a few beats

• also seen in patients on anticonvulsant therapy

evoked

• optokinetic: occurs when patient viewing a moving object

• vestibular: labyrinthine stimulation from thermal or rotatory movement

• unlike central lesions, vestibular nystagmus is suppressed by fixation

Abnormal Nystagmus

any nystagmus which occurs in the field of binocular vision persistently

vertical nystagmus

• always abnormal if persistent

• up-beating: usually due to acquired disease or lesion in medulla

• down-beating: usually due to lesion in lower brainstem or upper cervical cord

congenital nystagmus

• pendular, may cause amblyopia from poor fixation

gaze-evoked nystagmus

• in certain fields of gaze

• with a brainstem/cerebellar lesion, acoustic neuroma phenytoin, ethanol, barbiturates,

demyelinating diseases

spasmus nutans

• asymmetrical fine nystagmus of unknown pathogenesis

• in children 4-12 months of age, usually recover by 2 years

• head nodding to offset pathological eye movements

ataxic nystagmus

• one eye has more marked nystagmus than the other

• associated with internuclear ophthalmoplegias

INTRAOCULAR MALIGNANCIES

uncommon site for primary malignancies

eye usually affected secondarily by cancer or cancer treatments

MALIGNANT MELANOMA

most common primary intraocular malignancy

more prevalent in Caucasians

arise from uveal tract

hepatic metastases predominate

Management

choice is dependent on the size of the tumour

radiotherapy, enucleation, limited surgery

RETINOBLASTOMA

incidence: 1/1000; sporadic or genetic transmission

unilateral or bilateral (in 1/3 of cases)

malignant - direct or hematogenous spread

diagnosis

• may be detected by leukocoria (white pupil) in infant

• CT scan: dense radiopaque appearance (contains calcium)

Management

radiotherapy, enucleation(removal of globe from eye socket), or both

METASTASES

most common intraocular malignancy in adults

most common from breast and lung

usually infiltrate the choroid, but may also affect the optic nerve or extraocular muscles

may present with decreased or distorted vision, irregularly shaped pupil, iritis, hyphema

Management

local radiation, chemotherapy

enucleation if blind painful eye

MCCQE 2006 Review Notes

Ophthalmology - OP31

OCULAR MANIFESTATIONS OF SYSTEMIC DISEASE

HIV

up to 75% of patients with AIDS have ocular manifestations

ocular findings include: opportunistic infections, ocular vascular manifestations, neoplasms,

Lids/Conjunctiva

Kaposi's sarcoma

• affects conjunctiva of lid or globe

• numerous vascular skin malignancies

• DDx: subconjunctival hemmorhage (non-clearing), hemangioma

molluscum contagiosum

herpes zoster

Cornea

herpes simplex keratitis

herpes zoster

Retina

HIV retinopathy

• most common ocular manifestation of HIV

• cotton wool spots

• capillary abnormalities

• intraretinal hemorrhage

cytomegalovirus (CMV) retinitis(see Colour Atlas OP25)

• most common ocular opportunistic infection in HIV patients

• most common cause of visual loss in HIV patients, occurring in > 25% of patients

• develops in late stages of HIV when severely immunocompromised (CD4 count <= 50)

• a necrotizing retinitis, with retinal hemorrhage and vasculitis, brushfire or pizza pie appearance

• untreated infection will progress to other eye in 4-6 weeks

• symptoms and signs: scotomas related to macular involvement and retinal detachment,

blurred vision, and floaters

• treat with virostatic agents: gancyclovir IV or intravitreal injection, foscarnet IV

necrotizing retinitis

• from herpes simplex virus, herpes zoster, Pneumocystis carinii , toxoplasmosis

disseminated choroiditis

• Pneumocystis carinii, Mycobacterium avium intracellulare

, Candida

OTHER SYSTEMIC INFECTIONS

most common are herpes zoster and candidiasis

herpes zoster (see Cornea section)

Candida

• fluffy, white-yellow, superficial retinal infiltrate that may eventually result in vitritis

• may see inflammation of the anterior chamber

• treatment: amphotericin B

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 --> vitreous hemorrhage --> traction

--> retinal detachment

• Rubeosis Iridis (neovascularization of the iris) leading to neovascular glaucoma (poor prognosis)

Retina

background

• altered vascular permeability

• retinal vessel closure

non-proliferative: increased vascular permeability and retinal ischemia

• dot and blot hemorrhages

• microaneurysms

• retinal edema

• hard exudates (lipid deposits)

advanced non-proliferative (or pre-proliferative):

• non-proliferative findings plus

• venous sausaging (in 2 of 4 retinal quadrants)

• intraretinal microvascular anomalies-IRMA (in 1 of 4 retinal quadrants)

• IRMA: dilated, leaky vessels within the retina

• macular edema

• cotton wool spots (nerve fibre layer infarcts)

OP32 - Ophthalmology

MCCQE 2006 Review Notes

OCULAR MANIFESTATIONS OF SYSTEMIC DISEASE

. . CONT.

proliferative (see Colour Atlas OP23)

• 5% of patients with diabetes will reach this stage)

• neovascularization: iris, disc, retina to vitreous

• neovascular glaucoma (secondary to rubeosis iridis)

• vitreous hemorrhage, fibrous scarring, 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

• gestational diabetics not at risk for retinopathy

Management

Diabetic Control and Complications Trial (DCCT) (see Endocrinology Chapter)

- tight control of blood sugar decreases frequency and severity of microvascular complications

blood pressure control

focal laser for macular edema

panretinal laser photocoagulation, reduces neovascularization by decreasing retinal metabolic demand

- reduces risk of blindness

vitrectomy for vitreous hemorrhage and retinal detachment

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

Exrtra Ocular Movement (EOM) Palsy

usually secondary to CN III infarct

pupil usually spared in diabetic CN III palsy, but get ptosis

may involve CN IV and VI

usually recover within one year

Optic Neuropathy

visual acuity loss due to infarction of optic disc/nerve

MULTIPLE SCLEROSIS (see Neurology Chapter)

relapsing or progressive CNS disease characterized by disseminated patches of

demyelination in the brain and spinal cord resulting in varied symptoms and signs

many ocular manifestations

Symptoms

blurred vision secondary to optic neuritis

decreased colour vision secondary to optic neuritis

central scotoma, since papillomacular bundle of retinal nerve fibres tends to be affected

diplopia secondary to internuclear ophthalmoplegia (see Figure 5)

Signs

RAPD, ptosis, nystagmus, uveitis

optic atrophy (see Colour Atlas OP22)

, optic neuritis

internuclear ophthalmoplegia (INO)

Management

with optic neuritis, treatment with oral steroids leads to greater likelihood of getting MS

later on than treatment with IV steroids

HYPERTENSION

Keith-Wagener Grading

I: arteriosclerosis (slight narrowing of arterioles)

II: AV nicking, copper wire arterioles, cotton wool spots, hard exudates

III: flame hemorrhages (superficial), retinal edema, macular star

IV: papilledema (choked disc) (see Colour Atlas OP21)

AMAUROSIS FUGAX

sudden, transient blindness from intermittent vascular compromise

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)

MCCQE 2006 Review Notes

Ophthalmology - OP33

OCULAR MANIFESTATIONS OF SYSTEMIC DISEASE

. . CONT.

HYPERTHYROIDISM/GRAVES' DISEASE

mnemonic - NO SPECS

Grade 0: No signs or symptoms

Grade 1: Only signs are proptosis < 22 mm (measure by Hertel

exolphthalmometer) +/- lid lag; +/- lid retraction

Grade 2: Soft tissue involvement - conjunctival + lid miosis

Grade 3: P roptosis > 22 mm

Grade 4: Extraocular muscle involvement

Grade 5: Corneal involvement - exposure keratitis

Grade 6: Sight loss due to optic neuropathy from compression

ocular changes are often permanent

Management

treat the hyperthyroidism

proptosis can cause exposure of the cornea

• mild stage: use artificial tears

• more severe: steroids, surgery (lateral tarsorrhaphy, orbital decompression), radiation

CONNECTIVE TISSUE DISORDERS

most common ocular manifestation: dry eyes (keratoconjunctivitis sicca)

RA, JRA, SLE, Sjogren's syndrome

ankylosing spondylitis, polyarteritis nodosa (PAN), giant cell arteritis

GIANT CELL (TEMPORAL) ARTERITIS

abrupt monocular loss of vision

ischemic optic atrophy

- 50% lose vision in other eye if untreated

see Blurred Disc Margin section

SARCOIDOSIS

granulomatous uveitis with large "mutton fat" keratitic precipitates and posterior synechiae

neurosarcoidosis: optic neuropathy, oculomotor abnormalities, visual field loss

Management

steroids and mydriatics

STRABISMUS

non-alignment of eyes, found in 3% of children

object not visualized simultaneously by fovea of each eye

complications: amblyopia, cosmetic

TROPIA

a manifest (apparent) deviation

deviation not corrected by the fusion mechanism

Types

exo- (lateral deviation), eso- (medial deviation)

hyper- (upward deviation), hypo- (downward deviation)

esotropia = "crossed-eyes"; exotropia = "wall-eyed"

pseudoesotropia: epicanthal folds give appearance of esotropia but Hirschberg test is normal,

more common in Asians

Tests

Hirschberg: positive if the light reflex in the cornea of the two eyes is asymmetrical

• light reflex lateral to central cornea indicates esodeviation; medial to central cornea

indicates exodeviation

cover test (see Figure 6)

• ask patient to fixate on target

• cover the non-deviated eye, the deviated eye will then move to fixate on the target

• the covered eye will move in the same direction under the cover

• if deviated eye moves inward on covering the fixating other eye = exotropia

• if deviated eye moves outward on covering the fixating other eye = esotropia

the deviation can be quantified using prisms

PHORIA

a latent deviation

a deviation corrected in the binocular state by the fusion mechanism

(therefore deviation not seen when patient is using both eyes)

the Hirschberg test will be normal (light reflexes symmetrical)

very common - majority are asymptomatic

may be associated with asthenopia (eye strain)

OP34 - Ophthalmology

MCCQE 2006 Review Notes

STRABISMUS . . . CONT.

Tests

cover-uncover test (see Figure 6)

• placing a cover over an eye with a phoria causes a breakdown of fixation of that eye,

which allows it to move to a misaligned position

• then, uncovering the covered eye will allow it to return to a normal central position

• covered eye moves inward on removing cover = exophoria

• covered eye moves outward on removing cover = esophoria

alternating cover test

• alternating the cover back and forth from eye to eye detects both tropia and phoria

• maintain cover over one eye for 2-3 seconds before rapidly shifting to other eye

COVER TEST

TROPIA

COVER TEST

COVER-UNCOVER

TEST

PHORIA

COVER-UNCOVER

TEST

ET = ESOTROPIA

XT = EXOTROPIA

E = ESOPHORIA

X = EXOPHORIA

Figure 6. Cover and Cover-Uncover Tests for Detection of Tropias and Phorias

PARALYTIC STRABISMUS

non-comitant strabismus

deviation varies in different positions of gaze

Etiology

neural: arteriosclerotic (CVA), DM, MS, brain tumour

muscular: myasthenia gravis, Grave's disease

structural: orbital fracture due to trauma

Features

mostly in adults, acquired

diplopia (since adults do not get amblyopia)

greatest deviation in field of action of the weakened muscle

vision is usually unaffected in either eye, unless CN II is involved

NON-PARALYTIC STRABISMUS

comitant strabismus

deviation equal in all directions of gaze

Features

usually begins in infancy

no diplopia (child suppresses the image from the misaligned eye)

deviated eyes may become amblyopic (see Amblyopia section) if not treated when the child is young

i.e. 3-4 years old

amblyopia treatment rarely successful after age 8

amblyopia will not develop if child has alternating strabismus or intermittency -

allow neural pathways for both eyes to develop

Clinical Pearl

All children with strabismus should be promptly referred to Ophthalmology.

All children with defective vision should be promptly referred to detect and

treat non-strabismic amblyopia (e.g. from anisometropia: difference in

refraction between two eyes).

Accommodative Esotropia

normal response to approaching object is near reflex: convergence, accommodation, and miosis

hyperopes must constantly accommodate - excessive accommodation can lead to esotropia

usually reversible with correction of refractive error

Nonaccommodative Esotropia

accounts for 50% of childhood strabismus

most are idiopathic

may be due to ocular pathology (e.g. anisoemetropia, cataract, retinoblastoma)

MCCQE 2006 Review Notes

Ophthalmology - OP35

PEDIATRIC OPHTHALMOLOGY

AMBLYOPIA

Definition

decrease in visual acuity due to inappropriate visual stimulation during development

not due to ocular pathology and not correctable by refraction

note: pathology in visual cortex and lateral geniculate body

Detection

"Holler Test": younger child upset if good eye 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 8-9 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)

• surgery: recession (weakening) = moving muscle insertion further back on the globe;

or resection (strengthening) = shortening the muscle

• botulinum toxin for single muscle weakening

• cycloplegics or miotics (not commonly used)

• even after ocular alignment is restored (glasses, surgery, botulinum toxin),

patching is frequently necessary 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

• astigmatism

• treat with glasses to correct refractive errors

• patching is required if amblyopia persists > 4-8 weeks

other

• 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 cause

patching of good eye (duration is individually determined)

monitor vision until age 8-9 years

LEUKOCORIA

white pupil (red reflex is absent)

Differential Diagnosis

retinoblastoma, retinal coloboma

retinopathy of prematurity (ROP) (retrolental fibroplasia):

associated with supplemental oxygen use in premature infants

persistent hyperplastic primary vitreous (PHPV)

total retinal detachment

congenital cataract

corneal scar

NASOLACRIMAL SYSTEM DEFECTS

delay in duct formation for a few weeks after birth may be normal

increased tearing, crusting and discharge (sometimes mucopurulent)

treatment: massage over lacrimal sac

usually resolve within 8 months

consider referral for lacrimal probing if persistent at 9-12 months

OPHTHALMIA NEONATORUM

newborn conjunctivitis

Chlamydia is most common cause

other causes include: chemical (i.e. silver nitrate), bacterial (N. gonorrhea, S. aureus, Pseudomonas

), HSV

gonococcal infection is the most serious threat to sight

topical prophylaxis most commonly with erythromycin is required by law, less commonly with

silver nitrate or providone-iodine

RUBELLA

infection in the mother in first trimester

the infant may suffer from any or all of the following:

congenital cataract, heart disease, deafness, microcephaly, microphthalmos, mental deficiency

OP36 - Ophthalmology

MCCQE 2006 Review Notes

OCULAR TRAUMA

Clinical Pearl

Always test visual acuity (VA) first! - medicolegal protection.

BLUNT TRAUMA

e.g. 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 upgaze, diplopia

• ethmoid fracture: subcutaneous emphysema of lid

lids (swelling, laceration, emphysema)

conjunctiva (subconjunctival hemorrhage)

cornea (abrasions - detect with fluorescein and cobalt blue)

anterior chamber (assess depth, hyphema, hypopyon)

iris (prolapse, iritis)

lens (cataract, dislocation)

refer if you observe any of these signs of ocular trauma: decreased VA, shallow anterior chamber, hyphema,

abnormal pupil, ocular misalignment or retinal damage

PENETRATING TRAUMA

include ruptured globe +/- prolapsed iris, intraocular foreign body

be suspicious if history of "metal striking metal"

initial management: refer immediately

• ABCs

• don't press on eyeball!

• check vision, diplopia

• apply rigid eye shield to minimize further trauma

• keep head elevated 30-45 degrees to keep IOP down

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)

Management

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)

HYPHEMA

bleed into anterior chamber, often due to damage to root of the iris

may occur with blunt trauma

Management

refer to Ophthalmology

• patch, shield and bedrest x 5 days

may need surgical drainage if hyphema persists or if re-bleed occurs

Complications

risk of rebleed highest on days 2-5, resulting in secondary glaucoma, corneal staining, and iris necrosis

never prescribe aspirin as it will increase the risk of a rebleed

MCCQE 2006 Review Notes

Ophthalmology - OP37

OCULAR TRAUMA. . . CONT.

BLOW OUT FRACTURES(see Plastic Surgery Chapter)

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 may be damaged

Symptoms and Signs

pain and nausea at time of injury

diplopia, restriction of upgaze

infraorbital and upper lip paresthesia (CN V2)

enophthalmos, periorbital ecchymoses

Diagnosis

plain films: Waters view and lateral

CT: anteroposterior and coronal view of orbits

Management

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

SYMPATHETIC OPHTHALMIA

severe bilateral granulomatous uveitis

occurs after ocular trauma (usually penetrating and involving uveal tissue) or eye surgery,

10 days to years later

possibly due to a hypersensitivity reaction to uveal pigment

the injured eye becomes inflamed first and the other eye (sympathizing) second

Symptoms and Signs

photophobia

blurred vision

red eye

Management

if vision not salvageable in affected eye, enucleate to prevent sympathizing reaction

if inflammation in sympathizing eye is advanced, treat with local steroids and atropine --> cyclosporin

OCULAR EMERGENCIES

these require urgent consultation to an ophthalmologist for management

trauma, especially intraocular foreign bodies, lacerations

corneal ulcer

gonococcal conjunctivitis

orbital cellulitis

chemical burns

acute iritis

acute angle closure glaucoma

central retinal artery occlusion (CRAO)

retinal detachment

endophthalmitis

giant cell arteritis

OP38 - Ophthalmology

MCCQE 2006 Review Notes

OCULAR MEDICATIONS

TOPICAL OCULAR DIAGNOSTIC DRUGS

Fluorescein Dye

water soluble orange-yellow dye

green under cobalt blue light - ophthalmoscope or slit lamp

stains damaged corneal and conjunctival and mucus epithelium 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 and can lead to corneal ulceration and scarring with prolonged use,

therefore NEVER prescribe

Mydriatics

dilate pupils

cycloplegic

indications: refraction, ophthalmoscopy, therapy for iritis

cholinergic blocking

• paralyze iris sphincter i.e. dilation and cycloplegia

Table 6. Mydriatic Drugs and Duration of Action

Drugs

Duration of action

Tropicamide 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

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

GLAUCOMA MEDICATIONS

Beta-Adrenergic Blockers

decrease aqueous humour formation

nonselective beta-blockers (e.g. Timolol, Levobunolol, Metapranolol)

systemic side effects: bronchospasm, bradycardia, heart block, hypotension,

impotence, depression, exacerbation of congestive heart failure

Cholinergic Stimulating

increases aqueous outflow

e.g. pilocarpine, carbachol

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

Adrenergic Stimulating

decrease aqueous production and increase flow

e.g. epinephrine HCl, dipivifrin (Propine), brimonidine (Alphagan)

side effects: contact allergy, hypotension in children

Carbonic Anhydrase Inhibitor

decrease aqueous production

e.g. oral acetazolamide (Diamox), topical dorzolamide

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)

side effects: iris colour change, lash growth, trichiasis

TOPICAL OCULAR THERAPEUTIC DRUGS

Decongestants

weak adrenergic stimulating drugs (vasoconstrictor)

e.g. naphazoline HCl 0.012%, phenylephrine HCl 0.12%, tetrahydrazaline 0.05%

rebound vasodilation with over use can exacerbate angle closure glaucoma

MCCQE 2006 Review Notes

Ophthalmology - OP39

OCULAR MEDICATIONS. . . CONT.

Corticosteroids

never prescribed by primary care physician unless emergency indications

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)

Antibiotics

indications: bacterial conjuntivitis, keratitis, or blepharitis

commonly as topical drops or ointments, may give systemically

e.g. sulfonamide (sodium sulfacetamide, sulfisoxazole), gentamicin, erythromycin, tetracycline,

bacitracin, polymyxin

OCULAR DRUG TOXICITY

Table 7. Drugs with Ocular Toxicity

Amiodarone

Corneal microdeposits and superficial keratopathy

Chloroquine

Bull’s eye lesion at macula

Secondary keratopathy

Chlorpromazine

Anterior subcapsular cataract

Contraceptive Pills

Decreased tolerance to contact lenses

Migraine

Optic neuritis

Central vein occlusion

Digitalis

Yellow vision

Blurred vision

Ethambutol

Optic neuropathy

Haloperidol (Haldol)

Oculogyric crises

Blurred vision

Indomethacin

Superficial keratopathy

Isoniazid

Optic neuropathy

Nalidixic Acid

Papilloedema

Steroids

Posterior subcapsular cataracts

Glaucoma

Papilloedema (systemic steroids)

Increased severity of HSV infections (geographic ulcers)

Predisposition to fungal infections

Tetracycline

Papilloedema

Thioridazine

Pigmentary degeneration of retina

Vitamin A Intoxication

Papilloedema

Vitamin D Intoxication

Band keratopathy

REFERENCES

Coakes R, and Holmes Sellors P. Outline of Ophthalmology . 2nd Edition . 1995. Butterworth-Heinemann Ltd.: Oxford.

Stein R, Stein H, and Slat B. M anagement of Ocular Emergencies . 2nd Edition. 1994. An Allergen Handbook.

Vaugha D, Asbury T, and Piordan-Eva P. General Ophthalmology . 15th Edition . 1999. Prentice Hall Canada: Toronto.

OP40 - Ophthalmology

MCCQE 2006 Review Notes