Ophthalmology Easy Guide

OPHTHALMOLOGY
Dr. J.H. Fowler

Kylen McReelis and Daniel Weisbrod, editors
T.J. Lou, associate editor
THE OCULAR EXAMINATION . . . . . . . . . . . . . . . . 3 CONJUNCTIVA. . . . . . . . . . . . . . . . . . . . . . . . . . 12

Vision Assessment Pinguecula
Visual Fields Pterygium
Pupils Subconjuctival Hemorrhage
Anterior Chamber Depth Conjunctivitis
Extraocular Muscles Bacterial Conjunctivitis
External Examination Viral Conjunctivitis
Slit-Lamp Examination Chlamydia Conjunctivitis
Tonometry Allergic Conjuctivitis
Ophthalmoscopy Giant Papillary Conjunctivitis (GPC)
Vernal Conjunctivitis
OPTICS. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
Emmetropia SCLERA . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14
Refractive Errors Episcleritis
Myopia Scleritis
Hyperopia Scleromalacia Perforans
Astigmatism Blue Sclerae
Presbyopia Staphyloma
Refraction
Refractive Eye Surgery CORNEA . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15
Foreign Bodies
THE ORBIT. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7 Corneal Abrasion
Exophthalmos (Proptosis) Recurrent Erosions
Enophthalmos Corneal Ulcers
Preseptal Cellulitis Herpes Simplex Keratitis
Orbital Cellulitis Herpes Zoster
Keratoconus
LACRIMAL APPARATUS & LYMPH NODES . . . 8 Arcus Senilis
Lymph Nodes Kayser-Fleischer Rings
Lacrimal Apparatus
Keratoconjunctivitis Sicca (Dry Eyes) THE UVEAL TRACT. .. . . . . . . . . . . . . . . . . . . . . 18
Epiphora (Tearing) Uveitis
Dacryocystitis Anterior Uveitis
Dacryoadenitis Posterior Uveitis
LIDS AND LASHES. . . . . . . . . . . . . . . . . . . . . . . . . . 10
Lid Swelling GLOBE. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19
Ptosis Endophthalmitis
Trichiasis
Entropion LENS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20
Ectropion Cataracts
Hordeolum Dislocated Lens
Chalazion
Blepharitis
Xanthelasma
Lid Carcinoma
MCCQE 2000 Review Notes and Lecture Series Ophthalmology 1

OPHTHALMOLOGY . . . CONT.
RETINA AND VITREOUS. . . . . . . . . . . . . . . . . . . . . 21 OCULAR MANIFESTATIONS OF . . . . . . . . . . 32

Vitreous SYSTEMIC DISEASE
Vitreous Hemorrhage AIDS
Retina Other Systemic Infections
Central Retinal Artery Occlusion Diabetes Mellitus (DM)
Branch Retinal Artery Occlusion Multiple Sclerosis
Central Retinal Vein Occlusion Hypertension
Retinal Detachment 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 . . . . . . . . . . . . 24
Drusen STRABISMUS. . . . . . . . . . . . . . . . . . . . . . . . . . . . 35
Myelinated Nerve Fibres Tropia
Phoria
GLAUCOMA. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25 Paralytic Strabismus
Primary Open Angle Glaucoma Non-Paralytic Strabismus
Primary Angle Closure Glaucoma
Secondary Open Angle Glaucoma PEDIATRIC OPHTHALMOLOGY . . . . . . . . . 37
Secondary Angle Closure Glaucoma Amblyopia
Normal Pressure Glaucoma Leukocoria
Congenital Glaucoma Nasolacrimal System Defects
Ophthalmia Neonatorum
PUPILS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28 Rubella
Pupillary Light Reflex
Dilated Pupil: Differential Diagnosis OCULAR TRAUMA. . . . . . . . . . . . . . . . . . . . . . . 38
Constricted Pupil: Differential Diagnosis Blunt Trauma
Relative Afferent Pupillary Defect (RAPD) Penetrating Trauma
Chemical Burns
NEURO-OPHTHALMOLOGY. . . . . . . . . . . . . . . . . . 30 Hyphema
Visual Field Defects Blow Out Fractures
Bitemporal Hemianopsia Sympathetic Ophthalmia
Homonymous Hemianopsia
Internuclear Ophthalmoplegia COMMON COMPLAINTS . . . . . . . . . . . . . . . . . 40
Nystagmus Common Ocular Problems in the Elderly
Common Ocular Problems in Contact Lens Wearer
INTRAOCULAR MALIGNANCIES . . . . . . . . . . . . . 31
Malignant Melanoma OCULAR EMERGENCIES. . . . . . . . . . . . . . . . . 42
Retinoblastoma
Metastases OCULAR MEDICATIONS. . . . . . . . . . . . . . . . . 42
Topical Ocular Diagnostic Drugs
Glaucoma Medications
Topcial Ocular Therapeutic Drugs
OCULAR DRUG TOXICITY. . . . . . . . .. . . . . . . . 44
GLOSSARY AND DEFINITIONS . . . . . . . . . . . 45
Ophthalmology 2 MCCQE 2000 Review Notes and Lecture Series

THE OCULAR EXAMINATION Notes
sclera
choroid
aqueous outflow iris vitreous body retina
cornea fovea centralis
lens
anterior chamber
posterior chamber optic nerve
canal of Schlemm ciliary body
conjunctiva
rectus muscle
Diagram of the Eye
Drawing by Pascale Tranchemontagne
VISION ASSESSMENT
❏ always note best corrected vision first (i.e. glasses),
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)
❏ assess low vision starting with Snellen Acuity then ––>
count fingers/distance ––> hand motion/distance ––>
light perception ––> no light perception
Visual Acuity (VA) Near

❏ use Rosenbaum or Jaeger pocket vision chart
❏ record number and testing distance (usually 30 cm)
Visual Acuity for Children or Illiterate Adults

❏ Sheridan-Gardiner matching test (most 4 year olds able to do it)
❏ illiterate "E" chart
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 i.e. 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)
• tested by "swinging flashlight test"
❏ test pupillary constriction portion of near reflex
• bring object from far to near, observe
convergence and pupillary constriction
ANTERIOR CHAMBER DEPTH
❏ shine light tangentially from temporal side
❏ shallow = > 2/3 of nasal iris in shadow
THE OCULAR EXAMINATION . . . CONT. Notes
EXTRAOCULAR MUSCLES
Alignment
❏ examine in primary position of gaze (i.e. straight ahead)
❏ Hirschberg test (shine light into patient's eyes from 30 cm away)
• corneal light reflex should be symmetric and
near centre on each cornea
❏ strabismus testing as indicated - see Strabismus section
Movement
❏ examine movement of eyeball through the six cardinal
positions of gaze
❏ determine if diplopia present in any position of gaze
❏ observe for nystagmus
EXTERNAL EXAMINATION
❏ the four Ls
• 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), with cobalt blue filter
• Rose Bengal dye (stains devitalized corneal epithelium)
❏ can examine structures in the posterior segment with special lenses
TONOMETRY
❏ measurement of intraocular pressure
❏ normal range is 8-21 mm Hg
❏ commonly measured by
• indentation (Schiotz or Tonopen)
• applanation (Goldmann)
• non-contact (air puff)
❏ use topical anesthetic for Schiotz, Goldmann, Tonopen
OPHTHALMOSCOPY
❏ examination of the posterior segment of the eye
• vitreous
• optic disc (colour, cup, margins, cup/disc ratio)
• retinal vessels
• retina, macula
❏ best with pupillary dilatation (e.g. tropicamide)
❏ contraindications to dilatation
• narrow anterior chamber angles
• neurologic abnormality requiring pupillary evaluation
• iris supported anterior chamber lens implant

OPTICS Notes
❏ 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
❏ 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
❏ 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
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

OPTICS . . . CONT. Notes
ASTIGMATISM
❏ light rays not refracted uniformly in all meridians
❏ due to non-spherical surface of cornea or non-spherical
lens (i.e. 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
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
Emmetropia
Hyperopia corrected with positive lens
Myopia Hyperopia
Myopia corrected with negative lens
Figure 1. Refractive Errors and Emmetropia
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
• 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

OPTICS . . . CONT. Notes
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
❏ lid laceration
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
Etiology
❏ 2º to sinusitis, to facial and/or tooth infections
Symptoms and Signs
❏ lids swollen shut, chemosis
❏ ophthalmoplegia (due to pain on ocular movement)
❏ exophthalmos
❏ decreased VA, RAPD may occur
❏ adenopathy and fever
Management
❏ admit, IV antibiotics and blood cultures
❏ serious complications exist ie) cavernous sinus thrombosis
❏ surgical evacuation of abscess if it develops
THE ORBIT . . . CONT. Notes
Table 1. Differences between preseptal and orbital cellulitis

Finding Preseptal Cellulitis Orbital Cellulitis
Fever Present 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 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 i.e. CN VII palsy
❏ systemic diseases: rheumatoid arthritis, Sjögren's
syndrome, sarcoidosis, amyloidosis, leukemia, lymphoma
❏ vitamin A deficiency, especially in malnourished areas
❏ 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
Management
❏ artificial tears and ointments
❏ punctal occlusion
❏ tarsorrhaphy (sew lids together)
❏ treat underlying cause

LACRIMAL APPARATUS
AND LYMPH NODES . . . CONT. Notes
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 restoring lacrimal drainage
DACRYOCYSTITIS (see Colour Atlas H1)

❏ infection of the lacrimal duct
❏ 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. pneumoniae in chronic infections
Symptoms and Signs

❏ 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
❏ 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

❏ pain, swelling, redness of the outer region of the upper eyelid
Management
❏ +/– systemic antibiotics
❏ incision and drainage if required

LIDS AND LASHES Notes
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 (i.e. myxedema), trauma (i.e. 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
(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 Section):
• 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)
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 trichiasis with secondary corneal scarring
Etiology
❏ involutional (aging)
❏ scar contraction (burns, surgery)
❏ orbicularis oculi muscle spasm
Management
❏ lubricants, evert lid with tape, surgery
ECTROPION
❏ eversion of lower lid
❏ often bilateral
❏ symptoms: dry eye, tearing, cosmetic
❏ may cause exposure keratitis

LIDS AND LASHES . . . CONT. Notes
Etiology
❏ weak orbicularis oculi (aging)
❏ CN VII palsy
❏ scarring (burns, surgery)
❏ mechanical (tumour, herniated fat)
Management
❏ upward massage with ointment or surgery
HORDEOLUM
❏ painful, red swelling of lid
❏ usually S. aureus
❏ internal
• acute infection of meibomian gland
• chalazion in chronic stage
❏ external
• stye, pimple
• acute infection of hair follicle or of glands of Zeis or Moll
Management
❏ warm compresses
❏ topical antibiotics
❏ cellulitis may develop
❏ usually resolves in 2-5 days
CHALAZION
❏ due to chronic sterile granuloma of a meibomian gland (following
acute meidomitis), usually pointing towards the conjunctiva
❏ painless, often subsides
❏ differential diagnosis: basal cell carcinoma, sebaceous cell adenoma
Management
❏ warm compresses
❏ surgical incision and curettage if needed
BLEPHARITIS
❏ 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
Management (S. aureus)

❏ warm compresses and lid hygeine
❏ 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

LIDS AND LASHES . . . CONT. Notes
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
Management (see Dermatology/Plastic Surgery Notes)

❏ surgical excision
❏ irradiation for basal cell, sebaceous cell
❏ biopsy to confirm diagnosis
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 H8)

❏ fleshy triangular encroachment of epithelial tissue onto the cornea
❏ usually nasal and bilateral
❏ associated with wind, ultraviolet (UV) light exposure
Management
❏ surgery if threatens visual axis, causes irritation, or for cosmesis
❏ may recur (up to 40%) 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: ideopathic, 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
❏ tired or dry eyes
❏ allergy: pollutants, wind dust
❏ infection: bacterial, viral, chlamydial, fungal, rickettsial, parasitic

CONJUNCTIVA . . . CONT. Notes
❏ chemical
❏ irradiation associated with systemic disease
❏ immune reaction e.g. giant papillary conjunctivitis
especially in contact lens wearer
❏ secondary to dacryocystitis or canaliculitis
❏ see Table 4
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
BACTERIAL CONJUNCTIVITIS
❏ often has a purulent white-yellow discharge, and papillae
❏ causes: S. aureus, S. pneumoniae, and H. flu.
❏ may also be due to N. gonorrhea (in neonates and
sexually active people)
Management
❏ systemic antibiotics if indicated
VIRAL CONJUNCTIVITIS
❏ watery discharge, follicles, subepithelial infiltrates.
❏ associated with cold symptoms, (recent URTI history)
❏ preauricular node often palpable and tender
❏ initially unilateral, often progresses to the other eye
❏ cause: adenovirus
Management
❏ self-limiting
❏ adenovirus is highly contagious therefore proper hygiene is very
important
CHLAMYDIAL CONJUNCTIVITIS
❏ caused by Chlamydia trachomatis
❏ affects neonates on day 3-5, sexually active people
❏ causes trachoma and inclusion conjunctivitis
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
ALLERGIC CONJUNCTIVITIS
❏ intermittent
❏ chemosis/injection with itching and burning
❏ mucous discharge, lid edema, palpebral conjunctival papillae

CONJUNCTIVA . . . CONT. Notes
Management
❏ avoid irritants
❏ cold compresses
❏ topical medications: decongestant/antihistamines
(e.g. Albalon-A), mast cell stabilizer (e.g. Opticrom),
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
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)
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
EPISCLERITIS
❏ usually unilateral; simple or nodular
❏ non-specific immune response to irritants
Etiology
❏ mostly idiopathic
❏ associated with rheumatoid arthritis, gout, Sjögren's syndrome,
herpes zoster, tuberculosis, syphilis, coccidioidomycosis
Symptoms and Signs

❏ localized, elevated, segmental hyperemia, pink/purple-coloured globe
❏ pain, swelling, tenderness, photophobia, lacrimation
❏ topical vasoconstrictor reduces redness
❏ lasts for weeks, may recur
Management
❏ 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
❏ posterior scleritis: may cause exudative retinal detachment
❏ usually with episcleral involvement

SCLERA . . . CONT. Notes
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
❏ idiopathic
Symptoms and Signs

❏ 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, rarely occurs
❏ thinning of the sclera may lead to uveal dehiscence and
globe rupture with minor trauma
❏ prognosis poor, avoid steroids
BLUE SCLERAE
❏ rare, uveal pigment seen through thin sclera
❏ associated with: collagen vascular diseases
(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
❏ seen in rheumatoid arthritis, high myopia, glaucoma, trauma
CORNEA
❏ function
• transmission of light
• refraction of light (2/3 of total refractive power)
• barrier against infection, foreign bodies
❏ avascular, clear
❏ 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 H5)

❏ tearing, photophobia, foreign body sensation
❏ foreign body below lid may cause multiple vertical epithelial abrasions
due to blinking
❏ detected with fluorescein staining
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)

CORNEA . . . CONT. Notes
❏ pressure patch
❏ cycloplegia if iritis already present
❏ 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 H2)

❏ pain on blinking, conjunctival injection, tearing, photophobia
(after 24-48 hours)
❏ de-epithelialized area stains with fluorescein dye
Complications
❏ infection, ulceration, recurrent erosion, secondary iritis
Management
❏ +/– 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
❏ NEVER give topical analgesics - impedes epithelial healing
(unless needed to facilitate examination)
❏ systemic analgesics as needed
❏ most abrasions clear within 24-48 hours
RECURRENT EROSIONS
❏ localized area of superficial corneal edema 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 epithelium is
dislodged with eye opening due to poor adhesion
❏ examination reveals localized epithelial irregularity
Management
❏ as for corneal abrasion
❏ bandage contact lens, bed rest
❏ topical hypertonic 2% or 5% sodium chloride solution for epithelial edema
❏ anterior stromal needle puncture or YAG laser for chronic recurrence
Table 2. Corneal Abrasion vs. Corneal Ulcer

Abrasion Ulcer
time course acute (hours) subacute (days)

history of trauma yes 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
❏ central ulcers are most serious because can perforate or scar

❏ pain, photophobia, tearing, decreased visual acuity
❏ 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
❏ 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

❏ pain, tearing, foreign body sensation, redness,
❏ may have visual acuity loss
❏ corneal hypoesthesia
❏ occasional cold sore on lip, vesicles on skin
Complications
❏ geographic ulcer may often arise from inadvertent steroid use
❏ corneal scarring (can lead to loss of vision)
❏ chronic interstitial keratitis due to penetration of virus into stroma
❏ secondary iritis
Management
❏ 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
HERPES ZOSTER KERATITIS

❏ CN V1 territory
Symptoms and Signs

❏ neuralgia-type pain ( vesicular skin eruption (~ 2 weeks)
❏ ocular tearing, pain and photophobia
❏ corneal hypoesthesia
❏ Hutchinson's sign: if tip of nose involved, eye involvement likely
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 +/– 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
Management
❏ contact lens initially if spectacle correction unsatisfactory
❏ penetrating keratoplasty (corneal transplant) 90% successful
❏ post-operative complications: endophthalmitis, graft rejection
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 (green or brown) 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
ANTERIOR UVEITIS
❏ inflammation of iris (iritis) and ciliary body (cyclitis)
❏ usually unilateral
Etiology
❏ usually idiopathic
❏ connective tissue diseases: JRA, ankylosing spondylitis, Reiter's, IBD
❏ infectious: syphilis, Lyme disease, toxoplasmosis, TB, HSV, herpes zoster
❏ others: sarcoidosis, trauma
❏ ocular pain, photophobia, decreased visual acuity
❏ ciliary flush (perilimbal conjunctival injection), miosis
❏ anterior chamber cells (WBC) and flare (protein)
❏ occasionally keratitic precipitates (cells on corneal endothelium)
❏ cyclitis typically reduces intraocular pressure while
severe iritis may cause an inflammatory glaucoma
Complications
❏ inflammatory glaucoma
❏ anterior synechiae (rare): adhesions of iris to cornea ––> glaucoma
THE UVEAL TRACT . . . CONT. Notes
❏ posterior synechiae
• adhesions of the iris to the lens ––> angle closure glaucoma
• indicated by an irregularly shaped pupil
❏ 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
Symptoms and Signs

❏ decreased visual acuity
❏ floaters
❏ frequently there is no conjunctival or scleral injection
❏ vitreous cells and opacities
Management
❏ retrobulbar, or systemic steroids if indicated
(i.e. threat of vision loss)
GLOBE
ENDOPHTHALMITIS
❏ most commonly a postoperative complication of cataract surgery,
or due to post-penetrating injury to eye

❏ 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

LENS Notes
❏ 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), 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
❏ 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
❏ haloes around lights at night
❏ diagnose by slit-lamp exam and by eliciting red reflex with direct ophthalmoscope
Management
❏ surgical extraction of the cataract
❏ extracapsular: (more common)
• more common
• remove cataract nucleus (by expression or
phacoemulsification) and cortex, leaving the
posterior capsule and a peripheral rim of
anterior capsule
• 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 30-50% 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
Indication for Surgery
❏ when cataract interferes with daily pattern of living
DISLOCATED LENS
Etiology
❏ associated with Marfan's Syndrome, homocystinuria, syphilis, lens coloboma
❏ traumatic
Symptoms and Signs
❏ decreased visual acuity
❏ may get unilateral diplopia
❏ iridodenesis (quivering of iris with movement)
Complications
❏ cataract, glaucoma, uveitis
Management
❏ surgical correction +/– lens replacement

RETINA AND VITREOUS Notes
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 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
❏ if very large hemorrhage, may have RAPD
❏ ophthalmoscopy: retina not visible due to blood in vitreous
Management
❏ ultrasound to rule out retinal detachment
❏ expectant: in non-urgent cases (i.e. 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 ratio is < 0.5), retinal artery and vein pass through cup
CENTRAL RETINAL ARTERY OCCLUSION

Etiology
❏ emboli from carotid arteries or heart (e.g. arrhythmia, endocarditis,
valvular disease)
❏ thrombus
❏ temporal arteritis
❏ sudden, painless (except in temporal arteritis), unilateral loss of vision
❏ RAPD
❏ fundoscopy
• cherry red spot (macula), retinal pallor
• boxcars (segmentation of blood in arteries), narrowed arteries
• non-pulsatile empty veins
Management
❏ OCULAR EMERGENCY: attempt to restore blood flow within 2 hours
❏ if < 2 hours
• massage the globe
• decrease intraocular pressure
• anterior chamber paracentesis
• 100% oxygen at atmospheric pressure,
• IV Diamox (carbonic anhydrase inhibitor)
• IV Mannitol (draws fluid from eye)

RETINA AND VITREOUS . . . CONT. Notes
BRANCH RETINAL ARTERY OCCLUSION

❏ only part of the retina becomes ischemic resulting in partial loss of vision
❏ more likely than a central artery occlusion to be embolic; search for source
❏ management: ocular massage to dislodge embolus
if VA is affected
CENTRAL RETINAL VEIN OCCLUSION

❏ 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

❏ painless, unilateral, gradual or sudden visual loss
❏ 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 of iris (secondary
rubeosis), which can lead to secondary glaucoma
❏ iritis
Management
❏ retinal laser photocoagulation to reduce neovascularization
RETINAL DETACHMENT
❏ fluid collects between the neurosensory retina and the
retinal pigment epithelium
❏ three types
❏ rhegmatogenous
• 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, central
retinal vein occlusion, sickle cell disease, and retinopathy of prematurity
❏ exudative
• may be due to choroidal tumour, metastatic tumour, uveitis


❏ sudden onset
❏ flashes of light
• due to mechanical stimulation of the retinal photoreceptors
❏ floaters
• hazy spots in the line of vision, due to drops of blood in the
vitreous (blood vessels torn as the retina detaches)
❏ 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
❏ RAPD may be seen
Management
❏ prophylactic: if a symptomatic tear (flashes or
floaters) is detected, it can be sealed off with laser
therapy or cryotherapy, thereby preventing the
progression to detachment
❏ therapeutic: (late) scleral buckle with closure of all
tears and holes (by laser or cryotherapy), and intravitreal
injection of gas or oil
❏ 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 begining in
adolescence, with expanding ring scotoma 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 under the retinal
pigment epithelium (RPE), in Bruch's membrane
• 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% of ARMD resulting 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)
Investigations
❏ Amsler Grid: assesses macular function
❏ fluorescein angiography: see neovascularization, leaks
Management
❏ non-neovascular ARMD
• monitor
• low vision aids e.g. magnifiers, closed-circuit television
❏ 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
❏ antioxidant medication and photodynamic
therapy under investigation
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

BLURRED OPTIC DISC MARGINS . . . CONT. Notes
Table 3. Differential Diagnosis of Blurred Optic Disc Margins
Papilledema Optic Ischemic CRVO

(see Colour Atlas H11) Neuritis Neuropathy
Age any < 50 > 50 > 50
Etiology increased intracranial idiopathic, idiopathic, idiopathic

pressure associated with MS vascular, GCA
VA normal reduced reduced reduced
Other bilateral, enlarged unilateral, pain on altitudinal field loss, unilateral, hypertension,
sign or blind spot, eye movement, +/– GCA findings diabetes, increased
symptom neurological findings RAPD, reduced (e.g.jaw claudication, viscosity, arteriosclerotic
(e.g. headache) color vision, headache, tender vascular disease
+/– MS findings scalp)
Funduscopic swollen disc, hyperemic pale, swollen “blood and thunder”,

findings hemorrhage, swollen disc, disc, flame swollen disc,venous
dilated normal if hemorrhage engorgement,
retinal veins retrobulbar retinal hemmorhage
neuritis
Investigation CT head visual field, ESR, fluorescein

CT (if atypical VF biopsy temporal angiography,
or if no improvement artery medical
in 6 weeks) evaluation
Treatment neurosurgical steroids high dose panretinal laser

consult, steroids photocoagulation
treat underlying (for GCA) steroids
cause
GLAUCOMA
Definition
❏ progressive optic neuropathy involving characteristic
structural changes to optic nerve head with associated
visual field changes (commonly associated with high 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
❏ an isolated increase in intraocular pressure (IOP) is termed
ocular hypertension (or glaucoma suspect) and these
patients should be followed because 1-2% will develop glaucoma
❏ IOP has diurnal variation, higher in a.m.
❏ normal, average IOP is 16 +/– 2 mm Hg
❏ pressures > 21 are much more likely to be
associated with glaucoma
❏ normal C/D ratio < 0.4, if C/D ratio > 0.6, difference
between eyes > 0.2 or cup approaches disc margin, then
suspect glaucoma
❏ initially loss of peripheral vision is most common
❏ 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 or Goldmann visual field testing

GLAUCOMA . . . CONT. Notes
PRIMARY OPEN ANGLE GLAUCOMA

❏ most common form of glaucoma
❏ > 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 (> 21mm 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
❏ 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)
• 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
• topical beta-blockers (decrease aqueous production)
• topical cholinergics (increase aqueous outflow)
• topical adrenergics (decrease aqueous production and
increase aqueous outflow)
• topical and oral carbonic anhydrase inhibitor
(decrease aqueous production)
• topical prostaglandin agonist (increases aqueous outflow)
❏ surgical treatment
• laser: trabeculoplasty, selective destruction of ciliary body
• microsurgery: trabeculectomy, tube shunt placement
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)
Symptoms
❏ unilateral, but other eye predisposed
❏ 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 circumlimbal injection
GLAUCOMA . . . CONT. Notes
❏ 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
❏ iritis leading to iris bombé (posterior iris adheres to anterior
lens capsule, entrapping aqueous in posterior chamber)
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)
❏ 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% of general population (responders) after 4
weeks 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
SECONDARY ANGLE CLOSURE GLAUCOMA
❏ uveitis
• inflamed iris adheres to lens (posterior synechiae)
❏ neovascular glaucoma
• abnormal blood vessels develop on surface of iris
(rubeosis iridis) and trabecular meshwork
• due to retinal ischemia with proliferative diabetic retinopathy and CRVO
❏ treatment with laser therapy
NORMAL PRESSURE GLAUCOMA
❏ IOP in normal range but cupping and field loss typical of glaucoma are present
❏ often found in women > 60
❏ 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
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 Notes
PUPILLARY LIGHT REFLEX

❏ see Figure 2
❏ 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
❏ LGB = lateral geniculate body
1
6 6
5
2
2
4 4
3 3
LGB LGB
Figure 2. Pathway of direct light reflex from left eye and

consensual light reflex from right eye
❏ refer to text for explanation
Drawing by Aimée Worrell
DILATED PUPIL (MYDRIASIS)

DIFFERENTIAL DIAGNOSIS
Physiologic Anisocoria
❏ 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
❏ CN III palsy
• eye also deviated down and out with ptosis present
• etiology includes CVA, neoplasm, aneurysm, 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

❏ pupil reacts poorly to light (both direct and consensual)
constricts with accomodation
❏ hyporeflexic (Adie's syndrome)
PUPILS . . . CONT. Notes
❏ 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 eventually gets smaller than the unaffected eye
❏ 80% unilateral, females > males
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
❏ as for Dilated Pupil section above
Senile Miosis
❏ decreased sympathetic stimulation with age
Parasympathetic Stimulation
❏ local or systemic medications
❏ cholinergic agents: pilocarpine, phospholine iodide, carbachol
❏ 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
❏ 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)
RELATIVE AFFERENT PUPILLARY DEFECT (RAPD)

❏ defect in visual afferent pathway anterior to optic chiasm
❏ differential diagnosis: optic nerve compression, optic
neuritis, large retinal detachment, central retinal
artery/vein occlusion, 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
Clinical Pearl
❏ Even dense cataracts do not produce a relative afferent pupillary defect

NEURO-OPHTHALMOLOGY Notes
VISUAL FIELD DEFECTS

❏ lesions in the visual system have characteristic pattern losses
❏ several tests used: confrontation (screening), tangent screen,
Humphrey fields, Goldman perimetry
❏ refer to Figure 13 in Neurology section
BITEMPORAL HEMIANOPSIA
❏ a chiasmal lesion
❏ causes: craniopharyngioma (youth), pituitary mass, 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 VF defect in both eyes
INTERNUCLEAR OPHTHALMOPLEGIA
❏ commonly seen in MS - see Figure 3
❏ lesion of medial longitudinal fasciculus (MLF)
❏ delayed movement in ipsilateral adducting eye
❏ monocular nystagmus in contralateral abducting eye
Lateral Rectus M Medial Rectus M “Look left”
CN III
CN VI
PPRF
MLF
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 (not
shown) and travel to the left PPRF. The impulses then travel to the ipsilateral CN VI nucleus
and to the contralateral CN III nucleus via the MLF. In internuclear ophthalmoplegia, an MLF
lesion inhibits transmission from the PPRF to the contralateral medial rectus muscle.
Figure 3. Pathway for left lateral gaze, in patient with

right internuclear ophthalmoplegia
NYSTAGMUS
❏ 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
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
NEURO-OPHTHALMOLOGY . . . CONT. Notes
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, 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
OCULAR MANIFESTATIONS
OF SYSTEMIC DISEASE Notes
HIV
❏ up to 75% of patients with AIDS have ocular manifestations
❏ ocular findings include: ocular vascular manifestations, neoplasms,
opportunistic infections
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
❏ CMV retinitis (see Colour Atlas H15)
• 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
• a necrotizing retinitis, with retinal hemorrhage and vasculitis,
brushfire 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
Retina
❏ background
• altered vascular permeability
• retinal vessel closure
OF SYSTEMIC DISEASE . . . CONT. Notes
❏ non-proliferative: increased vascular permeability and retinal ischemia
• dot and blot hemorrhages
• microaneurysms
• retinal edema
• hard exudates
❏ advanced non-proliferative (or pre-proliferative):
• non-proliferative findings plus
• venous beading
• intraretinal microvascular anomalies
(IRMA): dilated, leaky vessels within the retina
• macular edema
• cotton wool spots (nerve fibre layer infarcts)
❏ proliferative (see Colour Atlas H13)
• (5% of patients with diabetes will reach this stage)
• neovascularization: iris, disc, retina to vitreous
• neovascular glaucoma
• 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 – see Endocrinology Notes
- tight control of blood sugar decreases frequency and severity of
microvascular complications
❏ blood pressure control
❏ focal laser for macular edema
❏ panretinal laser photocoagulation - 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
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 recovery within one year
Optic Neuropathy
❏ visual acuity loss due to infarction of optic disc/nerve
MULTIPLE SCLEROSIS
❏ 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 3)

OF SYSTEMIC DISEASE . . . CONT. Notes
Signs
❏ RAPD, ptosis, nystagmus, uveitis
❏ optic atrophy (see Colour Atlas H12), optic neuritis
❏ internuclear ophthalmoplegia
Management
❏ with optic neuritis, treatment with oral steroids leads
to greater likelihood of getting MS later on than
treatment with IV steroids
❏ see Neurology section
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)
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)
HYPERTHYROIDISM/GRAVES' DISEASE
❏ mnemonic - NO SPECS
Grade 0: No signs or symptoms
Grade 1: Only signs are proptosis < 22 mm +/– lid lag
+/– lid retraction
Grade 2: Soft tissue involvement - conjunctival + lid miosis
Grade 3: Proptosis > 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
❏ RA, JRA, SLE, Sjogren's syndrome
❏ ankylosing spondylitis, 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 Notes
❏ 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
• 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
❏ see Figure 4
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)
Tests
❏ cover-uncover test
• 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
• see Figure 4
❏ 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

STRABISMUS . . . CONT. Notes
ET
COVER TEST
XT
COVER TEST
E
COVER-UNCOVER
TEST
X
COVER-UNCOVER
TEST
ET = ESOTROPIA XT = EXOTROPIA
E = ESOPHORIA X = EXOPHORIA
Figure 4. 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, Graves' 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 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 - the neural paths for both eyes can develop
Clinical Pearl
❏ All children with strabismus should be promptly referred to opththalmology
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 anisometropia (difference in refraction between
two eyes) or ocular pathology (e.g. cataract, retinoblastoma)

PEDIATRIC OPHTHALMOLOGY Notes
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 thalamusor visual cortex
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
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
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 (retrolental fibroplasia):
associated with supplemental oxygen use in premature infants
❏ PHPV (persistent hyperplastic primary vitreous)
❏ 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

PEDIATRIC OPHTHALMOLOGY . . . CONT. Notes
OPHTHALMIA NEONATORUM
❏ newborn conjunctivitis
❏ Chlamydia is most common cause in USA
❏ 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:
congenital cataract, heart disease, deafness, microcephaly,
microphthalmos, mental deficiency
OCULAR TRAUMA
❏ always test visual acuity first!
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, because acids
coagulate tissue and inhibit further corneal penetration
❏ poor prognosis if cornea opaque, likely irreversible
stromal damage
Management
❏ IRRIGATE immediately, with water or buffered solution
• IV drip for at least 20-30 minutes with eyelids retracted
❏ 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)

OCULAR TRAUMA . . . CONT. Notes
❏ topical antibiotics and patching

❏ topical steroids 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
❏ patch and shield and bedrest x 5 days
❏ may need surgical drainage
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
BLOW OUT FRACTURES (see Plastic Surgery Notes)

❏ 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
❏ surgery if fracture > 50% orbital floor, diplopia
not improving within 6 weeks, or enophthalmos > 2 mm
❏ 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

COMMON COMPLAINTS Notes
Persistent Loss of Vision

❏ gradual (weeks to months)
• refractive error
• cataracts
• diabetes
• macular degeneration
• glaucoma
• 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
• optic neuritis
• multiple sclerosis (MS)
• papillitis or retrobulbar neuritis
• retinal detachment
Transient Loss of Vision (Amaurosis Fugax)

❏ transient ischemic attack (TIA), microemboli
❏ migrainous spasm of artery
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)

❏ anterior uveitis
❏ meningitis, encephalitis
❏ light dispersion by mucus, lens, corneal opacities
❏ retinal degeneration
Diplopia (Double Vision)

❏ binocular diplopia: strabismus, CN paresis (III,IV,VI), muscle entrapment
❏ monocular diplopia: dislocated lens, cataract, corneal scar

COMMON COMPLAINTS . . . CONT. Notes
Red Eye
Table 4. Differential Diagnosis of Red Eye

Acute Acute Angle Closure
Conjunctivitis Iritis Glaucoma Keratitis
discharge bacteria: pus no no profuse tearing

virus: serous
allergy: mucous
pain no ++ ++++ +++
(tender with nausea with blinking
globe)
photophobia no ++++ + ++
vision normal reduced reduced varies with
(cloudy (corneal edema) site of lesion
aqueous)
pupil normal smaller fixed same or
in mid dilation smaller
Clinical Pearl
❏ All red eyes are not necessarily conjunctivitis
Table 5. Additional Features of Red Eye

Acute Acute Angle Closure
Conjunctivitis Iritis Glaucoma
injection palpebral+bulbar ciliary flush diffuse

(limbal palor)
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

COMMON COMPLAINTS . . . CONT. Notes
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, temporal 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. aureus)
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
❏ CRAO
❏ retinal detachment
❏ endophthalmitis
❏ giant cell arteritis
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 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
❏ cholinergic blocking
• paralyze iris sphincter i.e. dilation and
cycloplegia
❏ indication: refraction, ophthalmoscopy, therapy for iritis

OCULAR MEDICATIONS . . . CONT. Notes
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
Corticosteroids
❏ never prescribed by primary care physician unless emergency indications
❏ complications
• potentiates herpes simplex keratitis and
fungal keratitis as well as masking symptoms
• posterior subcapsular cataract
• increased IOP, more rapidly in steroid responders
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 Notes
Table 7. Ocular Drug 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

GLOSSARY AND DEFINITIONS Notes
❏ anisocoria: unequal pupil sizes

❏ aphakia: absence of lens
❏ ARMD: age-related macular degeneration
❏ asthenopia: eye fatigue (blurred vision, diplopia, ache) from
excessive use of eye, associated with near work
❏ C/D ratio: ratio of optic cup to optic disc diameters
❏ cells: white blood cells found in the anterior chamber in anterior
segment inflammation
❏ chemosis: conjunctival swelling
❏ coloboma: congenital cleft due to failure of the eye or ocular
adenexae to complete growth
❏ cotton wool spots ("soft exudates"): "fluffy", pale areas in
retina representing micro-infarcts in the nerve fibre layer
❏ CRVO/CRAO: central retinal vein/artery occlusion
❏ CVA: cerebrovascular accident
❏ cycloplegia: paralysis of ciliary body = loss of accommodation
❏ DM: diabetes mellitus
❏ drusen: yellow-white deposits of collagen produced by retinal
pigment epithelium, associated with ARMD
❏ enucleation: removal of globe from eye socket
❏ EOM:
❏ epiphora: excessive tearing which overflows onto face
❏ evisceration: removal of globe's contents
❏ FB: foreign body
❏ flare: protein precipitates in the anterior chamber secondary to
inflammation, seen by slit-lamp exam
❏ floaters: dark spots in the visual field which move with eye
position, usually benign
❏ GCA: giant cell arteritis
❏ hard exudates: lipoprotein macromolecules found in localized
areas of retinal edema (hypertension, diabetes)
❏ IOP: intraocular pressure
❏ lid lag: seen on movement from up gaze to down gaze: upper
lid trails behind globe, allowing scleral rim to be visible above
limbus (Graves' disease)
❏ lid retraction: on normal gaze, scleral rim is visible
above/below limbal margins (Graves' disease)
❏ metamorphopsia: distortion of vision associated with
macular degeneration, "crooked" vision
❏ miosis: pupil constriction
❏ MS: multiple sclerosis
❏ mydriasis: pupil dilation
❏ photopsia: flashes of light due to retinal irritation
❏ RAPD: relative afferent pupillary defect
❏ scotoma: blind or partially blind islands in the visual field,
surrounded by areas of normal vision (abnormal blind spot)
❏ synechia: adhesion of the iris to cornea (anterior) or lens
(posterior) secondary to inflammation
❏ syneresis:liquefaction of vitreous, associated with age
❏ VA: visual acuity
❏ VF: visual fields

Drawing by Vince Mazzurco

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What are some of the important structures and components of the eye discussed in the document?

What are some of the important structures and components of the eye discussed in the document?

What are some common eye diseases and disorders mentioned?

What are some common eye diseases and disorders mentioned?

OPHTHALMOLOGY

Dr. J.H. Fowler

THE OCULAR EXAMINATION . . . . . . . . . . . . . . . . 3 CONJUNCTIVA. . . . . . . . . . . . . . . . . . . . . . . . . . 12

MCCQE 2000 Review Notes and Lecture Series Ophthalmology 1

RETINA AND VITREOUS. . . . . . . . . . . . . . . . . . . . . 21 OCULAR MANIFESTATIONS OF . . . . . . . . . . 32

OCULAR DRUG TOXICITY. . . . . . . . .. . . . . . . . 44

GLOSSARY AND DEFINITIONS . . . . . . . . . . . 45

Ophthalmology 2 MCCQE 2000 Review Notes and Lecture Series

Visual Acuity (VA) Far

Visual Acuity (VA) Near

Visual Acuity for Children or Illiterate Adults

Infant Visual Acuity

Ophthalmology 4 MCCQE 2000 Review Notes and Lecture Series

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

MCCQE 2000 Review Notes and Lecture Series Ophthalmology 5

Ophthalmology 6 MCCQE 2000 Review Notes and Lecture Series

REFRACTIVE EYE SURGERY

Symptoms and Signs

Table 1. Differences between preseptal and orbital cellulitis

Fever Present Present

KERATOCONJUNCTIVITIS SICCA (DRY EYES)

Ophthalmology 8 MCCQE 2000 Review Notes and Lecture Series

DACRYOCYSTITIS (see Colour Atlas H1)

Symptoms and Signs

Symptoms and Signs

MCCQE 2000 Review Notes and Lecture Series Ophthalmology 9

Ophthalmology 10 MCCQE 2000 Review Notes and Lecture Series

Management (S. aureus)

MCCQE 2000 Review Notes and Lecture Series Ophthalmology 11

Management (see Dermatology/Plastic Surgery Notes)

PTERYGIUM (see Colour Atlas H8)

Ophthalmology 12 MCCQE 2000 Review Notes and Lecture Series

Symptoms and Signs

MCCQE 2000 Review Notes and Lecture Series Ophthalmology 13

GIANT PAPILLARY CONJUNCTIVITIS (GPC)

Symptoms and Signs

Ophthalmology 14 MCCQE 2000 Review Notes and Lecture Series

Symptoms and Signs

FOREIGN BODIES (see Colour Atlas H5)

MCCQE 2000 Review Notes and Lecture Series Ophthalmology 15

Symptoms and Signs (see Colour Atlas H2)

Symptoms and Signs

Table 2. Corneal Abrasion vs. Corneal Ulcer

time course acute (hours) subacute (days)

Ophthalmology 16 MCCQE 2000 Review Notes and Lecture Series

❏ contact lens use (50% of ulcers)

Symptoms and Signs (see Colour Atlas H6)

HERPES SIMPLEX KERATITIS

Symptoms and Signs (see Colour Atlas H3)

HERPES ZOSTER KERATITIS

Symptoms and Signs

MCCQE 2000 Review Notes and Lecture Series Ophthalmology 17

THE UVEAL TRACT

Symptoms and Signs

Symptoms and Signs (see Colour Atlas H6)

MCCQE 2000 Review Notes and Lecture Series Ophthalmology 19

❏ consists of an outer capsule surrounding a soft

Ophthalmology 20 MCCQE 2000 Review Notes and Lecture Series

Symptoms and Signs