Ophthalmology

Ophthalmic History

History
1. Record age and gender

2. Presenting complaint
a. Visual disturbance
b. Pain
c. Red eye
d. Discharge
e. Itchy/dry/gritty eyes
f. Alteration in appearance
i. Ptosis, lid swelling, squint

3. History of presenting complaint?

a. How long?
b. Rate of onset?
c. Involving one or both eyes?
d. Any associated symptoms?
e. Any similar problems before?

4. Past ophthalmic history

a. Previous eye problems
b. Refractive errors (myopia, hyperopia, astigmatism)
c. Ocular surgery
d. Ocular trauma
e. Squint
f. Lazy eye

5. Past medical history

a. Diabetes?
b. Hypertension?
c. Rheumatoid arthritis?
d. Sarcoidosis?
e. Asthma?
f. Eczema or other skin problems?

6. Medications

7. Allergies

8. Family history
a. Squint
b. Glaucoma
c. Myopia
d. Cataracts
e. Poor vision
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9. Social History
a. Smoking
b. Alcohol
c. Occupation
Anatomy of the Eye and Visual Pathways

Orbit
o Thin walled, medial and floor
o Close proximity to paranasal air sinuses (sinusitis)
o Transmission of cranial nerves via fissures and foramen
o Susceptibility to trauma (blow-out fractures)
o Orbital fat swells in thyroid disease

Eyelids
o Protect ocular surface
o Facilitate spread of pre-corneal tear film
o Comprises skin and orbicularis muscle (anterior lamella) and tarsus
and conjunctiva (posterior lamella)
o Meibomian glands located in tarsus

Tears
o Important for maintenance of corneal clarity and refraction
o Contains important defence mechanisms against infection
o Requires integrity of lids and in correct position to spread tears and
drain (dryness vs. epiphora)

Conjunctiva
o Important to recognize extent of conjunctival covering
o Areas of redness important in differentiation causes of red eyes
(conjunctivitis, iritis, etc)

Cornea
o Transparency dependent upon hydration maintained by endothelial
pump
o Devoid of blood vessels
o Highly innervated from trigeminal nerve

Aqueous Humour (located in anterior chamber)

o Formed by ciliary body
o Maintains intraocular pressure (10-21 mm Hg)
o Constantly produced and drained via canal of Schlemm

Lens
o Normally transparent, refractive
o Reduced elasticity with age (presbyopia)
o Loss of transparency with age (cataract)
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Uveal Tissue
o Consists of iris, ciliary body, choroid
o Highly vascularized
o Immune competent
o Susceptible to inflammation

Pupil and Autonomic Control

o Constrictor and dilator muscles control pupil aperture
o Sympathetic control for dilation via sympathetic chain (Horner’s)
o Parasympathetic control for constriction cranial nerve III (oculomotor)

Retina
o Transparent innermost layer of globe
o Underlying melanin rich retinal pigment epithelium for maintenance of
photoreceptor health
o Cones are colour-sensitive and central
o Rods are night vision and peripheral
o Blood supply of inner 2/3 via ventral retinal artery (internal carotid) and
central retinal vein

Macula
o Highest concentration of cones
o More than one layer of ganglion cells
o Fovea is central and lacks blood vessels (nourished by choroid)

Muscles of the Eye + Innervation (LR6SO4)3

o Cranial Nerve III: superior rectus, medial rectus, inferior rectus, inferior
oblique
o Cranial Nerve IV: superior oblique
o Cranial Nerve VI: lateral rectus
o Movement: MR adducts, SR upward, IR downward, IO up and in, SO
down and in, LR abducts

Visual Pathway
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Emmetropia: normal
Myopia: short-sightedness, poor distance vision
 Eye is too long or cornea is too curved
 Common in teenagers
Hypermetropia: long-sightedness, poor near vision
 Eye is too short or cornea is too flat
 Common in infants
Anisometropia: refraction of the two eyes is different
Astigmatism: eye is short sighted in one plane and long sighted at 90o to
this
 Images distorted due to irregular cornea
Presbyopia: natural loss of accommodation power after age 40, resulting
in need for reading glasses
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Red Eye

 Nearly always due to inflammation

o Consider lids, conjunctiva, cornea, sclera, episclera, iris

Aetiology
1. Common
 Conjunctivitis
 Subconjunctival haem
 Episcleritis
 Trauma (foreign body, corneal abrasion)
 Allergy

2. Less Common
 Uveitis
 Acute angle closure glaucoma
 Corneal ulcers
 Endophthalmitis
 Scleritis
 Penetrating trauma
 Chemical injury

Conjunctivitis
o Diffuse conjunctival oedema and hyperaemia
o Involves palpebral (lid) and bulbar (eye) conjunctiva
o Bilateral/asymmetrical
o Vision is normal
 Infective
 Viral: adenovirus
o Watery discharge, +/- pain, lid swelling
o Conjunctival follicles
o Pre-auricular lymphadenopathy
 Bacterial: S. aureus (acute), Blepharoconjunctivitis (chronic)
o Purulent discharge
o Conjunctival papillae
 Allergic
o Itchy, watery discharge, atopy, more chronic
o Lid swelling, periocular eczematous skin changes
o Conjunctival papillae/cobblestoning
 Chemical
 Iatrogenic: drop toxicity (glaucoma drop allergy)
 Acids, alkalis, etc

Treatment
o Chloramphenicol drops QDS for 1-2 weeks
o Allergy: sodium chromoglycate drops QDS +/- olapatadine
(antihistamine) drops BD initially. Mild topical steroids may be required.
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Episcleritis
o Localised or diffuse redness
o Palpebral conjunctiva spared, only bulbar affected
o Mild discomfort and redness

Treatment
o Resolves spontaneously or with NSAIDs PO
o If not, refer for topical steroids

Blepharitis
o Chronic symptoms
o Crusting along lid margins/lashes
o Red lid margins
o Facial/lid rosacea

Management
o Warm lid compresses
o Lid hygiene
o Chloramphenicol ointment BD
o Doxycycline 50-100 mg OD x 3 months
o Artificial tears – symptom relief

Marginal Keratitis
o Peripheral corneal ulcer
o Stains with fluorescein
o Redness in adjacent conjunctiva
o Onset over days

Management
o Requires referral
o Responds well to steroid/antibiotic drop combination

DDx Red Eye + Foreign Body Sensation

1. Trichiasis (misdirected eyelash)
2. Corneal/conjunctival foreign body
3. Blepharitis
4. Marginal keratitis

DDx Painful Red Eye + Photophobia + Normal Vision

1. Iritis/Anterior Uveitis
o Increasing pain over 1-3 days, photophobia, blurring later
o Constricted pupil, circumcorneal redness, recurrent
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o Limbal injection
o a/w HLA-B27: ank spondylitis, Reiters, reactive arthritis, IBD,
psoriatic arthritis
o Urgent specialist management required
Treatment
o Intensive topical steroids
o Mydriatic (pupil dilating) drops (cyclopentolate)

2. Bacterial or herpetic keratitis

3. Scleritis (excruciating pain)

DDx Blurred Vision + Pain

1. Bacterial Keratitis/Corneal Ulcer
o Severe pain over 1-2 days, photophobia, reduced vision
o Contact lens or trauma
o Corneal opacity, fluorescein staining
Management: emergency referral – microbiology and intensive broad
spectrum topical antimicrobials (eg. Ofloxacin, vancomycin +
ceftazidime)

2. Herpetic Keratitis
o Pain, watering, photophobia, reduced vision
o Fluorescein staining Infective Keratitis
Investigations: corneal scrape for
o Urgent referral
gram stain and culture &
Treatment: ocular acyclovir 3% 5/day for 2-3 weeks
sensitivity and/or HSV PCR
3. Acute Angel Closure Glaucoma
o Severe pain, loss of vision, vomiting
o Diffuse redness, hazy cornea, mid-dilated unreactive pupil
o Rock hard eye to palpation
o Shallow anterior chamber
o Pathogenesis: angle narrows  aqueous drainage decreased 
pupil block  pupil iris bow forward  IOP rises
*Emergency Referral
Treatment
Immediate: IV acetazolamide (Diamox), pilocarpine drops, beta blocker
drops, steroid drops
Once IOP decreased: YAG laser peripheral iridotomy

4. Iritis
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Gradual Loss of Vision

Due to: cataract, age related macular degeneration, diabetic retinopathy,

glaucoma

Cataract
o Causes: increasing age, DM, steroids, trauma, uveitis
o Children: inherited AD, birth trauma, maternal infection (rubella,
toxoplasmosis), metabolic disease (galactosemia)
o Treat early to prevent amblyopia (lazy eye)

Treatment
o If reduction of vision is affecting activities of daily living
o Phacoemulsification of lens and intraocular lens implant under topical
or local anaesthetic
o Day case surgery

Leukocoria: white pupillary reflex

 DDx: cataract, retinoblastoma, toxocariasis, retinopathy of prematurity,
corneal opacity

Retinoblastoma
o Malignant embryonal tumour of retina
o 1:20,000 live births
o Usually presents < 2 years old with squint or leukocoria
o RB gene mutation // 13q14 in 40%

Age Related Macular Degeneration (ARMD)

o Leading cause of blindness
o Dry/atrophic (90%) vs. wet/exudative (10%)
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 Wet more damaging to vision, more rapid loss of vision +

distorted vision, submacular haemorrhage, oedema
o Pathology: retinal pigment epithelial (RPE) cell loss
 Drusen = deposits between RPE and photoreceptors
 Photoreceptor loss
Treatment
o Wet: intravitreal anti-VEGF therapy, vitamin supplements
o Dry: low vision magnifying aids, social services
o Stop smoking

Diabetic Retinopathy
o Pathogenesis: microvascular and macrovascular
 Pericyte loss
 Endothelial cell damage
 Occlusion and leakage
o Presentation (late disease): reduced visual acuity
 Macular oedema, vitreous haemorrhage, tractional retinal
detachment
o Risk Factors: hyperglycaemia, hypertension, hyperlipidaemia, smoking,
pregnancy, renal failure
o Classification: background, pre-proliferative, proliferative, maculopathy
 Background Diabetic Retinopathy
 Microaneurysms, dot haemorrhages, hard exudates
 Pre-proliferative: more extensive ischaemic change
 Deep retinal haemorrhages
 Venous change – beading and looping
 Cotton wool spots – nerve fibre layer infarcts
 Intra-retinal microvascular abnormalities (IRMA)
 Proliferative
 New vessels
- Disc = NVD
- Elsewhere = NVE
 Vitreous haemorrhage
 Vitreous traction can lead to tractional retinal detachment
 Diabetic Maculopathy
 Main cause of sight loss in DR
 Diabetic macular oedema: sight threatening macular
exudate/oedema at or near the fovea
 Macular ischaemia: severely damaging to vision and no effective
treatment

Management
o Optimise control of risk factors, stop smoking
o Laser photocoagulation
 Macula: reduces leakage and oedema
 Peripheral retina: reduces neovascular drive and risk of severe
sight threatening diabetic eye disease
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o Intra-vitreal anti-VEGF Therapy

o Vitrectomy

Principles of Laser Treatment

o Absorption of high energy light by retinal pigment epithelium (RPE)
produces thermal burn to RPE and retina
o Maculopathy: closure of leaking vessels and stimulation of RPE pump
reduces oedema
o Proliferative disease: destroys ischaemic retina and decreases
angiogenic growth factors
o Types:
 Argon Laser Retinal Photocoagulation: focal, grid, panretinal
photocoagulation (PRP)
o Side Effects:
 Focal/Grid: central field defects, burn spread, inadvertent foveal
burn
 PRP: loss of peripheral field, impaired night vision, implications
for driving license, pain during procedure

Severe Diabetic Eye Disease

o Rubeotic Glaucoma: severe refractory form of glaucoma with very high
intraocular pressures
o Persistent Vitreous Haemorrhage: requires vitrectomy surgery
o Tractional Retinal Detachment: requires vitrectomy surgery if threatens
macula

Glaucoma: optic nerve and visual field damage occurs often, but not
always as a consequence of raised IOP
Treatment
o Medical: topical agents, beta blockers, alpha agonists, prostaglandin
analogues, carbonic anhydrase inhibitors
o Surgical: trabeculectomy

Increase Outflow Decrease Secretion

 Prostaglandin analogues  Beta-Blockers
 Pilocarpine  Carbonic Anhydrase Inhibitors
 Trabeculectomy  Alpha Agonists
 Laser trabeculoplasty  Destruction of ciliary body
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o Types:
 Primary Open Angle Glaucoma
 Typical optic disc changes (“cupping”)
 Typical visual field loss (affects the peripheries first)
 Main risk factor is IOP
 Ocular Hypertension
 Normal disc and field, but elevated IOP
 Low Tension Glaucoma
 Glaucomatous disc and field, but normal IOP
 Secondary Glaucoma
 Variety of open or closed angle glaucoma with specific features
 Chronic Closed Angle Closure Glaucoma
 Diagnosis based on appearance of drainage angle
 Similar to POAG

Sudden Visual Disturbance

Presenting: sudden loss of vision/blurring, flashing lights (photopsia) and

floaters, double vision (diplopia)

Transient Loss of Permanent

Vision • Giant cell arteritis
• Amaurosis • Acute glaucoma
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fugax • Wet ARMD

• Giant cell • Anterior ischaemic optic neuropathy
arteritis • Central or branch retinal vein occlusion
• Ocular • Retinal detachment
migraine • Vitreous haemorrhage
• Optic neuritis
• Central retinal artery occlusion
• Occipital stroke
• Some/complete recovery may occur

Painless Painful
• Amaurosis fugax • GCA
• Wet ARMD • Raised intracranial pressure
• Anterior ischaemic optic • Migraine
neuropathy • Acute angle closure
• Central or branch retinal vein glaucoma
occlusion • Optic neuritis (dull ache)
• Retinal detachment
• Vitreous haemorrhage
• Central retinal artery
occlusion
• Occipital stroke

Monocular Binocular Either

• Acute glaucoma • Occipital stroke • Amaurosis fugax
• Anterior • Migraine • Giant cell
ischaemic optic • Raised arteritis
neuropathy intracranial • Wet ARMD
• Central or branch pressure
retinal vein
occlusion
• Retinal
detachment
• Vitreous
haemorrhage
• Optic neuritis
• Central retinal
artery occlusion

Amaurosis Fugax
o Painless, fleeting loss of vision
o Usually unilateral, last seconds to minutes
o Aetiology: arterial embolism (TIA) or giant cell arteritis – cardiovascular
risk factors
o Who: middle aged to elderly
o Normal eye exam after Work Up & resolution
Management
 CV exam, blood
pressure
 ESR, CRP, FBC,
carotid
ultrasound
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Ocular Migraine
o Variable visual disturbance – missing patches of vision, hemianopic
defects, scintillating colours of light, zig-zag lines
o Usually followed by headache, episodic
o Lasts 20-30 minutes
o Who: younger patient < 40 years
Management: lifestyle advice and reassurance

Raised ICP
o Bilateral blurring of vision
o Headache, morning nausea and vomiting
o Papilloedema: bilateral optic disc swelling due to raised ICP

Giant Cell Arteritis: vasculitis of medium and large sized arteries

o Most commonly superficial temporal, ophthalmic, and posterior ciliary
arteries
o Arteritic anterior ischaemic optic neuropathy
 Investigations
 ESR, CRP, FBC
 Temporal artery biopsy
 Treatment
 IV methylprednisolone
 Prednisolone 60-80 mg initially, tapering slowly to 5-10 mg
maintenance dose for 1-2 years
 Aspirin
o Who: age > 60
o Symptoms: sudden, permanent or transient loss in one eye usually
 Headache, jaw claudication, temporal tenderness, non-specific
constitutional symptoms, neck/shoulder acne
o Signs: RAPD; pale swollen disc; scalp tenderness; tender, nodular, non
pulsatile superficial temporal artery

Acute Angle Closure Glaucoma

o Painful loss of vision over 6-24 hours + headache + vomiting
o Who: elderly, female, hypermetropes (small eyes)
o Signs: fixed mid-dilated pupil, hazy cornea, hard eye, red eye

Non-Arteritic Anterior Ischaemic Optic Neuropathy

o Sudden painless loss of vision in one eye
o Mild to moderate visual loss, hypertension
o Who: age 45-65 years
o Findings: optic disc swelling with disc haemorrhages, RAPD, altitudinal
field loss, normal ESR
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Neovascular Age Related Macular Degeneration (Wet ARMD)

o Painless loss of vision in one eye over days
o Fellow eye commonly affected later
o Signs: pupils normal, exudate/haemorrhage at macula, distortion on
Amsler grid
Treatment: intravitreal anti-VEGF therapy

Retinal VEIN Occlusion: central or branch retinal vein

o Sudden painless unilateral vision loss
o Aetiology: diabetes, atherosclerosis, hypertension, glaucoma
- Macular oedema and ischaemia cause visual loss
o Who: > 50 years old
o Signs: haemorrhages in all four quadrants, haemorrhagic swollen optic
disc
Treatment:
 Retinal laser photocoagulation
 Intravitreal anti-VEGF injection

Central Retinal ARTERY Occlusion

o Sudden severe unilateral painless loss of vision
o Aetiology: embolus (eg, from carotid atheroma), giant cell arteritis
o Signs: RAPD, pale posterior pole with cherry red spot

Retinal Detachment
o Painless loss of peripheral field of vision followed by sudden central
visual loss
o Preceded by floaters and photopsia
Diplopia – true or just blurred vision?
o Elevated retina on ophthalmoscopy
True = second image disappears on
o Risk factors: increasing age, myopia,
closing one eye
trauma
o Aetiology:
Treatment: surgical repair
 Neurological: third, fourth, sixth
cranial nerve palsies  DM,
Vitreous Haemorrhage
hypertension, tumours, stroke,
o Sudden painless loss of vision
trauma, MS
accompanied by floaters
 Mechanical: orbital
o Usually caused by diabetic
inflammation, orbital infection,
retinopathy
trauma, orbital tumour
o Findings: loss of red reflex, no view of
 Other: decompensated latent
retina
squint
o Exam: cover test, examine position
Optic Neuritis
of corneal reflexes (Hirshberg test),
o Sudden loss of vision in one eye
examine eye movements and
associated with a dull ache or pain on
determine when diplopia is most
eye movement
prominent
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o Aetiology: MS, idiopathic, viral

o Who: young and middle aged adults
o Acute inflammation of optic nerve: papillitis (swollen disc), retrobulbar
optic neuritis (normal disc)
o Signs: RAPD, loss of colour vision, +/- swollen disc
Management: MRI scan to look for demyelination
 Gradual recovery over 3 months without treatment

Flashes and Floaters

o Syneresis: chronic mild floaters due to degenerative change in the
vitreous
o Aetiology:
 Posterior Vitreous Detachment: floaters +/- flashes
 Migraine: flashes, zig-zag lines, bizarre visual phenomena
 Vitreous haemorrhage and posterior uveitis: floaters and blurring

Posterior Vitreous Detachment

o Risk of retinal tear and retinal detachment
o In acute cases, retinal exam should be performed by ophthalmologist
within 2 days
o Occurs in 50% of people by later middle age, most are asymptomatic

Changes in Appearance

- Eyelid malposition (entropion, ectropion, ptosis), lumps and bumps

on lids, proptosis/exophthalmos, strabismus/squint

Eyelid malposition: entropion, ectropion, ptosis, lid retraction,

lagophthalmos
Entropion: an inward turning of the upper or lower eyelid
o Aetiology:
 Involutional: most common, results from age related changes and
laxity in lower lid
 Cicatricial: caused by scarring and contraction of lid
- Seen in trachoma, Steven-Johnson syndrome, ocular
pemphigoid, chemical burns, trauma

Ectropion: outward turning of the lower lid. If severe and prolonged may
cause conjunctival keratinisation
o Aetiology:
 Involutional: due to aged related tissue laxity
 Cicatricial: scarring resulting from burns or surgery
 Mechanical: excessive lid weight by lid mass, eg tumour
 Paralytic: associated with facial nerve palsy

Ptosis: drooping of upper eye lid

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o Aetiology:
 Congenital: weakness of levator muscle, uni or bilateral, surgical
correction is indicated for visual or cosmetic reasons
 Acquired: neurogenic 3rd nerve palsy, horner’s syndrome
- Aponeurotic: dehiscence of levator palpebrae superioris, can
be age related, traumatic or post-op
- Myogenic: myasthenia gravis, myotonic dystrophy, ocular
myopathies
- Mechanical: inflammation, tumour, vascular abnormality of
upper lid
Management
o Treat underlying condition
o Surgical correction

Lid retraction: may be unilateral or bilateral and is almost invariably due

to thyroid disease
Lagophthalmos: incomplete closure of the eyelids due to 7th nerve palsy,
resulting in exposure keratitis
o Treatment: lubricants, taping of lids, lateral tarsorraphy
Blepharospasm: involuntary spasm of orbicularis muscle causing lid
closure
o Aetiology: idiopathic, parkinsons, psychogenic
o Treatment: botox injection

Non-neoplastic Lid Lesions: meibomian cyst (chalazion), external

hordeolum (stye), cysts of Zeis and Moll, molluscum contagiosum

Benign Tumours of the Eyelid: papilloma (viral wart), seborrheic keratoses,

keratoacanthoma, naevi, capillary haemangioma, xanthelasma

Malignant Lid Tumours

1. Basal Cell Carcinoma
 Most common eye lid tumour
 Usually lower lid
 Invades locally
 Does not metastasize
 Treatment: local excision

2. Squamous Cell Carcinoma

 Metastasize to lymph nodes
 Treatment: excision/radiotherapy

Thyroid Eye Disease

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o Symptoms: redness, irritation, discomfort, wide eyed staring, double

vision, decreased vision in severe cases
o Signs: fullness of eyelids, conjunctival hyperaemia and chemosis,
proptosis may be uni- or bilateral, lid retraction, lid lag, restricted eye
movements, optic neuropathy
o Investigations: T3, T4, TSH, Thyroid autoantibodies raised
o Radiology:
 CT of orbit: enlarged extraocular muscles (tendons spared) and
enlarged soft tissue
 Optic nerve may be compressed in the canal
 Clinical and radiological findings more important than biochemical
profile in establishing diagnosis
Treatment:
 Lubricants and NSAIDs
 Prisms for double vision
 Systemic steroids
 Immunosuppressants (azathioprine, cyclophosphamide)
 Radiotherapy adjunctive to steroids
 Surgery
- Orbital decompression for acute optic nerve compression not
responding to immunosuppression and for cosmesis when
burnt out
- Strabismus surgery for double vision
- Surgery to correct lid retraction

Orbital Cellulitis: potentially life threatening acute bacterial infection of

the soft tissues of the orbit
o Aetiology: secondary to sinusitis, infected chalazion in children, or
following trauma or surgery
o Symptoms: acute lid swelling and redness, pain, malaise
o Signs: reduced visual acuity, lid oedema, erythema, chemosis,
proptosis, painful opthalmoplegia, optic disc swelling
o Complications: intra-cranial infection, cavernous sinus thrombosis,
blindness
Management:
 IV antibiotics
 Orbital CT to rule out abscess
 Surgery for abscess drainage or sinus washout

Strabismus: the eyes are not aligned, resulting in squint or heterotropia

o With squint, one eye is fixating upon a particular object and the other
is turned in another direction
o Deviating eye is not stimulated – lazy/amblyopic
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o Types of squint: esotropia/convergent, exotropia/divergent,

hypertropia (upward), hypotropia (downward)
o Diagnosis: decreased visual acuity in affected eye in most cases,
corneal light reflex, cover test, fully dilated fundal examination, early
referral in children
o Amblyopia Classification
 Strabismic: due to presence of manifest squint
 Stimulus deprivation: due to pathological obstacle to vision
 Anisometropic: unequal refractive errors in the two eyes
 Ametropic: bilateral high refractive errors
Treatment: correct refractive error, occlusion, start when <8 years
old
- Surgery: weakening procedure, muscle is detached from globe
and reattached further back
- Resection: strengthening procedure, section of muscle
removed and remained muscle reattached to original
insertion, over-resected muscle will produce limitations when
looking to opposite side

Leukocoria: white pupil

o Aetiology:
 Retinoblastoma: <3 years old, uni- or bilateral
 Toxocariasis: 3-10 years old, unilateral
 Persistant Hyperplastic Primary Vitreous: unilateral
 Cataract: unilateral or bilateral
 Retinopathy of Prematurity: bilateral
Examination: red reflex replaced by white pupil
 CT/MRI if full fundal exam not possible
*Urgent referral
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Ocular Trauma

Injury Types
1. Closed globe (blunt) 45%
2. Open globe (penetrating) 25%
3. IOFB 10%
4. Chemical injuries 10%
5. Lid/orbital 10%

Penetrating Eye Injury

o Young males greatest risk
o Elderly patients at risk from falls (especially if previous eye surgery –
wound rupture)
o Suspect if: eye shape deformed, shallow or flat AC, iris prolapse,
irregular pupil, severe visual loss
 Stop examination and cover the eye with plastic shield
 Immediate referral
Surgical Management
o Close the globe urgently under general anaesthetic
o Reposit/excise exposed intraocular contents
o Explore globe for unrecognized injuries
o Prophylaxis against infection
o Further surgery may be required later
Prognosis
o Isolated lacerations have a better prognosis than more extensive
posterior penetrating injuries
o If corneal scars involve the visual axis, corneal transplant may be
required in the future
o Poor prognosis: posterior segment lacerations, vitreous haemorrhage,
lens involvement, retinal detachment, endophthalmitis

Intraocular Foreign Body (IOFB)

o Hammering is main risk factor
o Minimal pain, blurring of vision
Management: referral, plain film or CT orbit, surgical removal

Blunt Eye Injury  Hyphema: accumulation of blood in the anterior

chamber
o Requires specialist management
o A/w increased IOP, cataract, iris injuries
Management: bed rest, control IOP, dilate pupil, topical steroid
(risk of rebleed 3-5 days later)
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Corneal or Conjunctival Foreign Body

o Painful red eye
o Assess with pen torch and stain with fluorescein
 If superficial, remove with cotton bud
 If deep or on visual axis, refer for removal using slit lamp and needle
after topical anaesthetic
Siedel test to ensure you haven’t punctured the cornea

Subtarsal Foreign Body (STFB)

o Painful, red, severe foreign body sensation
o Scratches cornea with each blink
o Evert lid to rule out/remove
Management: same as corneal abrasion

Corneal Abrasion
o Common, good prognosis
o Severe pain, photophobia, sometimes reduced vision
o Check with fluorescein drops
Treatment
o Broad spectrum topical antibiotics x5 days (eg. Chloramphenicol,
fuscidic acid)
o Patching for 1-2 days may help symptomatic relief
o Topical anaesthesia will delay healing
o Should heal within 72 hours

Chemical Eye Injury

o Ocular emergency
o Alkalis >> acids
Management
o Immediate copious irrigation after topical anaesthetic (eg. Normal
saline)
o Check for and remove FB
o Topical steroid and antibiotic +/- referral

Orbital Floor Fracture

o Due to high velocity blunt object
o Periorbital oedema, enophthalmost, diplopia, infra-orbital anaesthesia,
subcutaneous emphysema

Lid Laceration
o Repair must be perfect
o Poor repair can lead to entropion and trichiasis
o Full eye exam essential to rule out injury to globe
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Cataract

o Clouding of the lens in the eye that affects vision

o Uni- or bilateral
o Most are related to aging
o By 80, most people have a cataract or have had cataract surgery
o Aetiology: aging, DM, corticosteroids, trauma, uveitis
o Symptoms: cloudy or blurry vision, colours seem faded, glare, halo
around lights, poor night vision

Clinical
o History
o Visual Acuity
o Ophthalmoscopy – check red reflex
o Slit lamp distinguishes cataract subtype

Treatment
o Surgery – phacoemulsification of lens and intraocular lens implant
usually under topical or local anaesthesia

Cataracts in Children
o Inherited, autosomal dominant, birth trauma, maternal infection
(rubella, toxoplasmosis), metabolic disease (galactosemia)
o Diagnose and treat early to prevent amblyopia

Anatomy
o Zonules hold lens in place and mediate accommodative movements of
ciliary muscle, altering the lens shape and refractive power
 Ophthalmology

Glaucoma

o Common disease in which a characteristic pattern of optic nerve and

visual field damage occurs, often but not always as a consequence of
raised intraocular pressure.
o Initially loss of peripheral fields
o Visual acuity is only affected in advanced disease
o Visual field analysis and optic disc appearance are used to monitor
disease progression
o Risk factors for blindness: severity at presentation, life expectancy,
rate of progression

Aqueous Humour Physiology

o Intraocular pressure depends on balance btwn aqueous humour
production + drainage
o Produced in ciliary body
o Flows from posterior chamber through the pupil into the anterior
chamber and exits via trabecular meshwork in anterior chamber angle
o Elevated intraocular pressure is caused by reduction in aqueous
drainage through the trabecular meshwork
o Normal IOP is 10-21 mmHg

Classification of Glaucoma (see notes for gradual loss of vision)

 Ophthalmology

 Primary Open Angle Glaucoma Risk Factors: increasing age,

ethnicity,, family history, myopia, DM

Detection – Incidental
Diagnosis based on: intraocular pressure, visual field appearance, optic
disc appearance

Examination
1. Visual acuity and pupil reactions
2. Gonioscopy is done at the slip lamp to determine open or closed
mechanism
3. Intraocular Pressure measurement by Goldmann tonometry
(applanation, air puff)
4. Optic disc assessment – cupping of optic disc
5. Visual fields – automated visual field testing required, Humphrey
visual field test

 Optic Disc Cupping

 Optic disc is made up of pink neuro-retinal rim and of a central
pale optic cup
 Neuro-retinal rim is made up of axons of retinal ganglion cells
which converge to form the optic nerve
o Oral Anti-Glaucoma
 Optic cup: part of optic disc with no
Preparations
nerve fibres
 Carbonic anhydrase
 In glaucoma, loss of ganglion cells and
inhibitors for short term
their axons, leading to loss of the neuro-
Surgical Management:
retinal rim and enlargement of optic
 Trabeculectomy is gold
disc cup or cupping of disc
standard
 Some healthy people have a large optic
 Reserved for minority
cup with a healthy neuro-retinal rim and
of cases where
this is known as physiological cupping
condition progresses
Laser Treatment: certain
Aims of treatment: reducing intraocular pressure
Medical Management:
o Anti-Glaucoma Drops
 Prostaglandin analogues: increase outflow of aqueous
 Beta Blockers: reduce production of aqueous
 Alpha agonists: enhance outflow and decrease secretion of aqueous
 Carbonic anhydrase inhibitors: reduce production of aqueous
 Parasympathomimetic agents: enhance outflow of aqueous
Diabetic Retinopathy

Retinal Transparency
o Required for normal function, allows light through unmyelinated axons,
low density blood vessels, blood retinal barriers
o Loss of transparency: haemorrhage, oedema
 Ophthalmology

Retinal Disease
o Clinical Assessment: history, visual acuity, Amsler grid,
ophthalmoscopy
o Retinal imaging: FFA, OCT

Diabetic Retinopathy
o Microangiopathy
o Most common and serious ocular complication of DM
o Incidence
 Type 1: 86% after 15 years
 Type 2: 40%
 20% at diagnosis
 60% after 15 years
o Risk Factors: duration of disease, hyperglycaemia, hypertension,
hyperlipidaemia, smoking, anaemia, ethnicity, pregnancy, puberty

Pathophysiology
o Microvascular
 Increased vascular permeability – leakage
 Capillary occlusion
 Pericyte loss
 Endothelial cell damage
o Neuroretinal
 Impaired neurotransmission
 Increased apoptosis

Presentation
o Early disease asymptomatic, so screening is important
o Late disease presents with reduced visual acuity due to macular
oedema, vitreous haemorrhage, or tractional retinal detachment

Classification
1. Background
o Microaneurysms: focal dilations in capillary wall secondary to
endothelial cell proliferation
o Retinal haemorrhages
o Retinal oedema
o Hard exudates: usually close to a vessel, mainly around the
macula

2. Pre-proliferative (mild, moderate, severe)

More extensive ischaemic changes leading to:
o Cotton wool spots: disruptions in axonal transport, evidence of
ischaemia
o IRMAs: arteriolar-venular shunts, adjacent to capillary closure
o Venous changes: beading/sausaging, omega loops
o Extensive retinal haemorrhages
 Ophthalmology

o Arterial changes

3. Proliferative
o Progressive ischaemia
o Release of growth factors: VEGF
o New vessel formation: disc (NVD), elsewhere (NVE)
o Vitreous haemorrhage
o Vitreous traction can lead to tractional retinal detachment

4. Advanced
o Rubeotic glaucoma: severe refractory form of glaucoma with
very high IOP
o Persistent vitreous haemorrhage: requires vitrectomy surgery
o Tractional retinal detachment: requires vitrectomy surgery if
threatens macula

5. +/- Maculopathy
o Main cause of sight loss in diabetic retinopathy
o Diabetic macular oedema/exudate, variable visual impairment
o Macular ischaemia: severely damaging to vision, no effective
treatment
o Classification of Diabetic Maculopathy
i. Focal
ii. Diffuse
iii. Ischaemic
iv. Mixed

Management of Diabetic Retinopathy

o Systemic: Decrease HBA1c levels, reduction of 1% = 15% risk of
blindness decrease
 BP, lipids, smoking
o Screening: pre-symptomatic detection, annual digital photographic
grading, referral to eye services for treatment
 Laser, intravitreal therapy, surgery
Principles of Laser Treatment
o Absorption of high energy light (thermal burn) by retinal pigment
epithelium (RPE)
o Maculopathy: closure of leaking vessels, stimulation of RPE pump,
decreased oedema, stabilises vision
o Proliferative disease: destroys ischaemic retina, decreased
angiogenic growth factors, panretinal photocoagulation (PRP)
Side Effects of Laser Treatment
o Focal/Grid: central field defects, burn spread, inadvertent foveal
burn
o PRP: loss of peripheral field, impaired night vision, implications for
driving license, pain during procedure
Intra-Vitreal Anti-VEGF Therapy
 Ophthalmology

o Inhibition of VEGF: mediates vascular leakage and proliferation

o Diabetic Maculopathy: reduction of oedema, improvement in visual
function
o Proliferative Retinopathy: regression of new vessels, clearance of
vitreous haemorrhage
o Combined Therapy
 Intravitreal Therapy + Laser
 Diffuse DME
 Focal DME
 Combined DME and PDR
 PDR with vitreous haemorrhage
 Surgery: vitrectomy for persistent vitreous haemorrhage or
tractional retinal detachment
Age Related Macular Degeneration

o Risk Factors: age, Caucasian, smoking, diet

o Symptoms: distortion of vision, central scotoma (blind spot), reading
difficulties
o Pathology: retinal pigment epithelial (RPE) cell loss, drusen = deposits
between RPE and photoreceptors, photoreceptor loss

o Divided into dry/atrophic (90%) and wet/exudative (10%)

 Wet ARMD presents with more rapid loss of vision and distorted
vision over days compared with months for dry ARMD, wet more
damaging to vision
 Dry ARMD
 Drusen – lipofuscin in RPE
 Pigmentary changes
 Mild visual impairment at this stage
 Wet ARMD
 Choroidal neovascular membrane: haemorrhage, oedema,
inflammation
 Distortion
 Central visual loss
 Submacular haemorrhage
 Macular exudates and oedema (indicate choroidal neovascular
membrane)
 End Stage ARMD
 Geographical atrophy
 Scarring
 Irreversible loss of ventral vision
 Submacular fibrosis

ARMD Investigations
o OCT
 3D imaging
 Retinal thickness
 Ophthalmology

 Fluid
o Fluorescein Angiography
 Leakage
 Hyperfluorescence

Treatment
o Early
 Lifestyle changes, smoking cessation
 Diet: exogenous antioxidants (Vitamin C, E, B-carotene, zinc),
macular pigments (lutein, zeaxanthin)
o Wet ARMD
 Intra-vitreal anti-VEGF therapy
 Loading therapy x 3 months
 Maintenance therapy
 2/3 stabilize, 1/3 improve
o Dry ARMD
 Low vision magnifying aids
 Social services