Ophthalmology Mbchb4


1. Differential Dx
a. Conjunctivitis
b. Keratitis
c. Uveitis/iritis
d. Acute angle closure glaucoma
e. Scleritis/Episcleritis
f. Subconjunctival hemorrhage
g. Ocular trauma
2. Conjunctivitis
a. Definition
i. Aka pinkeye or bloodshot eyes
ii. Inflammation of the conjunctiva (outermost layer of eye and inner surface of eyelids)
b. Etiology
i. Infective – bacterial, chlamydial (3 month hx typical), viral (3 day hx, itchiness)
ii. Allergic – atopy, hayfever
c. Hx
i. Often bilateral
ii. Itching
iii. Gritty but Ø painful eye
iv. Discharge
1. purulent = bacterial
2. mucopurulent = chlamydial
3. mucoid/watery = allergic
4. watery = viral
v. Follicles or papillae
1. follicles = viral, chlamydial
2. papillae = bacterial, allergic, contact lens wear
vi. Assoc features
1. Viral = URTI, pre-auricular L/A
2. Allergic = atopy, hayfever, contact lens wear
3. Chlamydial = urethritis
d. Signs
i. Normal VA, pupil and cornea
ii. Diffuse (conjunctival redness) of ocular surface
e. Mgt
i. Swab and identify responsible organism
ii. Bacterial – chloramphenicol, Fucithalamic
iii. Viral – no specific tx
iv. Chlamydial – topical and systemic tetracycline
v. Ø referral necessary unless persistent with tx
3. Keratitis
a. Definition
i. Inflammation of the cornea
ii. Characterised by burning, blurring of vision and sensitivity to light
iii. Caused by an infectious or non-infectious agent
iv. SF keratitis involves the SF layers of the cornea (after healing, they type does not generally leave a scar)
v. Deep keratitis involves deeper layers of the cornea, leaving a scar upon healing that impairs vision if on or near the vis axis
b. Etiology
i. Multiple causes
ii. Eg – HSV infection 2ndry to upper respiratory infection, involving cold sores
c. Sxs (very similar pres to conjunctivitis)
i. Burning pain
ii. Photophobia / Sensitivity to light
iii. Decr vision
d. Signs
i. Decr vision
ii. D/C
iii. Ciliary redness and distribution
iv. Reduced corneal clarity
v. Normal – pupil size and mobility, IOC
e. Management
i. Corneal shape
ii. Mydriatic
iii. Start intensive antimicrobials immediately
iv. Bacterial – monotherapy = ciprofloxacin / dual therapy = fortified kefzol and tobrex
v. HSV – acyclovir ointment 5x daily
4. Anterior Uveitis
a. Defintion
i. Inflammation of the middle layer of eye (uvea)
ii. Common usage – may refer to any inflammatory process involving the interior of the eye
iii. Estimated to be responsible for approx 10% of blindness
iv. Categorised anatomically into anterior, intermediate, posterior and panuveitic forms
v. Anterior uveitis – 90% of cases (frequently termed iritis – inflammatin of iris or anterior chamber)
b. Presentation
i. Sxs
1. Pain
2. Photophobia (severe)
3. blurred vision
ii. Signs
1. ↓ VA (or normal)
2. Ciliary redness and distribution – diffuse or localiazed to lumbus (junction betw sclera and cornea)
3. Small and fixed pupil
4. Keratic precipitates on the posterior surface of the cornea
c. Etiology
i. Idiopathic – associated with autoimmune diseases, sometimes infections
ii. Many conditions can lead to the devt of uveitis incl systemic diseases and those syndromes confined to the eye
iii. Anterior uveitis is one of the syndromes assoc w HLA-B27
1. Ank spon
2. Reiters syndr
3. Juvenile arthritis
4. Psoriartic arthropathy
5. Sarcoidosis
d. Management
i. Tx inflammation – topical corticosteroids
ii. Prevent poster synechaiae – mydriatic eg cyclopentolate (mydriatic = causing or involving dilation of the eye)
iii. Reduce IOP if elevated – eg betablocker (timolol)
5. Acute closed angle glaucoma (ACAG)
a. Definition
i. Sudden severe ↑ in IOP due to reduced drainage of aqueous fluid
b. Risk Factors
i. 1/1000 at >40 yrs age
ii. F>M 4>1
iii. Short eye
iv. Narrow angle
v. Large lens
vi. Older hypermetropes at risk
c. Hx
i. Sudden onset sever eye pain
ii. Blurred vision
iii. Rainbow like halos around lights
iv. Photophobia (minimal)
d. Signs
i. ↓ VA
ii. Diffuse redness or ciliary distribution
iii. Pupil – semi-dilated, Ø reactive to light
iv. Cornea cloudy
v. High IOP
e. Acute Management
i. ↓ IOP
ii. Topical agents – pilocarpine, b-blockers
iii. Systemic agents – acetazolamide, mannitol
f. Surgical Management
i. Aim – re-establish N aqueous flows and maintenance of reduced IOP
ii. YAG laser iridotomy
iii. Surgical iridectomy
iv. Trabeculectomy
v. Cyrstalline lens extraction
6. Scleritis
a. Defintion
i. Inflammation of the sclera
ii. Most pts have an underlying vasculitis
iii. Rare
iv. Assoc w systemic dis – RA and herpes zoster ophthalmolicus
b. Hx
i. Mild to severe boring eye pain
c. Signs
i. VA – N
ii. Diffuse or localised injection of the visible conjunctiva
iii. Pupil and cornea are N
d. Management
i. Referral reqd – can lead to blindness if untx
7. Episcleritis
a. Definition - Inflammation of the episclera (thin membrane covering the sclera), usu idiopathic, common
b. Hx - Mild eye irritation and redness, Ø pain
c. Signs - VA N, Diffuse or localized injection of the visible conjunctiva
d. Management - Usu requires Ø tx, Seldom assoc w systemic dis
8. Subconjunctival Hemorrhage
a. Definition – focal bleeding under conjunctiva
b. Assoc w – severe coughing, valsalva manoeuvre, rarely systemic HTN
c. Mgt – no tx reqd



1. Definition
a. Opacification of the lens (partial or complete)
2. Lens Anatomy
a. Transparent, biconvex structure
b. Lies behind iris, suspended by zonules
c. Approx 10 mm diameter, 4 mm thick
d. Contributes approx 1/3 of focusing power of eye
e. Focusing dioptric power ↓ w age
i. 8D @ 40 yrs, 2D @ 60 yrs (Presbyopia)
f. Tends to opacity (cataract) w age
3. Epidemiology
a. >15 million blind due to cataract worldwide
b. 50% of aged 70+ yrs
c. 100% of aged 90+ yrs
d. 30% unhappy w their vision
4. Classification
a. Congenital
b. Adult
c. Older age
5. **Location
a. Nuclear cataracts – age related, change the lens refractive index
b. Cortical – age related
c. Posterior subcapsular – steroids, DM, trauma
d. Polar cataracts (ant and post) – commonly inherited
6. Etiology
a. Congenital cataracts
i. Inherited, no systemic abnormality – eg galactosaemia
ii. Inherited with systemic syndrome – eg Lowe (oculocerebral) syndrome, down syndrome
iii. Intrauterine infections – eg congenital rubella, varicella zoster, toxoplasmosis
b. Acquired cataracts
i. Senile
ii. 2ndry to systemic disease – eg DM
iii. Traumatic – direct trauma, irradiation
iv. Drug related – corticosteroids
v. 2ndry to ocular dis – chr uveitis
7. Risk factors
a. Age
b. DM
c. Steroid use
d. Atopy
e. Myopia
f. Uveitis
g. Ionizing radiation
h. UV light
i. Galactosaemia
8. Presentation
a. Sxs
i. Slow onset
ii. ↓ Vision / Blurred vision
iii. Glare – dazzling, esp in sunlight
b. Signs
i. ↓ snellen VA
ii. Attenuated red reflex (if dense, no red reflex)
iii. Slit lamp examination shows lens opacification
iv. Normal pupil response (no RAPD)
9. Ixs – snellen acuity, ophthalmoscope, slit lamp
10. Tx
a. Do nothing – if VA better than 6/12 and no sxs
b. Surgery
c. Phacoemulsification + Intraocular lens implantation (Phaco + IOL) – 95% of surgeries in NZ
i. Local anaesthetic
ii. 3mm incision made
iii. Lens is removed by phacoemulsification
1. U/S breaks up the lens
2. Aspiration of fragments into cannula
iv. Artificial lens then implanted (perspex, acrylic, silicon)
v. Some lenses are foldable so they can be placed through a smaller incision
vi. Posterior capsule remains to make surgery safer
vii. Pt can usu return home immed afterwards
viii. A dressing may be reqd for a few hours
ix. Full activities can be resumed the next day
x. A/B and anti-inflammatory eye drops for 3-6 wks post-operatively
xi. Will need to change spectacles to get full benefit from surgery
d. Extra-capsular cataract extraction + IOL
11. Prognosis
a. 80% 6/12 vision or better (legal driving limit)
b. Poor outcome if due to pre-existing dis
c. <1% have worse vision after surgery – infection, hemorrhage
d. 30% have posterior capsule opacification/thickening after surgery (months/years) → tx w laser capsulotomy


1. Anatomy
a. Layers
i. Epithelium 50-60 um
ii. Bowmans layer
iii. Stroma – 90% of corneal thickness
iv. Descemets membrane
v. Endothelium - monolayer
2. Functions
a. Optical – transparency, uniformity
b. Barrier – infections, ocular integrity
3. Corneal abnormalities
a. Congential
b. Acqd
i. Infection
1. Infective keratitis
a. RFs – contact lens wear, ocular surface dis, steroid eye drops, immunosuppression
b. Pathogens – bacterial, viral, fungal, protozoal
c. Lab tests – G stain, culture, PCR
ii. Inflammation
iii. Neoplasia
iv. Trauma
v. Deposits
vi. Dystrophies eg keratoconus


Diabetic retinopathy is the result of the micorvascular retinal changes



Early changes -
Death of retinal pericytes and microvascular endothelial cells
Basement membrane thickening

1. Formation of retinal capillary microaneurisms
2. Excessive vascular permeability → leakage / edema of protein (hard exudates) and lipid → macular edema
a. Pres – blurred vision (any stage of DR) → potential blindness
b. Difficult to detect so refer to specialist
3. ↑ vasoactive substances

Progressive microvascular obliteration and ischemic injury leading to eventual unregulated angiogenesis - due to repeated cycles of cell death and incr perm followed by cell renewal

Vascular occlusion (blockage) and rupture
1. Flame shaped blot hemorrhages
2. intraretinal infarcts (cotton wool spots) – soft exudates, sign of retinal ischemia

Progressively more severe ischemia → vasoproliferation (proliferative DR) → New vessels disc (NVD) and elsewhere (NVE)

Risks of new vessel formation
1. Initially – new vessels are fragile and prone to rupture → vitreous hemorrhage
2. As new vessels mature and becoming increasingly fibrotic → contraction and retinal detachment can occur

Risk of retinopathy – age, DM duration, glycaemic control, HTN, lipid status, obesity, smoking

1. General
a. Education
b. Diabetes control
c. Lifestyle changes – weight loss, dietary modification, exercise, smoking cessation
d. Carb control – diet, oral hypoglycaemics, insulin → ↓ HbA1c
e. ↓ BP
f. Lipid control
2. Laser photocoagulation (panretinal photocoagulation – PRP)
a. >80% of pts w abnormal new vessels to prevent hemorrhage and retinal detachment
b. Laser also used for leaking vessels at macula to prevent diabetic maculopathy


1. Introduction
a. Majority of diabetic eye disease almost exclusively at the retina where retinal blood vessels become blocked, leak or both
b. However, there are added risks to the cornea, lens (diabetic cataract), optic nerve (ischemic optic neuropathy) and others
c. Retinopathy is present in 1/3 of diabetics
d. Leading cause of blindess in the working age-group
e. Prompt recog and tx of sight-threatening eye dis can prevent sight loss
2. Pathophysiology
a. Blockage of the small vessels causes an ischemic reactive change, namely the prodn of abnormal vessels (neovascularisation)
i. Retinal hemorrhages
ii. Cotton wool spots (see picture) – disruption of axoplasmic flow at nerve fiber layer level
iii. Abnormal retinal vessels
1. Venous sausaging/irregularity
2. Intra-retinal microvascular anomalies
3. These new vessels typically develop –
a. on or at the optic nerve head – NVD (New vessels at the disc)
b. on other parts of the retina – NVE (New vessels elsewhere)
iv. New vessels can often bleed causing vitreous hemorrhage and can also cause fibro-vascular scar like tis to develop on the retina, which can contract leading to retinal detachment and may cause blindness
b. Leakage – at point of microaneurysms (earliest recognisable feature)
i. Protein (hard exudates)
ii. Hemorrhage
iii. Fluid (diffuse and local), intraretinal/subretinal
iv. Other blinding outcomes occur as a result of the leakage from the vascular sys
1. Leakage of blood vessels at the macula → diabetic maculopathy
2. Protein, fluid and blood leaking at the macula is not a good prognostic sign and accounts for considerable blindness in nz
3. Risk of Retinopathy
a. Age
b. Duration DM
c. Glycaemic control
d. HTN
e. Lipid status
f. Anemia
g. Pregnancy
h. Obesity
i. Smoking
j. Alcohol use
k. Other systemic dis
l. Ethnicity
4. General Management
a. Education and support
b. Good diabetic control
c. Lifestyle changes – weight loss, dietary modification, exercise, smoking cessation
d. Carbohydrate control – diet, oral hypoglycaemics, insulin
i. Lowering HbA1c from 7.9 to 7% reduces risk of micro-angiopathy by 25%
e. BP and Lipid control
i. Lowering BP <150/85 reduces risk of retinopathy by 34%
f. Monitoring of renal function
g. Management of the complications of diabetes
5. Tx
a. Laser Photocoagulation
i. Pan laser photocoagulation → lasering the retina such the majority of the peripheral retina is treated
1. Effective in dealing with >80% of eyes w abnormal new vessels
ii. Utilising focal laser for leaking vessels at the macula is v effective in preventing vis loss from diabetic maculopathy


1. Impt Structures
a. Tears – lubrication, O2 transmission, clarity of vision, immunity
b. Conjunctiva – mucous membrane investing anterior surface of eye and posterior surface of the lids betw the cornea and lids
i. O2 transmission, tear prodn, tear film adherent, defence, immunity
c. Eyelids – protection, tear film prodn and distbn, tear flow and drainage
d. Cornea – refractive surf of fixed power (2/3 of light to eye, 40 diopters), clarity, protection against micro-orgs, transparent smooth surface, ocular rigidity
i. Diopter = refractive power of lenses
e. Sclera – protection, ocular rigidity, opaque, attachment of extra-ocular muscles
f. Lens – refractive surface of variable power, accommodative mechanism, smooth interface w aqueous, transparency
i. Ø nuclei (would bend the light), Ø division/replication
ii. Long fibre cells
iii. Cortex, nucleus, ant and post poles
iv. Both lens and cornea are avascular (nutrients provided by aqueouos humour – ant and post chambers, Ø vitreous chamber)
g. Iris/Pupil – restriction of light to retina, reduction of light scatter within eye (pupil = circ orifice in centre of iris)
h. Ciliary body/Ciliary epith accom, attachment of lens, prodn of aqueous humour (nutrient supply to lens and cornea, waste metabolite removal from globe)
i. Relaxed muscle → low power lens, focus for distance
ii. Contracted muscle → high power lens, focus for close up
iii. Ciliary epith also produces aqueous humour, any blockage will cause ↑ IOP → glaucoma
i. Choroid – provides O2 and nutrition to outer retina (90% of blood supply to retina)
j. Vitreous chamber – vitreous humour maintains ocular shape, protection of ocular structures during trauma
k. Retina – visual sensation and conversion of light images into n impulses, supported by retinal pigment epith (layer of cells external to retina essential for formation of photopigments, renewal of photoreceptors, reduction of damage due to scattered light and transportation of water and nutrients to retina
i. Myopia
ii. Hypermetropia / Hyperopia / Long sightendess
l. Optic n – transmits electr signals to brain – optic n → optic chiasm → optic radiation → lateral geniculate nucleus → occipital cortex
2. Retinal Physiology
a. Electromagnetic spectrum that humans are visually responsive to = 400-700 nm
b. Scotopic conditions (low light)
c. Phototopic conditions (daylight)
d. When a photon collides w the retina, it is transmitted through the inverted retina to the photoreceptors where photochemical transduction results in conversion of the light into an electr signal
e. Blood vessels all eminate from optic disc (ie vessels travel with the optic nerve)
f. 3x retinal layers, 2x synapses
3. Rods and Cones
a. Process the visual signal in characteristic ways
b. Cones → daylight, colour (blue, green, red), fine details (visual acuity), concentrated in central VF
c. Rods → low light condition, peripheral mvment


1. Terminology
a. Phenotype = clinical description (inheritance, age of onset, clinical course, clinical feats)
b. Genotype – molecular description
c. Phenotypic heterogeneity – one gene, many diseases – eg corneal dystrophies caused by diff mutations in one gene (TGFB1)
d. Genetic (allelic) heterogeneity – one disease, many genes - eg primary open angle glaucoma
e. Variable expressivity – severity of dis varies betw individuals in a pedigree who are known to carry the dis causing mutation
i. Ex – NF1 → some minimally affected, others severely affected
f. Penetrance – whether an individual carrying a dis causing mutation manifests w the dis (mutation + non-dis = non-penetrance)
i. Ex – Retinoblastoma 90% penetrance
g. Lyonisation – x inactivation in all cells of female carrier
i. Ex – x-linked ocular albinism
h. Inheritance patterns
i. AD – a. Aniridia, b. Trinucleotide repeat expansion in muscular dystrophy
ii. AR – retinitis pigmentosa
iii. XL – ocular albinism
2. Ocular Genetics
a. Genetic dis of eye – dx, counselling, tx, understanding
b. Ocular manifestations of systemic diseases
c. Optimising visual outcome in syndromes
3. Primary open angle glaucoma (POAG)
a. 2 genes, 6 loci found
b. Molecular dx in POAG in up to 20%
c. Clear phenotype-genotype correlations exist
d. Eg Myocilin P370L mutation
i. Very early disease onset
ii. Very high pressures
iii. Aggressive dis responding better to surgical intervention than topical tx
4. Dx and Counselling
a. Two hit theory – hereditary cancers require two successive mutations in the same gene to affect a single cell
b. Ex - Retinoblastoma (RB) – germline vs somatic
i. 1st hit in germ cell results in bilateral multifocal tumors + other 2nd primary cancers
ii. 1st hit in somatic cell results in unilateral single tumor
c. Prenatal dx – PGD, reproductive choices, intensive monitoring, early delivery
5. Ocular manifestations of systemic disease
a. Eye exmn may be necessary to characterise any assoc eye findings that can help make or confirm a dx in multi-system d/os
b. Examples – Marfan’s syndr, Neurofibromatosis type 1 (NF1), Von hippel lindau dis
c. NF1 → variable expression – lisch nodules (major criterion)
d. Marfans → variable expression (ectopia lentis) – lens subluxation (major criterion)
6. Syndromes with ocular associations
a. Known assoc ocular dis – requires reg surveillance for detection, intervention and tx
b. Multiple other probs exist – aim to maximise visual functioning
c. Ex – Downs sydnr → keratoconus, strabismus, cataract, naso-lacrimal duct obstr


Case 1 – Neurofibromatosis (NF1 gene), (ocular manifestations of systemic dis)
1. PC – L ptosis, ‘S’ shaped lid, feels like bag of worms
2. O/E - café-au-lait spots, lisch nodules visible (multiple age by 10% - ie visible only in 50% of 5 year olds)

Case 2 – Aniridia (AD, Pax6 gene)
1. PC – 3 months old, shaking eyes, not seeing well, unusual pupil, under-developed iris
2. Dx – Aniridia (iris + macular hypoplasia)
3. Gene – PAX6 gene, AD transmission (ie - M=F, infected individuals have infected parents, 3x generations)

Case 3 – Marfans (ectopia lentis, ocular manifestations of systemic dis)
1. PC – 17 M, 1.98m tall, father died age 37, glasses no good
2. Dx – Marfans
3. Gene – FBN1 gene → fibrillin (assoc w CT dis) → zonules stretching causing lens to shift position (ectopia lentis)
4. Mgt – requires cardiology referral

Case 4 – Retinoblastoma (90% penetrance)
1. PC - 2 yr old boy, funny light reflex in photos, eyes started drifting out
2. O/E – leucocoria (white eye), calcium at back of eye
3. Dx – Retinoblastoma, 90% penetrance
4. Gene – 2 hit theory, prenatal dx via amniocentesis, chr villous sampling, pre-impl genetic dx (PGD) testing at 8 cell stage

Case 5 – Congenital glaucoma (AR, inbreeding)
1. 4 month old armish child, large white eyes
2. Congenital glaucoma – AR condition, often assoc w inbreeding

Case 6 – Albinism (AR and XL differences, lyonisation)
1. Fair skin, white hair/eyelashes, red eyes ++, nystagmus, ocular feats of translumination, macular hypoplasia
2. Gene – AR → oculocutaneous albinism, XL → ocular albinism (due to female lyonisation)

Case 7 – Glaucoma (Genetic Heterogeneity)
1. 17 year old, F.hx glaucoma, open angle, IOP >35
2. Glaucoma often is a genetic dis, many genotypes, clue lies in phenotypes

Case 8 – Downs (trisomy 21)
1. 4 yr old boy, rubs eyes, eyes crusting → Blepharitis (eyelid inflammation)
2. Downs – assoc w strabismus, cataract, keratoconus, refractive probs, naso-lacrimal duct obstr


1. Ocular pharmacology
a. Majority of ocular drugs exhibit 1st order (linear) kinetics – absorption and elimination rate varies depending on drug conc (drug ½ life is thus constant regardless of the amount of drug that is present)
b. Zero order kinetics – saturation may occur due to active t/port mechanisms
i. Examples – propane, fluorometholone, levobunolol
2. Ocular penetration
a. Majority of drugs obtain access via the cornea
b. Corneal permeability*
i. Epithelium → lipophilic (single greatest drug barrier, hence drugs need to be lipid sol)
ii. Stroma → hydrophilic
iii. Endothelium → lipophilic
c. Corneal permeability – biphasic properties (charged and non-charged) of topical drugs and lipid soluble drugs absorbed well, Ø water sol drugs
d. Example – Homatropine
i. Can lose its charge to become non-ionic and therefore penetrate the corneal epith
ii. Once through the epith, it can pick up a pos charge and behave in a hydrophilic manner to penetrate the stroma
iii. It then loses its charge at the endothelium to become non-charged and lipophilic
e. Conjunctiva has similar perm characteristics to corneal epithelium, however it is such a vascular structure that the majority of the drug does not penetrate the eye but is drained into systemic circ
3. Practical aspects of topical ocular medication
a. Tear film and cul de sac c/ments
i. Tear film vol = 7-10 ml
ii. Application of a topical drug, the cul-de-sac and tear film c/ment expands transiently to 30 ml
iii. The average commercially prepared topical drug has 40-70 ml vol → can not be accommodated by the cul de sac and tear film c/ments even when transient expansion of these c/ments occurs
b. Rate of tear film t/o varies but with application of a topical drug, the rate of tear fluid t/o more than doubles – from 15% to 50% per minute (this therefore increases the washout affect)
c. Washout effect
i. Adding a second drop within a short period will wash the original drops out of the eye – ideally, wait five mins and by this stage, the 2nd drug only produces a second drug washout effect of about 5%
d. Blinking
i. Normal blinking – only 15% of drug remains in eye after 5 mins
ii. 50% of drug will remain if pouch method utilised (lower lid pulled away from globe to create a pouch like repository for drops and the pt is then commended to close their eyes gently w/o force and w/o blinking
e. Summary of key points
i. Ave drop size vastly exceeds capacity of tear film and cul de sac
ii. Topical drops transiently double the tear fluid t/o
iii. Avoid 2nd drop washout effect – >5 min delay between instilling drops
iv. Pouch method w closed non-blinding eye reduces elimination
4. Advantages of topical drugs
a. Direct application to target organ
b. Ease of application
c. Rapid action
5. Disadvantages of topical drugs
a. Contamination of topical drops
b. Local toxicity due to drug preservatives
c. Limited penetration of most topical drugs via conjuctiva, cornea and anterior chamber
d. Systemic absorption which may act on other organs
6. Microsuspensions vs Solutions
a. Microsuspensions – prolong ocular residency time → higher drug peaks and longer duration of action
b. They also tend to settle in the bottle and therefore require shaking before application
7. Ophthalmic Ointments vs Topical Drugs
a. Advantages of ointments
i. Prolonged retention in cul de sac → longer duration of action
ii. Ø stinging on application (impt in children)
iii. Lack of preservatives
iv. ↓ risk of bacterial contamination
v. Lubricant nature prevents ocular surface drying → minimise morning lid stickiness in cases of infective conjunctivitis
b. Disadvantages of ointiments
i. ↓ speed of onset and ↓ peak concentration (due to drug tending to leave vehicle less readily)
ii. Greasy appearance on lid margins less acceptable
8. Intraocular injection
a. Reserved for post post op prophylaxis and tx of severe infection or uveitis where compliance is in doubt or high conc sustained release effort reqd
b. For many of the commonly used topical drugs – subconjunctival injection is not superior to intensive half hourly to hourly topical application
c. Injections are painful, pts are apprehensive, small risk of globe perforation
9. Elimination of topical drugs from the eye
a. Standard topical drop greater than the tear film and cul de sac can contain → sig fraction lost by initial overflow onto cheek
b. Naso-acrimal loss – due blinking (can be avoided by compression of the nasolacrimal sac during or immed after application of a topical drop)
c. Drug entering via the conjunctiva typically drains via blood vessels away from the eye
d. Drug reaching the anterior chamber via the cornea is drained by aqueous humour outflow
e. Drug also lost due to prodn of inactive metabolites
10. Local and systemic toxicity
a. Local toxicity
i. Inherent toxicity – eg topical anaesthetics and adrenaline
ii. Hypersensitivity reaction s- neomycin
iii. Preservatives – toxic to corneal epithelium (esp in dry eyes)
iv. Genetic predisposition to allergic reactions (esp in pts w atopy or allergy in other systems)
v. Some individuals have known but atypical undesirable reactions to topical drugs – eg ↑ IOP w topical corticosteroids
b. Systemic toxicity*
i. Topical b-blockers – resp and cardiac depr, exacerbation of respiratory conditions such as asthma
ii. Topical atropine – toxic to small children, fatal adult dose 100 mg, for a 4kg baby, lethal dose may be as little as 10 mg which represents only 20 drops, bottles must be kept safely out of reach of children
11. Compliance
a. Non-compliance estimated 30-40%
c. M>W
d. Non-attenders
12. *Corticosteroids and the eye
a. Therapeutic uses
i. Post-op inflammation
ii. Ocular inflammatory dis - eg uveitis
iii. External atopic dis – eg allergic conjunctivitis
iv. Corneal transplant allograft rejection
b. Complications
i. Steroid induced glaucoma
ii. Ocular HTN
iii. Corticosteroid induced posterior subcapsular cataract
iv. Exacerbation of infective keratitis eg HSV


1. PC
a. Vision Loss (or blurred vision)
i. Unilateral or bilateral
1. Unilat → ocular
2. Bilat → visual pways, cortical involvement
ii. Sudden or gradual
1. Gradual loss one eye → cataract
2. Sudden loss → vascular etiology
iii. Intermittent or constant
1. Transient loss → amaurosis fugax (premonitory sign of CVA)
iv. Extent of visual loss
v. Part of the field involved
1. Central VF loss w intact peripheral VF → age related macular degeneration
vi. Assoc sxs – eg headache, halos
1. Hx of flashing lights in 1 eye + a shower of floaters a wk prior to VL → retinal detachment
2. VL w sudden onset of dark or red blobs → vitreous hemorrhage
3. Headaches, temporal artery tenderness, jaw claudication → GCA
b. Red eye
i. Unilat or bilat
1. Conjunctivitis is more likely to be bilateral accompanied by purulentdischarge
2. Iritis or acute glaucoma → unilateral
ii. Distribution of redness
1. Diffuse → conjunctivitis
2. Sectorial on bulbar conjunctiva → episcleritis, scleritis
3. Localisation around cornea (circumcorneal) → more serious inflammation such as keratitis or ant uveitis
iii. Assoc sxs – eg pain, visual disturbance, discharge
c. Pain
i. Character – sharp, dull, intermittent or constant
1. Sharp pain or irritation → may suggest subtarsal or corenal FB or corneal abrasion
2. Deep boring pain → more serious dis
ii. Onset
iii. Exacerbating or relieving factors
1. Pain on reading or accommodation → iritis
iv. Assoc sxs – eg haloes, blurred vision
v. Past ocular trauma – eg trauma, shingles
vi. Systemic enquiry – consider referred pain
d. Photophobia (light sensitivity)
i. Usu due to keratitis or uveitis
ii. May be due to glare from a cataract
e. Double vision
i. Onset – eg after head injury
ii. Assoc sxs – eg headache, blurred vision
iii. Past hx – eg squint
iv. Systemic enquiry – eg diabetic, myasthenia
v. Binocular or monocular
1. Monocular → cataract
2. Binocular → misalignment of visual axes
vi. Where are they relative to each other
f. Flashers and Floaters (photopsia)
i. Flashes – originate from stimulation of the neurosensory retina by traction from the vitreous
ii. Floaters – due to degeneration of the vitreous
iii. Flashes in one eye with onset of floaters suggests vitreous degeneration and detachment from retina
iv. Large red floaters or ↓ vision suggest vitreous hemorrhage
g. Discharge
i. Purulent → infective conjunctivitis
ii. Mucous or watery → allergic conjunctivitis
h. Epiphora (overflow of tears) and lacrimation
i. ↑ tearing can result from any form of irritation or inflammation of the cornea
ii. Overflow can result from ↑ tearing or insufficient drainage through the naso-lacrimal sys
i. Itchiness
i. Hx of hayfever or allergic eye dis may cause itchy, gritty eyes as may blepharitis
j. Grittiness and irritation
i. Usu due to ocular surface abnormalities such as dry eye, small recurrent erosion or FB
2. Past Ocular Hx
a. Spectacle wear – myopia, hypermetropia, presbyopia
b. Contact lens wear
c. Squint or amblyopia
d. Surgery or trauma
3. Past M.Hx
a. Vascular hx – if acute VL
b. Locomotor hx – if suspect uveitis
c. DM
4. Meds and allergies
a. Idea of pts general state of health
b. Systemic meds can have ocular effects and vice versa
5. F.Hx – Glaucoma, Squint, Cataract, Poor vision
6. S.Hx
7. Examination
a. General inspection
b. VA - Reqd - snellen chart, near reading chart, pinhole
i. Check near and distance vision w pt’s own spectacles
ii. Test one eye at a time
iii. Improvement using a pinhole suggests a correctable refractive error
c. Colour vision
i. Use a red target to compare colour vision in each eye
ii. Optic n dis (eg optic neuritis) causes the red colour to appear desaturated or washed out
iii. Ishihara plates – used to identify congenital colour abnormalities but may also be used in acqd colour defects
d. VF – test on confrontation
i. Large white (and possibly) red pin is reqd
ii. Sit at same level as the pt, approx 1m apart
iii. Ask pt to look at your face and see if any parts are missing (may pick up hemianopias and central scotomas)
iv. Pt’s field in each eye is then compared with your own, using targets equidistant betw you and the pt
v. Use finger counting centrally then test the peripheral field using a white target coming in from the periphery
vi. Blind spot may be plotted using a red pin if reqd
e. Eye movements
i. Pen torch and occluder are used
ii. Corneal reflexes should be symmetrical if eyes are aligned
iii. Cover-uncover test on each eye will elicit a manifest squint
iv. Pt then follows a target into 9 positions of gaze (union jack) to see if this elicits diplopia
f. Pupil reactions – responses to light, direct and consensual, RAPD, response to accommodation
i. Inspect – pupils should be mobile, round and equal in size
ii. Is there a direct and consensual response
iii. Is there a RAPD on swinging flashlight test
iv. Lack of constrictive or relative dilation in one pupil indicates optic n or extensive retinal dis
v. Check accom
g. Exmn of external eye
i. Systematically examine the lids and anterior eye structures w a penlight
ii. Look for redness, swelling or discharge
iii. Is the cornea bright, shiny and clear
iv. Any opacities, abrasions, abnormal blood vessels or FBs
v. Fluorescein stain – any epithelial defects
h. At this point, dilate pupils w a drop of tropicamide 0.5 or 1% (onset <20 mins, duration 2-4 hrs) – examine red reflex and posterior segment of eye
i. Red reflex (use ophthalmoscope)
i. Assess eye from ~35cm
ii. Dial in plus lenses until iris and then the red reflex is seen clearly
iii. As some of the light entering the eye is reflected back by the retina, an even red glow is usu obtained
iv. Any opacity within the normally transparent structures of the eye will cause dark obscuration of the red reflex
v. Cataract is the most common cause of obscuration of part or the entire red reflex
j. Fundus examination – the posterior part of eye (use ophthalmoscope)
i. Ask pt to focus on a distant target then systematically examine the ocular fundus
ii. Start w the optic n head, follow the vessels along the arcades into each quadrant before examining the retina betw vessels
iii. Finally, examine the macula which is temporal to the optic disc

Pupil response to light
1. Parasym vs Sym
a. Parasym input → sphincter muscle (pupil constriction)
b. Sym input → dilator muscle (pupil dilation
2. Light reflex – 4 neurons
a. 1st – afferent pway – retinal ganglion cells via optic n to optic tracts before LGB and synapse in pretectal nucleus
b. 2nd – pre-tectal nucleus to EW nuclei (bilateral connections) – unilat light therefore evokes a bilat and symmetrical papillary constriction
c. 3rd – EW nucleus to ipsilateral ciliary ganglion (fibers travel via CN3 inf division; via the n to inf oblique mus)
d. 4th – ciliary ganglion via short ciliary nerves to sphincter pupillae mus
3. Near triad
a. Incr accommodation
b. Convergence
c. Pupillary constriction
4. The final pways of the near and light reflexes are the same (ie via CN3) and it’s the same mechanism underlying parasym input
5. Sym pway
a. 1st – central – hypothalamus down b/stem to ciliospinal centre of budge (lateral grey columns – C8-T2)
b. 2nd – preganglionic – ciliospinal centre of budge to superior cervical ganglion in neck
c. 3rd – postganglionic – superior cervical ganglion into skull to join nasociliary br of ophthalmic division CN5 to reach the ciliary body and dilatory pupillae mus
6. Afferent papillary defects (APD)
a. Total APD
i. Caused by complete optic n or retinal lesion
ii. Involved eye completely blind
iii. Pupils are equal
iv. Affected eye stimulated → neither pupils reacts
v. N eye stimulated → both pupils react normally
vi. Near reflex is normal in both eyes
b. RAPD (Marcus gunn pupil)
i. Caused by incomplete optic n lesion or severe retinal dis (Ø cataract)
ii. Equal pupils
iii. Swinging light test
1. shine light into normal eye – both pupils constrict
2. shine light into abnormal eye – both pupils dilate
iv. Mechanism – withdrawing light from normal eye outweighs the constriction produced by stimulating the abnormal eye


Aim – to u/stand ocular trauma eval and mgt in terms of a leading cause of acute visual morbidity in nz

1. Hx
a. Nature of injury
b. Trauma w sharp objects, high impact and potential foreign bodies (hammering) should raise concern
c. Chemical injuries – req elucidation of nature of causing agent, but 1st aid irrigation should be prioritised
2. Exmn
a. Unless, high suspicion of penetration, adequate exmn must be carried out
b. Pain relief via instillation of a topical LA drop – eg benoxinate, lignocaine, amethocaine
c. Use a bright light and slit lamp if available
d. Foreign bodies are often small but cause intense pain/irritation
e. Chemical injury – irrigate pt w saline and take hx subsequently
f. Specifically examine –
i. VA
ii. Conjunctiva incl lower fornix
iii. Subtarasal conjunctiva (evert upper lid)
iv. Corneal appearance, reflex on illumination
v. Instil fluorescein to show any abrasions or scratches
vi. Examine pupil shape + reaction
vii. Look for hyphaema (blood in ant chamber)
viii. Examine the red reflex (vitreous hemorrhage)
ix. Direct exmn by ophthalmoscopy of optic disc, retina and macula
3. Classifying ocular trauma
a. Injuries to eyelids and orbit
i. Blunt eyelid trauma
1. Black eye → massive bruising and lid swelling (eye may not be opened)
2. Blood may track across the nose, swelling may mask ocular or other orbital trauma
3. Always assess for diplopia
ii. Eyelid lacerations
1. Partial thickness or do not involve lid margin → suturing or gluing
2. If lid margin involved → specialist reconstruction of layers reqd
iii. Retro-orbital hemorrhage
1. Trauma can cause bleeding from orbital vessels → retrobulbar hemorrhage
2. Orbit has many fixed bony margins + bec the orbital septum anteriorly is essentially a restricted pyramidal space, a large hem may cause compression and permanent damage of orbital contents (esp the optic n)
3. Signs –
a. Proptosis (pushing forward on globe)
b. Altered pupil function
c. ↓ VA
iv. Blow out fractures
1. Blunt external trauma causing sudden intra-orbital pressure ↑ can cause blow-out of the thinnest part of the inf +/- thin medial bony orbital walls
2. Signs –
a. bruising of the lids
b. abnormal extra-ocular mvments (pt complains of diplopia)
c. enophthalmos (often masked initially by swelling) – recession of eyeball into socket
d. anaesthesia along infraorbital nerve
3. Advise pts not to blow their nose
4. Prophylactic A/Bs must be prescribed
5. Advanced cases require surgical reconstruction
v. Facial fractures
1. Trauma to facial bones (Le Fort #s) can cause damage to orbital walls and therefore impact on orbital contents and ocular func
b. Injuries to eyeball
i. Subconjunctival hemorrhage
1. Bright red, confluent blood beneath the transparent conjunctiva
2. Can occur after minor or no trauma
3. Visually striking but usu insig (see pic)
4. However, it can mask more serious path to underlying tis following injury
ii. Conjunctival laceration
iii. Corneal abrasion
1. Often invisible to naked eye
2. Bright green/yellow areas when stained w fluorescein dye and illuminated w blue light
3. Can cause intense pain, photophobia and blepharospasmus (invol spasms of orbicularis oculi mus)
4. Tx – topical A/B ointment w or w/o padding (self-repair)
5. Usu resolve within 1-3 days
iv. SF foreign bodies
1. Conjunctival FBs can be removed with a cotton bud
2. Upper eyelid must always be everted to seek for sub-tarsal FB
3. Corneal FBs are removed at the slit lamp, after topical anaesthetic w hypodermic needle
4. Ferrous FBs often leave a rust ring which is more difficult to remove
5. Following removal, tx as per corneal abrasion
6. Ensure FB not full thickness
v. Blunt ocular trauma
1. Hyphaema (see pic) is blood in the ant chamber
2. Hyphaema may fill the entire anterior chamber or more commonly may be partial w formed fluid level of blood
3. Uncomplicated hyphaema usu resolves
4. However, it may mask other ocular damage such as iris damage, angle recession, lens subluxation, retinal damage, globe rupture
5. Tx – rest to prevent re-bleed (occurs in 5-30%), usu 3-5 days post injury
a. Re-bleeding is usu more intensive and complicated by pain – pts must be instructed to return in case of painful episode
6. Hyphaema generally considered a sign of moderate to severe trauma
vi. Penetrating trauma incl intraocular FB
1. Scleral lacerations
a. May be partial or full thickness – they may be masked by hemorrhage
b. Full thickness corneal wounds lead to distortion of the ant segment –
i. Flattened ant chamber
ii. Pupil distortion
iii. Iris prolapse
c. Surgical tx reqd
2. Intra-ocular FBs
a. May be obvious or invisible
b. Hx of high velocity FB or fragments should raise concern
c. Ixs – b-scan echography and CT w high resol
i. If suspected magnetic FB → MRI is absolutely contraindicated
d. Tx – surgical (urgent as some can cause intense intra-ocular inflammation)
e. Intra-ocular inf is always a risk
vii. Chemical burns
1. Many chemicals are merely irritant (perfume, hair sprays) → only require irrigation
2. Strong chemical substances (acids, alkalis) → can cause serious LT ocular damage – urgent copious irrigation (saline or water 20-40 mins) is essential until pH is normal
3. If particles of solid subst are identified, they must be removed immediately
4. Urgent referral reqd – as they can cause permanent serious ocular problems
c. Combined injuries
i. Lid/orbit and eyeball injury +/- non-ophthalmic injury
4. Special Considerations
a. Subtarsal FBs
i. Material often becomes trapped under the upper lid
ii. Subtarsal sulcus – approx 2mm from lid margin
iii. Does not spontaneously dislodge
iv. Clues – hx of FB entry, FB sensation but no vis FB
v. Action – fluorescein, look for linear abrasions (usu involving sup part of cornea), evert upper lid, allocate + extract FB
b. Penetrating Injury
i. Serious life threatening injuries, must not be missed
ii. Clues – hx of high velocity or suspicious of intraocular FB injury, distorted pupil, hyphaema or haemophthalmus
iii. Action – protect the eye, ophthalmology referral
c. Children
i. May be difficult to examine and unless FB is v obvious should be referred
ii. May then even require exmn under anaesthetic
d. Type of FB material
i. Specific omplications may be assoc w certain types of FB
ii. All FB carry inf risk
iii. Organ FB may cause fungal inf
iv. Metallic FB contain iron → corneal rust ring if SF or serious intraocular complications (siderosis) if intra-ocular
v. Copper FBs → usu cause acute intraocular inflammation (endophthalmitis)
vi. Glass or plastic FB → are inert and may not require extraction
vii. SF FBs must be removed to avoid complications
viii. All suspicious intraocular FBs must be referred
5. Summary
a. Low velocity – injuries unlikely to have caused a penetrating injury (eg blown in by wind, riding a bike, grinding)
b. High velocity – must be treated w high index of suspicion for penetration (eg hammering, chiselling, drilling)
c. Thermal injuries – may cause sever ocular damage, referral (eg hot molten metal, liquids, hair irons)
d. Chemical injuries – extremely dangerous, must see an ophthalmologist (eg alkali (lime, cement), acid (battery)


1. Definition
a. Aka squint
b. Misalignment of the visual axes of the eyes
2. Significance
a. Cosmetic – sign pschosocial trauma, poor self-esteem
b. Visual –
i. Amblyopia - eye becomes lazy, never learns to see, incr risk of accident
ii. Binocular vision – depth perception affected, limits career choice
3. Classification
a. Congential vs Acqd
i. Congenital – present at or soon after birth, may be familial
ii. Acqd – develops later in childhood, may be due to factors such as high uncorrected refractive error, congenital cataract, retinoblastoma, devtal abnormalities of eye (basically anything that prevents a clear optical image forming on the retina and being relayed to the brain)
b. Phoria vs Tropia
i. Phoria – misalignment of eyes becoming apparent when eyes dissociated, controlled w binocular viewing conditions due to binocular and motor fusion (stimulus to reduce diplopia)
ii. Tropia – misalignment of eyes present under binocular viewing conditions, may initially be intermittent, suppression of image to overcome diplopia
c. Horizontal vs Vertical
i. Horizontal
1. Esotropia – convergent (eye turns inward)
2. Exotropia – divergent (eye turns outward)
ii. Vertical
1. Hypertropia – one eye turns up
2. Hypotropia – one eye turns down
iii. a
4. Other terminology
a. Orthophoric – straight
b. Pseudosquint – common, more obvious in young children, esp Asian children, due to wide nasal bridge, epicanthal folds, may become less apparent as child’s face grows, it APPEARS as if the eye disappears under the lid and more white shows on the other side, nasally – corneal reflexes symmetrical, eyes straight for near or distance
5. Normal Eye Development
a. Birth – poor vision 6/60
b. 6 months - ~6/6
c. Ocular control variable until about 3/12 in normal child
d. For optimum interaction w evt, req both eyes to look in same direction
e. Motor fusion – two eyes move together
f. Sensory fusion – double vis causes eyes to fuse images together (slight disparity of images, brain fuses into a single image)
6. Suppression and Amblyopia
a. In strabismus – difference betw the two images often too great too fuse at level of brain
b. Juvenile brain copes by suppressing the image made from the turned eye (ie – favours image from 1 eye while ignoring the oth)
c. But – whole visual system and neyral connections still developing
d. May result in amblyopia – reduced vision of otherwise anatomically normal eye (eye never learns to see, neural connections never developed)
e. If not tx at young age, amblyopia can become irreversible
7. Hx
a. PC – age of onset, duration, which eye, times of occurrence
b. Past ocular hx – injury, surgery
c. Pregnancy, Labour, Health – maternal illness, labour and delivery, prematurity, apgar, health
d. FHx - ?Squint, ?glasses
e. Devtal hx - milestones
8. Exmn
a. Ref reflex – means of testing whether light reaches back of eye
b. Corneal light reflex (Hirschberg)
i. Compares location of reflected light from cornea under binocular conditions
ii. Normally, the reflexes are positioned slightly nasal to centre of the pupil
iii. If the reflex is located more nasally, exotropia is suspected
iv. If reflex located more temporally, esotropia is suspected
c. Cover/Uncover test
i. Cover one eye
1. look at fixing eye (ie the uncovered eye)
2. Should remain in same position → Normal
3. If it moves and takes up fixation (strabismus) → exo if mvment in, eso if mvment out
ii. Uncover eye
1. Look at eye just uncovered
2. Normal = remains in fixation position
3. If it drifts back to take up fixation then strabismus → movement in exo, mvment out eso
d. Alternate cover test
i. Cover fixing eye – watch other eye to see the movement it takes to take up fixation
1. If other eye moves in → exotropic
2. If other eye moves out → esotropic
3. If wanders around but cant fixate → densely amblyopic
ii. Swing occluder over to other eye, watch uncovered eye as above (never allow binocular viewing conditions)
iii. Repeat back and forth betw the two eyes
e. Ocular motility – watch eye mvments in nine directions of gaze
9. Tx of Squint
a. Aim → binocular vision (fusion and stereopsis) and good cosmesis
b. Customised to type of squint, duration and age of child
i. Congential – early surgery aiming to establish some stereopsis
ii. Refractive error – accommodative, refraction, spectacle correction
iii. Must tx amblyopia – aim = good VA each eye, early intervention crucial
iv. Muscle surgery to align eyes properly
c. Tx of amblyopia
i. Patching – occlusion of good eye, forces lazy eye to develop neural connections, depends on age of child and depth of amblyopia
ii. Titrate – 2/6 hrs/day until vision in lazy eye picks up
iii. If intolerant of patch → atropine penalisation (atropine blurs image in good eye)
d. Squint surgery
i. Only after amblyopia has been treated
ii. Aim – align eyes to allow binocular vision
iii. Older children – cosmetic as squint present for a long time, binocular vision not possible
e. Notes
i. Not all children w squints require surgery, some squints can be prevented or helped by wearing glasses
ii. Some squints require early surgery eg congential esotropia, others can be delayed
10. Preschool screening for early detection
a. GP, plunket nurse, school vision tester
b. If suspect a squint, semi-urgent r/v to ophthalmologist
c. Early detection + tx key to success


Case 1 - Diplopia

58 M
PC – vision loss L eye
HxPC – better in morning, worse through the day, fluctuates, worse when tired, assoc w diplopia, then diploplia resolves and he has no vision in L eye

1. Differential dx
a. Trauma
b. Orbital cellulitis
c. CN3 palsy
d. Myasenthenia (most common presentation is diploplia) –ice on eye for 2 mins, cold decr cholinesterase activity and promotes efficiency of Ach at eliciting depol at end plate thus vision temporarily improves (mostly widely used test)
2. Approach to diplopia
a. Monocular v binocular (does diplopia disappear when each eye tested separately – if yes, then binocular)
b. Binocular = neurological
c. Monocular = cataract etc, not neurological

Case 2 - Chlamydia

21 year old
Incr difficulty seeing from R eye
Sticky d/c
Used A/Bs, little improvement
Vision improves with a blink – suggests something on front of eye (some form of conjunctivitis)
If no improvement with tx – then either not taking tx properly or tx is ineffective
Management – azithromycin 1 dose

Case 3 – Acute corneal infection from contacts lens

18 F
Sore L eye after a party
Poor vision
Light sensitive

Case 4 – Dendritic ulcer

Red painful eye
Loss of vision
Photophobic – suggests problem with front of eye
Recently under stress and quite tired
Fluorescin stain will reveal dendritic ulcer
Never give steroids – will take over eye and cause blindness
Tx - acyclovir

Case 5 – Optic Neuritis and MS

27 F
Sudden loss of vision L eye
Woke one morning, put her contact lens in and noticed she couldn’t see clearly
Developed assoc pain
No problems in R eye
Consider – has pt put in 2x contacts lens in same eye!
VA 6/6 6/36
Pupils Left RAPD
Colour vision 14/14 3/14
VF N Central defect

Fundus Examination

1. Diagnosis - Optic neuritis***
2. Clinical features suggesting swollen optic nerve (the afferent package)
a. Decr VA
b. Decr Colour perception
d. N or swollen optic n
e. Often assoc w multiple sclerosis
3. Hx
a. Rapidly progr VL
b. Sxs of underlying dis – usu MS or neuro ischemia due to atherosclerosis
4. Exmn
a. Decr VA, decr colour perception, RAPD, N or swollen optic disc, assoc w MS

Case 6 – Retinal Detachment

62 M
Loss of vision
Flashes 1/52
Spiders in front of eye
Shadows in front of eye

1. Diagnosis – Retinal detachment
a. 10x more likely in myopes (always ask for glasses, contacts lens, lasik hx)
2. Spiders – Vitreous floaters or blood
3. Shadow – sign of mvment of retinal detachment (emergency)
4. Hx
a. Flashing lights, floating spots (black or red)
b. VF loss – like a curtain coming down from periphery
5. Exmn
a. N or decr VA
b. Field defect usu
c. RAPD – pupil in affected eye dilates in response to light
d. Ophthalmoscopy – abnormal red reflex, detached retina looks grey and wrinkled, N exam does not excl detachment

Case 7 – Retinal Vein Occlusion

Loss of vision
Watching TV during rugby game
Previous days – had vision loss that lasted approx 5 mins in same eye
Sudden blackening of vision
PMHx – smokes 40/day, HTN, Hyperlipidemia
VA CF only 6/6
Pupils R RAPD
Colour vision Unable 14/14

Retinal Vein Occlusion
1. Hx
a. Sudden VL in all or part of VF
2. Exmn
a. Decr VA, decr VF, RAPD if severe
b. Ophthalmoscope – retinal hemorrhages, tortous dilated retinal veins, macular edema, cotton wool spots
3. Prognosis
a. Unlikely to recover any vision

***Differential Dx – Sudden painless vision loss
1. Retinal artery occlusion
2. Retinal vein occlusion (hemorrhagic)
3. Retinal detachment
4. Macular bleed
5. GCA (giant cell arteritis)

Note – Retinal artery occlusion
• Fundus examination – cherry red spot on background lightning of retina, ie macula becomes more prominent

Case 8 – Vitreous Hemorrhage

72 M
Big sneeze, when opened eyes, noticed flies all over
Only R eye
Flies moves with his eyes
IDDM 20 years

1. Huge bleed into vitreous
2. Flies represent blood, cells etc in the vitreous

Case 9 – Metamorphopsia, Age related macular degeneration

68 F
Noticing that knitting needles were bent rather than straight
Gradually become worse

Case 10 – Giant Cell Arteritis

LOV L eye, down to NLP (no light perception)
One day later, now NLP in both eyes

1. Clinical features
a. Majority have profound visual loss (first dx to consider in a pt w LOV and >70 yrs age)
b. 20% experience antecedent transient visual loss
c. Bilateral involve common
d. 1/3 lose vision in 2nd eye within 2 days
e. 1/3 within 1 week
f. 1/3 within 1 month
g. One of the few occasions when you can a person’s sight
2. Presentation
a. Non-specific sxs
i. Anorexia, weight loss
ii. Night sweats
iii. Fatigue
iv. Look and don’t feel well
b. Specific sxs
i. Jaw claudication – esp on eating/talking – GCA until proven otherwise
ii. New onset headache
iii. Scalp tenderness eg head on pillow
iv. PMR – pain in shoulders etc
v. Cardiac dysfunction
vi. GI infarction
3. Pathophysiology
a. Obstruction of lumen due to thickening
4. Start tx immediately – prednisone
6. Temporal artery biopsy (gold standard)


• Temporary blurring (bilat or unilat)
• Zig zag lines
• Other causes to consider – cerebrovasc lesions, tumors
• Attribute to migraine if hx typical of migraine headache, pt <50yrs and no other neuro s/s

Amaurosis fugax (severe temp vis loss)
• Transient lack of blood supply to retina or vis cortex
• May occur w TIA or temporal arterities
• Urgent tx reqd as sign of impending blindness or stroke

Causes of sudden or rapidly progressive VL
1. Acute retinal detachment
2. Retinal vein occlusion
3. Retinal artery occlusion
4. Acute optic neuropathy (optic neuritis)

Gradual Vision Loss
1. Slowly progressive optic atrophy
2. Chr glaucoma
3. Cataracts
4. Diabetic neuropathy
5. Macular degeneration
6. Chr retinal detachment

Unless otherwise stated, the content of this page is licensed under Creative Commons Attribution-ShareAlike 3.0 License