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Ophthalmology

By Dr Brenda Tam

Case Study 1

History 23 years old young lady Good past health c/o : floaters in both eyes for 2 months

What would you do ?

Flashes and Floaters

Majority of the case are benign in origin and are due to posterior vitreous detachment

However, in some cases they can indicate retinal hole formation, which may lead to retinal detachment later

Flashes and FloatersDDX Posterior vitreous detachment (PVD) +/-

retinal hole formation Vitreous haemorrhage Ocular migraine Posterior uveitis

(Pt may c/o rhythmicalflashing zigzag lines, or scintillating holes)

Basic referral guidelines

If the floater/flashes are of recent onset with decreased vision, an urgent referral is needed

With long-standing floaters/flashes, there is no need for referral

With floaters/flashes of less than 6 wks’ duration (especially in patients younger than 55years old,as this group of patients is too young to be affected by posterior vitreous detachment), referral is needed

Posterior Vitreous Detachment

PVD occurs in 75% of the population over the 55 years old, with around 30% being symptomatic

The vitreous body liquifies with increasing age, and eventually collapsed and detached from the retina

Condensations within the vitreous body cast shadows onto the retina, and are perceived as cobwebs or spider-shaped floaters

Retinal Hole Formation

PVD is the single most common event associated with retinal hole formation.

The vitreous in some eyes, especially myopes, is abnormally adherent to the retina in certain areas.

A retinal hole can result if the vitreous body fully detaches and pulls a piece of adherent retina with it.

Retinal Hole Formation

Retinal Detachment

Retinal Detachment

Typically, patient will presents with flashing light followed by large numbers of floater, and then a shade over the vision in one eye

If the detachment is extensive enough, it will reduce visual acuity, and also produce a relative afferent pupillary defect

Fundi exam may revealed an elevated retina, sometimes with folds, but this finding may not be obvious

Retinal Detachment

Other common presenting complaints Visual loss

– Acute– Chronic

Red eye Itchy eye Eye injury

History Vision—acuity, field, floaters Pain, discomfort, photophobia Discharge Halo (corneal edema) Mechanism of injury eg. FB possible chemical injuries? alkaline or acidic Associated symptoms eg.

- Headache—glaucoma, temporal arteritis

- Arthralgia—gonococcal conjunctivitis, autoimmune uveitis

Examination Test visual acuity: Snellen’ s chart Inspection eye lid—swelling, ecchymosis etc. conjunctiva : eversion of upper eyelid for small FB scleracornea : position of light reflection, fluorescence s

taininganterior chamberdepth by shining a torch sideways

Anterior Chamber Depth Assessment

Examination Inspectioniris— injection, irregularity, adhesionpupils —size, reaction to light, accommodation etc lens—opacity, position

Test ocular movements and visual fields

Ophthalmoscopic examinationred reflexoptic disc

Papillary Light Reflex

Swinging light test Afferent Papillary Defect

Afferent Papillary Defect

Examination Test ocular tension: - Tonometry by Schiotz or electronic tonometer- Finger palpation and ballotment is not a reliable

method

Slit lamp is a useful instrument for detail examination of the anterior segment of the eye e.g. corneal erosion, anterior hypopyon

NB: contact lens should be removed to facilitate examination

Acute Visual Loss

Anatomical approach– Optical : ciliary spasm– Tear film : Dry eye– Cornea : Ulcer– Lens : Cataract– Uvea : Uveitis– Vitreoretinal : Retinal detachment– Optic nerve : Optic neuritis

Acute Visual Loss

Transient visual loss (vision returns to normal within 24 hrs, usually within

1 hr)

- Few seconds : Dry eyes- Few mins : amaurosis fugax (unilateral)

vertebrobasilar artery insufficiency (bilateral)

- 10-60 mins : Migraine

Acute Visual Loss

Visual loss lasting longer than 24 hrs

Painful

- Acute glaucoma

- Optic neuritis

- Uveitis

- Corneal disease

Acute Visual Loss

Visual loss lasting longer than 24 hrs

Painless

- Retinal artery or vein occlusion

- Ischaemic optic neuropathy e.g. Giant cell arteritis

- Vitreous hemorrhage

- Retinal detachment

- Other retinal or CNS disease

Chronic Visual Loss

Anatomical approach– Optical : refractive error– Tear film : Dry eyes– Cornea : dystrophies, pterygium– Lens : Cataract– Uvea : Uveitis– Vitreoretinal : Retinal detachment, diabetic retinopat

hy– Optic nerve : glaucoma, chronic papilloedema– Cortical and functional blindness– Amblyopia

Cataract

It is the opacity of the lens of the eye causing partial or total blindness

The lens is made mostly of water and protein- The protein is arranged to let light pass through and focus on the retina- Sometimes some of the protein clumps together and cloud small areas of the lens, blocking some light from reaching the retina and interfering with vision

Anatomy

Cataract - Natural Course In its early stages, a cataract may not cause a

problem The cloudiness may affect only a small part of the

lens. However, over time, the cataract may grow larger and cloud more of the lens, making it harder to see

Because less light reaches the retina, your vision become dull and blurry

Some people may find their close-up vision suddenly improves, but this is temporary. Vision gets worse again as the cataract grows

Cataract - Symptoms

1. Blur vision

2. Glare

3. Monocular diplopia – with ghost image

4. Myopia shift

Cataract - Symptoms

1. Painless blurring or dimming of your vision

Cataract - Symptoms

2. Glare and Sensitivity to light

esp. in bright sunlight or while driving at night

Cataract - Symptoms

3. Distortion or ghost images in either eye

Cataract - Symptoms

4. Increased nearsightedness - requiring frequent changes in your eyeglass prescription

Causes of Cataract

1. Age-related : Most cataracts are related to aging

2. Congenital : Some babies are born with cataracts or develop them in childhood, often in both eyes. These cataracts may not affect vision. If they do, they may need to be removed.

Causes of cataract

3. Secondary causes: Cataracts are more likely to develop in people who have certain other health problems or related to drugs, e.g. DM, use of steroid or cytotoxic drug

4. Traumatic : Cataracts can develop soon after an eye injury, or years later

Types of Cataract

1. Nuclear type The cataract appears in the center of the lens It can bring about a temporary improvement in the

near vision, but the vision gradually worsen as it progresses

Distance vision typically affected much more than near vision

2. Cortical type Many DM patient develop this type of cataract

Types of Cataract

3. Post subcapsular type It tends to cause disabling glare in bright sunlight and

from headlights Acuity is degraded only slightly High farsightedness, DM, Systemic and topical steroi

d use are associated with formation of this type of cataract

It tends to progress quickly over a period of months rather than years

Complications of Cataract

1. Lens induced glaucoma- Swelling of cataract

- Leakage of denatured proteins from

hypermature cataract

2. Lens induced uveitis

Cataract Immature cataract

- A cataract that still allows view of the posterior pole and transmits a red reflex

Cataract

Mature cataract

- once the red reflex is loss, it becomes mature

Indications for Cataract Surgery

1. Reduced visual acuity sufficient to interfere with a patient’s desired activities

2. Cataract sufficiently dense to obscure fundus diagnosis and management (e.g. in diabetic retinopathy)

3. Complications of cataract (e.g. lens induced glaucoma)

Types of Cataract Surgery

1. Extracapsular Cataract Extraction (ECCE)- removal of lens nucleus and cortex through an opening in the anterior capsule, leaving the posterior capsule in place

2. Phaco-emulsification- the lens nucleus is emulsified using an ultrasonic needle and is aspirated through a small opening

3. Intracapsular Cataract Extraction (ICCE)

Visual Rehabilitation after Cataract Extraction Spectables Contact lenses Intraocular lenses Refractive surgery

Glaucoma

It is a condition in which the intraocular pressure (IOP) is sufficiently elevated to damage vision

Normal IOP is <= 21mmHg

Glaucoma - Types

1. Primary open-angle (POAG) glaucoma

2. Angle-closure glaucoma

3. Congenital glaucoma

4. Juvenile glaucoma

5. Secondary glaucoma

6. Pigmentary glaucoma

7. Normal pressure glaucoma

Primary open-angle Glaucoma(POAG) It is the most common type of glaucoma It accounts for 60%-70% of all

glaucoma cases Asymptomatic in early stage – it is often

called “the silent thief of sight” because you have no warning sign

Gradually impair the peripheral vision And then progress to tunnel vision and

blindness

Primary open-angle Glaucoma(POAG) In normal eye, aqueous humor flows through the pupi

l into the anterior chamger, where it is drained primarily through the trabecular meshwork to canal leading to the venous system

Primary open-angle Glaucoma(POAG) In POAG, there is increased resistance to outflow of

aqueous through the trabecular meshwork, hence IOP increases

Primiary open-angle Glaucoma(POAG) Risk factors- Elderly- Height of IOP is related to POAG prevalence- High myopia- Black race- Family Hx- DM, HT or cardiovascular disease

Primary open-angle Glaucoma(POAG) Screening of POAG :

IOP measurement (eg. By Schiotz tonometer)

+Optic disc evaluation

(increase in cup disc ratio, >0.9 – Highly suspicious 0.6-0.8 - moderately suspicious)

+Visual field testing

Treatment for Glaucoma

Because damage to the optic nerve cannot be reversed, treatment is aimed at preventing or slowing further damage.

The pressure is lowered to a level regarded as safe for a particular patient. This level is generally between 15-20 mmHg. In more severe glaucoma a lower pressure is required to prevent further damage.

Patients need to be followed up regularly while on treatment because overtime treatment changes may be required.

Treatment for GlaucomaEye Drops Eye drops lower the intraocular pressure by

either decreasing fluid production or increasing fluid outflow through the drainage angle.

They must be used regularly and continuously.

The effect of a medication only lasts a certain number of hours after which time the eye pressure may again rise, resulting in damage to the optic nerve.

Treatment for GlaucomaEye Drops The effectiveness of drops may be increased

by blocking the lacrimal ducts after putting the drop in. This is done by applying gentle pressure over the inside corner of the eyes, next to the nose, while closing your eyes for five minutes after each drop.

A patient on more than one drop should wait five minutes between drops to allow time for their absorption.

Treatment for GlaucomaEye Drops1. Topical cholinergic agonists

- increase aqueous outflow- duration of action from 6 hrs to 1 wk- Short-acting : Pilocarpine, Carbachol- Long-acting : phospholine iodide

S.E. : increase bronchial secretion, diarrhoea, nausea vomiting, increase myopia, brow pain and pupillary constriction (cause decreased vision)

Treatment for GlaucomaEye Drops2. Topical beta-blockers

- decrease aqueous production- Duration of action is 12-36 hrs- Treated with once daily or twice-a-day dosing- commonly used are : Timolol (Timoptic), levobunolol (Betagan), carteolol (Ocupress), metipranolol (OptiPranolol)

S.E. : bronchospasm, bradycardia, CHF, impotence

Treatment for GlaucomaEye Drops3. Topical adrenergic agonists

- decrease resistance to outflow and may decrease aqueous production- Duration of action 8-12 hrs- Treated with twice- or thrice-a-day dosing- commonly used are : epinephrine, Dipivefrin (Propine), Apraclonidine (Iopidine)

S.E. : tachycardia, tremor, anxiety, headachepupillary dilation, conjunctival injection

Treatment for GlaucomaEye Drops4. Carbonic anhydrase inhibitor

- decrease aqueous production by inhibiting ion transport associated with aqueous secretion- Currently available oral form are: acetazolamide (Diamox), methazolamide (Neptazane)

S.E. : malaise, anorexia, electrolyte disturbance, blood disorder : thrombocytopenia, agranulocytosis, neutropenia, aplastic anemia

Treatment for GlaucomaSurgery

If medical therapy fails, consider the surgical procedures :

Laser surgery Filtering surgery Cyclodestructive surgery Drainage device surgery

Acute angle closure Glaucoma

Accounts for about 10% of glaucoma cases High risk groups :

1. Elderly

2. Female

3. Family history

4. Hyperopia

5. Asians/Eskimos

Acute angle closure Glaucoma

Predisposing factors Lens size : growth of the crystalline

lens causes a shallow anterior chamber

Short eye Small corneal diameter

Acute angle closure Glaucoma

There is an excessive area of iris apposition to the lens, which impedes the flow of aqueous from the posterior chamber to the anterior chamber.

The iris bows forward because of the higher pressure in the posterior chamber, and the iris occludes the anterior chamber angle

the drainage angle of the eye becomes blocked. The blockage may be sudden and complete, raising eye pressure to a very high level quickly

Acute angle closure Glaucoma

Acute angle closure Glaucoma –Symptoms

Medical emergency Eye pain and redness Haloes around lights Rapidly progressive impairment of

vision Headache Nausea and vomiting

Acute angle closure Glaucoma –Signs Pupil fixed and dilated Shallow anterior chamber Corneal edema Optic disc : edematous and hyperemic Cup:disc ratio >= 0.5 IOP may range from 40-80 mmHg or

above

Acute angle closure Glaucoma –Treatment Urgent eye consultation Diamox (acetazolamide)

– 500mg IV stat, then 250mg QID P.O. Pilocarpine 4% eyedrops

– Q 30 mins x 4, then 1% Q4H Timolol eyedrops if not C.I. Miotic eyedrops to constrict pupil & facilitate o

utflow Analgesics and anti-emetics

Acute angle closure Glaucoma –Treatment After IOP under control, consider

- Laser iridotomy – with a hole in the iris, it provides an alternative channel for aqueous to reach the anterior chamber

- Drainage surgery

Case Study 2

67 years old man c/o : sudden onset of visual loss in Lt eye for 3

hrs PE :

- profound loss of vision in Lt eye – only finger counting- Rt pupil responds to light directly but not consensually, and Lt pupil responds to light consensually but not directly

Case Study 2

Fundi exam :

Case Study 2

The Lt eye shows a cherry-red spot in the macula, and the whole retina is infarcted and edematous, with narrowing of retinal arterioles and venules

Diagnosis : Central Retinal Artery Occlusion

Treatment within 48hrs advised Retinal tissue usually cannot survive ischaemia

for more than a few hrs

Case Study 2 Treatment :

- immediate ophthalmic consultation- Lie flat- Firm intermittent ocular massage for at least 15mins- re-breath in paper bag- I.V. acetazolamide (Diamox) 500mg

Need to exclude other associated disease : HT, DM, SLE, giant cell arteritis, and carotid stenosis

Central Retinal Vein Occlusion(CRVO) Painless loss of vision ranging from minimal t

o recongition of hand motion only

PE:

- Marcus Gunn pupil

- optic disc edema, hyperaemia, marked venous dilatation and tortuosity, flamed-shaped retinal haemorrhage, cotton wool spots

Central Retinal Vein Occlusion(CRVO)

Treat the underlying causes e.g. open angle glaucoma, DM, leukaemia

Look for ocular compications like proliferative retinopathies

Laser photocoaguation for neovascularization

Red Eyes

History :- Unilateral / bilateral- Any pain?

- Severity of pain

- Any discharge?- Any change of visual acuity?

Red Eyes

Examination- Visual acuity – if significantly reduced, it suggest

s corneal damage- Eyelids – any discharge- Conjunctiva – look for any follicles in the inferior f

ornix- Corneal sensation – if markedly decreased, it su

ggests a dendritic ulcer- Cornea – to exclude corneal ulcers- Pupil – to exclude acute glucoma

Case study 3 42 years old man presents with unilateral Lt

eye redness and with marked pain, blur vision photophobia, no response after taken topical antibiotic from GP for few days

No discharge, no headache, no vomiting PE : VA 20/60 on Lt eye, anterior chamber

depth not shallow,

IOP 20mmHg

Case Study 3

Ans : The photo shows ciliary flush- dilated deep conjunctival and episcleral vessels circumferential to corneal lumbus- signify inflammation of iris and ciliary body (anterior uveitis)- management : patient should be referred to eye immediately for topical corticosteroid drops- most cases respond rapidly and settle after 4-6 wks of treatment

Conjunctivitis

The hyperemia is produced by diffuse dilation of the conjunctival blood vessels, and tends to be less intense in the perilimbal region

Subconjunctival haemorrhage

Due to severe vomiting or coughing bouts; no clinical significance.

If no posterior border :- consider anterior fossa fracture

Maybe a first presentation of hypertension. Treatment :

- Gutt methylcellulose- Advise patients that it may take several weeks to clear

What are these ?

2.

3.

1.

Photo 1 : Pterygium– Most case occur in tropical climates– Sugical exicion is indicated if it starts to encroach on the visual axis or for cosmetic re

ason

Photo 2 : Stye– Acute inflammation of the glands or hair follicles in the eyelid, which cau

se pain and redness– Tx : hot compresses, for topical A/B if infected

Photo 3: Chalazion– Chronic inflammation of a meibomian gland in the eyelid, which is usuall

y non-tender

For stye and chalazion, most cases are sterile inflammatory reactions, and will resolve spontaneously. Incision and drainage is indicated only when lesions become persistent.

Eye Injuries

Chemical burns Check pH with pH paperDamage : alkaline acidDeeper penetration; coagulative necrosisTreatment : no place for chemical neutralizati

on.immediate copious irrigation with NS (IV drip

set) until pH back to normal, neutral range (around 7.4)

Eye Injuries Chemical burnremove chemical particles, esp. upper & lower fo

rnices.eyedrops local anaesthetics (stat only)

cycloplegic (eg gutt Mydriaticum) : for relief of ciliary spasm. antibotic eyedrops / ointment

eye paddingconsult ophthalmologist immediately

Eye Injuries

Corneal abrasion/ulcer

Positive staining with Fluorescein strip.

Eye Injuries Corneal abrasion/ulcerTreatment

Short-acting cycloplegic (stat only)

Antibiotics eyedrops / ointment

+/- eye padding, not proven to improve healing

NoteLocal anaesthetics eye drops delay re-

epithelization.

Steroid eyedrops - complication of penetrating ulcer

Refer to ophthalmologist for follow up (risk of scarring)

Eye Injuries Foreign bodiesIrrigation with NS.After LA eyedrops, remove with moist cotton tips, If ad

herent, carefully scrape with hypodermic needleCentral FB (along visual axis) should better be remove

d by the ophthalmologistNoteExcessive scraping can cause more damage to corn

ea & subsequent scarring.Refer to ophthalmologist e.g. Corneal abrasion,

rust ring

Eye Injuries

HyphemaBlood in anterior chamber

Hyphema should be regarded as a severe injury.Increase in IOP & glaucoma is a great risk with t

otal hyphaemiaManagement :

- pad eye- consult eye urgently- admit for bed rest & assessment.

The End