Vous êtes sur la page 1sur 98

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 Floaters
DDX
 Posterior vitreous detachment (PVD) +/-
retinal hole formation
 Vitreous haemorrhage
 Ocular migraine
 Posterior uveitis
(Pt may c/o rhythmical
flashing 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
− sclera
− cornea : position of light reflection,
fluorescence staining
− anterior chamber
− depth by shining a torch sideways
Anterior Chamber Depth
Assessment
Examination
• Inspection
− iris— injection, irregularity, adhesion
− pupils —size, reaction to light,
accommodation etc
− lens—opacity, position
• Test ocular movements and visual fields

• Ophthalmoscopic examination
− red reflex
− optic 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
retinopathy
– 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
• 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

• 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
steroid 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

 Itis 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
pupil 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 Glaucoma
Eye 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 Glaucoma
Eye 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 Glaucoma
Eye Drops
1. 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 Glaucoma
Eye Drops
2. 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 Glaucoma
Eye Drops
3. 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, headache
pupillary dilation, conjunctival injection
Treatment for Glaucoma
Eye Drops
4. 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 Glaucoma
Surgery
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 :
3. Elderly
4. Female
5. Family history
6. Hyperopia
7. 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
outflow
 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
to 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
suggests corneal damage
- Eyelids – any discharge
- Conjunctiva – look for any follicles in the
inferior fornix
- Corneal sensation – if markedly decreased, it
suggests 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 ?
1.
2.

3.
 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 reason

 Photo 2 : Stye
– Acute inflammation of the glands or hair follicles in
the eyelid, which cause 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 usually 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 paper
• Damage : alkaline > acid
• Deeper penetration; coagulative necrosis
• Treatment : no place for chemical
neutralization.
• immediate copious irrigation with NS (IV drip
set) until pH back to normal, neutral range
(around 7.4)
Eye Injuries
 Chemical burn
• remove chemical particles, esp. upper &
lower fornices.
• eyedrops
− local anaesthetics (stat only)
− cycloplegic (eg gutt Mydriaticum) : for relief
of ciliary spasm.
− antibotic eyedrops / ointment
• eye padding
• consult ophthalmologist immediately
Eye Injuries

 Corneal abrasion/ulcer
− Positive staining with Fluorescein strip.
Eye Injuries
 Corneal abrasion/ulcer
• Treatment
− Short-acting cycloplegic (stat only)
− Antibiotics eyedrops / ointment
− +/- eye padding, not proven to improve healing
• Note
− Local anaesthetics eye drops delay re-
epithelization.
− Steroid eyedrops - complication of penetrating
ulcer
− Refer to ophthalmologist for follow up (risk of
scarring)
Eye Injuries
 Foreign bodies
• Irrigation with NS.
• After LA eyedrops, remove with moist cotton tips, If
adherent, carefully scrape with hypodermic needle
• Central FB (along visual axis) should better be
removed by the ophthalmologist
• Note
− Excessive scraping can cause more damage to
cornea & subsequent scarring.
• Refer to ophthalmologist e.g. Corneal abrasion,
rust ring
Eye Injuries
 Hyphema
• Blood in anterior chamber
• Hyphema should be regarded as a severe
injury.
• Increase in IOP & glaucoma is a great risk
with total hyphaemia
• Management :
- pad eye
- consult eye urgently
- admit for bed rest & assessment.
The End