Ocular and Medical Emergencies

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Ocr emergenciesTrm

It is important that ocular injuries are

accurately assessed and the ndings

documented; good clinical records are

vital from a medico-legal standpoint.

A system for classifying ocular trauma

has been developed and is termed the

Birmingham Eye Trauma Terminology

System (BETTS). In this system, there

is standardisation of terminology. Aninjury is termed closed globe if there is

no full thickness wound of the eyeball.

The term ocular contusion is also used

in such cases. In an open globe injury,

there is a full thickness wound present.

MOdulE 13 PaRT 2: ClINICal OPTOMETRYCOuRSE COdE: C-13104/Od

loise OTooe FRCSI (Ophth), MRCOphth, MMeSci FEBO

There are some ocular emergencies which are visually threatening

and must be appropriately managed to prevent irreversible blindness.

There are also some medical emergencies which can present with

ocular signs and, if mismanaged, can result in death of the patient. It is

paramount that the attending optometrist is alert to these conditions

and administers appropriate action. This article discusses the most

likely conditions to be encountered by an optometrist in practice.

A partial thickness wound of the

eyewall is termed a lamellar laceration.

When the eyeball is struck by a blunt

object such as a squash ball, it will

cause a rupture of the eyewall rather

than a wound injury. When a blunt

object strikes the eye, there is a resultant

increase in intraocular pressure (IOP)

and the eye will split at its weakest point.

Certain patients are more vulnerable to

blunt object injury than others. Patientswith a history of extracapsular cataract

surgery have larger incisions compared to

those who have had phacoemulsication

surgery and are more prone to rupture

along these healed surgical lines. In

addition, patients who have had radialkeratotomies have an increased risk

of corneal perforation following blunt

injury compared to patients who

undergo LASEK for refractive correction.

The term penetrating injury refers

to an injury where there is only

an entrance wound. An example

of a penetrating injury would be a

hammering injury where a foreign body

enters and remains in the eye (Figure

1). In a perforating injury, there is

both an entry and exit wound causedby the same agent eg a bullet which

passes though the eyeball and lodges

in the brain. A bullet can also cause

extensive facial lacerations (Figure 2).

Common cases of minor trauma

include a subtarsal foreign body and

corneal foreign bodies and abrasions. A

subtarsal foreign body typically occurs

after walking past a building site on

a windy day. The patient complains

of ocular discomfort and the superior

bulbar conjunctiva will be injected.The cornea may show diffuse staining

or characteristic linear erosions. The

patient should have a topical anaesthetic

instilled (such as proxymethacaine,

amethocaine or tetracaine) and the

subtarsal foreign body should then be

removed by everting their upper lid. The

patient should be advised that when the

topical anaesthetic wears off, they will

still experience a foreign body sensation

until the cornea has completely healed.

A corneal abrasion often occurs

following a scratch or injury to the eye.

Typically, the patient strikes the eye

with a hairbrush or ngernail - often the

culprit is their own toddler. The patient

experiences intense pain secondary to

denudation of the corneal epithelium.

Because of this, patients should receive

topical anaesthesia in advance of an

ocular examination. On examination,

the cornea will stain with uorescein.

The treatment of a corneal abrasion is toadminister lubricants, a topical antibiotic

and a cycloplegic for pain relief. A

double pad is useful to aid healing

where the extent of the erosion is large.

Arc eye is essentially bilateral

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simultaneous corneal abrasions thisform of photokeratitis can occur during

welding and after skiing secondary

to prolonged exposure to high

concentrations of ultraviolet light. It is

managed as a supercial corneal abrasion.

A corneal foreign body may occur

following angle grinding. The metal

particle strikes the eye and lodges in

the cornea. If the foreign body is not

immediately removed, an iron rust ring

develops around the particle. When

treating such patients, it is importantto ascertain how the injury occurred

as well as performing a full dilated

ophthalmic examination to exclude an

intraocular foreign body. If the corneal

foreign body is relatively supercial, it

is often possible to dislodge it using a

cotton bud under topical anaesthesia.

A 19-gauge green needle is used to

dislodge foreign bodies which are more

deeply embedded and a mechanical rust

ring remover is helpful in clearing the

cornea of residual rusting. The patientis then treated with topical lubricants,

antibiotics and if required, cycloplegics.

It is important in any case of trauma

to rule out an ocular perforation and

exclude an intraocular foreign body. A

history of hammering would heighten

suspicion of a high velocity injury. All

patients with a high index of suspicion

for an intraocular foreign body should

have radiological investigation. X-rays

are performed in upgaze and downgaze

to detect intraocular metallic particlesand uorescein 2% dye is useful to

detect Seidel positivity aqueous

leakage from a corneal wound is seen

to dilute the topical dye. In addition,

the anterior chamber shallows when

there is a full thickness leaking wound.

If a patient is Seidel positive, the IOP

should not be checked and no external

pressure should be placed on the eye.

A shield should be applied but if no

shield is available, the eye should not be

padded while transferring the patient.When referring a patient to hospital

where surgery may be required (in order

to remove an intraocular foreign body or

to suture a ruptured globe) the patient

should be advised to fast, as these

cases are typically performed under

general anaesthesia. It is paramount

that in such cases, the ocular foreign

body is not removed. Although the

patient may be distressed to have a sh

hook embedded in their cornea, when

there is suspicion of a full thicknesscorneal laceration, such objects should

only be removed in the controlled

environment of an operating theatre.

Other alerting signs of an

intraocular foreign body include focal

transillumination of the iris and cataract

(a particle may traverse the lens). In

addition, gonioscopy should also be

performed because foreign bodies

may otherwise lie undetected in the

trabecular meshwork. It is important

that all intraocular metallic foreign

bodies are removed as they place the

eye at high risk of developing the

devastating condition of ocular siderosis

(chalcosis if copper is the foreign body)

in later years. Some objects such as

glass and eyelashes are inert and may

not cause any inammatory reaction.

Vegetable matter has the potential

to cause fungal endophthalmitis.

Blunt trauma to the eye can have

devastating effects (Figures 3 and 4).

The smaller the object and the higher

the velocity at impact, the greater the

trauma to the eye. A squash ball has the

potential for greater injury than a football

as a football will be deected back from

the orbital rim. A squash ball will cause

a direct contusional injury with the

eyeball. When assessing such an injury,

it is useful to work systematically from

anterior to posterior. The eyelids and

surrounding skin are often bruised (Figure

5) and Arnica (a homeopathic remedy)is useful in reducing such swelling.

A blunt injury may be severe enough to

cause an orbital oor blow out fracture.

The globe is displaced inferiorly and

the perimuscular fat tethers the globe

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Figre 1Corneal foreign body



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the extraocular muscles may become

avulsed following blunt trauma or

assault (Figure 7).3 Complications of

blunt trauma to the posterior segment

include vitreous haemorrhage, retinal

tears, commotio retinae and choroidal

rupture. Commotio retinae is caused by

neuro-retinal injury resulting in a cloudy

swelling 4. It has a grey/white appearance

and tends to resolve without sequelae.

Choroidal rupture is generally

concentric with the optic disc and may

be associated with retinal haemorrhages.

Patients should be carefully examined todetect peripheral retinal tears and advised

of the symptoms of a retinal detachment.

Chemical burns present an ocular

emergency in which the optometrist is at

the front line of treatment. Appropriate

management of this condition from

presentation has a direct impact on

the long-term outcome of the patient.

Common products containing alkalis

include cleaning products and fertilisers

(ammonia), drain cleaners and airbags

(sodium hydroxide), cement, plaster,mortar (lime) and reworks (magnesium

hydroxide). Common products

containing acids include battery acid

(sulfuric acid) and bleach (sulfurous acid).

Whether presenting with an alkali

or an acid burn, all patients should

have copious irrigation to remove the

chemical. Patients should receive

topical anaesthesia before such

irrigation. Ideally, the eye should be

irrigated with a sterile balanced buffered

solution, such as normal saline solution

or Ringers lactate solution. Immediate

irrigation with even plain tap water

is preferred, if these are not available.

The irrigation solution must contact the

ocular surface. This is best achieved with

a special irrigating tubing (eg, Morgan

lens) or a lid speculum. Irrigation shouldbe continued until the pH of the ocular

surface is neutralised, usually requiring

1-2 litres of uid. It is also important

to evert the eyelids and remove any

particulate matter from the subtarsal

space. If not removed, the residual

particles can serve as a reservoir for

continued chemical release and injury.

Alkalis saponify (hydrolyse esters to

form alcohol and carboxylic acid) cell

wall protein in cell walls so therefore

can cause extensive penetratingdamage. Alkalis penetrate into and

through the cornea and into the anterior

segment. Subsequent hydration of

glycosaminoglycans results in stromal

haze. Hydration of collagen causes

into position. The patient is unable

to gaze superiorly and may also

experience diplopia in the primary

position. There may be infraorbital

anaesthesia secondary to neural damage

and surgical emphysema secondary to

subcutaneous air, typically from the

ethmoidal sinuses.1 Any patient with

such a fracture needs a full medical

assessment as a matter of urgency.

Blunt injuries may cause bleeding of

the structures of the anterior segment

resulting in a hyphaema (Figure 6). If

blood lls the globe, it is termed aneight ball hyphaema and this requires

surgical evacuation of the clot. A simple

hyphaema is treated with bed rest and

cycloplegics to prevent the formation

of synechiae. Patients should not be

administered aspirin for pain relief

as this exacerbates a secondary bleed

patients should take paracetamol.

Complications of a hyphaema include

raised IOP and corneal staining.

Blunt trauma to the pupillary

sphincter will result in an irregularpupil and an iridodialysis (disinsertion

of the iris from the scleral spur) may

occur.2 The intraocular lens may

opacify causing a cataract or become

dislocated or subluxed. In addition,

Figre 2Lacerations to the skin following bullet trauma


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bril distortion and shortening, leadingto trabecular meshwork alterations

that can result in increased IOP. Acids

dissociate into hydrogen ions and

anions in the cornea. The hydrogen

molecule damages the ocular surface by

altering the pH, while the anion causes

protein denaturation, precipitation

and coagulation. Protein coagulation

generally prevents deeper penetration of

acids and is responsible for the ground

glass appearance of the corneal stroma

following acid injury. Hydrouoricacid is an exception; it behaves like an

alkaline substance because the uoride

ion has better penetrance through the

stroma than most acids, leading to more

extensive anterior segment disruption.

Chemical injuries cause ischaemia of the

peripheral cornea by damage to blood

vessels. The degree of limbal ischaemia

(blanching) is perhaps the most

signicant prognostic indicator for future

corneal healing because the limbal stem

cells are responsible for repopulatingthe corneal epithelium. In general,

the greater the extent of blanching,

the worse the prognosis. However, the

presence of intact perilimbal stem cells

does not guarantee normal epithelial

healing. Extensive burns can even

cause perforation of the globe. Both

acid and alkali chemical burns are a

true ocular emergency, which must take

precedent over all other waiting patients.

acte nge cosre gcomAcute angle closure glaucoma occurs

when a shift in aqueous humor outow

leads to structural changes in the eye and a

consequent rise in IOP. The most common

pathological mechanism is pupillary

block the shift in the transpupillary

aqueous humor outow produces a rise

in pressure in the posterior chamber.

Because of this, the peripheral iris is

pressed against the trabecular meshwork

and Schwalbes line. This obstructionof the trabecular outow causes a

rise in IOP to levels up to 80 mmHg.

Patients complain of a rapidly

progressive deterioration in vision

with pain and redness in the affected

eye. Nausea and vomiting, may beassociated with this condition. The

eye is injected, there is corneal oedema

and a shallow anterior chamber. The

pupil is mid-dilated and often oval

in shape and the disc is hyperaemic.

The lens may develop discrete

opacities termed glaucomecken. The

glaucomatous attack can be broken

by miotics and carbonic anhydrase

inhibitors and at a later stage bilateral

laser iridotomies are created. The

pupil may retain an anomalous shapeand there may be areas of iris atrophy.

Centr retin rtery occsionA central retinal artery occlusion (CRAO)

is an ophthalmic emergency, which if

treated appropriately may restore vision.

The incidence of retinal arterial occlusion

is estimated to be 0.85/100,000 per year.5

CRAO results in abrupt and massive

visual loss, with visual outcomes of

6/60 or lower. CRAO appears to be more

common in males than females at a ratioof 2:1 and is usually diagnosed too late

for effective therapeutic intervention.

The time required for irreversible loss

of vision in an experimental model

of CRAO was less than 250 minutes.6

CRAO mainly affects older people, with

a mean age of 60 years at presentation.In many cases, retinal arterial

obstruction is associated with general

cardiovascular disease risk factors:

hypertension (60%), smoking, diabetes

(25%) and hypercholesterolemia.

Giant cell arteritis (GCA) may

present in elderly people as a CRAO.

Retinal arterial occlusion is

characterised by a sudden, painless loss

of vision. The visual defect is unilateral.

Sometimes patients note the visual defect

on waking up in the morning, whichmay be due to reduced retinal perfusion

secondary to nocturnal hypotension.

Some patients may report antecedent

episodes of transient visual disturbance.

In a CRAO, the blockage may occur

at any point between the origin at the

ophthalmic artery and the optic disc head.

However, usually the blockage occurs at

the level of the lamina cribrosa. Vision is

usually reduced to the level of counting

ngers or hand movements, unless there

is a separate cilioretinal artery supplyingthe macula. A relative afferent papillary

defect is usually present and the retina

may initially appear normal. However,

within a few hours, the nerve bre

layer becomes thickened with retinal

whitening particularly in the macula.

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Figre 3Infraorbital bruising and subconjunctival haemorrhage following blunt injury



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A cherry red spot develops at the fovea

where the choroid is still visible. Embolimay be seen in the central retinal artery

in about a quarter of cases. Retinal

arteries become thin and attenuated

and may have breaks in the column of

blood (boxcarring or cattle-trucking).

The management of acute retinal

arterial occlusion is difcult and the

outcomes are often disappointing. There

are no proven treatments. This is because

retinal arterial occlusions are relatively

rare events, so studies have been either

retrospective or small case series withouta randomly allocated control group. The

aim of the treatment is to restore the

retinal blood supply as soon as possible,

increase oxygen delivery to the retina

or limit the damage from hypoxia.

For treatment to have any prospect of

success, it must be started immediately.

If a patient with a CRAO presents within

24 hours, it is reasonable to attempt

several of the non-invasive treatments

described below. In some ophthalmic

centres, if a CRAO is diagnosedwithin a few hours of onset, more

invasive treatments may be performed.

The simple act of lying the patient

at increases retinal perfusion pressure.

Ocular massage may also be useful as

it has been reported to occasionally

help to dislodge an embolus. Pressureis applied to the globe with the eyelids

closed for 10 seconds and then suddenly

released. This cycle is repeated for

up to 15 minutes. An emergency

anterior chamber paracentesis may

be performed to rapidly reduce the

IOP. In addition, drugs to lower the

IOP (eg, oral acetazolamide) are given

to try to augment the effect of massage

or anterior chamber paracentesis, in

the hope of dislodging an embolus

and improving the retinal perfusion.Improved retinal blood ow may be

achieved by vasodilatation of the vessels

and this can be achieved by asking the

patient to re-breathe into a paper bag.

Retin ter/etchmentA retinal detachment is a detachment

of the neurosensory retina from the

retinal pigment epithelium through

inux of uid into the subretinal space.

A rhegmatogenous retinal detachment

is produced by a full-thickness defect.It is an ophthalmological emergency,

which can lead to blindness if untreated.

The most common causes are age-

related destruction and liquefaction

of the vitreous body. The vitreous

detachment following degeneration cancause holes and tears through traction

on the peripheral retina, allowing the

liquid part of the vitreous to penetrate

and separate the neurosensory layer

from the pigment epithelial layer. Other

predisposing factors are high myopia,

cataract surgery and ocular trauma. The

incidence of rhegmatogenous retinal

detachment is 0.01%. It is diagnosed

most frequently between the ages of 50

and 70 years. The risk of rhegmatogenous

retinal detachment in the opposite eyeis 10%. The most important symptoms

are photopsia, oaters and an absolute

scotoma. Clinically, the detached

retina shows a whitish and creased

surface. Retinal defects, pigment cells

and erythrocytes are found in the

vitreous body often with subnormal IOP.

If the macula is still attached, it is

considered an ophthalmic emergency.

If the retinal detachment is complete

and has been present for weeks

or months, surgical interventionis not urgent. A retinal tear is

always treated as an emergency as

if left untreated, it will eventually

progress to a retinal detachment.

Corne emergenciesPatients with bacterial corneal

ulcerations need urgent referral.

These include contact lens wearers

or immunocompromised individuals

such as diabetic patients. The presenceof a hypopyon requires emergency

intervention. Pseudomonal infection

can progress rapidly and result in

corneal perforation within 48 hours.

Patients with a history of

penetrating keratoplasty must be

assumed to be rejecting their graft

until proven otherwise. They

require urgent referral for further

assessment and immunosuppression.

A herpetic corneal ulcer should

receive topical antiviral therapy toreduce scarring and visual loss. If

there is an associated anterior chamber

reaction, the patient should be

dilated by the referring optometrist

both for analgesia and to reduce the

Figre 4Extensive chemosis following blunt injury


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formation of posterior synechiae.Other ocular emergencies

include blebitis and postoperative

endophthalmitis. Blebitis occurs in

patients who have had a trabeculectomy

with formation of a ltering bleb. When

the bleb becomes infected, the eye is red

and the bleb has a milky appearance.

It is an ophthalmic emergency as

the infecting organisms can quickly

access the intraocular cavities.

Any patient with a history of recent

ophthalmic surgery (eg, postoperativecataract or post intravitreal injection)

who presents with a red and painful

eye should be treated as a potential

case of endophthalmitis and be

urgently referred back to the treating

surgeon. The sooner that intravitreal

antibiotics are administered to these

patients, the better the visual outcome.

Meic emergenciesGint ce rteritis

Temporal arteritis refers to inammation

of the supercial temporal artery

and is a feature of GCA. GCA causes

inammation of large to medium

sized arteries and typically involves

the supercial temporal, ophthalmic,

posterior ciliaries and proximal section of

the vertebral artery. Arteritic occlusion

of these vessels can result in blindness.

There may also be concomitant arteritis

of the aorta and other arteries resulting

in dissecting aneursyms, aorticincompetence, myocardial infarction,

brain stem stroke and renal failure. It

is for this reason that GCA is classied

not only as a neuro-ophthalmic

emergency but as an acute medical

emergency that can result in death.

The presentation of GCA may be abrupt

or insidious and typically occurs

during the seventh or eighth decade of

life. Constitutional symptoms include

anorexia, fever, malaise, depression,

myalgias, night sweats and weight loss.The hallmark symptom of GCA is a

recent-onset localised headache, usually

to the temporal or occipital area. This

headache occasionally may be diffuse or

bilateral. When palpating, the supercial

artery is tender, inamed and nodular.As the arteritis advances, no pulse

can be palpated. Patients commonly

complain of scalp tenderness which is

elicited when combing hair. They may

suffer jaw claudication as a consequence

of ischaemia to the muscles of mastication

chewing therefore becomes painful.

Visual symptoms are present in about 33%

of patients. Ophthalmic presentations of

GCA include arteritic anterior ischaemic

optic neuropathy (AAOIN), which may

be preceded by amaurosis fugax. Anynew onset nerve palsy in the elderly

patient should be considered GCA

until ruled out. In GCA associated

AAION, the optic nerve appears

swollen and chalky white with splinter

haemorrhages. There is an associated

profound reduction in visual acuity.

If GCA is clinically suspected, it is

important that patients are immediately

referred to Accident and Emergency

for clinical workup and treatment with

systemic steroids. If a patient haspresented with AAION in one eye, their

fellow eye is at high risk of becoming

affected. Unfortunately cases of bilateral

blindness are not uncommon 65% of

untreated patients become bilaterallyblind within weeks. The diagnosis of GCA

is made by a number of criteria including

an elevated erythrocyte sedimentation

rate (ESR), C reactive protein (CRP)

and positive temporal artery biopsy.7

Srgic (compressive) thir nerve psy

Patients presenting with a dilated,

unreactive pupil involving third nerve

palsy must be presumed to have an

intracranial aneurysm until proved

otherwise. The patient may have ahistory of associated headache and

examination may reveal a ptosis

secondary to weakness of the levator

palpebrae superiorus. The eye will be

diverged and inferiorly directed. There

will be weakness of adduction secondary

to palsy of the medial rectus. The

superior rectus and inferior rectus are

weak and the superior oblique remains

unopposed so there is ocular intorsion

on downgaze. Disruption of the pupillary

parasympathetic supply results ina xed dilated pupil. The patient

may not have any visual difculties

as the ptosis masks their diplopia.

An intracranial aneurysm of the


Figre 5Blunt trauma



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posterior communicating artery in

the Circle of Willis must be ruled out.

The patient should be immediately

referred for a neuro-surgical workup.

Ppioeem

If a patient is noted to have bilateral

disc swelling, papilloedema as a result

of raised intracranial pressure must

be suspected and excluded. In cases

of papilloedema, the patient may

complain of headache and nausea.

The patient may also experience

transient visual obscurations as well

as horizontal diplopia, which is a

consequence of involvement of the

abducens nerve. Patients with raised

intracranial pressure tend not to exhibit

spontaneous venous pulsations at the

optic disc and the blind spot is enlarged.

The patient requires neuro-imaging andassessment to rule out an intracranial

tumour. The term papilloedema is

reserved for optic disc swelling in the

presence of raised intracranial pressure.

Orbit ceitis

It is important to distinguish orbital or

postseptal cellulitis, which is a medical

emergency, from preseptal cellulitis.

The clinical picture is characterised by

severe general malaise, exophthalmos,

a motility decit and considerablelid and conjunctival swelling. Along

with persistent loss of function due

to damage to the optic nerve, there is

a risk of cavernous sinus thrombosis

leading to death. The treatment consists

of prompt broad-spectrum systemic

antibiotics and often debridement

of the paranasal sinuses is required.

Subperiosteal abscesses of the orbit

usually have to be drained. The most

common bacteria are Staphylococci,

Streptococci and Haemophilus

species. Orbital cellulitis is more

common in children than in adults.

Orbital cellulitis occurs in the

following three situations: (1) extension

of an infection from the periorbitalstructures, most commonly arising from

the paranasal sinuses (the face, globe

and lacrimal sac may also be a source

of infection); (2) direct inoculation

of the orbit from trauma or surgery;

and (3) haematogenous spread from

bacteraemia (bacteria in the blood).

In preseptal cellulitis, the

globe is white, vision is good

and the extraocular movements are

full. In orbital cellulitis, the globe

is injected, visual acuity and colourvision are compromised and there is

proptosis and ophthalmoplegia. The

infection can proceed very quickly and

therefore it is imperative to initiate

an urgent referral and intervention.

ConcsionThe attending optometrist should

be procient in detecting, treating

and appropriately referring ocular

emergencies. The inappropriate

management of these conditions increases

the patients risk of blindness and in

some cases may even lead to their death.

ReferencesSee www.optometry.co.uk/references

MSc in Cinic OptometryCITY UNIVERSITY and OT have

joined forces allowing readers to

achieve CET points through to a

full Masters in Clinical Optometry.

The content of this article is part of

the forthcoming Anterior Segment Eye

Disease module running May 16-18 2010.

Please note that the OT/City exam will

run on May 27 2010 and is based on

the City CET articles published in 2009 Diabetes and Vision in the Aged

For further information please

contact Dr Michelle L Hennelly

by emailing (m.hennelly@city.

ac.uk) or call 0207 040 8352.

Figre 7Avulsed lateral rectus

Figre 6Hyphaema following blunt trauma


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1.Which one of the foowing is FalSE?Gint ce rteritis:a. is treated with high dose topical steroidsb. is diagnosed by temporal artery biopsyc. is associated with jaw claudicationd. may be atal

2. Which one of the foowing is FalSE regring compete thir nervepsy?a. it may be associated with an intracranial aneurysmb. ptosis is a eaturec. the aected eye is hypertropicd. the parasympathetic supply to the pupil is interrupted

3. Which one of the foowing is FalSE?

Ppioeem is:a. associated with headache and nauseab. associated with transient visual obscurationsc. associated with diplopiad. synonymous with bilateral optic neuritis

4. Which one of the foowing is FalSE?Orbit ceitis my:a. ollow an inected styeb. ollow sinusitisc. ollow preseptal cellulitisd. be treated with topical antibiotics

5. Signs of penetrting eye injry o NOT ince:a. a Seidel negative resultb. ocal transillumination o the irisc. intraocular oreign body

d. traumatic cataract

6. Which one of the foowing is FalSE regring chemic injries?a. injuries should be immediately irrigated with copious fuidb. alkalis penetrate deeper then acidsc. limbal ischaemia is a poor prognostic signd. injuries should be neutralised with acid i the patient has an alkali burn

7. Which one of the foowing is FalSE?In cte nge cosre gcom:a. the eye is injectedb. vision is reducedc. there may be an associated posterior capsular cataractd. there is associated pain

8. Which one of the foowing is FalSE regring centr retin rteryoccsion (CRaO)?a. a cherry red spot is a eature o this conditionb. CRAO is associated with painul visual lossc. CRAO may be preceded by amaurosis ugaxd. CRAO may be treated by emergency paracentesis

9. Which one of the foowing is FalSE?

Tretment of CRaO inces:a. inhalation o high dose oxygenb. anterior chamber paracentesisc. oral acetazolamided. ocular massage

10. Which one of the foowing is FalSE?Rhegmtogenos retin etchment:a. is associated with pigmented cells in the vitreous cavityb. is associated with complaints o photopsiac. usually aects patients between the ages o 20 and 30 years o aged. is a eature o high myopia

11. Which one of the foowing is FalSE?Corne cers:a. are rapidly progressive in Pseudomonal inectionsb. are more common in contact lens wearers

c. may be more aggressive in diabetic patientsd. are treated with topical steroids

12. Which one of the foowing is FalSE?Enophthmitis is recognise compiction of:a. intravitreal injectionsb. cataract surgeryc. trabeculectomiesd. panretinal photocoagulation

Moe qestions Corse coe C13104/ Od

PlEaSE NOTE There is ony one correct nswer. a CET is now FREE. Enter onine. Pese compete onine by minight on Mrch 17 2010 Yo wi

be nbe to sbmit exms f ter this te nswers to the moe wi be pbishe on ww w.optometry.co.k


Ocular and Medical Emergencies

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