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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
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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
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