EYE EMERGENCIES

Jaybee Bautista, MD

OCULAR EMERGENCIES
Trauma
o Blunt
o Penetrating
Non-Trauma
OCULAR TRAUMA
ACUTE EYE CONDITION
SUBCONJUNCTIVAL HEMORRHAGE
not an
emergency case
EMERGENCY VERY URGENT URGENT
-

(Immediately) (few hours) (w/in the day) Leakage of blood between the conjunctiva and sclera
Causes
CRAO / central retinal artery AACG (acute angle closure Orbital cellulitis
occlusion )
glaucoma ) o Trauma, Hypertension
Chemical Burns Globe perforation Corneal abrasion
o Spontaneous
or rupture Hyphema
No Treatment
IOFB ( intraocular foreign body )
o Resolves within 2-3 weeks
Vaso constrict
0 apply wld compress for 24 hrs →

EVALUATION
0 hot compress after 24hr5
Acuteness of symptoms -

faster reabsorption
Accurate history
of blood
Complete eye examination

EYE EXAMINATIONS
Visual Acuity good for swtoma
External Eye: Orbit,
Periorbital skin, lids i CORNEAL ABRASION
Confrontation test / visual field
test
Ocular motility Scratch or scrape on the surface of the cornea (Fingernails,
Anterior Segment makeup brushes, tree branches)
o Conjunctiva SSx:
o Cornea o Pain, photophobia, foreign body sensation, tearing,
o Anterior Chamber conjunctival injection, swollen eyelid
o Iris Treatment: Topical Antibiotics prevent secondary bacterial infection
-

o Lens
o Pupil

sit lamp
-

cobalt -
blue / fluoresciendye )
-
detect corneal -

epithelial
detect
CONJUNCTIVAL AND CORNEAL FOREIGN BODIES

Eye pain, red eye, foreign body sensation

INTRAOCULAR PRESSURE MEASUREMENT Dx. Slit lamp Exam
Treatment:
Goldmann Applanation Tonometer o Removal of FB under slit lamp
o Topical Antibiotics
( gold
Normal IOP: 10-21 mmHg
] o Corneal wound healing agents, (odium hyaluronan
standard o Eye patch
pag↑ highly suggestive corticosteroids delay healing
-

✗ -

of glaucoma

FUNDUS EXAMINATION

A dilated pupil makes it easier to see the optic nerve, macula

and retina
o 1 % tropicamide
o 2.5 % phenylephrine can induce hypertensive crisis
-

WHISKY, PINKY, EXCELL, KANDRO EYE EMERGENCIES OPHTHA 1 | 4

 TRAUMA HYPHEMA CANALICULAR LACERATION

Blood in the Anterior Chamber hypopyon ( fungal infection ]

-
Refers to sudden physical injury that results in damage to the
Caused by injuries to the eye from accidents or playing sports lacrimal drainage system
Disruption of blood vessels in the iris or ciliary body Causes: direct injury (penetrating trauma with foreign objects
Management: such as glass metal)
o Elevate the patient’s head Treatment: Surgical Repair
o Bed rest May lead to scarring and stenosis -> EPIPHORA →
pag poorly repaired
control pain relief DX fluorescein dye
1-
o 1% atropine eye drops daily inject air nasal laminal duct is obstructed
-
- :
, ,

normal production
o Topical steroid cycloplegia ( paralyze)
-

of tears

( Kabali qtaran ng

overproduction
of Kaos )

OCULAR GLOBE INJURY

Rupture
ORBITAL TRAUMA/FRACTURE Laceration
o Penetrating
Results from a collision o Perforating
Coup and contra-coup injury o Intraocular Foreign Body (IOFB)
May present with periorbital teardrop sign
-

herniation OF
hematoma, pain, swelling, bleeding ' '

ocular contents and / or pen orbital fats

Dx: CT Scan, X-ray diplopia -

entrapment of inferior RUPTURED GLOBE

rectus muscle

Etiology: BLUNT injury caused by motor vehicular accidents,

Treatment :
sports activities, assault, or other trauma
2 weeks
of oral steroids Pathophysio: May occur when a blunt object impacts the orbit
-

compressing the globe and results in momentary increase in

IOP to a point that the sclera tears or ruptures
Diagnostics : CT scan- Imaging of choice →
lagisagot if unsure
Management: eye shield, tetanus prophylaxis, NPO, prepare
for patient surgical repair avoid unnecessary manipulation of eye
,
↑ IOP
can

LID LACERATIONS

Refer to partial or full thickness defects in the eyelids

Sharp or blunt trauma
R/O associated ocular injury -
rule out

Remove superficial FB
R/O deeper foreign body
Treatment: LACERATED GLOBE
o Tetanus prophylaxis
o Oral analgesics Injury to the eye caused by sharp object or projectile objects
o Surgical repair with the wound (full thickness defect) occurring at the impact
Repaired by an ophthalmologist or an oculoplastic surgeon site
Reapposition of anatomic detailed anatomic structures are Diagnostics: CT scan
important for normal functioning Management: eye shield, tetanus prophylaxis, NPO, prepare
Avoid aggressive suturing for patient surgical repair

realign / reap pose

WHISKY, PINKY, EXCELL, KANDRO EYE EMERGENCIES OPHTHA 2 | 4

 PENETRATING AND PERFORATING EYE TRAUMA ORBITAL CELLULITIS

These can result in severe vision loss or loss of the eye Etiology
o Penetrating injury – penetrates any part of the eye o Extension of sinus disease-90%
but not through and through, there is no exit wound o Penetrating trauma
o Perforating injury- have both entrance and exit o From infected adjacent structures
wound o Odontogenic origin (i.e severe dental caries or a
Etiology: Injury from sharp or high velocity object recent dental procedure)
hematogenous spread from distant site ( 417 )
°
a ex
Diagnosis: Ultrasound or CT scan to check for IOFB SSx: .

Management: Surgery, Globe exploration w/ possible o Limited Ocular Motility painful eye movements
-

Vitrectomy o Proptosis
o Chemosis ( edematous conjunctival
o Conjunctival hyperemia
o Fever
o Leukocytosis
Lab workups : CBC, Blood cultures
Imaging: CT Scan
Management:
o Medical: IV Broad spectrum Cephalosporin
(Cefuroxime or Cefriaxone) + Metronidazole or
Clindamycin
o Surgical: Drainage
PERFORATING INJURY Prognosis: Delayed management result to significant morbidity
(Cavernous sinus thrombosis, Meningitis, Intracranial abscess
formation, Death)

PENETRATING INJURY

chemo sis
-

topical steroids + antibiotics

CHEMICAL BURNS

TRUE OCULAR EMERGENCY!!!

Could be acid or alkali
INTRAOCULAR FOREIGN BODY ( 101=13 )
Presents with eye pain, redness, tearing, inability to keep eye
open, foreign body sensation, swelling of eyelids, BOV
In eyes with an open globe injury, Always suspect presence of Immediate intervention is warranted
IOFB
Can cause corneal scarring
Most common causes: Hammering and using power tools for
r liquefactive favor
carpentry or constructions
ALKALI BURN ACID BURN
Diagnostics :
o CT Scan- imaging study of choice
o Plain Xray- useful if a metallic IOFB is present and CT
scan is not available
o MRI- not recommended for metallic IOFB
o UTZ- useful in localizing the IOFB
Management: refer to Vitreo-Retina Specialist for Vitrectomy
and Removal of IOFB • More Severe • Less Severe
• Penetrate rapidly often in < 1 • Acids quickly denature
min proteins in the corneal
• Combine with cell membrane stroma, forming precipitates
lipids, mucopolysaccharides that retard additional
and to collagen disruption penetration
of cells and necrosis of the • Causing localized damage
tissues due to its:
• On the ocular surface - Coagulation effect
saponify cell membranes and - Protein
intercellular bridges rapid precipitations at
penetration - ischemic epithelium level
• Necrosis of conj. BV • Leading to:
“Cooked Fish Eye” - Physical barrier

WHISKY, PINKY, EXCELL, KANDRO EYE EMERGENCIES OPHTHA 3 | 4

 Treatment o Trabeculectomy if all else fails -

BEFORE ANY HISTORY TAKING OR PHYSICAL EXAMINATION, PROPHYLACTIC treatment to contralateral eye
normal eye
EMERGENCY TREATMENT MUST BE INSTITUTED FIRST! -
because there's higher chance na
magkaron AACG sa

Copious irrigation with clean water (at the sane of accident)

Irrigation with 2 liters of PNSS ( hospital ]
Topical antibiotics STOP IRRIGATION
Topical cycloplegic when the pH normalizes
-

Corneal wound healing agents normal 7.35 7.45

: -

Oral Analgesics

CHEMICAL BURN: Corneal Scarring -

can cause
astigmatism / blindness

CRANIAL NERVE 3 PALSY- PUPIL INVOLVING

Sudden onset of droopy eyelid and an inability to open the eye

If lid not completely closed- Double vision / diplopia
NON TRAUMATIC OCULAR EMERGENCIES Very limited movement of the eye upwards, downwards or
inwards, eye is deviated downwards and outwards
The pupil on affected side may be enlarged
CENTRAL RETINAL ARTERY OCCLUSION ( ( RAO ) Think of Posterior communicating Artery Aneurysm until
proven otherwise Kasi nakama mating
Sudden painless monocular loss of vision Refer to Neurosurgery service
Occurs in older patients as a complication of atherosclerosis
(90% from embolus usually from the ipsilateral carotid artery) Pupil- This is usually a sign that the third nerve palsy has been caused by
Other Risk Factor: Giant cell Arteritis direct pressure, rather than poor blood supply to the nerve as in the case
of CN 3 palsy on patients who are diabetic and hypertensive.
Presents with pale background retina and a cherry-red spot on
the macula
Irreversible damage after 90 minutes
-

usually in geriatrics
Management:
Brown bagging increase camion dioxide levels ( vaso dilate BV
-
retinal reperfusion) →

Lowering IOP with Anti-glaucoma meds (V mannitol )

Paracentesis decompress ↓ IOP
-

Ocular massage
Referral to a cardiologist and a neurologist for having a risk
macula factor for stroke and M.I.

\
optic nerve

- cherry
-

red spot

spina myelin defect / lipid storage

◦
-

- -

stands out Kasi Ito na

lang may
intact blood supply
retina

ACUTE ANGLE CLOSURE GLAUCOMA ( HAGG )

Blurring of vision, headache, nausea, vomiting, iridescent vision

P.E.- circumlimbal injection, hazy cornea, non-reactive pupil,
tense eyeball, Shallow Anterior Chamber 360 eye redness ,

50 80 mmHg *********END OF LECTURE*********

- -

Treatment
MEDICAL – Decrease the IOP Reference: PPT
o Beta Blocker
o IV Mannitol
o IV or Oral Acetazolamide or Topical CAI
SURGICAL l dorso tami del benzol amide

o Yag Laser Iridotomy (gold standard) daput clear cornea Muna

-

o Peripheral Iridectomy

WHISKY, PINKY, EXCELL, KANDRO EYE EMERGENCIES OPHTHA 4 | 4

 Quid Refert, Dummodo non Desinas, Tardius Ire

OPHTHALMOLOGY
Dr. Eirene Mapile

Acute Eye Conditions

EVALUATION

 The following are not considered emergency:

Emergency Very urgent Urgent
 Hypopion- pus in the anterior chamber
 Hyphema- blood is already in filling the anterior chamber
 Laceration of the lids
 Foreign Body 2 true emergency Perforation/rupture of
Orbital
globe-soft part eyeball
 Acuteness of symptoms  has something to do with time  the itself mas urgent cellulitis/orbital
injury- involves the
person will suffer the consequences unless you do something bone/endopthalmitis-
infection of the eye ,
immediately. (eye is a nutrient agar
 Accurate history  pertains to the eye chemical burns of the bacteria)
Sudden
 Complete eye exam congrestion/proptosis

 Visual acuity is one of the most important in evaluation

CRAO
Hyphema (blood in
TYPES OF ACUTE EYE CONDITIONS the ant
chamber)/IO
EMERGENCY Foreign
body/Retinal
detachment/macula
r edema
 Address immediately within minutes (MOST IMPORTANT)
 2 true ocular emergencies
o Chemical burns (don’t need complete hx) TRUE OCULAR EMERGENCY
 Liquid sosa injury- what do you do? CHEMICAL BURNS
 Dump her head in the pool
o CRAO (central retinal artery occlusion)  Immediate intervention is warranted
 Can cause corneal scarring
VERY URGENT  Could be ACID or ALKALI
 This one really looks more like an emergency compared to CRAO
 Address within a few hours kasi, pag pupunta ung patient sa ER, he is really in pain, di nya
 Includes mabuksan mata nya at sobrang sakit. Tapos pag tatangin mo,
o Acute glaucoma (the faster you drop the pressure, nabuhusan daw ng liquid sosa.
the better the prognosis)  Treatment
o Perforation o Copious irrigation with clean water
o Rupture of the globe (soft part, eyeball itself) o Topical antibiotics
o Sudden congestion o Corneal wound healing agents
o Proptosis o Pain reliever
o Eye touch
URGENT  QUESTION: Your neighbor is cleaning the swimming pool with a
very strong alkali agent like lye, and then, you were in the vicinity,
 Address within the day, 2 days or within the a week the neighbor accidentally splashed lye into her eye, what is the
 Includes best thing to do?
o Corneal abrasion o Never cause DELAY  Dump her head in the pool and
o Orbital cellulitis tell her to open her eyes! get as much as chemical out
o Orbital injury (bone involvement) of her eye para less ung damage.
o Hyphema (blood in anterior chamber) o Use any form of irrigating solution or flushing agent,
o Intraocular foreign body even BEER will do.
o Retinal detachment o Anything is better other than the liquid in her eye.
o Macular edema Because, even if you treat her promptly, the eye will still
have consequence, every second counts
o Do not try to neutralize: if it is ALKALI, then don’t put
ACID.
o Consume the 1-liter of irrigating solution, and then
check the pH.
o GOOD prognosis if the pH is neutral 6.5-

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is asked.
 ACID ALKALI o Brown Bagging
liquefaction Necrosislyses  Make patient breath from the BROWN bag w/
Coagulation Necrosis
the tissues faster nose and mouth covered  INCREASE CO2
Superficial Eschar More SEVERE inhalation CO2 dilate the blood vessels 
Prevents deeper penetration Penetrate more rapidly Dislodge the EMBOLUS
Extends thru submucosa , o Lowering of IOP with anti-glaucoma medications
More severe in the
esophagus tends to be more (normal IOP is 10 – 20 mmHg)
STOMACH
RESISTANT to acid burn  mannitol (diuretics)
Eats up the eye FASTER.  azetozolamide
Coagulation forms a barrier,
When you liquefy the soft  when you have pressure, everything inside is
its temporary but somehow
tissue you facilitate the masikip, so, when you release the pressure,
slows the spread of chemical
penetration FASTER you relieve the tightness so you have a chance
of dislodging the embolus.

CENTRAL RETINAL ARTERY OCCLUSION (CRAO) o Paracentesis - release some fluid, decrease pressure
 Procedure that lowers the IOP
 Looks benign but this is an emergency  Put the patient under slit lamp  Poke the
 SUDDEN monocular painless loss of vision  do fundoscopy eye with the needle in the cornea  aspirate
 If a patient with CRAO walks into the emergency room, you wont aqueous humor  decrease IOP
even know that this patient is in an emergency situation pero o Ocular massage
malalaman mo na emergency sya when you ask the chief  Use the heel of the palm to press eye for 10
complaint. sec  release after 10sec  alternate press
& release of eye  dislodge EMBOLUS
 DIFFERENTIAL DIAGNOSIS: (alternately put pressure using your index
o OPTIC NEURITIS finger)
 painful loss of vision o Streptokinase (thrombolytic)
o Other painless loss of vision  In order to lyse the thrombus
 Branch retinal artery Occlusion  Very expensive, refer to cardiologist/
 URGENT ocular assessment neurologist, thrombus may go anywhere
 Sectoral retinal whitening leading to stroke/ heart attack
 Anterior Ischemic Optic Neutopathy
VERY URGENT
 FUNDOSCOPY:
ACUTE GLAUCOMA
o Widespread retinal whitening or PALE retinal
background and a CHERRY-RED SPOT on the MACULA
 MANIFESTATIONS:
(supplied by the choriocapillaries underneath (choroid
o Eye pain
[Link]) kaya red sya saka it is also more heavily
o Blurring of vision / cloudy vision
pigmented.)
o Headache (mata naman talaga ung masakit, nagrerefer
 Macula for central vision
lang to the head)
 Retina for peripheral vision
o Nausea and vomiting
o Other conditions w/ CHERRY-RED SPOT
o Iridescent vision (halo of rainbow around light)
 Niemann-Pick DSE
o Mid-dilated pupil (5-6mm, normal is 3-4mm)
 Tay-sach’s syndrome
o Pag nasa ER sya tapos kukunan sya ng BP, they usually
 Sandhoff diseae
manage this patient as hypertension >_< but, since you
o The normal retina is transparent but it has red orange
attended the lecture, you should know better.
reflex (ROR) because of the REFLECTION of the
 How will you know na glaucoma?
CHOROID.
o Fundoscope – di pwede kasi you will further narrow the
o FOVEA has red orange reflex because of its blood supply
angles lalong tataas ung IOP
o Palpate!  tense eyeball  parang forehead (normally
 BLOOD SUPPLY OF RETINA:
firm sya tip of the nose.)
o 4 quadrants of the Inner RETINA – CRA (Central Retinal
 P.E.
Artery)  if BS is cut off ischemia  death  the
o Hazy cornea
ganglion cell layer is the most affected layer which is
o Non-reactive pupil
part of the nerve cell which does not regenerate.
o (N Pupil: 2-3mm) -> glaucoma, around 5-6mm dilated
o Outer RETINA – Choriocapillaries
o Penlight  mid?dilated, non reacting, non constricting
pupil
 CAUSE:
o Tense eyeball
o EMBOLUS (usually from the CAROTID ARTERY –
o Red eye  dt hyperemic vessles
ipsilateral)  can be a blood or a fat embolus
o Hard
o Thrombus
o Light reflex on the cornea looks like (normally round,
crisp, clear and no edges) in glaucoma, there are
 MANAGEMENT:

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 scattered bits and pieces of light because the cornea is whenever the pupil points to, kung may ___ doon, hindi
not clear and hazy kasi it is edematous yun foreign body, yun ung iris.
 PICTURE: Penetrating injury – fish hook O___O
 TREATMENT o Wag mo ng dalhin ung bait sa hospital, you cut it, pero
o Anti-glaucoma drugs Lowers IOP do not take out the hook
st
 Azetazolamine 1 line drugs o Can this still be saved? YES
o Laser iridectomy (“papillary plaque”) lowers IOP  PICTURE
 Definitive treatment URGENT
 Cut a portion of iris so that fluid can flow to INTRAOCULAR FOREIGN BODY
the cut part and drain to schlemm’s canal
o Trabeculoplasty – make filter for passage of fluid  Warrants a referral to a vitreoretinal surgeon
o Laser iridectomy and trabeculoplasty has the same  Do not TOUCH the eye
mechanism  you do a detour to bypass the flow and  Do not put pressure you might injure the eye
then you have another route for your aqueous flow.  Do not put OINTMENT
o Laser surgery – slit lamp  lens over the eye  use  Anterior tear drop shape + shallow chamber
laser to make a hole to the iris o IRIS is already touching the cornea
o Almost always with PERFORATION
 GLAUCOMA- increase IOP due to increase in production of o BROWN pigment extruding from the tear because
aqueous humor but decrease secretion represents the IRIS and CILIARY BODY are pigmented
st
o 1 thing to do is to decrease IOP  If with penetrating INJURY: put the patient on NPO for 8hours,
 Mannitol (20mg/kg, 10cc bolus then repeat start IV saline, then do SURGERY after 8 hours.
FAST DRIP)
 pilocarpine, steroids NON-URGENT
 timolol ORBITAL FLOOR FRACTURE
 acetazolamide (tablet)
 Results from collision
 OPTIC NERVE – most sensitive to INCREASE IOP o COUP/ direct (side)
o CONTRA-COUP / indirect (opposite the side) injury
RUPTURED OR LACERATED GLOBE  May present with PERIORBOTAL HEMATOMA (blackeye) 
resolves in 2-3 weeks
 Best left untouched until ophthalmologist arrives  You should rule out a BLOW-OUT fracture (FLOOR (weakest part
 Usually kasi, you usually, nasa OR ka, tapos, to prepare the  kasi, ung mga sinuses ung underneath nya, no solid support
patient, you have to put the patient on NPO for 8 hours to there, air lang nandun) usually ruptures)
prepare for general anesthesia  repair. o Do EOM, if the patient is unable to look up, the patient
 You have to place an eye shield (metal or plastic with holes in it - might have MUSCLE and FAT
hospital setting) or plastic/paper cup  bakit hindi patch or gauze
ung ginagamit?  para hindi madiinan, kasi pag diniinan mo, it  S/SX:
will aggravate the condition and maeexpress mo ung contents ng o Palpate mastoid, (+) crepitation
whole eyeball to protect the eye from the environment and the o Numbness of cheek because of the nerve entrapment
examiner. o Swelling around the eye
 Treatment
o Topical anesthetics  DIAGNOSIS
o Antibiotics o CT-scan
o Eye shield (for protection) should be initialized o X-ray
 Do not put pressure o Kasi you want to look at the indirect injury  what part
 If you do not have a shield get a paper cup and of the eye is the most vulnerable to indirect injury?
cut in cross wise, secure the bottom part with  The optic nerve
micropore/ tape.  If injured  loss of vision
 Diagnosis  PICTURE: other eye is looking straight and the other one is looking
o X-ray  ginagamit para malaman mo na walang foreign up, which one is the normal eye? Is the patient looking up? Why is
body. the other eye not looking up?
o CT-scan  ginagamit para malaman mo na walang o What makes the eye look up? Superior rectus and
foreign body. inferior oblique?
o B-scan ultrasound  di ginagawa kasi nilalagyan mo ng o When you have orbital fracture, di naglolook up yung
pressure pag nag uutz ka patient kasi nattrap sa floor ung muscle dahil sa
 PICTURE: Corneo-scleral laceration fracture, also, nattrap ung nerves that control the
o You have your limbus and your sclera, tapos may muscles tapos, there’s edema pa so, there is a lot of
ruptured globe, you can fix this but you will have to swelling underneath, tapos meron pang fat prolapse
undergo a wound exploration there so, everything is tight so, yung mga muscles, they
 PICTURE: Ruptured globe secondary to cannot move
o Pink/peaked??? pupil, there is a wound that proplapsed
out  a very good clue for globe perforation and

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  MANAGEMENT o Rust ring is hard to remove, it can stay in place because
o Wait for the inflammation to subside after few days it will drop on its own
o If inflammation subsides you can defer the surgery.  TREATMENT
o If it subsides but with double vision and the patient o Removal of foreign body under slit lamp
cannot look up then do surgery o Can be removed with with a spray of water and cotton
edges? but if you will be removing embedded foreign
CONJUNCTIVAL HEMORRHAGE body, like ung natalsikan ng apoy ng welding, then, you
have to use an instrument like your PV?? Syringe
 More likely to be subconjunctivalBetween the sclera and eyelid o Use anesthetic
o You have to watch out for your hyphema  blood in o Use topical antibiotic and corneal wound healing agents
your anterior chamber o Eye patch
 Very easy to manage kasi parang pasa lang sya. So how do you  If <10mm, put gauze, then press, and secure
manage? with micropore tape
o Warm compress  >10mm- DON’T PUT A PATCH because it can
o Even if you don’t do anything, the bruise will go away delay the healing. The normal blinking can
 It will resolve without treatment in 2-3weeks  just assure the facilitate healing though painful. Patch may
patient aggravate the infection
 It is correlated with TRAUMA
 Can be spontaneous  RETINAL DETACHEMENT
o If + weak vessel that suddenly rupture (seen in smokers) o Common symptom: kurtinang itim na bumababa
o After straining (coughing, sneezing, lifting heavy objects) o When you have a patient na yung complaint nya, is “I
 If it happened for the first time: it does not WARRANT medical could see half of your face or half of your body but not
treatment the lower part or I could see the lower part but not the
 If it happened repeatedly: do PT, PTT upper part”

LID LACERATION BOOK

INTRODUCTION
 Repaired by an ophthalmologist or an oculoplastic surgeon
 reapposition of anatomic detailed anatomic structures are  Prompt recognition and treatment of ophthalmic emergencies are
important for normal functioning. like your lid to lid margin. crucial to prevention of unnecessary visual impairment
You can do reapposition if the laceration involves only the skin  Important parameters:
 If it involves the lid margin or pag full thickness sya and involves o Intensity and duration of pain
the canaliculi, better refer to an ophthalmologist o Rapidity of onset and severity of visual loss
o Pag di mo nirepair ito, you will get tearing, so luha ng  Primarily assessed by:
luha tong patient na to.  Visual acuity  measured for each
 Avoid aggressive suturing (prolene or nylon) eye in all patients with ophthalmic
o 10-O nylon/ prolene  thinner than your hair emergencies
o Usually, use very fine sutures o Gross appearance of the globe
o Abnormalities on ophthalmoscopy
 TREATMENT  Ophthalmic emergencies are group according to their
o Surgical repair predominant symptom
o Antibiotics o Acute red eye
o Pain relievers o Acute orbital disease
o Anti-TETANUS o Acute painless visual loss
o Acute painful visual loss without a redeye
CANNALICULAR LACERATION o Double vision and eye movement abnormalities
o Pupil abnormalities
 Realign the inferior cannaliculi, where tear drains out o Bilateral optic disk swelling
 CANNALICULAR REPAIR
ACUTE RED EYE
CORNEAL ABRASIONS / FOREIGN BODIES
 MAJORITY: BENIGN little or no threat to vision
 Red eye with pain o Bacterial, viral, allergic conjunctivitis
 DIAGNOSIS o Subconjunctival hemorrhage
o Biomicroscopy o Blepharitis
o Fuorescein dye test  With risk of rapid progression (within a few hours or days) to
 Epithelial violation or if not intact it will severe visual impairment, even blindness
fluoresce under COBALT o Acute angle closure glaucoma
 FIRST THING TO DO o Intraocular infection (endophthalmitis)
o Anesthetize o Bacterial, viral, amoebic, or fungal corneal infection
o Use tuberculin syringe to remove foreign body o Acute uveitis
o Scleritis

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  Blepharitis
TRIAGE o Bluish redness (violaceous discoloration) of the globe
 Best identified in natural light
 Emergency or urgent ophthalmic evaluation in patients with:  Characteristic of scleritis
o A history (within the past few weeks) of intraocular o Vesicles or ulceration of the lids or periocular skin
surgery  Ophthalmic zoster (shingles)
 Predisposes to endophthalmitis  Less commonly
o Contact lens wear  Varicella
 Predisposes to corneal infection  Primary herpes simplex virus
o Recent or distant corneal transplantation infection
 Because of the possibility of graft rejection  Conjunctivitis
o Previous episodes of acute uveitis or scleritis such as o Usually causes purulent, mucoid or watery discharge
ankylosing spondylitis and rheumatoid arthritis  Allergic conjunctivitis
o In acutely ill patients o Typically causes itching
 Particularly with sepsis or  Conjunctivitis with profuse, purulent discharge
 Requiring prolonged intravenous cannulation o Characteristic of gonococcal conjunctivitis
such as intensive therapy units or for o Requires emergency treatment
parenteral nutrition
 Acute red eye due to bacterial or fungal  Any abnormality of the cornea on apparent gross examination
endophthalmitis such as:
o Ocular involvement in toxic epidermal necrolysis, o Ulceration
Stevens-Johnson syndrome or erythema multiforme o Focal opacity
 Pain, rather than discomfort should be regarded as inconsistent  May be due to infection or
with :  Diffuse cloudiness
o Conjunctivitis  May be due to markedly elevated
o Episclerits or intraocular pressure when
o Blepharitis associated with a semi-dilated
 Pain is suggestive of: unreactive pupil
o Keratitis  Warrants emergency ophthalmic
o Intraocular or scleral inflammation assessment unless it is known to be
o Elevated intraocular pressure longstanding, eg. pterygium
o *with the likelihood of serious cause increasing with  Instillation of fluorescein facilitates identification of an epithelial
increasing severity defect including
 Pain associated with nausea and vomiting o Dendritic ulceration due to herpes simplex virus keratitis
o Suggestive of markedly elevated intraocular pressure  A constricted pupil
 Deep boring pain, typically waking the patient at night o Suggestive of intraocular inflammation
o Characteristic of scleritis o Typically due to anterior uveitis
 Photophobia  Hypopyon  necessitates emergency ophthalmic assessment
o Characteristically occurs with keratitis and anterior o Pus within anterior chamber
uveitis o Feature of:
 Corneal infection
 Reduced vision in the absence of a pre-existing explanation is  Intraocular infection
inconsistent with:  Acute anterior uveitis (iritis)
o Conjunctivitis CLINICAL ASSESSMENT
o Episcleritis
o Blepharitis  Slitlamp examination
o Facilitates assessment of distribution of redness
o Identification of conjunctival abnormalities including:
 Severity of redness is not necessarily a guide to the seriousness of  Examination of the superior tarsal conjunctiva
the underlying condition following eversion of the upper eyelid
o Subconjunctival hemorrhage  bright red in color, o Diagnosis of episcleritis and scleritis
benign o Characterization of corneal lesions
 Distribution of redness is helpful o Detection of corneal keratic precipitates, anterior
o Redness predominating around the limbus chamber flare and cells and possibly hypopyon
(circumcorneal) indicative of anterior chamber inflammation due to
 Indicative of intraocular disease anterior uveitis, intraocular infection, or secondary to
o Diffuse redness involving the tarsal and bulbar corneal inflammation, including infection
conjunctiva  Dilated fundal examination
 Indicative of conjunctivitis o Used in cases of intraocular inflammation
o Focal or diffuse redness of the globe o Is essential to determine whether there is involvement
 Consistent with episcleritis of the vitreous, retina, or choroir which is important to
o Redness of the eyelid margins the diagnosis as well as the assessment of the severity.

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 MANAGEMENT  Acute angle closure glaucoma
o Prompt recognition and treatment are required if severe
 Acute conjunctivitis visual loss is to be avoided
o Most cases, benign, often self-limiting condition o Mainstay of initial treatment
 Care needs to be exercised in:  Intravenous and oral acetazolamide
o Neonates (ophthalmia neonatorum)  Topical agents  reduce intraocular pressure
 Because of the possibility of infection with  Supplemented by topical steroids  reduce
chlamydia which may be associated with non inflammation
ocular disease and needs systemic therapy  Topical pilocarpine constrict pupil
o Gonococcus or herpes simplex virus o Definitive treatment
 May be associated with encephalitis and  Laser peripheral iridotomy with prophylactic
requires hospitalization and parenteral treatment of the fellow eye
antiviral therapy o Emergency ophthalmic assessment is essential to
o Gonococcal conjunctivitis in neonates and adults establish the diagnosis, including exclusion of other
 Characteristically causing a purulent discharge causes.
as well severe conjunctival inflammation ACUTE ORBITAL DISEASE
 Necessitates emergency investigation by TRIAGE
microscopy and culture of the discharge
 Parenteral antibiotic therapy with ceftriaxone  Orbital cellulitis
to avoid progression to severe corneal o Usually a disease of childhood
damage o Due to spread of infection from the ethmoid sinuses
o Ophthalmic zoster (shingles) o Characterized by fever, pain, eyelid swelling and
 Parenteral antiviral therapy within 72 hours of erythema, proptosis, limitation of extraocular
the appearance of the rash reduces the movements, and systemic upset with leukocytosis
likelihood of the complications  Pre-septal cellulitis
 Huchinson’s sign o There is no proptosis or limitation of eye movement
 Skin lesions on the tip of the nose or o Due to a localized infection of the anteriour (pre-septal)
eyelid margins portion of the eyelid or may be the early manifestation
o Predictive of ocular of orbital cellulitis.
complications  In adolescents and young adults
 Acute keratitis o Orbital signs may be indicative of extension of infection
o Revolves around identification and treatment of from the fronto-ethmoidal sinus coplex
infection  In diabetics and immunocompromised
o Predisposing factors o Acute orbital disease may be due to fungal infection
 Contact lens wear (mucormycosis) with a high risk of death even with early
 Preexisting ocular surface disease treatment.
 Corneal anesthesia or exposure  Autoimmune hyperthyroidism (Grave’s disease)
o Occasionally, there is apparent straightaway that there o May lead to marked proptosis with the possibility of
is a non infectious inflammatory process, requiring corneal exposure or optic nerve compression and
other therapy, possibly topical or systemic steroids but limitation of eye movements
steroid therapy should not be started w/o ophthalmic  Pseudotumor
assessment. o Inflammatory orbital disease
 Acute intraocular inflammation (uveitis)  Carotid artery cavernous sinus fistula
o Revolves around identification and treatment of o Due to dural shunts that typically occur in patients with
infection particularly if there is: diabetes and /or systemic hypertension, or due to
 Posterior segment involvement spontaneous rupture of an intracavernous internal
 Vitritis carotid artery aneurysm, may present in a similar
 Retinitis manner.
 Choroiditis CLINICAL ASSESSMENT
 Recent history of intraocular surgery
 Non infectious inflammatory process is nore  Optic nerve dysfunction
common than in acute keratitis o Reduced vision unexplained by corneal exposure
o Topical or systemic steroid therapy o Especially if associated with impaired color vision and/or
 Should not be started without ophthalmic a relative afferent pupillary defect
assessment.  Non-axial proptosis
 Scleritis o If present in orbital cellulitis  implies abscess
o Infrequently caused by infection formation
o Autoimmune disease is commonly responsible  Other compliations
o Managed in the first instance by: o Cavernous sinus thrombosis
 Oral NSAIDS o Intracranial infection
 But ophthalmic assessment is necessary to  More likely if there is infection in the frontal
make diagnosis and exclude other entities sinus

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 MANAGEMENT  Patients aged 55 or older with acute or subacute unilateral central
visual loss, particularly if associated with distortion of images
 Orbital cellulitis o Should be assumed to have a neovascular related
o Clinical diagnosis macular degeneration unless another cause is apparent
o Requires hospitalization and immediate institution of o Urgent ophthalmic referral is arranged
antibiotic therapy, usually intravenously, together with  Abrupt onset of visual loss
early ophthalmic and otolaryngologic assessment o Very suggestive of an arterial vascular event
o Orbital imaging  Full recovery after a short period of impairment
 Taken in all cases o Suggestive of an embolic arterial event
 Reserved for those in whom orbital abscess or  Ask all patients with possible ocular vascular disease about the
another complication is suspected presence of vascular risk factors like:
 Usually by CT but possibly MRI, o Diabetes mellitus
 Is generally sufficient to o Systemic hypertension
differentiate between o Hyperlipidemia
o Graves opthalmopathy  Patients aged 55 or older with suspected arterial disease
o Orbital pseudotumor o Must be questioned about symptoms of giant cell
o Carotid artery-cavernous arteritis
sinus fistula o Check their ESR and CRP
 Orbital  Opthalmoscopy
ultrasound blood o Often provides the diagnosis of acute painless visual loss
flow studies is o Vitreous hemorrhage or retinal detachement
helpful  Lack of a red reflex with abnormal or absent
view of the retina
ACUTE PAINLESS VISUAL LOSS  Urgent or emergency ophthalmic referral is
required
 Sudden onset painless visual loss o Central or branch retinal vein occlusion
o Is a very important symptom  Widespread or sectoral retinal hemorrhages
o May be due to ophthalmic disease that requires  Urgent ophthalmic assessment is indicated
emergency or urgent treatment o Central retinal artery occlusion
o Ocular vascular disease with immediate or early threat  Widespread retinal whitening with a cherry
to the patient’s life or remaining vision red spot
o Acute intracranial disease  Emergency ophthalmic assessment must be
arranged
TRIAGE  Giant cell arteritis and embolic disease needs
to be excluded
 It is essential to determine whether the reported visual loss o Branch retinal artery occlusion
involves one or both eyes  Sectoral retinal artery whitening
 Distinguish monocular visual loss from loss of vision to one side in  Urgent ophthalmic assessment is important to
both eyes ie, homonymous hemianopia confirm diagnosis
o Ask the patient to close one eye and then the other  Prompt investigation of embolic disease needs
 Monocular visual loss to be undertaken.
o Indicates disease of the glove or optic nerve o Anterior ischemic optic neuropathy
 Bilateral visual loss  Optic disk swelling in an eye with recent acute
o Including homonymous hemianopia, indicates a lesion or subacute visual loss
at or posterior to the optic chiasm  Giant cell arteritis must be excluded in
 It is also essential to determine whether the visual loss is of recent patients aged 55 or over
onset or whether it has been longstanding and only recently
identified
 Retinal detachement CLINICAL ASSESSMENT
o (+) history of recent onset of black spots or shapes
(floaters) with flashing lights (photopsia) followed by a  Clarify whether the visual loss is monocular or binocular
field defect progressing upwards from below in one eye o Review the history
 Preservation of good central vision , implying that the central o Assess the visual acuity
retina (macula) has not yet detached, warrants emergency o Assess the visual field
ophthalmic referral,  Confrontation test
 Vitreous hemorrhage  Perimetry
o Sudden onset of floaters  Detection of bilateral visual field loss, including abnormality in a
o Main causes: subjectively unaffected fellow eye, may establish that the disease
 Retinal tear process involves the optic chiasm when there is bitemporal
 Proliferative retinopathy due to diabetes or hemianopia or a temporal hemianopia in the subjectively
retinal vein occlusion unaffected fellow eye or the retrochiasmal visual pathways when
there is homonymous hemianopia

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  Important in detection of optic nerve disease ACUTE PAINFUL VISUAL LOSS WITHOUT A RED EYE
o Assessment of color vision
o Pupillary reaction to light  Most of the time, they are retrobulbar in location
 Particularly looking for a relative afferent
pupillary defect TRIAGE
 Fundal examination following pupillary dilatation
o Best means of diagnosing:  Causes of optic neuritis
 retinal tears with or without retinal o Acute demyelinative optic neuropathy – MC
detachment,  Associated with multiple sclerosis, occurring
 Vitreous hemorrhage and its cause if the as the initial manifestation or part of a
hemorrhage is not too dense subsequent relapse
 Otherwise, ultrasound examination  Characteristically presents as subacute
is necessary monocular visual loss with peri- or retro-
 Age related macular degeneration ocular discomfort exacerbated by eye
 Including whether it has features of movements
the neovascular stage  Pituitary apoplexy
 Retinal vein or artery occlusion o Usually due to a hemorrhagic infarction of a pituitary
 And anterior ischemic optic neuropathy tumor
o Normal in giant cell arteritis when the visual loss is due o Rare but requires prompt recognition and treatment to
to choroidal ischemia or posterior ischemic neuropathy reduce risk of severe morbidity , possibly death, as well
as severe visual loss, possibly complete blindness
MANAGEMENT o Characteristically presents with suddne onset of
headache, unilateral or bilateral visual loss, sometimes
 Retina detachment impaired eye movements , and metabolic and
o Treated surgically circulatory derangement due to pituitary failure,
o With urgency primarily being determined whether the resulting in adrenal insufficiency
macula is detached but also the underlying cause  Sphenoid sinusitis
 Vitreous hemorrhage o Presents with headache typically localized to the vertex
o Treatment determined by the underlying cause and acute unilateral or bilateral visual loss
 Neovascular age-related macular degeneration  Diagnosis of posterior scleritis
o Standard treatment: repeated intravitreal injection of o Often delayed because of the frequent lack of specific
inhibitors of VEGF diagnostic features, including absence of apparent
 There is debate about the role of carotid endarterectomy in inflammation of the globe to suggest an inflammatory
patients with ocular TIAs due to carotid artery stenosis, but all condition
patients with transient monocular visual loss (amaurosis fugax)
likely to be due to retinal emboli should undergo investigations CLINICAL ASSESSMENT
for carotid and cardiac sourges
 Transient visual loss can also be due to:  Acute demyelinative optic neuropathy
o Giant cell arteritis or o There are features of optic nerve dysfunction
o Optic disk swelling due to raised ICP  Impaired color vision
 No treatment in the acute stage is established to alter visual  Visual field loss
outcome in central or branch retinal vein occlusion  A relative afferent pupillary defect
o Effective for long term complications o With progression of visual loss over a few days
 Intravitreal injections of VEGF inhibitors o Usually no opthalmoscopic abnormality
 Triamcinolone o With mild optic disk swelling in 1/3 of cases
 Retinal laser photocoagulation  Ophthalmic manifestations of pituitary apoplexy
 Various surgical techniques o Unilateral or bilateral, often severe visual loss
 Intra-arterial thrombolytic therapy o Impaired pupillary light reactions
o Advocated in the acute stage of CRAO o Sometimes impaired eye movements (external
o Evidence for their usefulness is lacking opthalmoplegia) due to ocular motor cranial nerve
 No treatment in the acute stage is established to alter the visual palsies
outcome in anterior ischemic optic neuropathy o Normal or pale optic disk depending upon whether the
 Failure to treat promptly could rapidly lead to complete bilateral pituitary tumor previously caused anterior visual
blindness pathway compression
o Giant cell arteritis causing anterior ischemic optic  Sphenoid sinusitis
neuropathy o Visual loss has features of optic nerve dysfunction
o CRAO o With normal or pale optic disks depending upon
 Emergency imaging and appropriate management  involves whether there has been chronic optic nerve
neurology or neurosurgery referral if there is compression from a pre-existing sphenoid sinus
o Sudden visual loss due to optic chiasmal or mucocele
o Retro chiasmal disease  Clinical signs in posterior scleritis
o Proptosis

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 o Limitation of eye movements  It is likely to be due to:
o Induced refractive error  Refractive error
o Choroidal folds  Lens opacity
o Fundal mass  Possibly macular disease
o Serious retinal detachement  Unless there are features that
o Optic disk swelling implicate cerebral disease, multiple
o Ultrasound is the best diagnostic test images on monocular viewing can
be assumed not to be due to
MANAGEMENT intracranial disease.
 You need to establish how long the double vision has been
 Acute demyelinative optic neuropathy noticed and whether there has been change in the pattern as
o In most cases, vision recovers spontaneously judged by direction of separation of images and the directions of
o Management centers on investigation of the likelihood gaze in which double vision has been present or severity as judged
of multiple sclerosis and the need for disease modifying by the distance separating the two images
therapy  Establish whether the double vision can be overcome with
o Exclude other entities that require urgent treatment voluntary effort
 Pituitary apoplexy o Implies a longstanding abnormality that has become
o An endocrine and neurosurgical emergency more difficult to overcome (decompensated
o Patient may require emergency resuscitation  Ocular motor cranial nerve palsy
o IV hydrocortisone should be given to all patients prior to o it is essential to determine whether it is isolated or part
investigation with MRI or CT if the patient’s condition is of multiple cranial nerve dysfunction
unstable o assess the trigeminal nerve as well as the optic nerve
o Urgent neurosurgery is frequently required, particularly function to provide anatomical localization of the
in patients with visual loss disease process and as a guide to the likelihood of a
 Sphenoid sinusitis causing visual loss serious underlying condition
o Requires surgical drainage as well as antibiotic therapy o presence of pupillary dysfunction
 Posterior scleritis  either anisocoria or a particularly and
o May respond to oral NSAIDS but oral steroid therapy impaired response to light
may be required  provides an important clue to the possibility of
a compressive lesion such as a posterior
DOUBLE VISION AND EYE MOVEMENT ABNORMALITIES communicating artery aneurysm.
TRIAGE  Severe pain
o Another important clue to the presence of an aneurysm
 In oculomotor ( third cranial) nerve palsy o May also occur in pituitary apoplexy
o There may be clues from associated ptosis or pupillary  Specific eye movement abnormalities provide precise anatomical
abnormality localization
 Unless the pattern of double vision reported by the patient or the  Internuclear opthalmoplegia
examination of the range of eye movements quickly leads to o Impairment of adduction of one or both eyes
identification of a specific entity such as an abducens nerve o Localizes to the medial longitudinal fasciculus within the
(lateral rectus) palsy, the non ophthalmologist will derive more brainstem
useful guidance to the urgency from information about the  Horizontal gaze palsy
features such as whether there is also impairment of vision, o There is loss of conjugate horizontal gaze to one or both
orbital signs such as lid swelling or proptosis, periocular pain or sides
headache, non-ocular neurologic abnormalities, or systemic o Localizes to the pons
illness.  Vertical gaze palsy
 Patients with multiple cranial nerve palsies or other neurologic o Localizes to the midbrain
features, severe headache, associated systemic illness or age  Myasthenia gravis
under 50 with single or multiple cranial nerve palsy are most o Variability of double vision during or between episodes
likely to have a serious underlying condition o With increasing severity with fatigue that may also
manifest as increasing ptosis
CLINICAL ASSESSMENT
MANAGEMENT
 Double vision
o Usually due to ocular misalignment  Isolated motor cranial nerve palsy in patients over 50
o First step in evaluation is to determine whether it is o Due to ischemic microvascular disease
monocular or binocular  Requires little investigation apart from
o Monocular exclusion of giant cell arteritis
 If double vision is present when the patient is  And review of vascular risk factors in which
viewing with only one eye, whether it is just spontaneous recovery is the rule
with one eye or with each eye alone, the  Isolated oculomotor nerve palsy suspicion of posterior
visual disturbance is not due to ocular communicating artery aneurysm due to pupillary involverment,
misalignment severity of pain, or age under 50

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 o Necessitates emergency imaging o **to avoid unnecessary investigations and ophthalmic
o Outcome being much better if treatment can be entities such as acute angle closure glaucoma , to direct
undertaken prior to subarachnoid hemorrhage due to management
aneurysm rupture  Tonic pupil
 Multiple cranial nerve dysfunction o May be identified by the delayed dilation following near
o Requires urgent investigation, usually guided primarily response from which it derives its name;
by a neurologist o Abnormal spiraling movements (vermiform)
 Management of orbital disease usually depends upon the movements of the iris when constricting to a light
outcome of imaging with CT or MRI stimulus
 When clinical evaluation suggests decompensation of a  Best seen on slitlamp examination or
longstanding abnormality, such as a congenital superior oblique  Constriction of dilute (0.125%) pilocarpine eye
(trochlear) palsy drops
o Further investigation may not be required  Pharmacological mydriasis
o Initial treatment will be with prisms o Characterized by lack of pupil constriction to bright light
 In any patient with suspected myasthenia gravis and standard strength (2%) pilocarpine eye drops
o It is important to establish whether there is a non-ocular
weakness suggesting generalized disease BILATERAL OPTIC DISK SWELLING
 Especially impairment of breathing or
swallowing for which emergency neurologic  Causes of optic disk swelling (usually unilateral)
assessment is essential. o Inflammatory
o Ischemic
PUPIL ABNORMALITIES o Optic neuropathy
TRIAGE o Central retinal vein occlusion
o Uveitis
 Acute isolated, dilated unreactive pupil in an otherwise well o Posterior scleritis
individual o Intraorbital optic nerve compression
o Rarely due to a serious underlying condition  Bilateral optic disk swelling
o Likely possibilities being: o Characteristic feature of:
 the benign entity of tonic pupil  Raised intracranial pressure
 pharmacological mydriasis from accidental  Malignant (accelerated) systemic
ocular inoculation with anticholinergic agent hypertension
in travel sickness medication o **both requiring emergency or urgent investigation and
 Isolated dilated, unreactive pupil in a patient with depressed treatment
conscious level due to head injury or other acute intracranial
disease is an ominous sign TRIAGE
o Suggestive of tentorial herniation
 Pupil involvement in oculomotor nerve palsy  Papillededema
o Important clue to the possibility of a compressive lesion, o Optic disk swelling due to raised ICP
including posterior communicating artery aneurysm o Usually identified as a part of examination of a patent
 Miosis with ptosis with neurological sx,ie headache.
o Characteristic of horners syndrome o Identified incidentally during routine opthometric
 Acute, painful horner’s syndrome, possibly following neck trauma examination
o Requires urgent exclusion of carotid dissection o Requires urgent head imaging to exclude intracranial
 Pupillary light-near dissociation mass lesion.
o Impaired pupillary constriction to light with better o Blood pressure should be checked even in a child
constriction to near CLINICAL ASSESSMENT
o Traditionally associated with CNS syphilis (Argyll  When abnormalities are florid, recognition is straightforward
Robertson pupils)  If the abnormalities are less marked, ophthalmological
o Can be due to midbrain dysfunction, typically assessment is crucial to identify:
compression from a pineal tumor or dilated third o Myelinated nerve fibers
ventricle in hydrocephalus, when usually there is also o Optic nerve head drusen
impairment of vertical eye movements o Congenitally small and crowded optic disks
(pseudopapilledema)
CLINICAL ASSESSMENT  ***so that unnecessary investigations and anxiety can be avoided
 Assessment of visual field is a crucial guide to urgency of
 Ophthalmologists role is to: treatment
o Confirm suspected diagnosis of oculomotor nerve palsy  Malignant hypertension
or horner syndrome o Optic disk swelling is usually accompanied by retinal and
o Identification of benign entities choroidal abnormalities
 Tonic pupil o An indication for urgent reduction of BP precipitous
 Pharmacological mydriasis reduction should be avoided to reduce risk of optic
nerve infarction.

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 OPHTHALMOLOGY | 2022
1
MIDTERMS CANVAS
Please use at your own risk
EYE EMER G EN CIES ( CAN VAS 2022) AS LEEP DU R IN G TH E PR OCEDU R E. TH E R EPAIR OF THE
G LOB E DEPEN DS ON TH E LOCATION AN D EXTEN T OF
1. Cherry-red spot on the macula, except
IN JU R IES .
a. Retinitis Pigmentosa
b. BRVO 5. Seidel’s test is
c. Sandhoff disease a. Used to test dry eyes
d. CRAO b. Used to assess the presence of anterior
chamber leakage in the cornea
CH ER R Y - R ED S POT ( CR S ) AT TH E MACU LA IS A CLIN ICALLY c. Used to test for scotomas
S IG N IF ICAN T S IG N OB S ER VED ON F U N DU S EXAMIN ATION
d. Used to check for angle closure
IN A VAR IETY OF PATH OLOG ICAL CON DITION S,
IN CLU DIN G R ETIN AL IN F AR CTION , R ETIN AL IS CH EMIA. AS TH E S EIDEL TES T AS S ES S ES F OR TH E PR ES EN CE OF
W ELL AS A VAR IETY OF LYS OS OMAL S TOR AGE AQU EOU S H U MOR LEAKAG E F R OM TH E AN TER IOR
DIS OR DER S . CH AMB ER .
DIS OR DER S : 6. Patient is a farmer and pricked his eye with a wooden
CEN TR AL R ETIN AL AR TER Y OCCLU S ION ( CR AO) stick. The following medications are safe to give for
G M1 G AN G LIODOS IS TYPE 1 ( LAN DIN G DIS EAS E) treatment, except
G M2 G AN G LIODOS IS TYPE 2 ( S AN DH OF F DIS EAS E) a. Moxifloxacin
N IEMAN N - PICK DIS EAS E b. Prednisone Forte
TAY - S ACH S DIS EAS E c. Tobramycin
F AR B ER DIS EAS E d. Eye lubricant
G ALACTOS IALIDOS IS ( G OLDB ER G COTLIER S YN DR OME) TH E U S E OF S TER OIDS CAN LEAD TO S IG N IF ICANT
B R AN CH R ETIN AL VEIN OCCLU S ION ( B R VO) OCU LAR S IDE EF F ECTS . IN TR AOCU LAR PR ES S U R E ( IOP)
2. Acute glaucoma can present as the following: ELEVATION F OLLOW IN G S TER OID U S E IS W ELL-
a. Eye discharge DOCU MEN TED. ( TAG ALOG : S IN CE TH IS IS AN EXAMPLE
b. Sudden painless visual loss OF B LU N T TR AU MA, CON TR AIN DICATED AN G S TER OIDS
c. Positive RAPD LIKE PR EDN IS ON E, KAS I KAPAG MAY B LU N T TR AU MA TO
d. Iridescent vision TH E G LOB E N AG KAKAR OON N G TR ANS IENT B UT S EVERE
S IG N S OF A CU TE AN G LE CLOS U R E G LAU COMA: INCR EAS E IN IOP¸ AT IEEXACER B ATE LAN G YU N NI
COR N EAL EDEMA - > IR IDES CE N T V IS ION PR EDN IS ON E S A CAS E N A TO. )
DEEP CON JU N CTIVAL H YPER EMIA 7. Retinal detachment presents with
N AR R OW DR AIN AG E AN G LE a. Acute painful visual loss
S H ALLOW AN TER IOR CH AMB ER b. lagophthalmos
H IG H IN T R AOCU LAR PR ES S U RE c. IOP of 5 mmHg
d. exophthalmos
S U DDEN PAIN LES S V IS U AL LOS S – R ETIN AL VEIN R ETIN AL DETACH MEN T IS TH E S EPAR ATION OF THE
OCCLU S ION S EN S OR Y R ETIN A ( IE, TH E PH OTOR ECEPTOR S AN D INNER
POS ITIVE R APD - DIF F ER EN CES B ETW EEN TH E TW O EYES R ETIN AL LAYER S ) F R OM TH E U N DER LYIN G R PE. TH ERE
IN TH E AF F ER EN T PATH W AY DU E TO R ETIN AL OR OPTIC AR E TH R EE MAIN TYPES : R H EG MATOG EN OU S , TR ACTION,
N ER VE DIS EAS E AN D EXU DATIVE ( S ER OU S ) , W H ICH MAY BE
3. Management of acute glaucoma, except H EMOR R H AG IC. TYPICALLY, R ETIN AL DETACH MEN T IS
a. Steroids AS S OCIATED W ITH LOW IOP, AS A R ES U LT OF IN CR EASED
b. Laser iridectomy OU TF LOW B Y ACTIVE PU MPIN G OF F LU ID TH R OU GH THE
c. Anti-glaucoma medication EXPOS ED R ETIN AL PIG MEN T EPITH ELIU M. IN S CH W AR TZ -
d. Trabeculoplasty MATS U O S YN DR OME ( ALS O R EF ER R ED TO AS
S TER OID- IN DU CED OCU LAR H YPER TEN S ION W AS "S CH W AR TZ ' S S YN DR OME") TH E OPPOS ITE IS OB S ER VED
R EPOR TED IN 1950, W H EN LON G - TER M U S E OF S YS TEMIC W ITH ELEVATED IOP.
S TER OID W AS S H OW N TO IN CR EAS E TH E IN TR AOCU LAR
PR ES S U R E ( IOP) . CH R ON IC ADMIN IS TR ATION OF
S TER OIDS IN AN Y F OR M W ITH R AIS ED IOP CAN CAU SE
OPTIC N EU R OPATH Y R ES U LTIN G IN S TER OID - IN DU CED
G LAU COMA.
4. Management for lacerated and ruptured globe
a. Give steroids
b. Give topical anesthetics
c. Do not put eye shields
d. Suture immediately
A R U PTU R ED G LOB E S H OU LD B E R EPAIR ED TH R OUGH
S U R G ER Y AS S OON AS POS S IB LE TO PR EVEN T S ER IOUS
COMPLICATION S . S U R G ICAL R EPAIR IS TYPICALLY DON E
U N DER G EN ER AL AN ES TH ESIA. TH IS MEAN S YOU W ILL BE

L
 OPHTHALMOLOGY | 2022
2
MIDTERMS CANVAS
Please use at your own risk
8. In lid lacerations, this/these should be included in
medications
a. Mefenamic acid
b. all of the choices
c. tetanus toxoid
d. tobramycin + dexamethasone eye ointment
EYELID LACER ATION S AR E MAN AG ED DIF F ER EN TLY
DEPEN DIN G ON TH E DEPTH , W IDTH , AN D LOCATION OF
TH E IN JU R Y. W ITH E YELID TR AU MA, TETAN U S S TATUS
S H OU LD B E AS CER TAIN ED.
MEF EN AMIC ACID – N S AID
TOB R AMYCIN + DEXAMETH AS ON E – AN TIB IOTIC, AN TI-
IN F LAMMATOR Y
9. This step in the ocular examination may be deferred if
globe rupture is suspected:
a. Extra ocular muscle movement test
b. Visual acuity
c. Tonometry
d. Direct fundoscopy
ON CE T H E DIAG N OS IS OF A R U PTU R ED G LOB E IS MADE,
F U R TH ER EXAMIN ATION S H OU LD B E DEF ER R ED U N TIL
TH E TIME OF S U R G ICAL R EPAIR IN TH E OPER ATING
R OOM. CON S IDER DIAG N OS IS VIA PEN LIG H T EXAM. S LIT
LAMP F IN DIN G S DES CR IB ED B ELOW , B U T CR U CIAL TO
AVOID AN Y PR ES S U R E ON EYE, W H ICH R IS KS EXTR U SION
OF IN TR AOCU LAR CON TEN TS .
N O PR ES S U R E MU S T B E APPLIED TO TH E G LOB E DU R IN G
EVALU ATION ; TH IS MEAN S TON OMETR Y AN D EVER S ION
OF TH E LIDS S H OU LD N OT B E PAR T OF TH E IN ITIAL
AS S ES S MEN T.
10. What clinical finding is not seen in a patient with orbital
floor fracture?
a. Ecchymosis
b. Diplopia
c. Hypesthesia
d. Exophthalmos
CLIN ICAL F IN DIN G S IN OR B ITAL F LOOR F R ACTU R E:
• DIPLOPIA
• VAR IAB LE ECCH YMOS IS
• S U B CU TAN EOU S EMPH YS EMA
• IN F AOR B ITAL N ER VE AN ES TH ESIA
• EN OPH TH ALMOS
• OCU LAR DAMAG E