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

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

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

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

Silence will fall when the question

Page 1 of 10
is asked.
 ACID
Coagulation Necrosis
Superficial Eschar
Prevents deeper penetration
More severe in the
STOMACH
Coagulation forms a barrier,
its temporary but somehow
slows the spread of chemical
ALKALI
liquefaction Necrosislyses
the tissues faster
More SEVERE
Penetrate more rapidly
Extends thru submucosa ,
esophagus tends to be more
RESISTANT to acid burn
Eats up the eye FASTER.
When you liquefy the soft
tissue you facilitate the
penetration FASTER
o Brown Bagging
 Make patient breath from the BROWN bag w/
nose and mouth covered  INCREASE CO2
inhalation CO2 dilate the blood vessels 
Dislodge the EMBOLUS
o Lowering of IOP with anti-glaucoma medications
(normal IOP is 10 – 20 mmHg)
 mannitol (diuretics)
 azetozolamide
 when you have pressure, everything inside is
masikip, so, when you release the pressure,
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
v.vascular) 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:

Silence will fall when the question

is asked Page 2 of 10
 scattered bits and pieces of light because the cornea is
not clear and hazy kasi it is edematous
 TREATMENT
o Anti-glaucoma drugs Lowers IOP
st
 Azetazolamine 1 line drugs
o Laser iridectomy (“papillary plaque”) lowers IOP
 Definitive treatment
 Cut a portion of iris so that fluid can flow to
the cut part and drain to schlemm’s canal
o Trabeculoplasty – make filter for passage of fluid
o Laser iridectomy and trabeculoplasty has the same
mechanism  you do a detour to bypass the flow and
then you have another route for your aqueous flow.
o Laser surgery – slit lamp  lens over the eye  use
laser to make a hole to the iris
 GLAUCOMA- increase IOP due to increase in production of
aqueous humor but decrease secretion
st
o 1 thing to do is to decrease IOP
 Mannitol (20mg/kg, 10cc bolus then repeat
FAST DRIP)
 pilocarpine, steroids
 timolol
 acetazolamide (tablet)
 OPTIC NERVE – most sensitive to INCREASE IOP
RUPTURED OR LACERATED GLOBE
 Best left untouched until ophthalmologist arrives
 Usually kasi, you usually, nasa OR ka, tapos, to prepare the
patient, you have to put the patient on NPO for 8 hours to
prepare for general anesthesia  repair.
 You have to place an eye shield (metal or plastic with holes in it -
hospital setting) or plastic/paper cup  bakit hindi patch or gauze
ung ginagamit?  para hindi madiinan, kasi pag diniinan mo, it
will aggravate the condition and maeexpress mo ung contents ng
whole eyeball to protect the eye from the environment and the
examiner.
 Treatment
o Topical anesthetics
o Antibiotics
o Eye shield (for protection) should be initialized
 Do not put pressure
 If you do not have a shield get a paper cup and
cut in cross wise, secure the bottom part with
micropore/ tape.
 Diagnosis
o X-ray  ginagamit para malaman mo na walang foreign
body.
o CT-scan  ginagamit para malaman mo na walang
foreign body.
o B-scan ultrasound  di ginagawa kasi nilalagyan mo ng
pressure pag nag uutz ka
 PICTURE: Corneo-scleral laceration
o You have your limbus and your sclera, tapos may
ruptured globe, you can fix this but you will have to
undergo a wound exploration
 PICTURE: Ruptured globe secondary to
o Pink/peaked??? pupil, there is a wound that proplapsed
out  a very good clue for globe perforation and
Silence will fall when the question
is asked Page 3 of 10
whenever the pupil points to, kung may ___ doon, hindi
yun foreign body, yun ung iris.
 PICTURE: Penetrating injury – fish hook O___O
o Wag mo ng dalhin ung bait sa hospital, you cut it, pero
do not take out the hook
o Can this still be saved? YES
 PICTURE
URGENT
INTRAOCULAR FOREIGN BODY
 Warrants a referral to a vitreoretinal surgeon
 Do not TOUCH the eye
 Do not put pressure you might injure the eye
 Do not put OINTMENT
 Anterior tear drop shape + shallow chamber
o IRIS is already touching the cornea
o Almost always with PERFORATION
o BROWN pigment extruding from the tear because
represents the IRIS and CILIARY BODY are pigmented
 If with penetrating INJURY: put the patient on NPO for 8hours,
start IV saline, then do SURGERY after 8 hours.
NON-URGENT
ORBITAL FLOOR FRACTURE
 Results from collision
o COUP/ direct (side)
o CONTRA-COUP / indirect (opposite the side) injury
 May present with PERIORBOTAL HEMATOMA (blackeye) 
resolves in 2-3 weeks
 You should rule out a BLOW-OUT fracture (FLOOR (weakest part
 kasi, ung mga sinuses ung underneath nya, no solid support
there, air lang nandun) usually ruptures)
o Do EOM, if the patient is unable to look up, the patient
might have MUSCLE and FAT
 S/SX:
o Palpate mastoid, (+) crepitation
o Numbness of cheek because of the nerve entrapment
o Swelling around the eye
 DIAGNOSIS
o CT-scan
o X-ray
o Kasi you want to look at the indirect injury  what part
of the eye is the most vulnerable to indirect injury?
 The optic nerve
 If injured  loss of vision
 PICTURE: other eye is looking straight and the other one is looking
up, which one is the normal eye? Is the patient looking up? Why is
the other eye not looking up?
o What makes the eye look up? Superior rectus and
inferior oblique?
o When you have orbital fracture, di naglolook up yung
patient kasi nattrap sa floor ung muscle dahil sa
fracture, also, nattrap ung nerves that control the
muscles tapos, there’s edema pa so, there is a lot of
swelling underneath, tapos meron pang fat prolapse
there so, everything is tight so, yung mga muscles, they
cannot move
  MANAGEMENT
o Wait for the inflammation to subside
o If inflammation subsides you can defer the surgery.
o If it subsides but with double vision and the patient
cannot look up then do surgery
CONJUNCTIVAL HEMORRHAGE
 More likely to be subconjunctivalBetween the sclera and eyelid
o You have to watch out for your hyphema  blood in
your anterior chamber
 Very easy to manage kasi parang pasa lang sya. So how do you
manage?
o Warm compress
o Even if you don’t do anything, the bruise will go away
 It will resolve without treatment in 2-3weeks  just assure the
patient
 It is correlated with TRAUMA
 Can be spontaneous
o If + weak vessel that suddenly rupture (seen in smokers)
o After straining (coughing, sneezing, lifting heavy objects)
 If it happened for the first time: it does not WARRANT medical
treatment
 If it happened repeatedly: do PT, PTT
o Rust ring is hard to remove, it can stay in place because
after few days it will drop on its own
 TREATMENT
o Removal of foreign body under slit lamp
o Can be removed with with a spray of water and cotton
edges? but if you will be removing embedded foreign
body, like ung natalsikan ng apoy ng welding, then, you
have to use an instrument like your PV?? Syringe
o Use anesthetic
o Use topical antibiotic and corneal wound healing agents
o Eye patch
 If <10mm, put gauze, then press, and secure
with micropore tape
 >10mm- DON’T PUT A PATCH because it can
delay the healing. The normal blinking can
facilitate healing though painful. Patch may
aggravate the infection
 RETINAL DETACHEMENT
o Common symptom: kurtinang itim na bumababa
o When you have a patient na yung complaint nya, is “I
could see half of your face or half of your body but not
the lower part or I could see the lower part but not the
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 conjunctivitis
o Most cases, benign, often self-limiting condition
 Care needs to be exercised in:
o Neonates (ophthalmia neonatorum)
 Because of the possibility of infection with
chlamydia which may be associated with non
ocular disease and needs systemic therapy
o Gonococcus or herpes simplex virus
 May be associated with encephalitis and
requires hospitalization and parenteral
antiviral therapy
o Gonococcal conjunctivitis in neonates and adults
 Characteristically causing a purulent discharge
as well severe conjunctival inflammation
 Necessitates emergency investigation by
microscopy and culture of the discharge
 Parenteral antibiotic therapy with ceftriaxone
to avoid progression to severe corneal
damage
o Ophthalmic zoster (shingles)
 Parenteral antiviral therapy within 72 hours of
the appearance of the rash reduces the
likelihood of the complications
 Huchinson’s sign
 Skin lesions on the tip of the nose or
eyelid margins
o Predictive of ocular
complications
 Acute keratitis
o Revolves around identification and treatment of
infection
o Predisposing factors
 Contact lens wear
 Preexisting ocular surface disease
 Corneal anesthesia or exposure
o Occasionally, there is apparent straightaway that there
is a non infectious inflammatory process, requiring
other therapy, possibly topical or systemic steroids but
steroid therapy should not be started w/o ophthalmic
assessment.
 Acute intraocular inflammation (uveitis)
o Revolves around identification and treatment of
infection particularly if there is:
 Posterior segment involvement
 Vitritis
 Retinitis
 Choroiditis
 Recent history of intraocular surgery
 Non infectious inflammatory process is nore
common than in acute keratitis
o Topical or systemic steroid therapy
 Should not be started without ophthalmic
assessment.
 Scleritis
o Infrequently caused by infection
o Autoimmune disease is commonly responsible
o Managed in the first instance by:
 Oral NSAIDS
 But ophthalmic assessment is necessary to
make diagnosis and exclude other entities
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 Acute angle closure glaucoma
o Prompt recognition and treatment are required if severe
visual loss is to be avoided
o Mainstay of initial treatment
 Intravenous and oral acetazolamide
 Topical agents  reduce intraocular pressure
 Supplemented by topical steroids  reduce
inflammation
 Topical pilocarpine constrict pupil
o Definitive treatment
 Laser peripheral iridotomy with prophylactic
treatment of the fellow eye
o Emergency ophthalmic assessment is essential to
establish the diagnosis, including exclusion of other
causes.
ACUTE ORBITAL DISEASE
TRIAGE
 Orbital cellulitis
o Usually a disease of childhood
o Due to spread of infection from the ethmoid sinuses
o Characterized by fever, pain, eyelid swelling and
erythema, proptosis, limitation of extraocular
movements, and systemic upset with leukocytosis
 Pre-septal cellulitis
o There is no proptosis or limitation of eye movement
o Due to a localized infection of the anteriour (pre-septal)
portion of the eyelid or may be the early manifestation
of orbital cellulitis.
 In adolescents and young adults
o Orbital signs may be indicative of extension of infection
from the fronto-ethmoidal sinus coplex
 In diabetics and immunocompromised
o Acute orbital disease may be due to fungal infection
(mucormycosis) with a high risk of death even with early
treatment.
 Autoimmune hyperthyroidism (Grave’s disease)
o May lead to marked proptosis with the possibility of
corneal exposure or optic nerve compression and
limitation of eye movements
 Pseudotumor
o Inflammatory orbital disease
 Carotid artery cavernous sinus fistula
o Due to dural shunts that typically occur in patients with
diabetes and /or systemic hypertension, or due to
spontaneous rupture of an intracavernous internal
carotid artery aneurysm, may present in a similar
manner.
CLINICAL ASSESSMENT
 Optic nerve dysfunction
o Reduced vision unexplained by corneal exposure
o Especially if associated with impaired color vision and/or
a relative afferent pupillary defect
 Non-axial proptosis
o If present in orbital cellulitis  implies abscess
formation
 Other compliations
o Cavernous sinus thrombosis
o Intracranial infection
 More likely if there is infection in the frontal
sinus
 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
o Assessment of color vision
o Pupillary reaction to light
 Particularly looking for a relative afferent
pupillary defect
 Fundal examination following pupillary dilatation
o Best means of diagnosing:
 retinal tears with or without retinal
detachment,
 Vitreous hemorrhage and its cause if the
hemorrhage is not too dense
 Otherwise, ultrasound examination
is necessary
 Age related macular degeneration
 Including whether it has features of
the neovascular stage
 Retinal vein or artery occlusion
 And anterior ischemic optic neuropathy
o Normal in giant cell arteritis when the visual loss is due
to choroidal ischemia or posterior ischemic neuropathy
MANAGEMENT
 Retina detachment
o Treated surgically
o With urgency primarily being determined whether the
macula is detached but also the underlying cause
 Vitreous hemorrhage
o Treatment determined by the underlying cause
 Neovascular age-related macular degeneration
o Standard treatment: repeated intravitreal injection of
inhibitors of VEGF
 There is debate about the role of carotid endarterectomy in
patients with ocular TIAs due to carotid artery stenosis, but all
patients with transient monocular visual loss (amaurosis fugax)
likely to be due to retinal emboli should undergo investigations
for carotid and cardiac sourges
 Transient visual loss can also be due to:
o Giant cell arteritis or
o Optic disk swelling due to raised ICP
 No treatment in the acute stage is established to alter visual
outcome in central or branch retinal vein occlusion
o Effective for long term complications
 Intravitreal injections of VEGF inhibitors
 Triamcinolone
 Retinal laser photocoagulation
 Various surgical techniques
 Intra-arterial thrombolytic therapy
o Advocated in the acute stage of CRAO
o Evidence for their usefulness is lacking
 No treatment in the acute stage is established to alter the visual
outcome in anterior ischemic optic neuropathy
 Failure to treat promptly could rapidly lead to complete bilateral
blindness
o Giant cell arteritis causing anterior ischemic optic
neuropathy
o CRAO
 Emergency imaging and appropriate management  involves
neurology or neurosurgery referral if there is
o Sudden visual loss due to optic chiasmal or
o Retro chiasmal disease
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ACUTE PAINFUL VISUAL LOSS WITHOUT A RED EYE
 Most of the time, they are retrobulbar in location
TRIAGE
 Causes of optic neuritis
o Acute demyelinative optic neuropathy – MC
 Associated with multiple sclerosis, occurring
as the initial manifestation or part of a
subsequent relapse
 Characteristically presents as subacute
monocular visual loss with peri- or retro-
ocular discomfort exacerbated by eye
movements
 Pituitary apoplexy
o Usually due to a hemorrhagic infarction of a pituitary
tumor
o Rare but requires prompt recognition and treatment to
reduce risk of severe morbidity , possibly death, as well
as severe visual loss, possibly complete blindness
o Characteristically presents with suddne onset of
headache, unilateral or bilateral visual loss, sometimes
impaired eye movements , and metabolic and
circulatory derangement due to pituitary failure,
resulting in adrenal insufficiency
 Sphenoid sinusitis
o Presents with headache typically localized to the vertex
and acute unilateral or bilateral visual loss
 Diagnosis of posterior scleritis
o Often delayed because of the frequent lack of specific
diagnostic features, including absence of apparent
inflammation of the globe to suggest an inflammatory
condition
CLINICAL ASSESSMENT
 Acute demyelinative optic neuropathy
o There are features of optic nerve dysfunction
 Impaired color vision
 Visual field loss
 A relative afferent pupillary defect
o With progression of visual loss over a few days
o Usually no opthalmoscopic abnormality
o With mild optic disk swelling in 1/3 of cases
 Ophthalmic manifestations of pituitary apoplexy
o Unilateral or bilateral, often severe visual loss
o Impaired pupillary light reactions
o Sometimes impaired eye movements (external
opthalmoplegia) due to ocular motor cranial nerve
palsies
o Normal or pale optic disk depending upon whether the
pituitary tumor previously caused anterior visual
pathway compression
 Sphenoid sinusitis
o Visual loss has features of optic nerve dysfunction
o With normal or pale optic disks depending upon
whether there has been chronic optic nerve
compression from a pre-existing sphenoid sinus
mucocele
 Clinical signs in posterior scleritis
o Proptosis
 o Limitation of eye movements
o Induced refractive error
o Choroidal folds
o Fundal mass
o Serious retinal detachement
o Optic disk swelling
o Ultrasound is the best diagnostic test
MANAGEMENT
 Acute demyelinative optic neuropathy
o In most cases, vision recovers spontaneously
o Management centers on investigation of the likelihood
of multiple sclerosis and the need for disease modifying
therapy
o Exclude other entities that require urgent treatment
 Pituitary apoplexy
o An endocrine and neurosurgical emergency
o Patient may require emergency resuscitation
o IV hydrocortisone should be given to all patients prior to
investigation with MRI or CT if the patient’s condition is
unstable
o Urgent neurosurgery is frequently required, particularly
in patients with visual loss
 Sphenoid sinusitis causing visual loss
o Requires surgical drainage as well as antibiotic therapy
 Posterior scleritis
o May respond to oral NSAIDS but oral steroid therapy
may be required
DOUBLE VISION AND EYE MOVEMENT ABNORMALITIES
TRIAGE
 In oculomotor ( third cranial) nerve palsy
o There may be clues from associated ptosis or pupillary
abnormality
 Unless the pattern of double vision reported by the patient or the
examination of the range of eye movements quickly leads to
identification of a specific entity such as an abducens nerve
(lateral rectus) palsy, the non ophthalmologist will derive more
useful guidance to the urgency from information about the
features such as whether there is also impairment of vision,
orbital signs such as lid swelling or proptosis, periocular pain or
headache, non-ocular neurologic abnormalities, or systemic
illness.
 Patients with multiple cranial nerve palsies or other neurologic
features, severe headache, associated systemic illness or age
under 50 with single or multiple cranial nerve palsy are most
likely to have a serious underlying condition
CLINICAL ASSESSMENT
 Double vision
o Usually due to ocular misalignment
o First step in evaluation is to determine whether it is
monocular or binocular
o Monocular
 If double vision is present when the patient is
viewing with only one eye, whether it is just
with one eye or with each eye alone, the
visual disturbance is not due to ocular
misalignment
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 It is likely to be due to:
 Refractive error
 Lens opacity
 Possibly macular disease
 Unless there are features that
implicate cerebral disease, multiple
images on monocular viewing can
be assumed not to be due to
intracranial disease.
 You need to establish how long the double vision has been
noticed and whether there has been change in the pattern as
judged by direction of separation of images and the directions of
gaze in which double vision has been present or severity as judged
by the distance separating the two images
 Establish whether the double vision can be overcome with
voluntary effort
o Implies a longstanding abnormality that has become
more difficult to overcome (decompensated
 Ocular motor cranial nerve palsy
o it is essential to determine whether it is isolated or part
of multiple cranial nerve dysfunction
o assess the trigeminal nerve as well as the optic nerve
function to provide anatomical localization of the
disease process and as a guide to the likelihood of a
serious underlying condition
o presence of pupillary dysfunction
 either anisocoria or a particularly and
impaired response to light
 provides an important clue to the possibility of
a compressive lesion such as a posterior
communicating artery aneurysm.
 Severe pain
o Another important clue to the presence of an aneurysm
o May also occur in pituitary apoplexy
 Specific eye movement abnormalities provide precise anatomical
localization
 Internuclear opthalmoplegia
o Impairment of adduction of one or both eyes
o Localizes to the medial longitudinal fasciculus within the
brainstem
 Horizontal gaze palsy
o There is loss of conjugate horizontal gaze to one or both
sides
o Localizes to the pons
 Vertical gaze palsy
o Localizes to the midbrain
 Myasthenia gravis
o Variability of double vision during or between episodes
o With increasing severity with fatigue that may also
manifest as increasing ptosis
MANAGEMENT
 Isolated motor cranial nerve palsy in patients over 50
o Due to ischemic microvascular disease
 Requires little investigation apart from
exclusion of giant cell arteritis
 And review of vascular risk factors in which
spontaneous recovery is the rule
 Isolated oculomotor nerve palsy suspicion of posterior
communicating artery aneurysm due to pupillary involverment,
severity of pain, or age under 50
 o Necessitates emergency imaging
o Outcome being much better if treatment can be
undertaken prior to subarachnoid hemorrhage due to
aneurysm rupture
 Multiple cranial nerve dysfunction
o Requires urgent investigation, usually guided primarily
by a neurologist
 Management of orbital disease usually depends upon the
outcome of imaging with CT or MRI
 When clinical evaluation suggests decompensation of a
longstanding abnormality, such as a congenital superior oblique
(trochlear) palsy
o Further investigation may not be required
o Initial treatment will be with prisms
 In any patient with suspected myasthenia gravis
o It is important to establish whether there is a non-ocular
weakness suggesting generalized disease
 Especially impairment of breathing or
swallowing for which emergency neurologic
assessment is essential.
PUPIL ABNORMALITIES
TRIAGE
 Acute isolated, dilated unreactive pupil in an otherwise well
individual
o Rarely due to a serious underlying condition
o Likely possibilities being:
 the benign entity of tonic pupil
 pharmacological mydriasis from accidental
ocular inoculation with anticholinergic agent
in travel sickness medication
 Isolated dilated, unreactive pupil in a patient with depressed
conscious level due to head injury or other acute intracranial
disease is an ominous sign
o Suggestive of tentorial herniation
 Pupil involvement in oculomotor nerve palsy
o Important clue to the possibility of a compressive lesion,
including posterior communicating artery aneurysm
 Miosis with ptosis
o Characteristic of horners syndrome
 Acute, painful horner’s syndrome, possibly following neck trauma
o Requires urgent exclusion of carotid dissection
 Pupillary light-near dissociation
o Impaired pupillary constriction to light with better
constriction to near
o Traditionally associated with CNS syphilis (Argyll
Robertson pupils)
o Can be due to midbrain dysfunction, typically
compression from a pineal tumor or dilated third
ventricle in hydrocephalus, when usually there is also
impairment of vertical eye movements
CLINICAL ASSESSMENT
 Ophthalmologists role is to:
o Confirm suspected diagnosis of oculomotor nerve palsy
or horner syndrome
o Identification of benign entities
 Tonic pupil
 Pharmacological mydriasis
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o **to avoid unnecessary investigations and ophthalmic
entities such as acute angle closure glaucoma , to direct
management
 Tonic pupil
o May be identified by the delayed dilation following near
response from which it derives its name;
o Abnormal spiraling movements (vermiform)
movements of the iris when constricting to a light
stimulus
 Best seen on slitlamp examination or
 Constriction of dilute (0.125%) pilocarpine eye
drops
 Pharmacological mydriasis
o Characterized by lack of pupil constriction to bright light
and standard strength (2%) pilocarpine eye drops
BILATERAL OPTIC DISK SWELLING
 Causes of optic disk swelling (usually unilateral)
o Inflammatory
o Ischemic
o Optic neuropathy
o Central retinal vein occlusion
o Uveitis
o Posterior scleritis
o Intraorbital optic nerve compression
 Bilateral optic disk swelling
o Characteristic feature of:
 Raised intracranial pressure
 Malignant (accelerated) systemic
hypertension
o **both requiring emergency or urgent investigation and
treatment
TRIAGE
 Papillededema
o Optic disk swelling due to raised ICP
o Usually identified as a part of examination of a patent
with neurological sx,ie headache.
o Identified incidentally during routine opthometric
examination
o Requires urgent head imaging to exclude intracranial
mass lesion.
o Blood pressure should be checked even in a child
CLINICAL ASSESSMENT
 When abnormalities are florid, recognition is straightforward
 If the abnormalities are less marked, ophthalmological
assessment is crucial to identify:
o Myelinated nerve fibers
o Optic nerve head drusen
o Congenitally small and crowded optic disks
(pseudopapilledema)
 ***so that unnecessary investigations and anxiety can be avoided
 Assessment of visual field is a crucial guide to urgency of
treatment
 Malignant hypertension
o Optic disk swelling is usually accompanied by retinal and
choroidal abnormalities
o An indication for urgent reduction of BP precipitous
reduction should be avoided to reduce risk of optic
nerve infarction.
 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

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 OPHTHALMOLOGY | 2022
2
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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