Eye Emergencies
Done by : Dr. Obadah Abu Thawabeh
Supervisor : Dr. Ghadeer Rbehat
Dr. Juma Taha
At the end of this presentation we should able
to :
1 . Differentiate the types of eye emergency
which need immediate intervention
2 . Recognize the signs and symptoms
associated with each eye condition
3 .be able to perform a basic eye examination
to assess the situation
4 . Perform the suitable first aid to save the eye
and the vision as well
Sign and symptoms that require
immediate referral :
•
Sudden decrease or loss of vision

Hyphaema
•
Loss of visual field

Halos around light
•
Pain on eye movement

•
Photophobia
Laceration of the lid margin or near
medial canthus
•
Diplopia

Subconjunctival hemorrhage
•
Proptosis of the eye

•
light flashes and floaters
Broken contact lens or shattered eye
glasses
Suspected globe perforation
•
Irregular shape pupil

•
foreign body sensation
•
Red eye and infected eye
Relative Afferent Pupillary Defect (RAPD)
done by swinging flashlight test in Dark
room.
A 7 Years old Female present with painful
swelling and redness of upper and lower lid of
her right eye. She report having a bug bite
near her Right eye .
On examination , her eyelid are extremely
edematous with well demarcated area of
erythema . Ocular examination is normal and
normal vision , no RAPD, no proptosis and No
motility deficit .
What is most likely
diagnosis :
A) Orbital cellulitis
B) Preseptal cellulitis
C)Anaphylactic
reaction to the
insect bite
D) Blepheritis
Orbital Cellulitis
Orbital cellulitis
Peri – Orbital cellulitis
Post septal cellulitis.
Emergency
Pre - septal cellulitis
Only affects
eyelids
Orbital cellulitis :
Definition :
Infection that
spreads post orbital
septum
Etiology :
 Direct extension ( sinusitis esp. ethmoiditis ,
dacrocystitis , hordeolum , dental
infection)
 Complication of trauma ( skin trauma with
inoculation )
 Hematogenous ( if immunocompromised )
Age :
Organisms :
 Mostly in children as
orbital septum not fully
developed .
 Gram positive cocci :
( fully developed at age 8 –
9 years old )
 H. influenza previously
 Common also in elderly
and
immunocompromised .
Staphylococcus
Streptococcus
 Aspergillus in DM and
immunocompromised
Clinical features :
 Preseptal cellulitis :
Lid induration , warm erythema , tenderness ,
unable to open eye.
 Additional features seen in orbital cellulitis :
Fever
Proptosis
Chemosis
Red flag signs of optic nerve
compromises :
 Reduce vision
 Reduce color vision ( cons )
 RAPD ( specific for optic nerve
compromised )
 Reduce visual field .
 Ophthalmoplagia ( pain on eye
movement )
Investigation :
Management :
 CBC , CRP , ESR .
 Admission
 Blood culture .
 Broad spectrum antibiotics ( IV
for 72 hours then PO for one
week )
 Imaging ( CT Head = the gold
slandered)
 ENT review to assess for sinus
drainage .
 Repeat CT if any deterioration
to exclude posterior extension
( abscess , cavernous sinus
thrombosis ).
Remember : management of preseptal
cellulitis :
Warm compresses .
PO (10-14 days) and Topical
Antibiotics .
Complication :
Optic nerve inflammation
Cavernous sinus thrombosis
Meningitis
Brain abscess with possible loss of vision
Death
A 67 years old white man with a history of Coronary
artery disease , HTN , DM and a PVD . Present with
sudden PAINLESS loss of vision in right eye several hour
ago . On examination he has light perception vision ,
presence of a RAPD and normal anterior segment of
the eye . By fundoscopy , fundus appear diffusely
white with reddish hue within the macula ( cherry red
spot ) .
What is the most likely diagnosis ?
A ) central retinal artery occlusion
B) Anterior ischemic optic neuropathy
C) Choroidal ischemia
D) Retinal Detachment
Central Retinal
Artery Occlusion
Etiology :
Occlusion of blood flow by :
1. Emboli from carotid artery or heart ( AF .
Endocarditis , valvular disease )
2. Thrombus
3. Temporal arteritis
Result in acute painless loss of vision due to
oxygen starvation of the retinal tissues and
eventual cell death .
Clinical features :
Symptoms :
Sudden PAINLESS
unilateral loss of
vision
Signs:
RAPD
By fundoscopy :
- Chery red spot
- Retinal pallor
- Cotton wool spot
(retinal infarct)
- Cholesterol emboli
(hollenhorst plaque )
Cholesterol emboli (hollenhorst plaque )
Cotton wool spot
Chery red spot
Treatment :
 Attempt to restore blood flow within 2 hours ( irreversible retinal damage if
> 90 min of complete CRAO )
 Massage the globe to dislodge embolus ( compress eye with heel of
hand for 10 seconds , release for 10 seconds , repeat for 5 min )
 Decrease IOP
- topical BB, IV acetazolamide , IV mannitol
- or drain aqueous fluid by anterior chamber paracentesis ( carries risk of
infection , lens puncture .
 Nd:YAG laser embolectomy
 Intra arterial or intra venous thrombolysis .
 In embolus is seen refer to an internist or neurologist for stroke
management.
A 56 years old white male with a history of hypertension
and DM , complains of double vision and pain for the
past 2 days .
On examination , his vision is OD 20/50 and OS 20/25 .
He has a larger pupil with a RAPD OD . The lid of his right
eye is slightly lower than the left . His right eye is
deviated slightly temporally and inferiorly and he has
difficulty adducting and elevating the eye .
What is the most likely diagnosis ?
A)grave’s disease
B)Horner syndrome
C)3rd nerve palsy
D)Myasthenia gravis
Third Nerve Palsy
What are the nerves that are
responsible for eye movement ??
CN 3 : occulomotor
nerve
CN 4 : Trochlear nerve
CN 6 : abducent nerve
Extra ocular muscles
Remember LR6 SO4
Occulomotor Nerve also supply levator
palpebrae superioris. ( elevate eye lid )
and
have connection with neurons in ciliary
ganglion which innervate the pupillary
sphincter ( control constriction of the pupil )
What you see in
rd
3 nerve palsy ?
 Ptosis
 dilated pupil
 an eye that is down
and out.
 diplopia with or
without pain
Etiology
Aneurysm ( posterior communicating
artery aneurysm )
Intraocular tumor
Ischemia ( DM )
Trauma
Work up :
Complete ocular examination
CNS imaging to R/O aneurysm or
mass
ESR and CRP to R/O GCA
Treatment :
Treat the underlying causes if present .
Patch or prism over affected eye if there is
symptomatic diplopia ( but not for < 11 years old
for the risk of amblyopia )
What is the most likely diagnosis?
A) anterior uveitis
B) Optic neuritis
C) Acute Angle glaucoma
D) Giant cell arteritis
Glaucoma
Definition :
Two main types :
Optic nerve Damage due
to increase IOP.
1. Open angle glaucoma.
2. Closed angle glaucoma .
Normal aqueous pathway
 Aqueous is made by the ciliary body and secreted into posterior
chamber .
 Aqueous passes through the pupil into the anterior chamber .
 Most of the aqueous leaves the eye via the trabecular
meshwork -> schlemm’s canal -> bloodstream .
 Small portion ( 4%) drains via uveoscleral pathway .
acute angle closure glaucoma
 Pathogenesis = pupil block
mechanism
In response to pupil dilatation (e.g. dark
condition ) -> peripheral iris bunches up
-> increase resistant to aqueous flow .
Build up of aqueous in posterior chamber
-> bows iris forward -> closes drainage
angle .
Risk factors :
 Female
 Family history
 Small eye ( long sighted , hypermetropic )
 Asian ethnicity .
 Age >70 years old
 Mature cataract
 Shallow anterior chamber
 Pupil dilation ( topical and systemic anticholinergic ,
stress , darkness )
Acute angle glaucoma is
about 5% of all glaucoma
cases .
Clinical features :
 IOP > 40 mmHg ( by tonometry )
 Cloudy, injected cornea ( seen by slit lamp ) .
 Fixed , oval , mid - dilated pupil ( seen by slit lamp )
 Halos around the light.
 Red painful unilateral eye .
 Reduced vision .
 Watering .
 Nausea, vomiting , abdominal pain .
Halos around light
Complication :
 irreversible loss of vision within
hours to days if untreated .
Permanent peripheral anterior
synechia result in permanent
angle closure .
Ocular emergency :
aqueous suppressants and hyperosmotic
agents :

-
Decrease aqueous humor formation :
Topical BB ( timolol )
Topical alfa adrenergic agonist ( brimonidine )
Topical carbonic anhydrase inhibitor (dorzolamide )
Systemic carbonic anhydrase inhibitor ( acetazolamide IV or oral )

-
Increase aqueous outflow :
topical prostaglandin analog ( latanoprost ) .
Topical carbonic anhydrase inhibitor
Topical cholinergic ( pilocarpine : mitotic drops to reserve pupillary block )
 Hyperosmotic agent : mannitol ( rarely used now , mostly OR cases ) , or oral
glycerin .
Definitive treatment :
Laser peripheral iridotomy
(bilaterally)
What is the diagnosis you would
most worry about ??
A) Cataract
B) Endophthalmitis
C) GCA
D) Retinal detachment
E) Vitreous detachment
Retinal Detachment
Definition
The potential space
between the
neuroretina and the
retinal pigment
epithelium (loosely
attached in the eye )
become separated .
Risk factors :
 Recent eye trauma
 Retinal detachment in other
eye
 High myope ( short sighted ,
large eye ).
Clinical features :
 Flashing light .
 > 100 floaters
 Shadow over vision ,
curtain of blackness .
 RAPD
 Decrease IOP 4 – 5
mmHg lower than the
other eye
 Most common
presentation is unilateral
blurry vision without pain
or redness (PAINLESS
acute loss of vision )
Treatment
 Prophylactic : symptomatic tear ( flash or floaters ) can be sealed off with laser /
cryotherapy .
 Therapeutic :
 Rhegmatogenous :
-
Scleral buckle procedure
-
Pneumatic retinopathy
-
Vitrectomy plus injection of gas ( silicone oil in recurrent detachment )
 Tractional :
Vitrectomy +/- membrane removal / scleral buckling/ injection of intraocular gas
or silicone oil as necessary
 Exudative : nonsurgical , any underlying disease should be treated if possible .
What is your most likely diagnosis ??
A)Endophthalmitis
B) Orbital cellulitis
C)Acute closed angle glaucoma
D)Keratitis
E) Retinal detachment
Endophthalmitis
Definition :
Serious but rare
inflammation of
the interior eye.
Risk factors :
Recent ocular surgery
Complicated surgery
Immunocompromised
Poor lid hygiene
Clinical features :
Present within one week of surgery with :
- Severe pain
- Loss of vision
- Red eye
- Hypopyon
Organisms :
Staph aurues
Staph epidemidis
Treatment
IV broad spectrum antibiotics
Take sample from aqueous
and vitreous
Ischemic optic
neuropathy
It is the most common cause of
optic nerve pathology causing
visual loss in patients older than
50 years .
Caused by blockage of optic nerve blood
supply
Blockage can be due to :
• Inflammation of the arteries as a part of Giant cell
arteritis = Arteritic Type
or
• Without inflammation of arteries = non arteritic type
( most cases are idiopathic ) .
Blood supply to the optic nerve
Anterior part : optic nerve head , which is
supplied primarily by the posterior ciliary
circulation .
Posterior part : supplied by multiple
sources other than posterior ciliary
circulation .
Classification of ION :
1 - Anterior ION : involve 1mm segment of the optic
disc so it will cause disc swelling or edema
2 – Posterior ION : involve any portion of optic nerve
posterior to the optic disc so will not cause disc
edema .
Anterior ION :
Arteritic
Non arteritic
Posterior ION
Arteritic
Non arteritic
Surgical : as a
complication from
a surgical
complication .
Non Arteritic is more common than Arteritic type
 Arteritic ION is much more emergent than Non
Arteritic .
Anterior ION is more common than Posterior
ION.
PION is very rare and is generally a diagnosis of
exclusion.
Arteritic Ischemic Optic Neuropathy
( GCA )
Symptoms :
 Amaurosis fugax is an early
sign .
 Proximal muscle and joint aches
(polymyalgia rheumatic)
 Sudden PAINLESS visual loss
 Anorexia
 Unilateral (may become
bilaterally )
 Weight loss
 Age : >= 55
 Headache
 Jaw claudication
 Scalp tenderness
 Fever ( may occur )
Signs :
 Relative Afferent pupillary Defect
(RAPD)
 Visual loss ( counting fingers or
worse )
 Pale swollen disc
 High ESR , CRP markedly and may
be platelets
 Visual field defect
 Palpable tender non pulsatile
temporal artery .
 CRAO or CN ( esp. 6th ) may occur
Workup :
History : age is a critical
Complete ocular examination .
ESR , CRP , Platelet.
Temporal Artery Biopsy : one week
after initiation of systemic steroid .
Treatment :
 Systemic steroid immediately once GCA is suspected
 Methylprednisolone 250mg IV q 6 h for 12 doses then prednisolone
80-100 mg PO daily .
 Note that without steroid , other eye can become involved within 1
to 7 days .
 Treatment should last at least 6 to 12 months with smallest steroid
dose that suppresses the disease .
 Don’t forget to give the patient PPI or H2 blockers and medication to
help prevent osteoporosis ( vit D and Ca )
NON Arteritic ION
Etiology :
Mostly Idiopathic .
Risk factors :
 Atherosclerosis
 DM
 HTN
 Dyslipidemia
 Anemia
 Nocturnal hypotension
(esp. in pt. with antiHTN
medications.
Symptoms :
Signs :
 Sudden painless loss of vision
(moderate degree)
 RAPD
 Unilateral (may become
bilateral)
 Normal ESR and CRP.
 Age 40 to 60 .
 Pale optic disc swelling .
Treatment :
Observation .
Consult internist to rule out CVD , DM, HTN
and sleep apnea .
Avoid antiHTN medications at bedtime to
avoid nocturnal hypotension.
A 42 year old bookkeeper presents with a complaint of red
painful eye and she feels like there is something in her right
eye . Discharge and blurry vision. On examination her pupils
are equal, round, reactive to light but her right eye has diffuse
injected. She also complains photophobia. You perform
fluorescein staining, which reveals an area of focal corneal
uptake .
Which of the following is the most likely diagnosis ?
A)Acute angle closure glaucoma
B) Corneal abrasion
C)Subconjuctival hemorrhage
D)Uveitis .
Corneal abrasion
Definition :
Scratch on your eye .
 injury is limited to the
epithelium of the cornea .
Clinical features :
Symptoms :
Signs :
 History of scratching or
hitting the eye .
 Epithelial defect that
stains with fluorescein .
 Sharp pain
 Absence of underlying
corneal opacification
that indicates infection or
inflammation .
 Photophobia
 Foreign body sensation
 Tearing
 Discomfort with blinking
Investigation :
 Slit lamp examination : use fluorescein dye
 Evert the eye lid to ensure no foreign body is present
Treatment :
 Topical antibiotic :
- Non contact lens wearer : ointment or drops
e.g.
Ointment ( erythromycin , bacitracin q 2 - 4 hours )
Drops ( fluroquinolones q 6 hours .
- Contact lens wearer : should have antipseudomonas coverage (
fluroqinolones q 6 hours , ointment or drops )
• Patching is rarely necessary : can
cause serious abrasions if not used
properly .
• Cycloplegic agents for traumatic irtis
which may develop 24 – 72 hour post
trauma .
• Consider topical NSAID for pain
control
Ointment vs. Drops
Ointment offer better barrier and
lubrication between eyelid and abrasion
Ointment tend to blur vision temporarily .
May use the ointment to augment drops
at bedtime .
Prefer frequent ointment .
Corneal Ulcer
Etiology :
 Local necrosis of corneal tissue due to infection.
 Injury extend to the stroma of the cornea .
 Infection is usually bacterial , rarely viral , fungal or protozoa
 2ry to corneal exposure to abrasion . Foreign body , contact lens use
( 50% of ulcers)
 Also associated with conjunctivitis , blepharitis , keratitis , vit A deficiency
Clinical picture :
• Pain , photophobia , tearing , foreign body sensation ,
decrease visual acuity if central ulcer
• Corneal opacity
• Corneal epithelial defect that stains with fluorescein .
• May develop corneal edema
• Bacterial ulcers may have purulent discharge , viral ulcers
may have watery discharge .
Complication
Investigations
Decrease vision .
Fluorescein
stain .
Corneal
perforation
Iritis
Endophthalmitis
Treatment :
Must treat vigorously to avoid
complications
Culture prior to treatment
Topical antibiotic every hour
What is your most likely diagnosis ?
A)Acute angle closure glaucoma
B) Bacterial keratitis
C)Viral keratitis
D)Anterior uveitis
E) Endopthamitis
Bacterial Keratitis :
Definition :
 Inflammation of the
cornea .
 Commonly infective
(bacterial , viral , fungal )
Risk Factors :
 Contact lenses .
 A breech in the corneal
epithelium ( e.g. Trauma )
 Dry eye .
 Prolonger use of steroid
drops.
Etiology :

Pseudomonas ( most
common in CL
wearer )
 Staphylococcus
 Streptococcus
 Moraxella
 Serratia species
Clinical features
 Painful eye
 Red eye
 Purulent discharge
 Blurred vision
 Hypopyon ( collection of WBCs)
 White corneal opacity = corneal ulcer
 Photophobia
Investigation :
Stain with fluorescein see epithelial defect
Corneal scrape : gram stain and culture
Management :
Stop wearing contact lenses until healed .
Topical antibiotic drops : ciprofloxacin ,
ofloxacin .
A 35 years old woman comes to your office with an
acutely inflamed and painful left eye . Her symptoms
started 2 days ago. There is some visual blurring . On
examination there is a diffuse inflammation of the left
conjunctiva. On fluorescein staining , dendritic ulcer
is seen in the center of the cornea. Visual acuity is
intact
 What is the most likely diagnosis ?
A) Corneal abrasion
B) Herpetic corneal ulcer
C) Adenoviral ulcer
D) Bacterial keratitis .
Dendritic ulcer
Viral keratitis :
Herpes simplex keratitis
( HSV 1, 90% of
population are carriers )
May be triggered by
stress , fever , sun ,
exposure ,
immunosuppression .
Clinical features
• Reduced vision ( depend on the
location and the size of the ulcer )
• Pain
• Photophopia
• Red eye
• Watery discharge
Fluorescein staining :
Dendritic ulcer
Complication :
Corneal scarring ( can lead to loss of
vision )
Chronic interstitial keratitis due to
penetration of virus into stroma
Secondary iritis , secondary glaucoma .
Treatment :
Antiviral eye drops ( acyclovir )
Oral acyclovir for sever infection
Cycloplagic drops (cyclopentolate) to
relive pain caused by ciliary spasm.
 topical antibiotics for ulcers suspected of
being infected by bacteria .
Topical corticosteroids are absolutely
Contraindicated in dendritic ulcer .
A 55 years old man presented to ER complaining of ocular pain
and irritation . He reports accidently splashing ammonia in both
eyes . His visual acuity is OD 20/100 and OS 20/80 . Both eyes are
injected with corneal edema .
What is the immediate first step in treatment of chemical injuries to
eye ??
A)Complete ocular examination
B)Manual removal of particulate material followed immediately by
irrigation with water or saline until the PH is 7
C)Application of topical glycerin to clear corneal edema
D)Topical anesthetic with debridement of surface epithelium
Chemical injury to the eye
Accidently or intentional exposure of the eye to
chemical agent with potentially blinding
complications.
Most patients will remember a chemical insult .
Alkali injury are frequently more severe than acids
as it can penetrate deep into the eye and lead to
substantial intraocular inflammation and damage .
Clinical features :
Pain
Photophobia
Reduced vision
Difficulty in eye opening
Investigations :
PH measurement
Complications :
Glaucoma
Cataract
Permanent corneal
opacification
Treatment :
Immediate irrigation of the eye wilt normal
saline
A drop of topical anesthetic after PH
measurement .
Irrigation should continue until PH is 7.0 – 7.5
Swab should be used to sweep any particular
matter
Remember : NEVER neutralize.
A 20 years old male presents to the ER with bloody eye
after he was hit in it. His visual acuity is hand motion only ,
he also has moderate lids edema but still can open his eye
. By slit lamp the pupil appears normal . Motility is normal
and no diplopia .
what is the most important first step in evaluation of this
patient :
A)Detection of a RAPD
B) Patching until the heme clears
C)Evaluation for possible open globe
D)CT scanning to evaluate for an orbital fracture
Traumatic Hyphema
Open globe:
Clinical features :
Symptoms
History of eye Trauma
blunt or penetrating
Signs :
 Hyphema ( blood )in the
anterior chamber
Pain
 Full thickness scleral or
corneal laceration
Decrease vision
 Severe subcongunctival
hemorrhage
Loss of fluid from the
eye
 Irregular pupil
 Intraocular contact may be
outside of the globe .
Investigations :
CT scan of brain and orbits
to rule out intraocular
foreign body
 Seidal test .
Treatment :
Admission to the hospital
Systemic antibiotics within 6 hours of the injury
Tetanus toxoid if needed
Antiemetic PRN for Nausea and vomiting
Pain killers
Arrange for surgery ASAP .
Eyelid laceration
 Partial or full thickness defect in the
eyelid after facial trauma .
 Often associated with other ocular
injuries ( corneal abrasions, foreign
bodies , open globe ….
Symptoms :
• Peri orbital pain
• Tearing
• Bleeding
Investigations :
• Complete ocular examinations
• CT scan of brain , orbits , midface if
history of severe blunting or
penetrating injury to rule out fracture,
retained FB , rupture globe or
intracranial injury .
Treatment :
 Consider Tetanus prophylaxis
 Systemic antibiotics for 7 – 10 days if contamination or FB
is suspected ( amoclan 625 1x2 or 1x3 , 1gm 1x2 ..)
 For human or animal bites consider penicillin and rabies
prophylaxis .
 Repair eyelid laceration in minor room surgery
Corneal and conjuctival
foreign body
Clinical features :
Foreign body sensation
Tearing
History of trauma
Work up :
• Visual acuity
• Slit lamp
examination
• Evert the eyelids
to exclude
retained foreign
bodies
Treatment
Apply topical anesthetic
Remove the FB
Treat the corneal abrasion if present (
epithelial defects
Topical antibiotics and preservative free
artificial tears my be given in case of
conjunctival FB
Blowout fracture
A 14 years old boy is bought to the emergency
after suffering a high impact injury when football
his right eye , no loss of consciousness but
complaining of right facial pain .
By imaging , orbital blowout fracture is seen .
Which bone most likely to be involved ??
a)Maxillary bone
b)Zygomatic bone
c)Frontal bone
d)Sphenoid bone
Definition :
break of one or more of the bones that
surrounds the eye .
Why does it occur ?
Object strikes the eye -> force is
transmitted into the orbit -> thinnest orbital
bones fracture .
the release of this force protects the eye
from more serious injury .
Most common fracture
sites :
 Orbital floor ( esp.
maxillary bone )
 Medial wall .
Clinical Feature :
 Eyelid swelling
 Pain
 Reduced vision
 Diplopia ( if inferior rectus affected)
 Surgical emphysema
 Enophthalmous or proptosis (
retrobulbar hemorrhage )
 Hypoesthesia bellow lower lid
 ( infraorbital nerve injury )
Investigations
Imaging :
Management :
 ABC (multitraum )
- facial XR
 Antibiotics : broad
spectrum
- CT
 Tetanus vaccine if open
wound.
 Refer to ophthalmology
and oromaxillofacial .