Ocular Emergencies

Professor Dr Amany El-Shazly

It is important for medical
practitioners to recognize
emergency eye conditions as
delays in treatment can
cause vision impairment.
These require urgent consultation to an
ophthalmologist for management.
 Taking an
ophthalmic
history
Clinical
approach to a
patient
presenting
with an eye
problem
Clinical
examination
 Onset and duration of symptoms
including previous Trauma.
In general, the
following areas Previous ocular history e e.g.,
act as basic road Cataract surgery, previous
sign in ophthalmic inflammation.
Taking an history-taking:
ophthalmic
history Red eye (DD).

Pain, photophobia and decreased

vision.

Contact lens wear.

Causes of a red eye
Unilateral +ve Intraocular
Conjunctival
Cause or Pain fluorescein Vision Pupil pressure
injection
bilateral stain (IOP)
Bilateral
Conjunctivitis Diffuse, mainly (often
Gritty -ve Normal Normal Normal
Forniceal unilateral
initially)
Circumcorneal
Stitching or Normal or
Keratitis ciliary Unilateral +ve Diminished Normal
Pricky raised
injection
Circumcorneal
Constricte Normal or
Uveitis ciliary Unilateral Dull aching -ve Diminished
d raised
injection
Acute attack
Mid-
of angle Circumcorneal Severe pain
dilated,
closure ciliary Unilateral with colored -ve Diminished Raised
vertical &
glaucoma injection haloes
sluggish
 The involvement
of foreign objects.

With
trauma,
determine: The types of
& the mechanism object (e.g.,
of injury. Metallic, organic
material).
1. Assessment of vision using a Snellen chart at 6 m
2. Pupil examination to determine the afferent and
efferent pathways:
o Size of the pupils
o Reactivity of the pupils
o Any relative afferent pupillary defect (RAPD)
3. Integrity of the eyelids, including any lumps, bumps or
lacerations (partial or full thickness, involvement of the
canaliculi) in cases of trauma
4. Periorbital redness and swelling; if present, temperature
measurements must be documented
5. Eye redness: generalized or localized
6. Corneal ulcers and haze
7. Results of fluorescein staining and examination under
a blue light to help determine integrity of the corneal
epithelium. If full-thickness corneal injury is present
after trauma, aqueous humour may be seen to leak
(Seidel test)
8. Presence of blood (hyphema) or pus (hypopyon) in
the anterior chamber of the eye
9. Fundus examination with cycloplegic eye drops such
as tropicamide 1% or cyclopentolate 0.5% or 1%.
 Overall view of the
time factors involved
in referral to an
ophthalmologist
Retrobulbar hemorrhage
 Retrobulbar
hemorrhage (RBH)

Is a rare, rapidly That results in an

progressive, sight- accumulation of blood That lead to an
threatening in the retrobulbar increased IOP
emergency space

 IOP  stretching of the optic nerve & blockage of ocular perfusion

leading to venous or arterial occlusive process
 Orbital trauma

Use of
Complication of
anticoagulation
orbital surgery
medication
Etiology of
retrobulbar
hemorrhage
(RBH)
Arteriovenous
Lymphangiomas
malformations

Orbital
varicosities,
 Pain

Visual loss
Symptoms
Nausea

Vomiting

Periorbital ecchymosis

Eyelid hematoma

Signs Proptosis

Subconjunctival hemorrhage

 IOP
lateral canthotomy with cantholysis has been shown to be an
effective first line treatment if IOP > 40mmHg or vision loss
Cantholysis
lateral canthotomy with cantholysis has been shown to be an
effective first line treatment if IOP > 40mmHg or vision loss
Transcutaneous transseptal
incisions → evacuate the
hematoma + release the
periorbital pressure.

Alternative methods such as:

Transconjunctival pressure
release and/or lateral canthotomy
+ inferior cantholysis should be
considered according to patient
condition.
 Management
 If a retrobulbar hematoma leads to a tense, proptotic globe,
emergency decompression should be considered
 lateral canthotomy with cantholysis has been shown to be an
effective first line treatment if IOP > 40 mmHg or vision loss
 Surgical management is preferred over medical management
due to better results. However, medical management can be
used in conjunction with surgery. Some recommend IV
acetazolamide 500 mg or IM/IV hydrocortisone 100 mg to be
used to decrease pressure.
 Proper management of patients can prevent permanent vision
loss.
Chemical burn (check PH & irrigate 1st)
 Chemical Burn
Treatment should be instituted IMMEDIATELY
(Immediate Within minutes), even before talking
history
Treatment • Copious but gentle irrigation using saline or Ringer
1. Early and energetic lactate solution. Or Normal saline for 15-30 minutes
wash: until pH is normalized.

2. Mechanical removal
of any particles of • Especially in the fornices, (e.g.. in cases of lime)
caustic substance • Followed by thorough irrigation with saline
present in the eye.

• Atropine ointment
• Local antibiotic drops, ointment
[Link] of corneal
• Bandage
ulcer if present by
• Systemic antibiotics to guard against secondary
infection
 • Consider topical steroids as adjunctive treatment
4. Corticosteroid eye with topical antibiotic for a week even if epithelial
drops and ointment. defect is present, especially if alkali injury.

• Ascorbate & citrate for alkali burns has been

reported to speed healing time and allow better
5. Could use: visual outcome. Caution in patients with renal
compromise secondary to potential renal
toxicity.

• Prevention of symblepharon can be done by

6. Could use: using a glass shell or sweeping a glass rod in the
fornices twice daily.
Wash With Water
Contact
shell
 Corneal ulcer with +ve
fluorescein stain induced by
chemical trauma
Symblepharon

Symblepharon = adhesion between bulbar &

palpebral conjunctiva
Symblepharon
Sweeping the fornices
with glass rod in
symblepharon
Clinical picture:
Symptoms: Signs
Immediate severe ocular  Severe edema of lids and chemosis of
pain with photophobia, conjunctiva with stromal opacification.
lacrimation and  Hazy, lustreless cornea.
blepharospasm and redness  Intense ciliary injection and positive
fluorescein test & conjunctival injections
as well

Amany El-Shazly
 Alkali Burn

• Cornea  hazy. Lusterless

• Ciliary Injection
• Cornea  hazy.
Lusterless
• Ciliary Injection
• Cornea opacity
• Conjunctival chemosis
Complications:
1. In mild injuries: 1. In moderate or severe injuries:
Superficial corneal a. Dense corneal scarring with symblepharon.
scars superficial (especially of lower lid and fornix)
opacities. b. Perforation of the eye with loss of substance. due
to severe corneal ulcer corneal and scleral melting
may occur.
c. Uveitis and secondary glaucoma
d. Atrophia bulbi (following corneal ulcer
perforation or if perforation occurred from the
start accompanying loss of substance)
Amany El-Shazly
 Complicated corneal ulcer

•Ciliary injection.
•Very thinned cornea.
•Corneal edema.
Corneal
vascularization
Central retinal artery occlusion
CRAO
BRAO
CRAO
 Signs
Symptoms
Perform a dilated fundal
 Painless sudden profound loss examination to detect:
of vision (NB: may be painful [Link] red spot at
with temporal or scalp macula.
tenderness in giant cell arteritis
[Link] occasionally
(GCA). visible at optic disc.
[Link] of arterioles.
 Profound sudden drop in visual [Link] pallor.
acuity (unless cilioretinal artery
sparing).
[Link] pupillary defect
(RAPD).
Amany El-Shazly
54
OCULAR EMERGENCY: attempt to
restore blood flow within 2 h

The sooner the treatment = better prognosis

(irreversible retinal damage if > 90 min of
complete CRAO)
  may be tried in
The following treatments
patients with occlusions of less than 24–48
hours’ duration at presentation, though
evidence of benefit is limited.

56
 Treatment
The aim is to re-establish circulation within the CRA.
This is attempted by:
 Lowering the intraocular pressure (IOP) using:
[Link] 500 mg I.V.;
[Link] the globe (compress eye with heel of hand
for 10 s, release for 10 s, repeat for 5 min) to dislodge
embolus
[Link] chamber paracentesis (1 ml aqueous
withdrawn).
1. Sublingual isosorbide dinitrate (Vasodilation to
increase blood oxygen content).
2. Intra-arterial or intra-venous thrombolysis:
thrombolysis eg. Streptokinase or rtPA in very
selective cases. (Thrombolytic therapy to dissolve
clot)
3. Vasodilation: sublingual nitrate (Nitroglycerin
sublingual) or rebreathe into a paper bag (carbon
dioxide increases). {mixture of 5%CO2 + 95%
O2 or amyle nitrite}
 Protect other eye, e.g., treat
underlying GCA with systemic
steroids immediately
It is essential to check the erythrocyte
sedimentation rate (ESR) & CRP to investigate
for an inflammatory cause for CRAO, since
GCA is often a bilateral condition with
catastrophic visual loss if not treated
appropriately.
Other investigations
• Examine for carotid bruits, heart murmurs &
irregular pulse (atrial fibrillation is a cause needs
anticoagulation).
• Arrange carotid Doppler studies,24h Holter
monitor and echocardiogram.
• Follow-up by a physician
Acute glaucoma
Usually present as an
emergency
Sudden severe
periocular pain
and headache

Symptoms
of ACG
Rapid severe
Nausea and
visual impairment
vomiting from the
due to corneal
severe pain
edema
Very poor VA: HM or finger Misty cornea  stromal
counting &epithelial edema.

Ciliary congestion Very shallow AC with

iridocorneal touch
 Other signs
The eye is stony If the fundus is
Pupil is
hard on digital visible
assessment of
Vertically oval, ocular tension
semidilated & Pulsations of the CRA
sluggishly reactive to
light
Venous congestion
Assumes a bluish
coloration

Disc edema
Vertically oval, semidilated
pupil
 The patient must be
hospitalized.

IOP must be controlled

medically before surgery
is attempted to avoid the
Management risk of IO hemorrhage.
during the
attack
 Hyperosmot
ic agents

Medical Carbonic
Beta
blockers preparation anhydrase
for surgery inhibitors

Miotics
1. Acetazolamide 500 mg I.V.
2. Hyperosmotic agents - if appropriate
• Oral glycerol 1-1.5 g/kg of
50% solution in lemon juice
• Intravenous mannitol 2g/kg of 20% solution
3. Topical therapy
• Pilocarpine 2% to both eyes
• Beta-blockers
• Steroids
4. YAG laser iridotomy
• To both eyes when cornea is clear
Hyperosmotic agent (Mannitol)

Rapid IV drip
(1-2 g/kg body weight)
Most effective during
The acute attack
Hyperosmotic agent (Glycerol)

Oral (add lemon)

(1ml/kg body weight)
effective during
The acute attack
Hyperosmotic agent (Glycerol)

Diabetes Mellitus???
Carbonic anhydrase inhibitors

2 Tablets initially
1 tablet / 6 hours
Decrease aqueous secretion.
Pilocarpine 2% eye drops

Withdrawal of the

Iris from the angle

Higher concentrations congestion &

vascular permeability particularly.
Timolol maleat 0.5% eye drops

Beta Blocker

Every 12 hours

Decrease aqueous secretion

 Management after the attack

Gonioscopy is done

If a significant part
If the angle is mostly
(50% or more) of the The other eye
open, with minimal PAS
angle is closed by PAS

Peripheral iridectomy Prophylactic

Filtering surgery
or laser iridotomy iridotomy
Corneal laceration
Globe perforation

Intraocular FB
Iris prolapse (cover with an eye shield)
 Very URGENT Within hours
 Trauma leads to corneal or scleral disruption and
extravasation of intraocular contents. Can lead to:
o Irreversible visual loss
o Endophthalmitis
Manifestations
1. Hypotony
2. Pain, decreased vision
3. Hyphema
4. Loss of AC depth
5. “tear-drop” pupil which points toward laceration
6. Subconjunctival hemorrhage
Management:
Stop the examination
Cover with eye shield, DO NOT PATCH.
CT head and orbit to evaluate for concomitant
facial/orbital injury.
Tetanus
Systemic Antibiotics
Repair.
Refer if You Observe Any of These Signs
Decreased VA
Shallow anterior chamber
Hyphema
Abnormal pupil
Ocular misalignment
Hypopyon (pus in anterior chamber)
Endopthalmitis

89
Endopthalmitis

90
 Endophthalmitis

If the eye is a blind

Vitrectomy (to
painful one (no
remove the vitreous
If fungal perception of light),
that allows the flare
endophthalmitis evisceration is
up of infections)
is suspected, indicated to prevent
with intravitreal
intravitreal the spread of
injection of broad-
amphotericin is infection to the
spectrum antibiotics
usually outer coat
(usually a
(evisceration is
combination of added. better than
vancomycin
enucleation in this
/cephalosporin).
case).
 Examinations & Investigations
Vitreous tap
•Topical anesthesia
•Trans conjunctively
•23-guage needle
•0.1ml aspirated
 Gram staining
 Sensitivity test
 culture
 Investigations

B scan-Ultrasound
 Surgical treatment

Pars Plana Vitrectomy

• Two port

• Three port
 Panophthalmitis
Suppurative inflammation of all 3 coats of the eye. {eyeball is filled with pus + inflamed
uveal tract → infiltrated with cells (mainly polymorphs) }

Management Clinical picture:

Intensive antibiotic therapy for 24 hours Symptoms:
↓↓ 1. Severe ocular pain
No response 2. Headache + fever
3. Loss of vision
↓↓
Signs:
Evisceration
1. Lid edema + mild proptosis
{enucleation → meningitis} 2. Conjunctival chemosis
3. Corneal edema & haziness
4. Hypopyon
5. No light perception
6. Self evisceration → shrinks
Panophthalmitis

96
 Endophthalmitis Panophthalmitis
Definitions Suppurative inflammation of the Suppurative inflammation of all 3
entire uveal tract + adjacent tissues coats of the eye.
Symptoms 1. Pain 1. Severe ocular pain
2. Lacrimation 2. Headache + fever
3. ↓↓ vision 3. Loss of vision
Signs 1. Injected eye 1. Lid edema + mild proptosis
2. conjunctival chemosis 2. Conjunctival chemosis
3. KPs + hypopyon 3. Corneal edema & haziness
4. yellow reflex 4. Hypopyon
5. ± No light perception 5. No light perception
Management 1. Intensive antibiotics Intensive antibiotic therapy for 24
2. Vitrectomy → in early hours
cases ↓↓
3. Enucleation → blind No response
painful eye ↓↓
Evisceration 97
 Anti-
inflammatory
analgesic

Treatment of
panophthalmitis
Broad spectrum
Evisceration
antibiotic
Microbial keratitis

99
 Sharp Stitching
Pain

Pricking
Pain
 Pain

Blurring of
Blepharospasm
vision

Symptoms

Photophobia lacrimation

Frontotemporal
headache
 Management

Antibiotic eye Atropine

Scrapings
drops

by frequent topical to relieve the

Culture and
instillation of spasm of the
sensitivity
fortified, sphincter
commercially
available antibiotic & prevent the
agents complications of
toxic iritis.
Uveitis
Uveitis
 Painful
Defective Vision
 Forehead

Around the eye

Eyeball

Severe Neuralgic Pain

Lacrimation And Photophobia
 1. Circumferential ciliary injection

2. Keratic precipitates {KPs}

3. Aqueous flare

4. Miotic pupil with sluggish reaction

5. Lost iris pattern

6. Exudation into vitreous

7. ↑↑ intraocular pressure
108
Orbital cellulitis
Periorbital Cellulitis
Periorbital Cellulitis
Orbital Cellulitis...
Infection of the
Orbital Soft Tissue
POSTERIOR to the
orbital septum
Orbital Cellulitis...
Infection of the
Orbital Soft Tissue
POSTERIOR to the
orbital septum
 1. The patient should be hospitalized

2. Local and systemic broad-spectrum

Management: antibiotics (IV or IM broad spectrum
G+ve, G-ve and anaerobes).

Prophylaxis and
treatment of corneal 3. Hot fomentations
exposure (antibiotic
ointment)
 4. CT scan of the orbit and paranasal
sinuses should be ordered, especially
with cases that are not responding to
treatment. One of the main reasons
to order for CT scan in such cases is
to exclude that orbital cellulitis may
Management: be a masquerade syndrome for an
intraocular tumor (as retinoblastoma
in children).
Prophylaxis and
treatment of corneal 5. If an abscess is formed, it should be
exposure (antibiotic drained.
ointment)
 1. Hospital admission

2. Systemic antibiotic therapy

Pre-treatment 3. Monitoring of optic nerve

function

4. Indications for surgery

• Resistance to antibodies

• Orbital or subperiosteal abscess

Post-treatment • Optic neuropathy

• Raised intraocular pressure.
• Retinal vasculature occlusion.
• Optic neuropathy.
Orbital :
• Orbital or subperiosteal abscess .

Intracranial :

• Meningitis, brain abscess.

• Cavernous sinus thrombosis.
Complications of orbital cellulitis

Panophthalmitis
Complications of orbital cellulitis

Panophthalmitis
Complications of orbital cellulitis

Brain abscess
Preseptal cellulitis: Orbital Cellulitis
Inflammation and infection confined Active infection of the orbital soft
to the eyelids & periorbital structures tissue is present posterior to the
anterior to the orbital septum. orbital septum
1. Edematous lids with skin redness 1. Edematous lids with redness of
2. Conjunctival chemosis the skin.
3. The vision is not affected and 2. Chemosis of the conjunctiva.
pupil reactions are intact 3. Decreased visual acuity, sluggish
pupil reactions.
4. Proptosis: This is axial and
irreducible.
5. Limitation of ocular movements
in all directions.
The three ocular cranial
nerves pass inside it.

The right & left

cavernous sinuses
communicate with each
other 'to entirely the
pituitary gland
 Orbital cellulitis

Septic wounds of the face

1. Extension of
infection along
tributaries & Infective conditions of the
connections e.g. mouth, pharynx , ear , nose,
paranasal sinuses ,
Etiology
Or the other cavernous sinus

2. Blood born Metastatic infections

Clinical picture:

General Ocular
Fever Severe pain in the orbit
which increases during
ocular movement.
Malaise
Diplopia: because of
limitation of ocular
Headache movement .
Sometimes cerebral symptoms;
delirium, drowsiness &
convulsions
 1. Edematous lids

2. Chemosis and congestion of the conjunctiva

3. Rapidly increasing axial proptosis

4. Limitation of ocular movements due to paralysis ,
starting by the abducent nerve ( which is present inside the
sinus itself)
5. Oedema in the mastoid region due to congestion of the
emissary vein
6. Transference of signs to the opposite eye . occurs in 50%
of the cases .
General Ocular
l .Central retinal vein
1. Meningitis
occlusion .
2. Exposure corneal
2. Encephalitis
ulcer .

3. Brain abscess

4. pyaemia
 1. The patient should be hospitalized

2. Intravenous intensive broad-spectrum antibiotics (IV

broad spectrum G+ve/G-ve and anaerobes)

3. Intravenous anticoagulants : heparin 5000 1.U .every

6 hours

4. Antibiotic ointment to the exposed cornea

5. Treatment of the causative septic focus or infective

area
Giant cell arteritis with visual disturbance
 Giant cell arteritis with visual disturbance
GCA – inflammation of the lining of large and medium
sized arteries. Immediate treatment with corticosteroids
usually relieves symptoms and prevents loss of vision
 Elderly patient
 Non pulsatile tender temporal artery
 ± Headache (may be painless)
 ± Jaw claudication
 ± Weight loss
 High ESR and CRP
 Swollen disc of arteritic anterior ischaemic optic neuropathy
⁂ Affects about 25% of untreated patients with giant cell arteritis.
⁂ Severe acute visual loss.
⁂ Induce altitudinal field defect.
⁂ Treatment - steroids to protect fellow eye.
⁂ Bilateral in 65% if untreated
Acute 3rd cranial nerve palsy if pupil involvement or pain
 Acute 3rd cranial nerve palsy if pupil
involvement or pain
Acute 3rd cranial nerve palsy: an acute 3rd nerve palsy
associated with headache is a medical emergency.

The etiology is more likely to be the result of a posterior

communicating artery aneurysm if there is pain.

It is more likely caused by a compression if the pupil is dilated.

Other symptoms include diplopia and lid droop. Once

examination, there is ptosis, and the eye points down and out
 Within 24 hours
 Hyphema
Hyphema: usually absorbed spontaneously in 1 - 7 days.
Types Complications
1. Subtotal or 1. 2ary glaucoma may be open angle(RBCs clogging the
Layered angle) or closed angle: fibrosis of blood causing PAS or
organization of blood at pupil with pupillary block
2. Total 2. Corneal blood staining due to the increased IOP.
Clearing occurs from periphery to center . May lead to
amblyopia in children and hence require keratoplasty
3. Eight ball 3. Iritis (use cyclopentolate eye drops to prevent synechiae
(if pupillary block) formation)
4. Rebleeding (common on 1st 5 days after the injury,
can be avoided by anti-fibrinolytic drugs as oral
aminocaproic acid).
Hyphema
Total Hyphaema
 Semi sitting is the best position for
the patient.

Strict follow up of IOP, CAI & β

blockers are prescribed to treat rise
of the IOP
Treatment Uncontrolled high
Topical steroids to  inflammation IOP
& risk of 2ary haemorrhage.
Early blood staining
Surgical drainage
Total hyphaema
Eye shield (no patching)
Eight ball hyphaema
 Screen for sickle cell esp. in
dark race.

 Antifibrinolytic drugs e.g.,

Oral aminocaproic acid
(Amicar) may be given in
high-risk cases to avoid
rebleeding
Avoid
Aspirin – NSAID - Miotics
Carbonic anhydrase inhibitors in
sickle cell anemia
Globe compression in the first 2
weeks e.g., retinal indentation or
gonioscopy
 Trauma (most common)

Rubeosis iridis (rare)

Spontaneous with iris tumors (Juvenile

Etiologies of Xanthogranuloma)
hyphaema
Neoplastic as melanoma & retinoblastoma

Hemorrhagic uveitis

Leukemia & blood diseases

 Eye
shield
 Within 24 hours

 Retinal detachment/tear
It is separation of neurosensory layer of retina
from underlying retinal pigment epithelium
with macula on (Very URGENT Within
hours).
KEY MANAGEMENT POINT- know
“classic” presentation so you can refer to an
ophthalmologist quickly.
Amany El-Shazly
Amany El-Shazly
 Appears to be
more Arises from
Photopsias = noticeable in the mechanical
perception of dim stimulation of
flashing VR traction on
Stage of lights by the the retina
tear patient. + eye
without movements
New floaters
RD Musca
are opacities
Symptoms (small blood
volitantes
clots) in the
vitreous

Massive V
Marked ↓↓ of hge or
vision detached
macula
 Corresponding to
the detached area
Patients
Stage of Visual often
RD field describe a
defect. black
Symptoms curtain
Especially
Marked when the
↓↓ of macula is
vision
detached
 • Detached retina is grey, white
with surface blood vessels,
Fundus picture loss of red reflex

• The intraocular pressure is

IOP usually lower in the eye with a
RD.

Visual field • Corresponding to the detached

defect area
 • Detached retina is grey, white with
Fundus picture surface blood vessels, loss of red reflex

• The intraocular pressure is usually

IOP lower in the eye with a RD.

Visual field • Corresponding to the detached area

defect
Slit lamp • The anterior vitreous might show
pigment = Tobacco dusting ( +ve
examination Shaffer sign)
 Sealing with two rows of
laser to induce
chorioretinal scarring
results in strong adhesion
between the sensory
retina and the
RPE/choroid preventing Argon laser
In case of the development of RD photocoagulation
breaks
without RD Cryotherapy
 1. Drainage of SR fluid
Conventional 2. Sealing of the break
Scleral buckle 3. Application of a scleral
surgery buckle to indent the sclera at
the site of break by using an
explant sutured to the sclera
In case of
RD
1. Posterior breaks e.g.,
Vitrectomy with Macular hole
silicone oil 2. Giant breaks
injection
3. Multiple (at different sites )
 Pneumatic Perfluorocarbonwas injected
retinopexy to seal the tear

Indentation of sclera (buckle),

In case of approximation of RPE and
Scleral buckles neurosensory retina and
RD serves as scaffold for tear and
reduce vitreo-retinal traction)

To remove the membranes

Vitrectomy and abnormal vitreoretinal
attachments
 Within 24 hours

 Orbital fractures
 Fracture floor
Increased
intraorbital pressure,
which causes
the orbital bones
to break at their
weakest point.
Fracture floor
 Epistaxis, ptosis, localised tenderness

Restricted eye movements (particular on

vertical gaze)  in diplopia

looking for evidence of ocular injury, e.g.

Hyphema, subconjunctival hemorrhage,
retro-orbital hemorrhage, RD & vitreous
hemorrhage
 Check for infraorbital nerve involvement —
anaesthesia of the affected cheek, & the upper
teeth & gums on the affected side. This nerve
passes along the floor of the orbit and be
stretched or otherwise damaged.

Palpate the eyelid for crepitus

There may be no other significant facial injury

Infraorbital
nerve

Anaesthesia of:
 Cheek
 The upper teeth &
gums on the affected
side
 Center of lower lid)
branch of maxillary
Describe the investigation and management of a blowout
fracture?
 A CT scan of the orbits and brain may be required + the
Caldwell (occipitofrontal) and Waters (occipitomental) facial
radiographic views are often sufficient.
 Early treatment includes
o Nasal decongestants for 1 week
o Prophylactic antibiotics, e.g. Cephalexin 500mg .
o Instruct the patient to avoid nose blowing and Valsalva
manoeuvres; and to avoid driving until diplopia resolves.
o Apply an ice pack to the orbit for 1-2 days
REFER TO OPHTHALMOLOGIST for
further management
 Within 24 hours
Corneal abrasion

 Corneal FB
Corneal Abrasion & FB
 Discomfort, profuse
watering + redness in
the eye.
A foreign body
produces
immediate: Pain and photophobia
are more marked in
Symptoms corneal FB than the
conjunctival.

Defective vision occurs

when it is lodged in the
centre of cornea.
 Marked blepharospasm and conjunctival
congestion.

A foreign body can be localized on the conjunctiva

or cornea by oblique illumination.

Slit-lamp examination after fluorescein staining is

the best method to discover corneal foreign body.

Double eversion of the upper lid is required to

discover a foreign body in the superior fornix.
 2.
Fluorescein
1. Careful test.
3. Slit lamp
clinical
examination
examination

Diagnosis:
 Within 24 hours

 Photophthalmia
 Radiation Injuries
i. Photo-ophthalmia (occurrence of multiple
epithelial erosions, severe pain)  photo
keratoconjunctivitis. occurs on acute
Ultra-violet rays. exposure accompanied by photophobia,
Along seashores or headache, and in case of edema/bullae 
welders or treatment seeing haloes
of some skin diseases [Link] be responsible for:
a)Pterygium
b)Senile Cataract.
c)AMD.
 Punctate epithelial erosions
with +ve flourecein stain

Circumcorneal ciliary
injection
Photo-ophthalmia
 Radiation Injuries
i. Solar macular burns (up to macular hole
and detachment)
Infra-red rays in glass [Link] cataract (posterior cortical or
blowers and bakers nuclear cataract or posterior subcapsular)
up to posterior polar
[Link] exfoliation of the anterior capsule
 Within 1 week
 Sudden/recent onset of diplopia
 Entropion that is painful
 Herpes zoster Ophthalmicus (HZO) with eye
involvement
 Episcleritis (if cannot manage appropriately)
 Scleritis
 Within 1 week

Bell’s palsy
 Optic neuritis
 Severe infective conjunctivitis
 Vein occlusions

 Posterior vitreous detachment