Ocular emergency
Ocular emergency
 True



emergency
Chemical burn
Central retinal artery occlusion
Rx should be instituted within
minutes
 Urgent











situations
Acute narrow angle glaucoma
Endophthalmitis
Penetrating injury of the globe
Orbital cellulitis , Preseptal cellulitis in children
Cavernous sinus thrombosis
Corneal ulcer
Gonococcal conjunctivitis
Giant cell arteritis with acute ischemic of optic nerve
Acute retinal detachment
Hyphema
Rx should be instituted within
one to several hours
 Semi-urgent







situations
Optic neuritis
Ocular tumors
Acute exophthalmos
Old retinal detachment (involve macular >1 wk)
Strabismus in young children
Blow-out fracture of the orbit
Rx should be instituted within
days
CRAO
Unilateral, sudden, painless loss of vision
VA: FC (counting finger) to PL (light
perception) in about 90% of cases
better vision in cases of cilio-retinal artery
sparing (~ 15%)
NPL (no light perception) in cases
of ophthalmic artery occlusion
Fundus finding
Cherry-red spot appearance
opaque or whitened and edematous retina,
particularly in the posterior pole due to retinal
ischemia
Causes
Emboli or thrombosis (mostly)
Connective tissue diseases
- Giant cell arteritis
- SLE
- Rheumatoid arthritis
Others
Management
Treat without delay, before work up
irreversible damage within about 90 minutes of
complete occlusion
Reduce intraocular pressure (IOP)
- ocular massage
- anterior chamber paracentesis
- antiglaucoma drugs
Inhalation therapy: carbogen (mixture of 95%
oxygen and 5% carbon dioxide)
Prognosis
Permanent severe loss of vision from
retinal infarction despite reopening or
recanalization of the central retinal artery
Irreversible damage within about 90
minutes of complete occlusion
Prognosis
Questionable efficacy of treatments
Cardiovascular disease is
the leading cause of death
in patients with CRAO!!
Chemical burn

The severity depends on



the volume and duration of contact
the pH
the inherent toxicity of the chemical
Alkali
Alkalis cause saponification of fatty acids in
cell membranes and ultimately cellular disruption
lye (NaOH)
caustic potash (KOH)
fresh lime [Ca(OH)2]: plaster, cement
ammonia (NH3): househole cleaner,
fertilizer, refrigerant
Acid
 Acids denature and precipitate proteins in
tissues they contact
battery acid (H2SO4)
bleach
fruit & vegetable preservatives
industrial solvents
Degree
 Corneal
haziness
 Perilimbal blanching
 Cells in anterior chamber
Mild degree
Erosion of corneal epithelium
Faint haziness of cornea
No ischemic necrosis of perilimbal conjunctiva
and sclera (no blanching)
Moderate degree
Markedly hyperemic eye
Corneal opacity with blurring of iris detail
Corneal edema
Slight limbal ischemia (partial blanching)
Anterior uveitis
Severe degree
Marked corneal opacity with blurring of the
pupillary outline
Marked corneal edema
Marked limbal ischemia (total blanching)
Whitening of
the external eye
Severe uveitis
Ocular adnexa
Long term complications
 Superficial
neovascularization of the cornea
 Persistent epithelial defect
 Corneal thinning and perforation
 Permanent visual impairment from corneal
scar
Corneal transplantation
PKP (corneal transplantation)
Management

Immediate and copious irrigation
relief pain: topical anesthetic agent
at least 1,000-2,000 cc of NSS , test pH
avoid direct pressure if rupture suspected
remove any foreign bodies
careful examination after irrigation
for other ocular injuries
Management
 Decreasing


Antiglaucoma drugs
Limiting matrix degradation


Topical steroid
Monitoring IOP


inflammation
Ascorbate, collagenase inhibitor
Promoting reepithelialization

Tear (non-preservatives)
 Prophylaxis
topical antibiotic
Acute glaucoma
Acute attack or acute angle-closure
glaucoma
Unilateral, sudden, painful loss of vision
Risk factors:
- elderly age, female>male
- small, hyperopic eye
- familial risk
- previous attack of the fellow eye
- dark environment
Sign & symptom
Aching pain, +/- nausea & vomiting
Decrease vision +/- halos due to corneal edema
Red eye (conjunctival congestion maybe ciliary injection
or mixed injection)
Very tense eyeball (IOP often > 40-50 mmHg)
Sami dilated fixed pupil
Narrow angle in both eyes
Management
Rapidly lower high IOP by hyperosmotic agents
(oral acetazolamide, 50%glycerine or 20%mannitol)
Other anti-glaucoma drugs:
- b adrenergic antagonist
- parasymmatomimetic agent
- carbonic anhydrase inhibitor (CAI)
- selective a 2 adrenergic agonist
- prostaglandin analog
Management
Treatment of choice: peripheral iridectomy;
PI, (laser or surgical PI) for both eyes
indicated when the cornea is clear enough
Other surgical treatments:
filtering surgery
tube implant surgery
Orbital cellulitis
 Clinical appearance
 eyelid edema and erythema
 proptosis, chemosis , pain on eye movement ,
external ophthalmoplegia, decreased vision ,
RAPD +
 malaise , headache , fever
Orbital cellulitis
 Causes

Periorbital structures
• most commonly from the paranasal sinuses
• the face, the globe, and the lacrimal sac


Trauma or surgery
Hematogenous spread from bacteremia
Orbit: Infection





(Preseptal cellulitis)
Orbital cellulitis
Subperiosteal
abscess
Orbital abscess
Cavernous sinus
thrombosis
Preseptal
Inflammation
Fever
Lid edema
EOM limitation
Proptosis
Hospitalization
Anterior to
septum
Mild
+
No
No
Only children
Orbital
Beyond septum
++
+++
Yes
Yes
Yes
Management



Vision loss due to high orbital pressure :
lateral cantholysis, rarely in very severe case,
orbital decompression
Systemic ATB : 10-14 days, longer in severe
case
Treat causes
Complication and sequelae

Corneal exposure with secondary ulcerative
keratitis

Facial cellulitis, necrotizing fasciitis

Brain abscess, meningitis, osteomyelitis

Panophtalmitis

Sepsis
Endophthalmitis
 Postoperative,



posttraumatic, endogenous
Painful visual loss
Ciliary injection, chemosis, corneal edema,
and eyelids edema
Cells in A/C, vitreous