Central Retinal

Artery Occlusion

Causes painless catastrophic visual
loss occurring over a period of
seconds;
Antecedent transient visual loss
(amaurosis fugax) may be reported.
Visual acuity ranges between
counting fingers and light
perception in 90% of eyes at initial
examination.

Classic presentation:

extremely sudden, acute unilateral
nonpainful visual loss.
Causes: Branch retinal artery is usually
embolic in origin and results in visual field
loss and atherosclerosis.

Visual acuity is only reduced if there is
foveal involvement.

Ocular exam: cherry red spot on fundoscopic
examination.

Acute central
retinal artery
occlusion with
cherry-red
spot (arrow)
and preserved
retina due to
cilioretinal
arterial supply
(arrowheads)
superficial retina
becomes opacified
due to ischemia.
A foveal cherry-red
spot is evident as a
result of visualization
of the choroidal
pigment and retinal
pigment epithelium
through the extremely
thin retina overlying
foveola.
This resolves within
46 weeks,leaving a
pale optic disk as the
major ocular finding
Remember!!!
Irreversible retinal damage occurs after 90
minutes of complete central retinal artery
occlusion in the subhuman primate model,
leaving little time in which to begin
therapy.
Treatment
Embolic central retinal artery occlusion - Sudden
decrease in intraocular pressure resulting in increased
retinal perfusion can be achieved with anterior
chamber paracentesis and intravenous acetazolamide.
nhaled oxygencarbon dioxide mixture induces retinal
vasodilation and increases the PO2 at the retinal
surface.
Thrombolytic therapy, infused directly into the
ophthalmic artery or administered systemically,
continues to be evaluated.
Systemic anticoagulants are generally not employed.

Chemical
Burns
Alkali
Liquifactive necrosis

Will denature collagen and destroy
vessels

More common and worse than acid
burns.

Require immediate ophthalmologic
consultation.

Found in: household cleaners, fertilizers

Alkali burns more severe than acid

Rapidly penetrates through ocular tissues
and will continue to cause damage long
after the injury is sustained, prolonged
lavage and repeated Ph checks are
needed.



Acid
Coagulative necrosis

Found in: automobile
batteries (sulfuric acid),
industrial cleaners.

Acids form a barrier of
precipitated necrotic
tissue that tends to limit
further penetration and
damage.

Other ocular burns

Thermal usually local effect
Electrical and Lighting Systemic
and wide spread effect coagulation of
proteins (cataract)

Remember!!!
White eye is a bad
eye!
If conjunctiva and
cornea appears
white, sign of very
severe burn.
ACUTE MANAGEMENT

pH determination
Immediate ocular irrigation: plain
NSS, lactated ringers or BSS sol.
2-3L in 1 hour
Repeat pH determination after
5mins.
Cul de sac cleaning and swabbing
Repeat irrigation

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