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MANAGEMENT OF CENTRAL RETINAL ARTERY OCCLUSION

YOGI PRATAMA
VITREORETINA SUBDIVISION DEPARTMENT OF
OPHTHALMOLOGY FACULTY
OF MEDICINE ANDALAS UNIVERSITY
2021
INTRODUCTION
Central Retina Artery Occlusion (CRAO) is a condition in
which a sudden decrease in blood flow in the central retinal
artery causes ischemia in the inner of the retina.

This condition is a true ocular emergency


that requires immediate treatment

This disorder is generally found in


patients with an average age of 60 years

Almost all cases of CRAO are unilateral


and only 1%-2% of cases are bilateral
• CRAO has a close relationship with various
systemic diseases, including hypertension, heart
disease, vascular disease, diabetes mellitus, sickle
cell disease, and giant cell arteritis.

• Typical clinical picture of CRAO is a history of a


sudden decrease in visual acuity, the posterior
retina appears whiter, and a cherry red spot is
found in the central fovea.

• Even with prompt treatment, it is said that the


prognosis for CRAO remains poor
• Management of CRAO consists of acute management and secondary prevention to
prevent ischemic events
• Complete improvement < 10%
• Conventional therapy can include ocular massage, reducing intraocular pressure,
increasing retinal blood flow, vasodilatation of retinal blood vessels, reducing retinal
edema, maintaining oxygenation until spontaneous reperfusion, and treating
thrombus with thrombolytics.
RETINA ANATOMY
02
The retina gets its blood supply from Occlusion in the central retinal
two sources, the first from branches artery only affects the inner part of
of the central retinal artery, which the retina
supplies blood to the inside of the
retina, and the second from the 01
choriocapillary choroid, which
supplies blood to the outside of the 03
retina.

04
A= Arachnoid, C = koroid, CRA = arteri retina
sentralis, Col. Br. = cabang kolateral, CRV =
vena retina sentralis, D = duramater, LC =
lamina kribrosa, ON = nervus optikus, PCA =
arteri siliaris posterior, PR = daerah prelaminar,
R = retina,
S = sklera; SAS = ruang subarachnoid

The central retinal artery pierces the medial inferior portion of the optic nerve sheath, about 12 mm posterior to the eyeball. It then
continues on to the optic disc and divides into superior and inferior papillary branches.
Retinal vessels are end
vessels that do not
normally anastomose
The silioretinal artery is
present in approximately
14% of the population and
as many as 25% of patients

The silioretinal artery is present in approximately 14% of the population and as many as 25% of patients with central retinal artery
occlusion have silioretinal arteries. Branches of the cilioretinal artery, which arise from the short posterior ciliary artery, supply the
macula via the choroidal circulation.
PATHOPHYSIOLOGY

In CRAO, the occlusion is caused by emboli originating in the carotid arteries, platelet-fibrin emboli are associated
with atherosclerosis of the great vessels and calcific emboli from valvular heart disease.

? Embolic phenomena in the carotid


distribution area, which may include
transient ischemic attack on the retinal
circulation, are the most common cause
of amaurosis fugax.
CLASSIFICATION

• Non arteritic CRAO

• Non-arteritic CRAO constitutes


2/3 of all cases of CRAO,
caused by platelet fibrin
thrombus and embolism. This
type shows the classic picture
of CRAO in the form of retinal
whitening/opacification, cherry
red spots
This type has the
classic clinical
features of non-
arteritic
permanent CRAO
and the presence
Non-arteritic CRAO with Name Here of a patentName Here
cilioretinal artery sparing Programmer
Programmer
cilioretinal artery
Transient non arteritic CRAO

• Causes transient monocular blindness,


occurring in about 15-17% of CRAO cases.
Transient non-arteritic CRAO is analogous to
transient ischemic attack (TIA), with the best
visual prognosis.
Arteritic CRAO is present in only
5% of cases of CRAO. Giant cell
arteritis (GCA) is a major cause of
arteritic CRAO. GCA is also
associated with anterior arteritic
ischemic optic neuropathy
(AAION).

Arteritic CRAO
Management

 Management The ideal therapy is still debated, acute treatment


should be given within 3 hours of vision loss to prevent
permanent retinal ischemia

 > 12 hours result poor visual function


Ocular massage

Ocular massage is performed by compressing the eyeball with pressure on the ocular
either digital over closed eyelids for 10-15 seconds, followed by sudden release.
Laser or Embolectomy Surgery

Embolisms seen in CRAO can be removed using an


Nd:Yag laser or surgery (vitrectomy with cannulation)

the procedure was complicated by the occurrence of vitreous


hemorrhage in 50% of patients and the formation of a central
retinal artery false aneurysm in 1 case.
Use of drugs to lower intraocular
pressure, either drugs or systemic drugs
for treatment (oral or intravenous or
acetazolamide)

Acetazolamide used for acute


management of CRAO to increase
retinal artery perfusion pressure
 Anterior chamber Parasentesis

 Anterior chamber paracentesis is performed by inserting a small gauge syringe through the corneal
limbus into the anterior chamber and withdrawing a small amount of aqueous humor. This is
expected to reduce intraocular pressure rapidly, resulting in retinal artery dilatation and an increase
in retinal artery perfusion pressure
Hyperventilation or Drugs That Induce
Vasodilation or Increase

1 2
Carbogen Inhalation
Erythrocyte Flexibility

Increased CO2 Systemic drugs, such as


concentration prevents sublingual isosorbite
oxygen-induced dinitrate (ISDN) and
vasoconstriction of retinal pentoxifylline, can also
blood vessels and be used for the treatment

3 4
causes retinal arteriolar of CRAO. ISDN can
dilatation, thereby cause retinal vascular
increasing retinal dilatation and can slightly
perfusion. lower intraocular
pressure
• Hyperbaric Oxygen
• Thrombolytic
Thrombolytics such as urokinase, streptokinase, and tissue plasminogen activator
(tPA) have as much efficacy in the acute management of CRAO as they are in acute
cerebral ischemia.
• Corticosteroids
Corticosteroids are given in cases of arteritic CRAO suspected of being caused by
GCA .
conclusion
• CRAO is an ocular emergency which is a secondary effect of certain systemic diseases. The main complaint
in CRAO patients in general is a drastic decrease in visual acuity in one eye and is not accompanied by pain.

• CRAO is closely related to systemic diseases such as hypertension, atherosclerosis, diabetes mellitus, heart
valve disease and giant cell arteritis. The pathophysiology is the occurrence of embolism, thrombosis, vascul
ar spasm and hypertensive arterial necrosis associated with this systemic disease.

• Management of CRAO that needs to be considered is the acute management of CRAO and secondary preve
ntion of retinal circulation ischemia.

• Therapies for CRAO include ocular massage, laser embolectomy surgery, medications to increase retinal art
ery perfusion, COA paracentesis, inhaled carbogen, vasodilator agents, hyperbaric oxygen, thrombolytic ther
apy and corticosteroids. All of the above measures were selected based on the associated systemic disease.

• Management of CRAO aims to improve central retinal artery perfusion, overcome embolic occlusion, reduce I
OP and retinal arteriolar vasodilation.
Thank you

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