a brief slide of Retinal artery occlusion

1. Retinal Artery
Occlusion
Dr. Laxmi Dhawal
2nd
year resident
LEIRC,NAMS

2. 2
Introduction
• The blood supply to the inner layers of the retina is derived entirely
from the central retinal artery unless a cilioretinal artery is present.
• Retinal ischemia results from disease processes that affect the vessels
anywhere from the common carotid artery to the intraretinal arterioles.
• The signs and symptoms of arterial obstruction depend on the vessel
involved: occlusion of a peripheral arteriole may be asymptomatic,
whereas an ophthalmic artery occlusion can cause total blindness.

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BLOOD
SUPPLY OF
EYE

4. Central retinal artery
• First branch of Ophthalmic Artery
• Arises near optic foramen and
courses ahead as
 outside optic nerve
 in sub arachnoid space
 centre of optic nerve
 optic nerve head
 in Retina

5. Outside optic nerve ; runs a wavy course forward , below optic nerve , adherent to dural
Sheath about 10-15 mm behind eyeball , bends upwards to pierce dura and
Arachnoid
Subarachnoid space ; again bends upwards at right angle and invaginates
Pia to reach centre of optic nerve
Centre of optic nerve ; passes anteriorly and pierces lamina cribrosa to
Appear inside the eye
Optic nerve head ; lies superficially in nasal part of physiological cup , divides into
Superior and nasal branch and subdivides into temporal and nasal branch

6. In retina : the four terminal branches they
divide dichotomously as they proceed
towards ora serrata

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Blood supply of optic nerve head

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RETINAL CAPILLARIES

9. Cilioretinal artery

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Epidemiology
• 1-2 cases in 100,000 people per year
• Older adults (early 70s)
• Men> Women
• 1-2% B/L
• Comorbidities: HTN,DM, Smoking, Lipid disorder
• The life expectancy of patients with central retinal artery occlusion
(CRAO) is significantly lower (5.5 years) compared to an age-
matched population without CRAO (15.4 years).
Reference - Retinal artery occlusion epidemology

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CAUSES OF RETINALARTERY
OCCLUSION

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Retinal artery occlusion types
CRAO BRAO
Cilioretinal artery
occlusion
CRAO+CRVO
RAO

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Mechanisms of Occlusion
Embolic
80%
• Either from carotid or heart
• More common cause
• Site of obstruction is usually at the
site where the CRA pierces the dura
matter around the optic nerve
Thrombotic
20%
• Due to atherosclerosis
• Less common than embolus
• Site of obstruction is mainly at the
lamina cribrosa

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• Vasospastic
• Extravascular Compression
• Vasculitis

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Types of emboli
thrombus
calcific

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cholesterol
fat

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PATHOGENESIS FOR THROMBOTIC
COMPONENT
VIRCHOW’S
TRIAD

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Vasospastic

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Vasculitis
• Giant cell arteritis:1-2% of CRAO
• RA
• IBD
• Kawasaki disease
• SLE
• Toxoplasmosis
• PAN

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CENTRAL RETINALARTERY

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Pathophysiology
Acute obstruction of retinal artery
Axoplasmic stasis , intracellular edema & ischemic necrosis of inner
retina
Secondary collapse of capillary flow

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Cherry-red spot appearance of foveola , as foveola is nourished by the choroidal
circulation
NFL & inner retina opacified, more denser in the posterior
pole as a result of increased NFL thickness

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CRAO TYPES
CRAO
Non-Arteritic
Permanent
Transien
t
Non-Arteritic with
cilioretinal artery
sparing
Arteritic

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Clinical features
• Symptoms:
Sudden, severe, painless (except in GCA), unilateral visual loss,
occurring over seconds
History of amaurosis fugax (10%)
Relapsing and remitting course of visual loss (in arterial spasm)

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• Signs:
VA: CF to light perception (>90%)
VA of NPL usually suggests either GCA or ophthalmic artery
obstruction
Afferent pupillary defect
Anterior segment: Normal unless rubeosis develops

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Factors responsible for visual prognosis
Duration of retinal ischemia
• Complete recovery can occur if ischemia reversal & reperfusion
started in 90 minutes
• Some improvement possible upto 240 min (4 hours)
• Beyond that irreversible , massive damage occurs

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Types of CRAO
• Transient NA-CRAO :Best improvement, can improve by 82%
• NA-CRAO with cilioretinal artery sparing : can improve by 67%
• NA-CRAO : can improve by 22 %
• Arteritic CRAO : no improvement possible
source : Central retinal artery occlusion, Hayreh, Sohan Singh (10.4103/ijo.IJO_1446_18)

29. Fundus examination
• May be normal during the 1st
hour
Subsequently, posterior pole becomes opaque and edematous
except the foveola
Cherry red spot macula: Pale retina with reddish hue of fovea.
Box-carring or segmentation of the blood column in the
arterioles(cattle trucking)
• Occasionally, cilioretinal artery sparing is evident – part of macula
remains normal in colour.

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Chronic stages of CRAO (As retina
recovers)
Retina opacification
disappears
Arterial
attenuation in
58%
Optic atrophy in
91%
Cilioretinal
collaterals in 18%
Pigmentary
changes at macula
11%
1 month
3 month

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INVESTIGATION
• FUNDUS PHOTO

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FFA
ACUTE CRAO
• In NA CRAO- sluggish filling of
the retinal vasculature , & a
variable amount of residual
circulation
• Transient CRAO – almost
normal retinal circulation
• In arteritic CRAO- evidence of
posterior ciliary artery occlusion
LATE CRAO
• Complete restoration of retinal
arterial circulation(except for the
delayed arm to retina time)
within a few days to several
weeks of a CRAO

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In a patient with cilioretinal
artery

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OCT

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OCTA

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• Visual field
– Central scotoma –most common
– Paracentral scotoma
– Improve in 28% , remain stable in 57% and worsen in 7%
• Electroretinogram
– Inner retinal layers are more affected :↓ B-wave more than A-wave
– Ophthalmic artery occlusion: attenuation of both A wave & B wave due to
global ischemia

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Systemic work up
• History-medical,drugs,ocular disease
• Blood pressure
• Blood tests:
• FBS, HbA1c,CBC with differentials,platelets,
• PT/PTT,ESR
Lipid profile,serum homocysteine level,
ANA,FTA-ABS,VDRL or RPR
• Hb electrophoresis,cryoglobulins
• Coagulation profiles

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• HS-CRP,lipoprotein(a)
• Antiphospholipid Abs,lupus anticoagulant
• Sr,protein electrophoresis
Complete medical evaluation with careful attention to CVS disease or
hypercoagulability
ECHO,transesophageal echocardiography (TEE)
Carotid & vertebral doppler
Magnetic resonance imaging (MRI) including diffusion weighted imaging
(DWI) is the preferred imaging modality

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Treatment
• CRAO is an ocular Emergency
• Treatment Goals:
Increase retinal oxygenation
Increase retinal arterial blood flow
Reverse arterial obstruction
Prevent hypoxic retinal damage

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Within 24 hour of occlusion
Ocular massage
Anterior chamber
paracentesis

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Rebreathing
• Breathing a high oxygen (95%) and carbon
dioxide (5%) mixture, “carbogen”
• Lowering IOP

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• Hyperosmotic agents. Mannitol or glycerol have been used for their
possibly more rapid IOP-lowering effect as well as increased
intravascular volume.
• Sublingual isosorbide dinitrate
• Transluminal Nd:YAG laser embolysis/embolectomy
• Thrombolysis

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Systemic Management Following Retinal
Artery Occlusion
• Urgent referral to a specialist stroke clinic is advisable
• General risk factors as discussed above should be addressed and
smoking should be discontinued.
• Antiplatelet therapy
• Oral anticoagulation (e.g. warfarin) : Atrial fibrillation
• Carotid endarterectomy : indicated in patients with symptomatic
stenosis greater than 70%.
• Obstruction associated with temporal arteritis: High-dose
corticosteroids

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On Follow Up
• Follow as directed by managing internist and/or neurologist.
• Repeat eye examination in 1 to 4 weeks, checking for
neovascularization of the iris/disc/angle/retina (NVI/NVD/NVA/NVE)
• Photocoagulation: Iris neo-vascularization
• Long-term management aims are to identify and address the
underlying cause in order to prevent further ischaemic events (e.g.
investigate and treat hypertension and reduce risk factors for
atherosclerosis) and low-dose aspirin may be beneficial.

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Prevention
• Raising awareness “BE FAST”
• Warning sign : amaurosis fugax.
• Some basic first aid measures should be explained to the patient :
ocular massage , breathing in a bag
• Patient can be instructed to sublingial sorbitrate or use a nitroglycerin
patch
• Report to an ophthalmologist without any delay

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Prognosis
• Vision remains stable ( unless associated with NVG)
• Risk of cerebral stroke is high
• Life expectancy after CRAO : 5.5 years compared to 15.4 years for an
age-matched population
• For patient with visible emboli , the mortality rate is 56% for the next
9 years compared to 27% for an age matched population

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Intravenous Thrombolysis With Low-dose
Recombinant Tissue Plasminogen Activator
in Central Retinal Artery Occlusion
“American Journal of Ophthalmology, August-2008”
• Purpose:
To evaluate the beneficial effect of intravenous thrombolysis aiming at
rapid restoration of blood flow during the early hours of a central retinal
artery occlusion (CRAO).
• Conclusions:
Thrombolytic treatment with intravenous low-dose rt-PA is of value for
an improved visual recovery in patients with acute CRAO, if
administered within the first 6.5 hours after the onset of symptoms.

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European assessment group for lysis in the
eye (EAGLE)
• In 2010 the EAGLE study group published the results of the first
prospective, randomized clinical trial evaluating the effect of local intra-
arterial fibrinolysis (LIF) using recombinant tissue plasminogen activator
(rtPA) compared with conservative treatment(CST) for acute non arteritic
CRAO.
• At 1 month, the mean best-corrected visual acuity improved significantly
in both groups (60% among CST and 57.1% among LIF)
• Adverse reaction was noted in 4.3 % in CST group and 37.1% in LIF
group.
• In light of these 2 therapies,similar outcomes and the higher rate of adverse
reactions associated with LIF, we cannot recommend LIF for the
management of acute CRAO.

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Recent Advances
• PPV endovascular surgery
• Digital Subtraction Angiography (DSA)

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Branched retinal artery occlusion
• An abrupt diminution of blood flow through one or more
of the branches of central retinal artery causing ischemia
of the inner retina of the supplied territory
Epidemiology
• Less common than CRAO
• Mean age: 60 years
• M>F=2:1 above 50 years, but equal in below 50 years
• Laterality: R>L=60:40
• More incidence in temporal retina than nasal

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Etiopathogenesis
• More than 2/3rd
of cases are due to emboli
• Risk factors:
Non-modifiable: Positive family history , race, ethinicity
Modifiable:
Hypertension
Elevated lipid levels
Cigarette smoking
Diabetes mellitus

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Clinical features
• Symptoms :
Abrupt, painless loss of vision in the visual field corresponding to the
territory of the obstructed artery(altitudinal or sectoral field loss)
Amaurosis fugax in about 1/4th
of patients
• Signs :
VA is variable
Intact central visual acuity in about 50% of patients
RAPD may be present, but determined by extent of retinal
involvement

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Fundus examination
• Retinal whitening, resulting from oedema corresponding to the area
of ischemia
• Retinal emboli can be seen
• Flame shaped hemorrhages at the margin of ischemia may be
present
• Narrowing of arteries and veins with segmentation of blood
column.

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Contd…
• In chronic case, loss of the nerve fiber layer in the affected area may
be apparent
• Arteriolar collaterals on the optic disc or at the site of obstruction may
develop

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Diagnosis
• Mainly clinical, based on history and clinical findings
• FFA
Will show non perfusion distal to the site of embolus or obstruction
Extreme delay of arterial phase
Late staining or even leakage from the embolus site and arterial walls

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Investigation
• FFA: useful in diagnosis
• Goldman Perimetry: will show
the extent of visual field loss
• Other investigations for risk
factors as in CRAO should be
done

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Treatment
• No proved treatment
• Ocular massage or paracentesis may be successful in dislodging an embolus
• Laser photocoagulation has been employed to 'melt' an embolus, without
improvement in the vision
• systemic anticoagulation may prevent further events in patients with
coagulopathy

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Course and outcome
• Most patients remain with a fixed visual field defect, but intact central
acuity
• About 80% of eyes recover to 6/12 or better central acuity
• Retinal neovascularization has been reported, but uncommon
• Iris neovascularization does not occur

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Branch Retinal Artery Occlusion: Visual
Prognosis
July 2008,American Journal of Ophthalmology
• Purpose : To evaluate the visual prognosis in eyes with branch retinal
artery occlusion (BRAO).
• Conclusions: Visual prognosis after BRAO seems to be correlated to
presenting VA. Eyes with initial VA of 20/40 or better usually
remained at 20/40 or better. Individuals with poor VA of 20/100 or
worse generally did not show the significant improvement reported in
previous studies.

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Cilioretinal artery obstruction
• Presents in 18-32% of population and arises from
posterior ciliary circulation.
• Supplies the macula and papillomacular bundle.
• Cilioretinal arteries enter on the temporal aspect
of optic disc
• Cilioretinal artery obstruction appears as areas of
superficial retinal whitening along the distribution
of these vessels

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Clinical variants
• Isolated cilioretinal obstruction (40%)
In young individuals with
A systemic vasculitis
Usually good prognosis

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Cilioretinal obstruction with CRVO (40%)
Generally behaves as a nonischemic central
retinal vein obstruction with a good central
visual prognosis.
The scotoma from the artery obstruction is
usually permanent.
Cilioretinal artery obstruction with ischemic
optic neuropathy (15%)
Affects patients with giant cell arteritis
Carries good prognosis

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Ophthalmic artery obstruction
• Very rare,5% of patients with apparent CRAO
have in reality an acute ophthalmic artery
occlusion.
• Causes:
Associated local orbital or systemic diseases,
which include orbital mucormycosis, orbital
trauma, retrobulbar anesthesia, depot
corticosteroid injection, atrial myxoma, or carotid
artery disease.
Funduscopy; Intense retinal opacification
resulting from inner and outer retinal ischemia.

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• OAO can be differentiated clinically from CRAO by the following
features:
Severe visual loss - bare or no light perception.
Intense ischemic retinal whitening that extends beyond the macular
area.
Little to no cherry-red spot.
Marked choroidal perfusion defects on fluorescein angiography.
Non-recordable electroretinogram.
Late retinal pigment epithelium alterations.

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Combined Artery And Vein Obstructions
• Central retinal artery obstruction combined with
simultaneous central retinal vein obstruction
rarely occurs.
• Present with acute, severe loss of vision, usually
to no light perception.
• The visual prognosis is generally poor
• the risk of neovascularization of the iris is about
75%

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Cotton wool spots
• Acute obstruction in the distribution of the radial
peripapillary capillary net leads to the formation of an
NFL infarct, or CWS, which causes impaired
axoplasmic transport in the NFL
• These inner retinal ischemic spots are superficial, white,
and typically 1/4th
disc area or less in size
• They usually fade in 5–7 weeks, although spots present
in association with DR (MCC) often remain longer

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• Fluorescein angiography demonstrates a lack of filling of the capillaries
in the area of the cotton-wool spot, although this appearance may be due
in part to masking by the overlying opaque retina
• OCT

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Paracentral acute middle
maculopathy(PAMM)
• In patients with partial or incomplete CRAO,
ophthalmoscopy may show a more subtle and non-diffuse
retinal whitening in the middle layers of the perifoveal
macula, with peri-arterial sparing.
• This pattern of ischemia, known as paracentral acute
middle maculopathy (PAMM),
• The primary etiology in PAMM may be ischemia of the
deep capillary system
• The typical presentation is acute onset of diminished
central visual acuity or paracentral scotoma.

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Arterial macroaneurysm
• Retinal arterial macroaneurysms are acquired ectasias of the first 3
orders of retinal arterioles.
• Large macroaneurysms can actually traverse the full thickness of the
retina.
• Vision loss may occur from embolic or thrombotic occlusion of the
end arteriole (white infarct) or from hemorrhage in any retinal layer.
• Often, there are multiple arterial macroaneurysms, although only 10%
of cases are bilateral.

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• Arterial macroaneurysms are associated with systemic arterial
hypertension in approx. 2/3rd
of cases
• Typically, the macroaneurysm closes and scleroses spontaneously,
with accompanying resorption of related hemorrhage
• Initial management is usually observation. In most instances, closure
can be achieved with moderate- intensity laser treatment of the retina,
performed immediately adjacent to the macroaneurysm

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Ocular ischemic syndrome

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RAO in young
• Protein S deficiency , protein C deficiency
• Cannabis smoke inhalation
• Sickle cell anemia
• Homocystinuria
• Cystic fibrosis
• Chronic alcoholism
• OCP, SLE, Sleep apnoea ,Sjogren syndrome, multiple myeloma
• Splenectomy , intense exercise, Factor V leiden mjutation
• Migraine , spherocytosis, CNS TB ,cat scratch disease, Trauma
• DM,HTN( arterial,pulmonary), ocular surgeries
• Antiphospholipid antibody syndrome , pregnancy , thrombophilia

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Bibiliography
• AAO, Retina and vitreous 2023-2024
• Myron yanoff- Duker ophthalmology-5th
edition
• Central retinal artery occlusion, Hayreh, Sohan Singh (10.4103/ijo.IJO_1446_18)
• Albert and Jakobiec’s Principles and Practice of Ophthalmology
Fourth Edition
• Kanski’s clinical ophthalmology, a systemic approach-9th
edition

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Thank you