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11/11/20 November 6, 2020 Page 1
Contents
11/11/20 November 6, 2020 Page 2
Introduction
• Common vascular disorder
• 2nd most common cause of blindness after
Diabetic retinopathy
• Cause ….obstruction to venous flow
• Associated risk factors: Multifactorial
• Classification
• -Site of involvement
• -Extent of retinal perfusion
11/11/20 November 6, 2020 Page 3
Demographics
• InAustralia,prevalenceof RVO…
– 0.7%inptsaged49-60yearsto4.6%inptsolder than80
years a
• Seasonalvariationfound…greaterthan20,000patientsinthe
monthofJanuary
a. MitchellP, SmithW, ChangA. PrevalenceandassociationsofretinalveinocclusioninAustralia.TheBlueMountainsEye
Study.Arch Ophthalmol. Oct 1996;114(10):1243-7
b. HoJD,TsaiCY, LiouSW, etal.Seasonalvariationsintheoccurrenceofretinalveinocclusion:afive-year nationwidepopulation-
basedstudyfromTaiwan.Am J Ophthalmol. Apr 2008;145(4):722-728.
11/11/20 November 6, 2020 Page 4
Common mechanism
Severe non perfusion leads to edema
Edema / hemorrhages
Dysfunction leakage of fluid and blood
Back pressure on capillaries endothelial junction
Venous blockage
11/11/20 November 6, 2020 Page 5
Predominant associations
• Royalcollegeofophthalmologistsguidelines:Feb. 2009
Patient
Group
NoObvious
Cause
Age<50
yrs
40%
Age>50
yrs
21%
Asian 10.7%
West
Indian
8.3%
Recurren
tcases
Hypertensio Hyperlipidemia Diabetes
n Mellitus
25% 35% 03%
64% 34% 4-15%
64% 50% 29%
83% 33% 38%
88% 47% 3%
6%
11/11/20 November 6, 2020 Page 6
Pathogenesis
• Virchowtriad:
– Lossofvesselwallintegrity
– Alteredbloodflow
– Hypercoagulablestate
• Disturbanceleadstothrombusformation&
vesselocclusion
11/11/20 November 6, 2020 Page 7
• Klein&Olwinpostulated:
– Compressionofveinbyscleroticcentralretinalartery
– Occlusionbyprimaryvesselwalldisease(degenerativeor
inflammatory)
– Hemodynamicdisturbance
KleinBA,OlwinJH.Asurveyofthepathogenesisofretinalvenousocclusion.ArchOphthalmol1956;56:207.
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RVO resistancetovenousflow
blood stagnation &ischemia stimulates
productionof VEGF (vascularendothelial growthfactor)
neovascularization
capillaryleakage (edema)
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Etiology
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Any factor which directly or indirectly activates
virchowtraid….
External compression
– Arteriosclerosisof CRA (HTN, DM,
Hyperlipidemia)
– Glaucoma(5 timesmorelikelytohave CRVO)
– Papilledema
– Thyroideye disease
– Orbitalspaceoccupying lesions
– Cavernoussinus thrombosis
– Closed-Head trauma
– Retrobulbarinjections
* Morganetal.ocularcomplicationsassociatedwithretrobulbarinjections.Ophthalmology1988;95:660.
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– SystemicVasculitis
• TB
• AIDS
• Syphilis
• SLE
– Localized inflammation
• Sarcoidosis
• Serpiginouschoroiditis *
* Bluemenkranzetal.atypicalserpiginouschoroiditis.Archophthalmol1773;1982:100.
Disease of vessels wall
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Hematological disorders
•
resistance
– Lupus anticoagulant
deficiency
– Anticardiolipin antibodies
– Protein C & Protein S
deficiency
– Antithrombin III def
– Antiphospholipid
antibodies
• Nephrotic syndrome
•Clotting disorders Paraproteinemia
– Activated protein C – Multiple myeloma
– Cryoglobulinemia
• Drugs
– Oral contraceptive
– Diuretics
• Blood dyscrasia
– Lymphoma
– Leukemia
– Polycythemia vera
– Sickle cell disease
11/11/20 November 6, 2020 Page 15
MANAGEMENT
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History
• Symptoms
– Painlesslossof vision(mild tosevere)
– Usually unilateral
• Past&Personal Hx
– HTN,DM, smoking
– Hyperlipidemia
– Bleedingorclotting disorders
– Glaucoma
– Oralcontraceptive use
– Headtrauma/ retrobulbarinj
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Examination
– VA&BCVA
– Pupillary reactions
– Congestionof conjunctivaor cornea
– Iris…neovessels
– AC angle…neovessels
– IOP
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• Fundus findings
– Retinalhemorrhages
– Extensivehemorrhages…blood&thunder
appearance
– Dilatedtortuous veins
– Cottonwoolspots,macular edema
– Opticdisc
• Edema/ optociliaryshunts/ atrophy
– Neovessels
• NVD/ NVE……vitreous hemorrhage
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Differential diagnosis
• Ocularischemic syndrome
• Diabetic retinopathy
• Papilledema
• Radiation retinopathy
• Retinopathydueto anemia
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Ocular investigation
• ERG
– Reducedb-wave amplitude
– reducedb:a ratio
– b:aratio< 1suggestsan I-CRVO
• OCT
– Formacular thickness
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• Fluoresceinangiography
– Veryusefulfor detecting…
• Capillary nonperfusion
• Neovascularization
• Macularedema
– ReliabletodifferentiatebtwI-CRVO &NI-CRVO
– >10DD retinalnonperfusionistermedas I-CRVO*
* TheCentralVeinOcclusionStudyGroup Arandomizedclinicaltrialofearlypanretinalphotocoagulationforischemic
centralveinocclusion:TheCentralRetinalVeinOcclusionStudyGroup NReport.Ophthalmology1995;102: 1434-44.
11/11/20 November 6, 2020 Page 22
Treatment
• Systemictreatment a
– Anticoagulants…Heparin, warfarin
– Fibrinolyticagents…Streptokinase,tissue
plasminogen activator
– Antiplatelets…Aspirin, prostacyclin
– Hemodilution
• Nofavorableeffectsonnaturalhistory b
a MahmoodT. CRVO: currentmanagementoptions.PakJOphthalmol2009.25(1):56-9.
b Mohamed Q etal. interventionsfor CRVO. an evidence-basedsystematic review. Ophthalmology. 2007; 114:507-19
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• Ocular treatment
– Pharmacotherapy
– Photocoagulation
– Newtechniques(Surgical)
• Certainclinicaltrialsneedsattention
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CENTERAL RETINAL VEIN OCCLUSION
• It is more common than the artery occlusion.
• It typically affects > 6th or 7th decade of life.
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Etiology
• 1. Pressure on the vein by a sclerotic retinal artery
where the two share a common adventitia (e.g., just
behind the lamina cribrosa and at arteriovenous
crossings).
• 2. Hyperviscosity of blood as in polycythemia,
hyperlipidemia and macroglobulinemia.
.
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• 3. Periphlebitis retinae which can be central or
peripheral.
• 4. Raised introcular pressure. Central retinal vein
occlusion is more common in patients with
primary open-angle glaucoma.
• 5. Local causes are orbital cellulitis, facial
erysipelas and cavernous sinus thrombosis
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Classification
• Centralretinalveinocclusion(CRVO)
– Non-ischemic CRVO
– Ischemic CRVO
• Branchretinalveinocclusion(BRVO)
– Major BRVO
– Macular BRVO
• Hemicentralretinalveinocclusion(HCRVO)
– Non-ischemic HCRVO
– Ischemic HCRVO
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Central retinal Vein occlusion
• Painlesslossof vision
• Site:occlusionatorposteriortolamina
cribrosa
• Twoclinicaltypes
– IschemicCRVO(I-CRVO)
– Non-ischemic (NI-CRVO)
• ‘Research into CRVO is fraught with challenges, from
accurate disease classification to its treatment; even the
most prestigious trials have become controversial’
• MadhusudhanaKC,NewsomRS.Centralretinalveinocclusion:thetherapeuticoptions.CanJOphthalmol.Apr2007;42(2):193-5.
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Demographics
• NI-CRVO morecommonthanI-CRVO
• Noracial predilection
• Men> women
• >90%CRVO occursin> 50yrs age
a KleinR etal.Theepidemiologyofretinalveinocclusion:theBeaverDamEyeStudy.TransAmOphthalmolSoc2000;98:133–41. b
MitchellPetal.PrevalenceandassociationsofretinalveinocclusioninAustralia.TheBlueMountainsEye Study. Arch
Ophthalmol1996;114:1243–7.
c KleinR etal.The15-yearcumulativeincidenceofretinalveinocclusion:theBeaverDamEye Study.Arch
Ophthalmol. Apr2008;126(4):513-8.
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Non-ischaemic CRVO (venous stasis Retinopathy)
Most common clinical variety (75%).
Characterized by mild to moderate visual loss.
Fundus examination
 In early cases :Mild venous congestion and tortuosity, a few
superficial flame-shaped hemorrhages more in the peripheral
than the posterior retina,
 In late stage (after 6-9 months) : Mild papilloedema and mild or no
macular oedema. There appears sheathing around the main
veins, and a few cilioretinal collaterals around the disc. Retinal
haemorrhages are partly absorbed. Macula may show chronic
cystoid oedema in moderate cases or may be normal in mild
cases.
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Treatment
is usually not required.
The condition resolves with almost normal vision in
about 50 percent cases.
Visual loss in rest of the cases is due to chronic
cystoid macular oedema, for which no treatment is
effective.
However, a course of oral steroids for 8-12 weeks
may be effective.
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Ischaemic CRVO (Hemorrhagic retinopathy)
1. Acute (sudden) complete occlusion of central retinal
vein.
2. It is characterized by marked sudden visual loss.
Fundus examination in early cases:
1. Massive engorgement,
2. Congestion and tortuosity of retinal veins,
3. Massive retinal hemorrhages (almost whole fundus is full of
hemorrhages giving a ‘splashed-tomato’ appearance),
4. Numerous soft exudates, and papilledema.
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• Macular area is full of hemorrhages and is severely
edematous.
• In late stages:
• Marked sheathing around veins &collaterals is seen
around the disc.
• Neovascularisation may be seen at the disc (NVD) or
in the periphery (NVE).
• Macula: shows marked pigmentary changes and
chronic cystoid oedema.
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Complications
• Rubeosis iridis
• Neovascular glaucoma (NVG) (occur in more than 50 percent cases within 3
months (so also called as 90 days glaucoma).
• A few cases develop vitreous hemorrhage & proliferative
retinopathy.
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Natural history of CRVO
• NI-CRVO
– Completelyresolution…10% a
– ME resolves…30%in6-15 monthsb
– About50%...VAis6/60 orworse a
– 1/3rd progressto I-CRVO in6-12 monthsa
– Neovesselsdevelop…33%in12-15 months b
a. Central Vein Occlusion Study Group. Baseline and early natural history report. Arch Ophthalmol. Aug 1993;111(8):1087-95
b. McIntoshRL etal.NaturalHistoryofCentralRetinalVeinOcclusion:AnEvidence-BasedSystematicReview.Ophthalmology
2010;117:1113–1123
11/11/20 November 6, 2020 Page 37
Treatment
• Panretinal photocoagulation (PRP) or cryo-application, if the
media is hazy, may be required to prevent neovascular
glaucoma in patients with idespread capillary occlusion.
Photocoagulation should be carried out when most of the
intraretinal blood is absorbed, which usually takes about 3-4
months.
11/11/20 November 6, 2020 Page 38
(2) Branch retinal vein occlusion (BRVO)
• It is more common than the central retinal vein
occlusion.
• It may occur at the following sites: main branch at the
disc margin causing hemispheric occlusion, major
branch vein away from the disc,
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1. AT A-V crossing causing quadrantic occlusion and
small macular or peripheral branch occlusion.
2. In BRVO oedema and haemorrhages are limited to
the area drained by the affected vein Vision is
affected only when the macular area is involved.
3. 2nd ry glaucoma occurs rarely in these cases.
4. Chronic macular oedema and neovascularisation
may occur as complications of BRVO in about 1/3
cases.
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Treatment
• Grid photocoagulation may be required in
patients with chronic macular oedema. In
patients with neovascularisation, scatter
photocoagulation should be carried out.
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Non-Ischemic Ischemic
Frequency 75-80% 20-25%
VA betterthan 6/60 Worsethan 6/60
RAPD Slightor nil Marked
VF defect rare Common
Fundus Lesshemorrhages &
cottonwool spots
Extensivehemorrhages &
cottonwool spots
FFA Good perfusion Non-perfusion> 10 DD
ERG Normal Reducedb-wave amplitude,
reducedb:a ratio
Prognosis 50%...6/60 or better 60%...Rubeosis &NVG
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• Principlecausesof visualmorbidity
– Macularedema (ME)
– Neovascularization(NVI>NVD>NVE)&
Neovascularglaucoma(100 days)
– Vitreoushemorrhage
– Opticatrophy
Complications
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Differential diagnosis
• Ocularischemic syndrome
• Diabetic retinopathy
• Papilledema
• Radiation retinopathy
• Retinopathydueto anemia
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– Limitations
• Itprovideslittleinformationinearlystagesbczof
extensivehemorrhages
• Poorqualityof angiograms
• Inabilitytovisualizeperipheral retina
• Interpretationissubjective&hence variable
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FFAfindings
– Delayedarteriovenous transit
– Macular edema
– Stainingalongtheretinalveins
– Microaneurysms,Arteriovenous collaterals
– NVD, NVE
– Dilatedopticnervehead capillaries
– Nonperfusion…hypofluorescence
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Initial medical investigations
•
– FBC &ESR
– Renalfunction tests
– Randomblood glucose
– Lipidprofile
– Plasmaprotein
electrophoresis
– Thyroid function
– ECG
Royalcollegeofophthalmologistsguidelines:Feb. 2009
•ALL PATIENTS ACCORDING TO
CLINICALINDICATION
– Thrombophilia screen
– Anticardiolipinantibody
– CRP
– SerumACE
– Autoantibodies
– CXR
– Fasting homocystine
levels
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• Systemictreatment a
– Anticoagulants…Heparin, warfarin
– Fibrinolyticagents…Streptokinase,tissue
plasminogen activator
– Antiplatelets…Aspirin, prostacyclin
– Hemodilution
• Nofavorableeffectsonnaturalhistory b
a MahmoodT. CRVO: currentmanagementoptions.PakJOphthalmol2009.25(1):56-9.
b Mohamed Q etal. interventionsfor CRVO. an evidence-basedsystematic review. Ophthalmology. 2007; 114:507-19
Treatment
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Medical treatment:
• In hypercoagulopathy – anticoagulant may be given, (no
role in prevention and management in most cases). So
generally not indicated
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Laser treatment:
BRVO study for macular edema:
• Argon laser photocoagulation (grid pattern) may reduce visual
loss from macular edema
Results in thinning of retina (outer retina)
Reducing oxygen consumption and increasing choroidal
delivery of oxygen to the inner retina
Produces auto regulatory constriction of the retinal vasculature in
the leaking area
decreases the edema
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• Wait 3 – 6 months before considering laser therapy.
• If the vision is reduced to 20/40 or worse, wait 3 – 6
months for sufficient clearing if retinal hemorrhage to
permit high quality FAand then evaluate for macular
edema and macular ischemia
• If perfused macular edema accounts for the vision loss
and vision continues to be 20/40 or worse without
spontaneous improvement consider grid macular
photocoagulation
• If macular ischemia accounts for the visual loss no laser
treatment is recommended.
General guideline from BRVOS for Macular edema
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•For grid treatment – argon blue green wavelength is
used
•Krypton red and argon green are absorbed less than
blue green by the xanthophyll pigment of the inner
retina that is present in increased concentration close
to the foveal center.
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BRVOS for new vascularization
• Prophylactically scatter laser photocoagulation can lessen
subsequent neovascularization complications
• If neovascularization already exists that laser can lessen
subsequent vitreous hemorrhage
• But it is recommended that laser be applied
only after neovascularization is observed
• BRVOS – strongly suggests that laser after development of
neovascularization is as effective in preventing vitreous
hemorrhage as is laser before the development of
neovascularization
• After laser vitreous hemorrhage incidence reduced from 60 %
to 30%
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Steroidtreatment
SCORE study (standard care vs corticosteroid for retinal vein
occlusion study)
• Effective and safety of intravitreal triamcinolone acetate for
the treatment of macular edema
• IVTA not recommended as 1st line therapy for macular edema in
BRVO. However can be considered if laser or anti VEGF are
ineffective
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GENEVA study (Global evaluation of implantable dexamethasone in
retinal vein occlusion with macular edema in BRVO and CRVO.
• Dexa implant is an alternative treatment to macular grid laser
in the appropriate patient (i.e. no glaucoma and
pseudophakic)
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Anti VEGF
retinal
ischemia
secretion of
VEGF
increased
vascular
permeability
vasodilatation
migration of
endothelial cells
and
neovascularization
Increased vascular
permeability
and vasodilatation
leads to retinal
edema
BRAVO (Branch retinal vein occlusion study)
• Efficacy and safety of ranibizumab in the treatment of macular edema from BRVO
• Study shows ranibizumab is superior to traditional laser for the treatment of
macular edema
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Current recommendation
Macular edema from BRVO
Monthly injection of 0.5mg
Ranibizumab If treatment fails after 3 months
Traditional grid macular laser
If capillary non perfusion
explains vision loss then
laser is not indicated)
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Experimental treatment
FAVOR study
• Intravitreal implant of fluocinolone
acetonide
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Surgical management
Vitrectomy with or without sheathotomy
• Removal of the compressive factor by sectioning the
adventitial sheath may be effective
• Due to risk of intraoperative complications and availability of
less invasive alternatives this is not indicated as 1st line
treatment
• Vitreous surgery: in non clearing vitreous hemorrhage,
epiretinal membranes or TRD with macular involvement
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Central retinal vein occlusion (CRVO)
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Epidemiology
• M:F – equal
• More above 65 years old
• Prevalence in population based study: 0.1 – 0.4%
• Usually U/L disease but may develop RVO in fellow eye in 1 %
patient within 1 year and estimated 7 % of patient within 5
years
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Associations and risk factors with CRVO:
• Systemic vascular disease: DM, HTN, carotid insufficiency
• Ocular disease: POAG, ischemic optic neuropathy,
pseudotumor cerebri, tilted optic disc, optic nerve head
drusens
• Hematological alterations: hyperviscocity syndromes
(polycythemia vera, lymphoma, leukemia, sickle cell disease),
anemia, elevated plasma homocysteine, factor XII def,
antiphosphilipid antibody syndrome, protein c and s
deficiency.
• Inflammatory/autoimmune vasculitis: SLE
• Medications: oral contraceptions, diuretics, Hep B vaccine
• Infectious vasculitis: HIV, syphilis, herpes zoster, sarcoidosis
• Others: after retrobulbar block, dehydration, pregnancy
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Clinical features
• Sudden painless loss of
vision
• Hemorrhage radiate from the
optic nerve head are variable
in quantity and may result in
the classic “blood and
thunder” appearance
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• Cilioretinal artery occlusion can occur in association with CRVO
Together these occlusion have been hypothesized to constitute a
distinct clinical entity arising from a sudden increase in the
intraluminal capillary pressure due to CRVO
Inducing relative occlusion of the cilioretinal artery whose
perfusion pressure is lower than the central retinal artery
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CVOS
• VA at the time of presentation was variable but an
important prognostic indicator of final visual outcome
• Of those initial VA 20/40 or better – majority maintain VA
• Intermediate VA (20/50 to 20/200) – variable outcome
• Poor VA at onset (20/200 or less) – 20% chance of
improvement
• In CVOS – worse VA correlated with development of
NVI/NVA
• NVA may be present without NVI in 12%.
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Perfusion status
• CVOS classified perfusion status of CRVO – perfused, non
perfused or indeterminate based on FA characters
Perfused CRVO (non ischemic/incomplete/partial)
• Demonstrates less than 10 disc areas of retinal capillary
nonperfusion on FA
• These eyes typically have less intraretinal hemorrhage and
better initial VA
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Non perfused CRVO (ischemic/hemorrhagic/complete)
• Demonstrates 10 or more disc areas of retinal capillary
nonperfusion on FA
• Greater degree of intraretinal hemorrhage, macular and disc
edema and worse VA at onset
Indeterminate:
• When there is sufficient intraretinal hemorrhage to
prevent angiographic determination of perfusion
status.
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Other examination features that may help in determining the
perfusion status in the acute phase of CRVO include:
• Baseline VA
• RAPD
• Electro-retinography (negative wave form is seen)
• Goldmann perimetry
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CVOS classification of initial perfusion status of the
CRVO was important for determining the natural history
of the disease
• Poor VA and larger areas of non perfusion – Increased risk of
NVI/NVA
• Perfused – 10% chance of NVI/NVA
• Non perfused or indeterminate: 35% chance of NVI/NVA
• At 3 years – 45% chance of developing neovascular
glaucoma after onset of ischemic CRVO
• Overall – 34% of initially perfused eyes converted to non
perfused after 3 years.
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Pathogenesis
• Pathophysiology not clearly
understood
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Within the retrolaminar portion of optic nerve
Central retinal artery and vein are aligned parallel to each
other in common tissue sheath
CRA and vein are naturally compressed as they cross the rigid
shieve like openings in the lamina cribrosa but typically gives
off branching collaterals vessels just piercing the lamina
These vessels may compress from mechanical stretching of
lamina as with increase in IOP which may cause a post bowing
of the lamina and subsequent impingement on the vein
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• Furthermore, local factors may predispose to occlusion of
veins, including compression by an atherosclerotic central
retinal artery or primary occlusion of the central retinal vein
from inflammation
• Hemodynamic alterations: produce stagnant flow and
subsequent thrombus formation in the CRV including
diminished blood flow, increased blood viscocity and an altered
lumen wall (Virchow’s triad)
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• In experimental trial – occlusion of both retrolaminar CRA and
vein posterior to lamina and prior to the branching of collateral
channels from the main trunk was required to produce
ischemic CRVO
• It is hypothesized that a non ischemic CRVO may be due to
occlusion of the CRV at a site further posterior, allowing normal
collateral channels to provide alternatives routes of venous
drainage
• Neovascularization of the anterior and posterior segment and
severity of macular edema are modulated by growth factors
released from ischemic retina.
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Treatment
• Treatment of CRVO is directed at treating the sequelae of
CRVO particularly macular edema and neovascularization
Treatment of systemic medical conditions
if any:
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Treatment of macularedema
• CVOS – grid laser photocoagulation not recommended
Corticosteroid therapy
• Maintain anti-inflammatory effects with modulation of production
of cytokines and growth factors including VEGF
• Also thought to stabilize BRB with reduction of vascular
permeability
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Score
• Showed significant improvement in VA with intravitreal
triamcinolone compared to observation
• The limited duration of the response to IVTA therapy has
prompted the development of sustained release steroids
(intravitreal fluocinolone acetonide)
• But with sustained release all phakic pt developed visually
significant cataracts and 92% developed increase IOP
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Intra vitreal Anti VEGFtherapy
VEGF
cause capillary endothelium cell proliferation
Progressive vascular closure and non perfusion in
CRVO
• Anti VEGF – enhance blood flow, lower intravenous
pressure and normalize venous diameter and tortuosity.
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Treatment of ocularneovascularization
Laser photocoagulation:
• CVOS recommends PRP be delivered promptly after the
development of NVI/NVA but not prophylactically in eyes with
nonperfused CRVO
• In 90% cases, NVI/NVA resolve in 1 to 2 months
after PRP Persistent neovascularization after PRP
Close observation
Additional PRP may be applied to halt its progression.
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• Patient with NVD/NVE without NVI/NVA should be treated with
PRP to prevent anterior segment neovascularization
Medical therapy
• Topical/systemic anti glaucoma agents to reduce IOP
• Topical steroids to reduce inflammation
• Cycloplegics to prevent from posterior synechiae
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Alternative treatment
Chorioretinal venous anastomosis:
• In eyes with perfused CRVO – investigators have bypassed the
occluded central retinal vein by creating a chorioretinal
anastomosis between nasal branch retinal vein and choroidal
circulation.
Tissue plasminogen activator:
• Thrombolytic agents in suspected thrombus in the central retinal
vein
• TPA converts plasminogen to plasmin which destabilize
intravascular thrombi
• Can be administered systemic, intravitreal and by
endovascular cannulation of retinal vessels
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Surgical treatment
Vitrectomy
• PPV may be useful to address complication of CRVO and
even to attempt to alter the natural course of the disease
Indicated:
• Non clearing vitreous hemorrhage
• Removal of epiretinal membranes and fibrovascular proliferation
if present and placement of complete endolaser PRP at the
time of PRP
• In eyes with extensive anterior segment neovascularization and
neovascular glaucoma, PPV and endolaser may be combined
with pars plana placement of a glaucoma drainage device to
avoid anterior chamber hemorrhage at the time of tube
placement
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• Potential role for PPV with peeling of ILM has also been
investigated for treatment of CME secondary to CRVO
Radial optic neurotomy:
• Combined with PPV with radial optic neurotomy (RON) involving
transvitreal incision of the nasal scleral ring to release pressure
on the central retinal vein at the level of scleral outlet
11/11/20 November 6, 2020 Page 87
Generalguideline for CRVO
• Treat any associated intraocular neovascularization with PRP
• Treat associated macular edema, if visually significant, with an
intra vitreal Anti VEGF or steroids
• VA loss from macular edema does not improve with grid laser
• Lower IOP if elevated
• Treat underlying medical conditions
11/11/20 November 6, 2020 Page 88
References
• Ryan’s 5th edition
• Myron yanoff 4th edition
• American academy of Ophthalmology-sec 12,
2013,2014
• Kanski’s clinical ophthalmology 8th edition
11/11/20 November 6, 2020 Page 89
CentralVeinOcclusionStudy (CVOS)
• Morethana decade
• Purpose
– To determine whether photocoagulation therapy
can help prevent iris neovascularization in eyes
withCVO andevidenceof ischemicretina.
– Toassesswhethergrid-patternphotocoagulation
therapywillreducelossof centralvisualacuitydue
tomacularedemasecondarytoCVO.
– Todevelopnewdatadescribingthecourseand
prognosisforeyeswithCVO.
11/11/20 November 6, 2020 Page 90
•
Eligibleptsweredividedin4groups:
– Group N: Eyeswithextensiveretinalischemia
(atleast10discareasof nonperfusion)were
randomlyassignedtoreceive panretinal
photocoagulationornotreatmentunlessiris
neovascularizationdeveloped.
– Group M: Eyeswithvisuallossascribable to
macularedemawererandomlyassignedto
receivegrid-patternphotocoagulationorno
treatment.
TheCentralVeinOcclusionStudyGroup: Evaluationofgridpatternphotocoagulationformacularedemaincentralvein
occlusion.The CVOS Group M Report. Ophthalmol102: 1425-1433, 1995
11/11/20 November 6, 2020 Page 91
– Group P: Eyeswith
relativelyperfused retinas
• werefollowedtoprovideinformationaboutthe natural
historyofthedisease.
• – Group I: Indeterminateeyesinwhichtheretina
couldnotbevisualizedaccuratelybecauseof
hemorrhagewerefollowedinanaturalhistory study.
TheCentralVeinOcclusionStudyGroup: Naturalhistoryandclinicalmanagementofcentralretinalveinocclusion.Arch
Ophthalmol115: 486-491, 1997.
11/11/20 November 6, 2020 Page 92
• GreenargonlaserwasusedforallTx
• Followedfor3yrswithphotographic images
• Visualacuitywasprimaryoutcomefactorin
macularedemagroup
• ClarksonJG, Central Vein Occlusion Study Group: Central vein occlusion study: Photographic protocol and early natural history. .
TransAmOphthalmolSoc92:203-215, 1994
 TheCentralVeinOcclusionStudyGroup: Baselineandearlynaturalhistoryreport.ArchOphthalmol111:1087-1095, 1993.
11/11/20 November 6, 2020 Page 93
• Results
– Group M-- MacularEdema:Maculargrid
photocoagulationwaseffectiveinreducing
angiographicevidenceof macularedemabutdid
notimprovevisualacuityineyeswithreduced
visionduetomacularedemafromCVO.
– Group I-- Indeterminate:Eyeswithsuch
extensiveIntraretinalhemorrhagethatitisnot
possibletodeterminetheretinalcapillary
perfusionstatusactasif theyareischemicor
nonperfused
11/11/20 November 6, 2020 Page 94
– Group N-- PRP forIschemicCVO: Prophylactic
PRP didnotpreventthedevelopmentof NVIin
eyeswith>10discareasof retinalcapillary
nonperfusionconfirmedbyFFA. Rather,resultsof
thisRCT demonstratethatitissafetowaitforthe
developmentof earlyirisneovascularizationand
thenapply PRP
11/11/20 November 6, 2020 Page 95
SCORE-CRVOstudy
• Standardcarevs. COrticosteroids for
REtinal veinocclusion study
• FundedbynationaleyeinstituteinMay 2003
• Multicentered RCT
• 271 participants
SCORE studyReport#5. ArchOphathalmol. 2009;127:1101.
11/11/20 November 6, 2020 Page 96
11/11/20 November 6, 2020 Page 97
11/11/20 November 6, 2020 Page 98
11/11/20 November 6, 2020 Page 99
11/11/20 November 6, 2020 Page 100
11/11/20 November 6, 2020 Page 101
11/11/20 November 6, 2020 Page 102
11/11/20 November 6, 2020 Page 103
11/11/20 November 6, 2020 Page 104
11/11/20 November 6, 2020 Page 105
TheRoyalCollegeof Ophthalmologists
Guidelines
• PublishedinFeb. 2009.
• Macular edema
– Gridlaserimprovestheedemabutno
improvementinVA… sonotrecommended
– IVTAproduceanatomical&functional
improvementbuteffectsareshort lived.
– Commondoseof IVTA…4mg
– RepeatedIVTAmaynotimprovevision.*
* WangL, Song H. Effectsofrepeatedinjectionofintravitrealtriamcinoloneonmacularoedemaincentralretinalvein occlusion.
ActaOphthalmol2008 May 27. [Epub ahead of print] PMID: 18507724.
11/11/20 November 6, 2020 Page 106
– Posurdex*in350or700g also
improvesvision.
– Intravitrealanti-VEGF therapy(CRIUSE) trialwas
goingonbutnotpublishedatthattime.
– However,nowitsapprovedbyFDA for RVO.
* Clinicaltrials.govIdentifierNCT 00485836/00486018
11/11/20 November 6, 2020 Page 107
• Anteriorsegment neovascularization
– I-CRVO shouldbemonitoredmonthlyfornew
vesselsatiris&/or angle
– Pan-retinalphotocoagulationisadvisedwhenNVI
orNVAare visible
– If logisticallynotpossible…2-3monthsfollow-upis
adequate
11/11/20 November 6, 2020 Page 108
– Ifregularfollow-upnot
practical…prophylactic
treatmentisappropriatea
– IVTA…noprovenprotectiveeffectonanterior
neovascularization
– Anti-VEGFcanbeusedasanadjuvanttoPRP in
ptswithanteriorsegmentneovascularization
secondarytoI-CRVO b
a. Laatikainen,L. Aprospectivefollow-upstudyofpanretinalphotocagulationinpreventingneovascularglaucomafollowing
ischaemiccentralretinalveinocclusion.Graefe’s ArchClinExpOphthalmol1983; 220:236-239.
b. DavidorfFH, MouserJG, DerickRJ. Rapidimprovementofrubeosisiridisfromasinglebevacizumab(Avastin)injection.Retina
2006; 26(3):354-6.
11/11/20 November 6, 2020 Page 109
• Establishedneovascular glaucoma
– Aim…keepeyepain free.
• Topical steroids
• Atropine
– If there’svisual potential
• Topicalpressurelowering agents
• Cycloablation
– IntravitrealandIntracameralanti-VEGF show
regressionof irisvessels&angle obstruction
11/11/20 November 6, 2020 Page 110
Recommendationsforfurther follow-up
• Follow-upafter6monthsforischemiashould
beevery3monthsfor1 year
• Non-ischemiceyes…every3monthsfor6
months.
• Subsequentfollow-upwilldependonlaserTx
&complications.
• Developmentof disccollaterals+/- resolution
of CRVO shouldleadtodischargefrom
clinical supervision
11/11/20 November 6, 2020 Page 111
Summary
• CRVO…potentially blinding
• Local&systemicriskfactors
• Youngptsneedspecialworkup
• Manytreatmentoptions…difficulttodecide
• Guidelinesare helpful
11/11/20 November 6, 2020 Page 112
THANKS
11/11/20 November 6, 2020 Page 113

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Retinal vein occulision

  • 1. 11/11/20 November 6, 2020 Page 1
  • 3. Introduction • Common vascular disorder • 2nd most common cause of blindness after Diabetic retinopathy • Cause ….obstruction to venous flow • Associated risk factors: Multifactorial • Classification • -Site of involvement • -Extent of retinal perfusion 11/11/20 November 6, 2020 Page 3
  • 4. Demographics • InAustralia,prevalenceof RVO… – 0.7%inptsaged49-60yearsto4.6%inptsolder than80 years a • Seasonalvariationfound…greaterthan20,000patientsinthe monthofJanuary a. MitchellP, SmithW, ChangA. PrevalenceandassociationsofretinalveinocclusioninAustralia.TheBlueMountainsEye Study.Arch Ophthalmol. Oct 1996;114(10):1243-7 b. HoJD,TsaiCY, LiouSW, etal.Seasonalvariationsintheoccurrenceofretinalveinocclusion:afive-year nationwidepopulation- basedstudyfromTaiwan.Am J Ophthalmol. Apr 2008;145(4):722-728. 11/11/20 November 6, 2020 Page 4
  • 5. Common mechanism Severe non perfusion leads to edema Edema / hemorrhages Dysfunction leakage of fluid and blood Back pressure on capillaries endothelial junction Venous blockage 11/11/20 November 6, 2020 Page 5
  • 6. Predominant associations • Royalcollegeofophthalmologistsguidelines:Feb. 2009 Patient Group NoObvious Cause Age<50 yrs 40% Age>50 yrs 21% Asian 10.7% West Indian 8.3% Recurren tcases Hypertensio Hyperlipidemia Diabetes n Mellitus 25% 35% 03% 64% 34% 4-15% 64% 50% 29% 83% 33% 38% 88% 47% 3% 6% 11/11/20 November 6, 2020 Page 6
  • 7. Pathogenesis • Virchowtriad: – Lossofvesselwallintegrity – Alteredbloodflow – Hypercoagulablestate • Disturbanceleadstothrombusformation& vesselocclusion 11/11/20 November 6, 2020 Page 7
  • 8. • Klein&Olwinpostulated: – Compressionofveinbyscleroticcentralretinalartery – Occlusionbyprimaryvesselwalldisease(degenerativeor inflammatory) – Hemodynamicdisturbance KleinBA,OlwinJH.Asurveyofthepathogenesisofretinalvenousocclusion.ArchOphthalmol1956;56:207. 11/11/20 November 6, 2020 Page 8
  • 9. 11/11/20 November 6, 2020 Page 9
  • 10. RVO resistancetovenousflow blood stagnation &ischemia stimulates productionof VEGF (vascularendothelial growthfactor) neovascularization capillaryleakage (edema) 11/11/20 November 6, 2020 Page 10
  • 11. 11/11/20 November 6, 2020 Page 11
  • 12. Etiology 11/11/20 November 6, 2020 Page 12 Any factor which directly or indirectly activates virchowtraid….
  • 13. External compression – Arteriosclerosisof CRA (HTN, DM, Hyperlipidemia) – Glaucoma(5 timesmorelikelytohave CRVO) – Papilledema – Thyroideye disease – Orbitalspaceoccupying lesions – Cavernoussinus thrombosis – Closed-Head trauma – Retrobulbarinjections * Morganetal.ocularcomplicationsassociatedwithretrobulbarinjections.Ophthalmology1988;95:660. 11/11/20 November 6, 2020 Page 13
  • 14. – SystemicVasculitis • TB • AIDS • Syphilis • SLE – Localized inflammation • Sarcoidosis • Serpiginouschoroiditis * * Bluemenkranzetal.atypicalserpiginouschoroiditis.Archophthalmol1773;1982:100. Disease of vessels wall 11/11/20 November 6, 2020 Page 14
  • 15. Hematological disorders • resistance – Lupus anticoagulant deficiency – Anticardiolipin antibodies – Protein C & Protein S deficiency – Antithrombin III def – Antiphospholipid antibodies • Nephrotic syndrome •Clotting disorders Paraproteinemia – Activated protein C – Multiple myeloma – Cryoglobulinemia • Drugs – Oral contraceptive – Diuretics • Blood dyscrasia – Lymphoma – Leukemia – Polycythemia vera – Sickle cell disease 11/11/20 November 6, 2020 Page 15
  • 17. History • Symptoms – Painlesslossof vision(mild tosevere) – Usually unilateral • Past&Personal Hx – HTN,DM, smoking – Hyperlipidemia – Bleedingorclotting disorders – Glaucoma – Oralcontraceptive use – Headtrauma/ retrobulbarinj 11/11/20 November 6, 2020 Page 17
  • 18. Examination – VA&BCVA – Pupillary reactions – Congestionof conjunctivaor cornea – Iris…neovessels – AC angle…neovessels – IOP 11/11/20 November 6, 2020 Page 18
  • 19. • Fundus findings – Retinalhemorrhages – Extensivehemorrhages…blood&thunder appearance – Dilatedtortuous veins – Cottonwoolspots,macular edema – Opticdisc • Edema/ optociliaryshunts/ atrophy – Neovessels • NVD/ NVE……vitreous hemorrhage 11/11/20 November 6, 2020 Page 19
  • 20. Differential diagnosis • Ocularischemic syndrome • Diabetic retinopathy • Papilledema • Radiation retinopathy • Retinopathydueto anemia 11/11/20 November 6, 2020 Page 20
  • 21. Ocular investigation • ERG – Reducedb-wave amplitude – reducedb:a ratio – b:aratio< 1suggestsan I-CRVO • OCT – Formacular thickness 11/11/20 November 6, 2020 Page 21
  • 22. • Fluoresceinangiography – Veryusefulfor detecting… • Capillary nonperfusion • Neovascularization • Macularedema – ReliabletodifferentiatebtwI-CRVO &NI-CRVO – >10DD retinalnonperfusionistermedas I-CRVO* * TheCentralVeinOcclusionStudyGroup Arandomizedclinicaltrialofearlypanretinalphotocoagulationforischemic centralveinocclusion:TheCentralRetinalVeinOcclusionStudyGroup NReport.Ophthalmology1995;102: 1434-44. 11/11/20 November 6, 2020 Page 22
  • 23. Treatment • Systemictreatment a – Anticoagulants…Heparin, warfarin – Fibrinolyticagents…Streptokinase,tissue plasminogen activator – Antiplatelets…Aspirin, prostacyclin – Hemodilution • Nofavorableeffectsonnaturalhistory b a MahmoodT. CRVO: currentmanagementoptions.PakJOphthalmol2009.25(1):56-9. b Mohamed Q etal. interventionsfor CRVO. an evidence-basedsystematic review. Ophthalmology. 2007; 114:507-19 11/11/20 November 6, 2020 Page 23
  • 24. • Ocular treatment – Pharmacotherapy – Photocoagulation – Newtechniques(Surgical) • Certainclinicaltrialsneedsattention 11/11/20 November 6, 2020 Page 24
  • 25. CENTERAL RETINAL VEIN OCCLUSION • It is more common than the artery occlusion. • It typically affects > 6th or 7th decade of life. 11/11/20 November 6, 2020 Page 25
  • 26. Etiology • 1. Pressure on the vein by a sclerotic retinal artery where the two share a common adventitia (e.g., just behind the lamina cribrosa and at arteriovenous crossings). • 2. Hyperviscosity of blood as in polycythemia, hyperlipidemia and macroglobulinemia. . 11/11/20 November 6, 2020 Page 26
  • 27. • 3. Periphlebitis retinae which can be central or peripheral. • 4. Raised introcular pressure. Central retinal vein occlusion is more common in patients with primary open-angle glaucoma. • 5. Local causes are orbital cellulitis, facial erysipelas and cavernous sinus thrombosis 11/11/20 November 6, 2020 Page 27
  • 28. Classification • Centralretinalveinocclusion(CRVO) – Non-ischemic CRVO – Ischemic CRVO • Branchretinalveinocclusion(BRVO) – Major BRVO – Macular BRVO • Hemicentralretinalveinocclusion(HCRVO) – Non-ischemic HCRVO – Ischemic HCRVO 11/11/20 November 6, 2020 Page 28
  • 29. Central retinal Vein occlusion • Painlesslossof vision • Site:occlusionatorposteriortolamina cribrosa • Twoclinicaltypes – IschemicCRVO(I-CRVO) – Non-ischemic (NI-CRVO) • ‘Research into CRVO is fraught with challenges, from accurate disease classification to its treatment; even the most prestigious trials have become controversial’ • MadhusudhanaKC,NewsomRS.Centralretinalveinocclusion:thetherapeuticoptions.CanJOphthalmol.Apr2007;42(2):193-5. 11/11/20 November 6, 2020 Page 29
  • 30. Demographics • NI-CRVO morecommonthanI-CRVO • Noracial predilection • Men> women • >90%CRVO occursin> 50yrs age a KleinR etal.Theepidemiologyofretinalveinocclusion:theBeaverDamEyeStudy.TransAmOphthalmolSoc2000;98:133–41. b MitchellPetal.PrevalenceandassociationsofretinalveinocclusioninAustralia.TheBlueMountainsEye Study. Arch Ophthalmol1996;114:1243–7. c KleinR etal.The15-yearcumulativeincidenceofretinalveinocclusion:theBeaverDamEye Study.Arch Ophthalmol. Apr2008;126(4):513-8. 11/11/20 November 6, 2020 Page 30
  • 31. Non-ischaemic CRVO (venous stasis Retinopathy) Most common clinical variety (75%). Characterized by mild to moderate visual loss. Fundus examination  In early cases :Mild venous congestion and tortuosity, a few superficial flame-shaped hemorrhages more in the peripheral than the posterior retina,  In late stage (after 6-9 months) : Mild papilloedema and mild or no macular oedema. There appears sheathing around the main veins, and a few cilioretinal collaterals around the disc. Retinal haemorrhages are partly absorbed. Macula may show chronic cystoid oedema in moderate cases or may be normal in mild cases. 11/11/20 November 6, 2020 Page 31
  • 32. 11/11/20 November 6, 2020 Page 32
  • 33. Treatment is usually not required. The condition resolves with almost normal vision in about 50 percent cases. Visual loss in rest of the cases is due to chronic cystoid macular oedema, for which no treatment is effective. However, a course of oral steroids for 8-12 weeks may be effective. 11/11/20 November 6, 2020 Page 33
  • 34. Ischaemic CRVO (Hemorrhagic retinopathy) 1. Acute (sudden) complete occlusion of central retinal vein. 2. It is characterized by marked sudden visual loss. Fundus examination in early cases: 1. Massive engorgement, 2. Congestion and tortuosity of retinal veins, 3. Massive retinal hemorrhages (almost whole fundus is full of hemorrhages giving a ‘splashed-tomato’ appearance), 4. Numerous soft exudates, and papilledema. 11/11/20 November 6, 2020 Page 34
  • 35. • Macular area is full of hemorrhages and is severely edematous. • In late stages: • Marked sheathing around veins &collaterals is seen around the disc. • Neovascularisation may be seen at the disc (NVD) or in the periphery (NVE). • Macula: shows marked pigmentary changes and chronic cystoid oedema. 11/11/20 November 6, 2020 Page 35
  • 36. Complications • Rubeosis iridis • Neovascular glaucoma (NVG) (occur in more than 50 percent cases within 3 months (so also called as 90 days glaucoma). • A few cases develop vitreous hemorrhage & proliferative retinopathy. 11/11/20 November 6, 2020 Page 36
  • 37. Natural history of CRVO • NI-CRVO – Completelyresolution…10% a – ME resolves…30%in6-15 monthsb – About50%...VAis6/60 orworse a – 1/3rd progressto I-CRVO in6-12 monthsa – Neovesselsdevelop…33%in12-15 months b a. Central Vein Occlusion Study Group. Baseline and early natural history report. Arch Ophthalmol. Aug 1993;111(8):1087-95 b. McIntoshRL etal.NaturalHistoryofCentralRetinalVeinOcclusion:AnEvidence-BasedSystematicReview.Ophthalmology 2010;117:1113–1123 11/11/20 November 6, 2020 Page 37
  • 38. Treatment • Panretinal photocoagulation (PRP) or cryo-application, if the media is hazy, may be required to prevent neovascular glaucoma in patients with idespread capillary occlusion. Photocoagulation should be carried out when most of the intraretinal blood is absorbed, which usually takes about 3-4 months. 11/11/20 November 6, 2020 Page 38
  • 39. (2) Branch retinal vein occlusion (BRVO) • It is more common than the central retinal vein occlusion. • It may occur at the following sites: main branch at the disc margin causing hemispheric occlusion, major branch vein away from the disc, 11/11/20 November 6, 2020 Page 39
  • 40. 1. AT A-V crossing causing quadrantic occlusion and small macular or peripheral branch occlusion. 2. In BRVO oedema and haemorrhages are limited to the area drained by the affected vein Vision is affected only when the macular area is involved. 3. 2nd ry glaucoma occurs rarely in these cases. 4. Chronic macular oedema and neovascularisation may occur as complications of BRVO in about 1/3 cases. 11/11/20 November 6, 2020 Page 40
  • 41. Treatment • Grid photocoagulation may be required in patients with chronic macular oedema. In patients with neovascularisation, scatter photocoagulation should be carried out. 11/11/20 November 6, 2020 Page 41
  • 42. 11/11/20 November 6, 2020 Page 42
  • 43. Non-Ischemic Ischemic Frequency 75-80% 20-25% VA betterthan 6/60 Worsethan 6/60 RAPD Slightor nil Marked VF defect rare Common Fundus Lesshemorrhages & cottonwool spots Extensivehemorrhages & cottonwool spots FFA Good perfusion Non-perfusion> 10 DD ERG Normal Reducedb-wave amplitude, reducedb:a ratio Prognosis 50%...6/60 or better 60%...Rubeosis &NVG 11/11/20 November 6, 2020 Page 43
  • 44. • Principlecausesof visualmorbidity – Macularedema (ME) – Neovascularization(NVI>NVD>NVE)& Neovascularglaucoma(100 days) – Vitreoushemorrhage – Opticatrophy Complications 11/11/20 November 6, 2020 Page 44
  • 45. Differential diagnosis • Ocularischemic syndrome • Diabetic retinopathy • Papilledema • Radiation retinopathy • Retinopathydueto anemia 11/11/20 November 6, 2020 Page 45
  • 46. – Limitations • Itprovideslittleinformationinearlystagesbczof extensivehemorrhages • Poorqualityof angiograms • Inabilitytovisualizeperipheral retina • Interpretationissubjective&hence variable 11/11/20 November 6, 2020 Page 46
  • 47. FFAfindings – Delayedarteriovenous transit – Macular edema – Stainingalongtheretinalveins – Microaneurysms,Arteriovenous collaterals – NVD, NVE – Dilatedopticnervehead capillaries – Nonperfusion…hypofluorescence 11/11/20 November 6, 2020 Page 47
  • 48. 11/11/20 November 6, 2020 Page 48
  • 49. 11/11/20 November 6, 2020 Page 49
  • 50. 11/11/20 November 6, 2020 Page 50
  • 51. 11/11/20 November 6, 2020 Page 51
  • 52. Initial medical investigations • – FBC &ESR – Renalfunction tests – Randomblood glucose – Lipidprofile – Plasmaprotein electrophoresis – Thyroid function – ECG Royalcollegeofophthalmologistsguidelines:Feb. 2009 •ALL PATIENTS ACCORDING TO CLINICALINDICATION – Thrombophilia screen – Anticardiolipinantibody – CRP – SerumACE – Autoantibodies – CXR – Fasting homocystine levels 11/11/20 November 6, 2020 Page 52
  • 53. • Systemictreatment a – Anticoagulants…Heparin, warfarin – Fibrinolyticagents…Streptokinase,tissue plasminogen activator – Antiplatelets…Aspirin, prostacyclin – Hemodilution • Nofavorableeffectsonnaturalhistory b a MahmoodT. CRVO: currentmanagementoptions.PakJOphthalmol2009.25(1):56-9. b Mohamed Q etal. interventionsfor CRVO. an evidence-basedsystematic review. Ophthalmology. 2007; 114:507-19 Treatment 11/11/20 November 6, 2020 Page 53
  • 54. Medical treatment: • In hypercoagulopathy – anticoagulant may be given, (no role in prevention and management in most cases). So generally not indicated 11/11/20 November 6, 2020 Page 54
  • 55. Laser treatment: BRVO study for macular edema: • Argon laser photocoagulation (grid pattern) may reduce visual loss from macular edema Results in thinning of retina (outer retina) Reducing oxygen consumption and increasing choroidal delivery of oxygen to the inner retina Produces auto regulatory constriction of the retinal vasculature in the leaking area decreases the edema 11/11/20 November 6, 2020 Page 55
  • 56. • Wait 3 – 6 months before considering laser therapy. • If the vision is reduced to 20/40 or worse, wait 3 – 6 months for sufficient clearing if retinal hemorrhage to permit high quality FAand then evaluate for macular edema and macular ischemia • If perfused macular edema accounts for the vision loss and vision continues to be 20/40 or worse without spontaneous improvement consider grid macular photocoagulation • If macular ischemia accounts for the visual loss no laser treatment is recommended. General guideline from BRVOS for Macular edema 11/11/20 November 6, 2020 Page 56
  • 57. •For grid treatment – argon blue green wavelength is used •Krypton red and argon green are absorbed less than blue green by the xanthophyll pigment of the inner retina that is present in increased concentration close to the foveal center. 11/11/20 November 6, 2020 Page 57
  • 58. BRVOS for new vascularization • Prophylactically scatter laser photocoagulation can lessen subsequent neovascularization complications • If neovascularization already exists that laser can lessen subsequent vitreous hemorrhage • But it is recommended that laser be applied only after neovascularization is observed • BRVOS – strongly suggests that laser after development of neovascularization is as effective in preventing vitreous hemorrhage as is laser before the development of neovascularization • After laser vitreous hemorrhage incidence reduced from 60 % to 30% 11/11/20 November 6, 2020 Page 58
  • 59. Steroidtreatment SCORE study (standard care vs corticosteroid for retinal vein occlusion study) • Effective and safety of intravitreal triamcinolone acetate for the treatment of macular edema • IVTA not recommended as 1st line therapy for macular edema in BRVO. However can be considered if laser or anti VEGF are ineffective 11/11/20 November 6, 2020 Page 59
  • 60. GENEVA study (Global evaluation of implantable dexamethasone in retinal vein occlusion with macular edema in BRVO and CRVO. • Dexa implant is an alternative treatment to macular grid laser in the appropriate patient (i.e. no glaucoma and pseudophakic) 11/11/20 November 6, 2020 Page 60
  • 61. Anti VEGF retinal ischemia secretion of VEGF increased vascular permeability vasodilatation migration of endothelial cells and neovascularization Increased vascular permeability and vasodilatation leads to retinal edema BRAVO (Branch retinal vein occlusion study) • Efficacy and safety of ranibizumab in the treatment of macular edema from BRVO • Study shows ranibizumab is superior to traditional laser for the treatment of macular edema 11/11/20 November 6, 2020 Page 61
  • 62. Current recommendation Macular edema from BRVO Monthly injection of 0.5mg Ranibizumab If treatment fails after 3 months Traditional grid macular laser If capillary non perfusion explains vision loss then laser is not indicated) 11/11/20 November 6, 2020 Page 62
  • 63. Experimental treatment FAVOR study • Intravitreal implant of fluocinolone acetonide 11/11/20 November 6, 2020 Page 63
  • 64. Surgical management Vitrectomy with or without sheathotomy • Removal of the compressive factor by sectioning the adventitial sheath may be effective • Due to risk of intraoperative complications and availability of less invasive alternatives this is not indicated as 1st line treatment • Vitreous surgery: in non clearing vitreous hemorrhage, epiretinal membranes or TRD with macular involvement 11/11/20 November 6, 2020 Page 64
  • 65. Central retinal vein occlusion (CRVO) 11/11/20 November 6, 2020 Page 65
  • 66. Epidemiology • M:F – equal • More above 65 years old • Prevalence in population based study: 0.1 – 0.4% • Usually U/L disease but may develop RVO in fellow eye in 1 % patient within 1 year and estimated 7 % of patient within 5 years 11/11/20 November 6, 2020 Page 66
  • 67. Associations and risk factors with CRVO: • Systemic vascular disease: DM, HTN, carotid insufficiency • Ocular disease: POAG, ischemic optic neuropathy, pseudotumor cerebri, tilted optic disc, optic nerve head drusens • Hematological alterations: hyperviscocity syndromes (polycythemia vera, lymphoma, leukemia, sickle cell disease), anemia, elevated plasma homocysteine, factor XII def, antiphosphilipid antibody syndrome, protein c and s deficiency. • Inflammatory/autoimmune vasculitis: SLE • Medications: oral contraceptions, diuretics, Hep B vaccine • Infectious vasculitis: HIV, syphilis, herpes zoster, sarcoidosis • Others: after retrobulbar block, dehydration, pregnancy 11/11/20 November 6, 2020 Page 67
  • 68. Clinical features • Sudden painless loss of vision • Hemorrhage radiate from the optic nerve head are variable in quantity and may result in the classic “blood and thunder” appearance 11/11/20 November 6, 2020 Page 68
  • 69. • Cilioretinal artery occlusion can occur in association with CRVO Together these occlusion have been hypothesized to constitute a distinct clinical entity arising from a sudden increase in the intraluminal capillary pressure due to CRVO Inducing relative occlusion of the cilioretinal artery whose perfusion pressure is lower than the central retinal artery 11/11/20 November 6, 2020 Page 69
  • 70. CVOS • VA at the time of presentation was variable but an important prognostic indicator of final visual outcome • Of those initial VA 20/40 or better – majority maintain VA • Intermediate VA (20/50 to 20/200) – variable outcome • Poor VA at onset (20/200 or less) – 20% chance of improvement • In CVOS – worse VA correlated with development of NVI/NVA • NVA may be present without NVI in 12%. 11/11/20 November 6, 2020 Page 70
  • 71. Perfusion status • CVOS classified perfusion status of CRVO – perfused, non perfused or indeterminate based on FA characters Perfused CRVO (non ischemic/incomplete/partial) • Demonstrates less than 10 disc areas of retinal capillary nonperfusion on FA • These eyes typically have less intraretinal hemorrhage and better initial VA 11/11/20 November 6, 2020 Page 71
  • 72. Non perfused CRVO (ischemic/hemorrhagic/complete) • Demonstrates 10 or more disc areas of retinal capillary nonperfusion on FA • Greater degree of intraretinal hemorrhage, macular and disc edema and worse VA at onset Indeterminate: • When there is sufficient intraretinal hemorrhage to prevent angiographic determination of perfusion status. 11/11/20 November 6, 2020 Page 72
  • 73. Other examination features that may help in determining the perfusion status in the acute phase of CRVO include: • Baseline VA • RAPD • Electro-retinography (negative wave form is seen) • Goldmann perimetry 11/11/20 November 6, 2020 Page 73
  • 74. CVOS classification of initial perfusion status of the CRVO was important for determining the natural history of the disease • Poor VA and larger areas of non perfusion – Increased risk of NVI/NVA • Perfused – 10% chance of NVI/NVA • Non perfused or indeterminate: 35% chance of NVI/NVA • At 3 years – 45% chance of developing neovascular glaucoma after onset of ischemic CRVO • Overall – 34% of initially perfused eyes converted to non perfused after 3 years. 11/11/20 November 6, 2020 Page 74
  • 75. Pathogenesis • Pathophysiology not clearly understood 11/11/20 November 6, 2020 Page 75
  • 76. Within the retrolaminar portion of optic nerve Central retinal artery and vein are aligned parallel to each other in common tissue sheath CRA and vein are naturally compressed as they cross the rigid shieve like openings in the lamina cribrosa but typically gives off branching collaterals vessels just piercing the lamina These vessels may compress from mechanical stretching of lamina as with increase in IOP which may cause a post bowing of the lamina and subsequent impingement on the vein 11/11/20 November 6, 2020 Page 76
  • 77. • Furthermore, local factors may predispose to occlusion of veins, including compression by an atherosclerotic central retinal artery or primary occlusion of the central retinal vein from inflammation • Hemodynamic alterations: produce stagnant flow and subsequent thrombus formation in the CRV including diminished blood flow, increased blood viscocity and an altered lumen wall (Virchow’s triad) 11/11/20 November 6, 2020 Page 77
  • 78. • In experimental trial – occlusion of both retrolaminar CRA and vein posterior to lamina and prior to the branching of collateral channels from the main trunk was required to produce ischemic CRVO • It is hypothesized that a non ischemic CRVO may be due to occlusion of the CRV at a site further posterior, allowing normal collateral channels to provide alternatives routes of venous drainage • Neovascularization of the anterior and posterior segment and severity of macular edema are modulated by growth factors released from ischemic retina. 11/11/20 November 6, 2020 Page 78
  • 79. Treatment • Treatment of CRVO is directed at treating the sequelae of CRVO particularly macular edema and neovascularization Treatment of systemic medical conditions if any: 11/11/20 November 6, 2020 Page 79
  • 80. Treatment of macularedema • CVOS – grid laser photocoagulation not recommended Corticosteroid therapy • Maintain anti-inflammatory effects with modulation of production of cytokines and growth factors including VEGF • Also thought to stabilize BRB with reduction of vascular permeability 11/11/20 November 6, 2020 Page 80
  • 81. Score • Showed significant improvement in VA with intravitreal triamcinolone compared to observation • The limited duration of the response to IVTA therapy has prompted the development of sustained release steroids (intravitreal fluocinolone acetonide) • But with sustained release all phakic pt developed visually significant cataracts and 92% developed increase IOP 11/11/20 November 6, 2020 Page 81
  • 82. Intra vitreal Anti VEGFtherapy VEGF cause capillary endothelium cell proliferation Progressive vascular closure and non perfusion in CRVO • Anti VEGF – enhance blood flow, lower intravenous pressure and normalize venous diameter and tortuosity. 11/11/20 November 6, 2020 Page 82
  • 83. Treatment of ocularneovascularization Laser photocoagulation: • CVOS recommends PRP be delivered promptly after the development of NVI/NVA but not prophylactically in eyes with nonperfused CRVO • In 90% cases, NVI/NVA resolve in 1 to 2 months after PRP Persistent neovascularization after PRP Close observation Additional PRP may be applied to halt its progression. 11/11/20 November 6, 2020 Page 83
  • 84. • Patient with NVD/NVE without NVI/NVA should be treated with PRP to prevent anterior segment neovascularization Medical therapy • Topical/systemic anti glaucoma agents to reduce IOP • Topical steroids to reduce inflammation • Cycloplegics to prevent from posterior synechiae 11/11/20 November 6, 2020 Page 84
  • 85. Alternative treatment Chorioretinal venous anastomosis: • In eyes with perfused CRVO – investigators have bypassed the occluded central retinal vein by creating a chorioretinal anastomosis between nasal branch retinal vein and choroidal circulation. Tissue plasminogen activator: • Thrombolytic agents in suspected thrombus in the central retinal vein • TPA converts plasminogen to plasmin which destabilize intravascular thrombi • Can be administered systemic, intravitreal and by endovascular cannulation of retinal vessels 11/11/20 November 6, 2020 Page 85
  • 86. Surgical treatment Vitrectomy • PPV may be useful to address complication of CRVO and even to attempt to alter the natural course of the disease Indicated: • Non clearing vitreous hemorrhage • Removal of epiretinal membranes and fibrovascular proliferation if present and placement of complete endolaser PRP at the time of PRP • In eyes with extensive anterior segment neovascularization and neovascular glaucoma, PPV and endolaser may be combined with pars plana placement of a glaucoma drainage device to avoid anterior chamber hemorrhage at the time of tube placement 11/11/20 November 6, 2020 Page 86
  • 87. • Potential role for PPV with peeling of ILM has also been investigated for treatment of CME secondary to CRVO Radial optic neurotomy: • Combined with PPV with radial optic neurotomy (RON) involving transvitreal incision of the nasal scleral ring to release pressure on the central retinal vein at the level of scleral outlet 11/11/20 November 6, 2020 Page 87
  • 88. Generalguideline for CRVO • Treat any associated intraocular neovascularization with PRP • Treat associated macular edema, if visually significant, with an intra vitreal Anti VEGF or steroids • VA loss from macular edema does not improve with grid laser • Lower IOP if elevated • Treat underlying medical conditions 11/11/20 November 6, 2020 Page 88
  • 89. References • Ryan’s 5th edition • Myron yanoff 4th edition • American academy of Ophthalmology-sec 12, 2013,2014 • Kanski’s clinical ophthalmology 8th edition 11/11/20 November 6, 2020 Page 89
  • 90. CentralVeinOcclusionStudy (CVOS) • Morethana decade • Purpose – To determine whether photocoagulation therapy can help prevent iris neovascularization in eyes withCVO andevidenceof ischemicretina. – Toassesswhethergrid-patternphotocoagulation therapywillreducelossof centralvisualacuitydue tomacularedemasecondarytoCVO. – Todevelopnewdatadescribingthecourseand prognosisforeyeswithCVO. 11/11/20 November 6, 2020 Page 90
  • 91. • Eligibleptsweredividedin4groups: – Group N: Eyeswithextensiveretinalischemia (atleast10discareasof nonperfusion)were randomlyassignedtoreceive panretinal photocoagulationornotreatmentunlessiris neovascularizationdeveloped. – Group M: Eyeswithvisuallossascribable to macularedemawererandomlyassignedto receivegrid-patternphotocoagulationorno treatment. TheCentralVeinOcclusionStudyGroup: Evaluationofgridpatternphotocoagulationformacularedemaincentralvein occlusion.The CVOS Group M Report. Ophthalmol102: 1425-1433, 1995 11/11/20 November 6, 2020 Page 91
  • 92. – Group P: Eyeswith relativelyperfused retinas • werefollowedtoprovideinformationaboutthe natural historyofthedisease. • – Group I: Indeterminateeyesinwhichtheretina couldnotbevisualizedaccuratelybecauseof hemorrhagewerefollowedinanaturalhistory study. TheCentralVeinOcclusionStudyGroup: Naturalhistoryandclinicalmanagementofcentralretinalveinocclusion.Arch Ophthalmol115: 486-491, 1997. 11/11/20 November 6, 2020 Page 92
  • 93. • GreenargonlaserwasusedforallTx • Followedfor3yrswithphotographic images • Visualacuitywasprimaryoutcomefactorin macularedemagroup • ClarksonJG, Central Vein Occlusion Study Group: Central vein occlusion study: Photographic protocol and early natural history. . TransAmOphthalmolSoc92:203-215, 1994  TheCentralVeinOcclusionStudyGroup: Baselineandearlynaturalhistoryreport.ArchOphthalmol111:1087-1095, 1993. 11/11/20 November 6, 2020 Page 93
  • 94. • Results – Group M-- MacularEdema:Maculargrid photocoagulationwaseffectiveinreducing angiographicevidenceof macularedemabutdid notimprovevisualacuityineyeswithreduced visionduetomacularedemafromCVO. – Group I-- Indeterminate:Eyeswithsuch extensiveIntraretinalhemorrhagethatitisnot possibletodeterminetheretinalcapillary perfusionstatusactasif theyareischemicor nonperfused 11/11/20 November 6, 2020 Page 94
  • 95. – Group N-- PRP forIschemicCVO: Prophylactic PRP didnotpreventthedevelopmentof NVIin eyeswith>10discareasof retinalcapillary nonperfusionconfirmedbyFFA. Rather,resultsof thisRCT demonstratethatitissafetowaitforthe developmentof earlyirisneovascularizationand thenapply PRP 11/11/20 November 6, 2020 Page 95
  • 96. SCORE-CRVOstudy • Standardcarevs. COrticosteroids for REtinal veinocclusion study • FundedbynationaleyeinstituteinMay 2003 • Multicentered RCT • 271 participants SCORE studyReport#5. ArchOphathalmol. 2009;127:1101. 11/11/20 November 6, 2020 Page 96
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  • 106. TheRoyalCollegeof Ophthalmologists Guidelines • PublishedinFeb. 2009. • Macular edema – Gridlaserimprovestheedemabutno improvementinVA… sonotrecommended – IVTAproduceanatomical&functional improvementbuteffectsareshort lived. – Commondoseof IVTA…4mg – RepeatedIVTAmaynotimprovevision.* * WangL, Song H. Effectsofrepeatedinjectionofintravitrealtriamcinoloneonmacularoedemaincentralretinalvein occlusion. ActaOphthalmol2008 May 27. [Epub ahead of print] PMID: 18507724. 11/11/20 November 6, 2020 Page 106
  • 107. – Posurdex*in350or700g also improvesvision. – Intravitrealanti-VEGF therapy(CRIUSE) trialwas goingonbutnotpublishedatthattime. – However,nowitsapprovedbyFDA for RVO. * Clinicaltrials.govIdentifierNCT 00485836/00486018 11/11/20 November 6, 2020 Page 107
  • 108. • Anteriorsegment neovascularization – I-CRVO shouldbemonitoredmonthlyfornew vesselsatiris&/or angle – Pan-retinalphotocoagulationisadvisedwhenNVI orNVAare visible – If logisticallynotpossible…2-3monthsfollow-upis adequate 11/11/20 November 6, 2020 Page 108
  • 109. – Ifregularfollow-upnot practical…prophylactic treatmentisappropriatea – IVTA…noprovenprotectiveeffectonanterior neovascularization – Anti-VEGFcanbeusedasanadjuvanttoPRP in ptswithanteriorsegmentneovascularization secondarytoI-CRVO b a. Laatikainen,L. Aprospectivefollow-upstudyofpanretinalphotocagulationinpreventingneovascularglaucomafollowing ischaemiccentralretinalveinocclusion.Graefe’s ArchClinExpOphthalmol1983; 220:236-239. b. DavidorfFH, MouserJG, DerickRJ. Rapidimprovementofrubeosisiridisfromasinglebevacizumab(Avastin)injection.Retina 2006; 26(3):354-6. 11/11/20 November 6, 2020 Page 109
  • 110. • Establishedneovascular glaucoma – Aim…keepeyepain free. • Topical steroids • Atropine – If there’svisual potential • Topicalpressurelowering agents • Cycloablation – IntravitrealandIntracameralanti-VEGF show regressionof irisvessels&angle obstruction 11/11/20 November 6, 2020 Page 110
  • 111. Recommendationsforfurther follow-up • Follow-upafter6monthsforischemiashould beevery3monthsfor1 year • Non-ischemiceyes…every3monthsfor6 months. • Subsequentfollow-upwilldependonlaserTx &complications. • Developmentof disccollaterals+/- resolution of CRVO shouldleadtodischargefrom clinical supervision 11/11/20 November 6, 2020 Page 111
  • 112. Summary • CRVO…potentially blinding • Local&systemicriskfactors • Youngptsneedspecialworkup • Manytreatmentoptions…difficulttodecide • Guidelinesare helpful 11/11/20 November 6, 2020 Page 112
  • 113. THANKS 11/11/20 November 6, 2020 Page 113