2. Common mechanism
Venous blockage
back pressure on capillaries
endothelial junction dysfunction
leakage of fluid & blood
(edema / hemorrhages)
■ Severe nonperfusion leads to ischemia
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3. Predominant Associations
Patient
Group
Hypertension Hyperlipidemia Diabetes
Mellitus
No Obvious
Cause
Age<50
yrs
25% 35% 03% 40%
Age>50
yrs
64% 34% 4-15% 21%
Asian 64% 50% 29% 10.7%
West
Indian
83% 33% 38% 8.3%
Recurrent
cases
88% 47% 3% 6%
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4. Central retinal vein occlusion
■ Painless unilateral sudden loss of vision
■ Occlusion at or posterior to lamina cribrosa
■ Two clinical types
– Ischemic CRVO (I-CRVO)
– Non-ischemic (NI-CRVO)
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5. Pathogenesis
■ Virchow triad:
– Loss of vessel wall integrity
– Altered blood flow
– Hypercoagulable state
■ Disturbance leads to thrombus
formation & vessel occlusion
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6. ■ Klein & Olwin postulated:
– Compression of vein by sclerotic central retinal
artery
– Occlusion by primary vessel wall disease
– Hemodynamic disturbance
Klein BA, Olwin JH. A survey of the pathogenesis of retinal venous occlusion. Arch Ophthalmol 1956;56:207.
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7. CRVO resistance to venous flow
blood stagnation & ischemia stimulates
production of VEGF (vascular endothelial growth factor)
neovascularization
capillary leakage (edema)
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8. Etiology
■ Any factor which directly or indirectly
activates virchow triad….
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9. External compression
– Arteriosclerosis of CRA (HTN, DM,
Hyperlipidemia)
– Glaucoma (5 times more likely to have CRVO)
– Papilledema
– Thyroid eye disease
– Orbital space occupying lesions
– Cavernous sinus thrombosis
– Closed-Head trauma
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13. History
■ Symptoms
– Painless loss of vision (mild to severe)
– Usually unilateral
■ Past & Personal Hx
– HTN, DM, smoking
– Hyperlipidemia
– Bleeding or clotting disorders
– Glaucoma
– Oral contraceptive use
– Head trauma / retrobulbar inj
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14. Examination
– VA & BCVA
– Pupillary reactions
– Congestion of conjunctiva or cornea
– Iris…neovessels
– AC angle…neovessels
– IOP
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23. Differential diagnosis
■ Ocular ischemic syndrome:dilated veins
without tortuosity,no disc edema,patients
have history of visual loss.
■ Diabetic retinopathy:hemorrhages on
posterior pole and bilateral.
■ Papilledema:bilateral disc swelling with
hemorrhages surrounding disc.
■ Radiation retinopathy:history of
radiation,disc swelling,more cotton wool
spots than hemorrhages.
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24. Ocular Investigations
■ ERG
– Is depressed
– Extent of this is used to assess neovascular
risk
■ OCT
– For macular thickness.Enables quantification
of cystoid macular edema.
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25. ■ Fluorescein angiography
– Very useful for detecting…
■ Capillary nonperfusion
■ Neovascularization
■ Macular edema
– Reliable to differentiate btw I-CRVO & NI-CRVO
– >10 DD retinal nonperfusion is termed as I-CRVO*
– Limitations
■ It provides little information in early stages bcz of
extensive hemorrhages
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29. TREATMENT
■ Treat the underline cause
■ It is the responsibility of the diagnosing
physician or ophthalmologist to:
– Investigate and interpret results.
– Refer the patient for appropriate medical
advice with urgency according to the severity of
underlying risk factor(s).
– Ensure that initiation of medical management
occurs within 2 months of diagnosis
Royal college of ophthalmologists guidelines: July, 2015
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30. Initial medical investigations
■ ALL PATIENTS
– FBC & ESR
– Renal function tests
– Random blood
glucose
– Lipid profile
– Thyroid function
– ECG
Royal college of ophthalmologists guidelines: JULY,
2015
■ ACCORDING TO
CLINICAL INDICATION
– Thrombophilia screen
– CRP
– Serum ACE
– Autoantibodies
– CXR
– Fasting homocystine
levels
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31. Natural history of CRVO
■ NI-CRVO
– Completely resolution…10% a
– ME resolves…30% in 6-15 months b
– About 50%...VA is 6/60 or worse a
– 1/3rd progress to I-CRVO in 6-12 months a
– Neovessels develop…33% in 12-15 months b
a Central Vein Occlusion Study Group. Baseline and early natural history report. Arch Ophthalmol. Aug 1993;111(8):1087-95
b McIntosh RL et al. Natural History of Central Retinal Vein Occlusion: An Evidence-Based Systematic Review. Ophthalmology
2010;117:1113–1123
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32. ■ I-CRVO
– >90%...VA is 6/60 or worse a
– ME resolves…73% in 15 months b
– NVG…>60% in 1-2 yrs a
– About 10% develop RVO in same or fellow eye in 2 yrs
■ Vitreous hemorrhage…10 % of CRVO by 9 months
b
a Central Vein Occlusion Study Group. Baseline and early natural history report. Arch Ophthalmol. Aug 1993;111(8):1087-95
b McIntosh RL et al. Natural History of Central Retinal Vein Occlusion: An Evidence-Based Systematic Review. Ophthalmology
2010;117:1113–1123
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33. Treatment
■ Systemic treatment a
– Anticoagulants…Heparin, warfarin
– Fibrinolytic agents…Streptokinase, tissue
plasminogen activator
– Antiplatelets…Aspirin, prostacyclin
– Hemodilution
a Mahmood T. CRVO: current management options. Pak J Ophthalmol 2009. 25(1):56-9.
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35. Central Vein Occlusion Study (CVOS
■ Results
– Group M--Macular Edema: Macular grid
photocoagulation was effective in reducing
angiographic evidence of macular edema but
did not improve visual acuity.
– Group N--PRP for Ischemic CVO: Prophylactic
PRP did not prevent the development of NVI in
eyes with >10 disc areas of retinal capillary
nonperfusion confirmed by FFA
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36. THE SCORE STUDY
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■ The SCORE study showed an improvement
of three or more lines of vision at one year
in over 25% of patients (versus 7% of
controls) treated with an average of two
injections of 1 mg triamcinolone, using a
preservative-free preparation developed for
intraocular use. There was a slightly higher
rate of IOP elevation and cataract than with
observation.
37. CRUISE Study
■ In June 2010, the FDA approved a new
indication for Ranibizumab(0.5 mg)
intravitreal injection…for the treatment of
macular edema after retinal vein occlusion.
■ Ranibizumab may initially be given monthly
for 6 months and subsequently less
intensively, with typically a two- to three-
line gain in VA.
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38. The GENEVA study
■ Evaluated safety and efficacy of an intravitreal
implant of dexamethasone (Ozurdex; Allergan Inc.,
Irvine, California, USA).
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39. The Royal College of Ophthalmologists
Guidelines
■ Treatment Algorithm: Published in JULY 2015.
■ NON-ISCHAEMIC CRVO
■ If no iris or angle NV and there is OCT evidence of MO:
If visual acuity is 6/96 or better Anti VEGF or OZURDEX
If visual acuity is less than 6/96, potential ↑ in VA is low
and high risk of developing NVI/NVA… Treatment can be
offered.
If visual acuity is better than 6/12…. Observation
*
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40. ISCHAEMIC CRVO
■ If iris or angle neovascularisation occurs and the
anterior chamber angle is open:
■ Urgent PRP is recommended and with review at two
weeks initially and then less frequently as regression
occurs ± Bevacizumab.
■ If iris or angle NV are present with a closed angle and
raised intraocular pressure
■ Urgent PRP is recommended with cyclodiode laser
therapy / tube shunt surgery ± Bevacizumab.
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41. If an ischaemic CRVO is present without
NVI/NVG
■ Patient should be seen monthly for 6
months.Prophylactic PRP is generally not
recommended even with marked ischaemia
unless iris new vessels develop, though may
be considered in patients unlikely to attend
scheduled review.
■ FFA shows > 30 DD non-perfusion.
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42. Recommendations for further follow-up
■ Follow-up after 6 months for ischemia should
be every 3 months for 1 year
■ Non-ischemic eyes…every 3 months for 6
months.
■ Subsequent follow-up will depend on laser Tx
& complications.
■ Development of disc collaterals +/- resolution
of CRVO should lead to discharge from clinical
supervision
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43. Experimental treatments
– Chorio-retinal anastomosis
– Radial optic neurotomy with PPV
■ Currently…these are not recommended
except as part of clinical trials.
a
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44. Take home message
■ Emphasis should be on:
– Differentiating ischemic & Nonischemic CRVO
– Exploring the risk factors (local & systemic)
– Treating CRVO and Referral to physician for
risk factors
– Proper follow-up
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