Central retinal vein occlusion (CRVO) occurs when the central retinal vein gets blocked, causing fluid and blood to leak into the retina. It can be either ischemic or non-ischemic depending on the extent of blocked blood flow. Risk factors include hypertension, diabetes, hyperlipidemia, and various hematological disorders. Treatment involves managing underlying conditions, treating macular edema with anti-VEGF injections or steroids, and laser photocoagulation if neovascularization develops. The goal is to preserve vision by reducing edema and preventing complications like glaucoma. Regular follow up is needed to monitor for recurrence or progression.

1. CENTRAL RETINAL
VEIN OCCLUSION
Dr. SALMAN AHMAD KHAN
FCPS Resident
Ophthalmology Unit-1
SIMS/SHL
13-Jan-24

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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10. Disease of vessel wall
– Systemic Vasculitis
■ TB
■ AIDS
■ Syphilis
■ SLE
– Localized inflammation
■ Sarcoidosis
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11. Hematological disorders
■ Clotting disorders
– Activated protein C
resistance
– Lupus anticoagulant
deficiency
– Anticardiolipin
antibodies
– Protein C & Protein S
deficiency
– Antithrombin III def
– Antiphospholipid
antibodies
■ Nephrotic syndrome
■ Paraproteinemia
– Multiple myeloma
■ Drugs
– Oral contraceptive
– Diuretics
■ Blood dyscrasia
– Lymphoma
– Leukemia
– Polycythemia vera
– Sickle cell disease
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12. MANAGEMENT
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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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15. ■ Fundus findings
– Retinal hemorrhages in 4 quadrants
– Extensive hemorrhages…blood & thunder
appearance
– Dilated tortuous veins
– Cotton wool spots, macular edema
– Optic disc
■ Edema / optociliary shunts / atrophy
– Neovessels
■ NVD / NVE……vitreous hemorrhage
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16. ISCHEMIC CRVO
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17. OPTICOCILIARY SHUNTS
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18. NVIs
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19. ■ Diagnosing CRVO is not difficult
■ Main task…differentiate btw ischemic &
non-ischemic CRVO
■ No single criterion is helpful
■ Various useful tools…
– Visual acuity, pupillary reflex
– Ocular neovascularization, Fundus findings
– ERG, FFA
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20. Non-Ischemic Ischemic
Frequency 75-80% 20-25%
VA better than 6/60 Worse than 6/60
RAPD Slight or nil Marked
VF defect rare Common
Fundus Less hemorrhages &
cotton wool spots
Extensive hemorrhages &
cotton wool spots
FFA Good perfusion Non-perfusion > 10 DD
Prognosis 50%...6/60 or better 60%...Rubeosis & NVG
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21. NON ISCHEMIC CRVO
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22. Complications
■ Principle causes of visual morbidity
– Macular edema (ME)
– Neovascularization (NVI>NVD>NVE) &
Neovascular glaucoma (100 days)
– Vitreous hemorrhage
– Optic atrophy
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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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26. ■ FFA findings
– Delayed arteriovenous transit
– Macular edema
– Staining along the retinal veins
– Micro aneurysms, Arteriovenous collaterals
– NVD, NVE
– Dilated optic nerve head capillaries
– Nonperfusion…hypofluorescence
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27. Extensive hypofluorescence due
to capillary non-perfusion On
FFA
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28. Wide-field FA showing
Extensive Peripheral
Ischaemia
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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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34. ■ Ocular treatment
– Pharmacotherapy
– Photocoagulation
– New techniques (Surgical)
■ Certain clinical trials needs attention
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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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THANKS