CENTRAL RETINAL

VEIN
OCCLUSION
DR. SIDDHARTHA KAR
INTRODUCTION
• Retinal Veinous Occlusion is the 2nd most common retinal vascular
disorder, after Diabetic Retinopathy
• It is caused by a thrombus located at any point along the veinous
circulation and is named accordingly
VENOUS DRAINAGE OF EYE
CLASSIFICATION
• Branch RVO occurs when venous thrombosis and obstruction occur at
an AV crossing, mostly in Superotemporal Quandrant
- Major
- Macular
• Hemicentral RVO occurs in eyes with a persistent vestigial bifurcation
of the retrolaminar portion of central retinal vein
- Ischaemic
- Non-ischaemic
• Central RVO arises from thrombosis in the retrolaminar portion of the
vein. - Ischaemic
- Non-ischaemic
RISK FACTORS AND CAUSES
1. Increased age
2. Hypertension
3. Cigarette smoking
4. Hyperlipidemia
5. Diabetes mellitus
6. Open Angle Glaucoma
7. Oral Contraceptive Pills
8. Diseases leading to thrombophilia- APLA, Hyperhomocysteinemia,
Factor V Leiden mutation, Protein C and S deficiency
PATHOGENESIS
• Pathogenesis of RVO mirrors Virchows triad
for thrombosis
• Normally, retinal arteries and veins share a common
adventitial sheath
• Progressive arteriosclerosis leads to
thickening of arterial wall which in turn leads to
compression and inelasticity of venous wall.
• As a result, it may produce turbulent flow
of blood and stasis, which predispose to
venous thrombosis
PATHOGENESIS (contd.)
• At a cellular level, retinal ischaemia leads to upregulation and release of
hypoxia-related factors
• The most salient of these are vascular endothelial growth factor(VEGF)
and various mediators of inflammation
• VEGF has 2 profound effects on retinal vasculature
1. Increased vessel wall permeability
2. Neovascularization
SYMPTOMS AND SIGNS
• Sudden, painless, monocular loss of vision (CRVO>BRVO)
• Paracentral or peripheral scotoma may be present
• Metamorphopsia
• Transient blurring of vision
• RAPD may be present(More in ischaemic CRVO than Non-ischaemic)
Non-Ischaemic (perfused)CRVO
• Most common type(75%)
• Sudden, unilateral blurred vision
• Mild to moderate loss of acuity, usually 6/60 or better, and an absent or
mild RAPD
• Fundoscopy - tortuosity and dilatation of all branches of the central retinal vein,
dot/blot and flame-shaped hemorrhages and macular edema
• Some cotton-wool spots, particularly in hypertensive patients, may be present.
Transient retinal vessel wall sheathing may occur
• The acute signs resolve over 6-12 months, with disc collaterals and pigmentary
changes at the macula as residual findings
• Prognosis is reasonably good with return of vision to normal or near normal in
about 50%
Ischaemic CRVO
• Rapid onset venous obstruction resulting in decreased retinal perfusion, capillary
closure and retinal hypoxia
• VA less than 6/60, marked afferent pupillary defect; severe tortuosity and
engorgement of all branches of the central retinal vein; extensive dot blot and
flame-shaped hemorrhages involving the peripheral retina and posterior pole;
and severe disc edema and hyperemia.
• Profound vascular leakage, Rubeosis iridis and raised intraocular pressure
• Prognosis is extremely poor due to macular ischemia
• Rubeosis iridis develops in about 50% of eyes, usually between 2 and 4 months
(90-day glaucoma), and there is a high risk of Neovascular Glaucoma.
 Ischaemic Vs Non-Ischaemic
Ischaemic Non-ischaemic
Visual Acuity <6/60 >6/60
Rapd Present Mostly Absent
Visual Field Defect Present Rare
Fundus More disc/macular edema, Less disc/macular edema, hemorrhage, cotton-
hemorrhage, cotton-wool spots wool spots
Severe venous tortuosity and Mild venous tortuosity and dilation
dilation
FFA Retinal capillary nonperfusion more Less area of capillary nonperfusion
than 10 disc areas
ERG Reduced b wave amplitude Normal

Prognosis Poor, high chance of anterior Good, less chance of anterior segment
segment neovascularization/neovascular glaucoma
neovascularization/neovascular
glaucoma
EVALUATION
• History –
- Hypertension, DM, Smoking, h/o OCP use, Hyperlipidemia, h/o
Glaucoma, h/o Blood dyscrasias
• Clinical Examination –
- VA
- IOP
- Gonioscopy
- Fundoscopy
Investigations
Laboratory
Erythrocyte sedimentation rate (ESR)
Complete blood count (CBC)
Random blood glucose
Total and HDL cholesterol
Plasma protein electrophoresis (dysproteinemias such as multiple myeloma)
Urea, electrolytes and creatinine (renal disease in association with hypertension)
Thyroid function tests (associated with dyslipidemia)
ECG (left ventricular hypertrophy secondary to hypertension)
 Investigations
Ocular
1. Fluroscein Angiography – Delayed AV transit,
Haemorrhages, CNP areas,leakage, Macular edema, AV
collaterlas, Neovascularization
2. Optical Coherence Tomography – Evidence of Macular
Edema and ERM
3. Fundus Autoflouroscence – Characteristic ‘fern’ like
hypoflouroscence due to masking of background by
oedema
4. ERG – Reduced “b” wave amplitude
5. Perimetry (Goldman)
 Treatment
1. Treament of Underlying cause
2. Treatment of Complications (Macular Edema and Neovascularization, VH)
A. Treatment of Macular Edema
- Generally indicated in VA <6/9
- Intravitreal anti-VEGF :
• Monthly Injection of Ranibizumab for 6 months (BRAVO & CRUISE) results in increase of VA
• Monthly injection of 2mg aflibercept for 6 months (GALILEO & COPERNICUS) followed by
efficacy assessment at week 16. If VA is good and OCT is dry, interval is raised by 2-4 weeks.
No recurrence of ME after 12 weeks-> can be shifted to PRN regimen (as and
when needed)
- Intravitreal Dexamethasone implant : 0.7mg Dexamethasone Implant
(GENEVA) results in increased VA and decrease of ME over first 2 months.
Effect wanes over 6 months, can be repeated. But chances of raised IOP and
Cataract formation is there.
- Intravitreal Triamcinolone : 2 Injections of 1mg triamcinolone(SCORE) results
in increase of VA over 1 year. But increased chances of raised IOP and
cataract formation is there.
- Macular Grid Laser : Although macular edema is anatomically improved, it
doesn’t improve visual acuity by much
B. Treatment of Neovascularization
- Laser Photocoagulation : Scatter Photocoagulation in
BRVO and Pan-Retinal Photocoagulation is done in CRVO.
- Adjunctive intra-vitreal anit-VEGF administered every
6 weeks, leads to more rapid resolution of NV
C. Treatment of Vitreous Haemorrhage
- Vitrectomy and endolaser
DIFFERENTIAL DIAGNOSIS
• Proliferative DR
• Hyperviscosity Retinopathy
• Ocular Ischaemic Syndrome
THANK
YOU