MEANT FOR POST GRADUATES

1. Central retinal vein thrombosis
Dr. K. Vasantha M.S., F.R.C.S.
Director RIO Chennai (Rtd)

2. • Retinal venous occlusions can be
• Central – CRVO
• Branch retinal – BRVO
• Hemicentral vein occlusion – rare. Usually
upper or lower part of the retina is affected.
Very rarely nasal or temporal part can be
affected. This depends on the type of
anatomical variation.

3. Signs and symptoms
• Commonest cause of sudden loss of vision in
the elderly.
• In typical CRVO extensive superficial and
deep hemorrhages are seen. Hemorrhages
extend from to the disc to the periphery.
• Edema of the disc and retina
• Dilated and tortuous retinal veins.

4. • In mild cases only few hemorrhages, mild
disc edema and slight dilatation of veins are
seen.
• If associated with ischemia cotton wool
spots, severe macular edema and capillary
non perfusion areas will be seen.
• Ischemia – severe loss of vision along with
RAPD

5. • In CRVO the thrombus formation is at the
retro laminar level.
• There is narrowing of vessels
• And the artery and vein are closely placed at
this location.
• There is turbulent blood flow – endothelial
damage – thrombus called Virchow’s triad

6. Predisposing factors
• Old age group – POAG, hypertention, cardio
vascular and collagen vascular dis., diabetes,
smoking and more common in males
• Thrombus – due to alterations in blood flow
• Abnormal cellular products- leukemia, sickle cell
disease
• Abnormal plasma – Lupus, factor V Leiden
mutation, low plasminogen (birth control pill)
• Excess cells – polycythemia, thrombocytosis

7. • Abnormal plasma- hyper proteinemia and
homocyteinemia
• Alterations in blood vessel – atherosclerosis,
compression due to tumors, vessel wall
derangement in diabetes
• Abnormal blood flow currents – low flow in
cavernous sinus thrombosis, dural cavernous
fistula
• Compression of blood vessels
• Endothelitis – syphilis, multiple sclerosis, Eales’,
sarcoidosis, parsplanitis, autoimmune, TB

8. • Risk of CRVO decreases with postmenopausal
estrogen
• Increases with increased ESR
• In polycythemia and Waldenstrom’s
macroglobulinemia bilateral CRVO may be
seen.
• Presence of anti cardiolipin and
antiphospolipid antibodies.

9. • Protein C and protein S (anticoagulant)
deficiency. History of abortions and
involvement of other arteries and veins will
be present.
• Activated protein C resistance – AD trait
• In younger age group phlebitis must be
suspected.

10. Types
• Ischemic
• Non ischemic

11. CRVO / tomato splash

12. Ischemic CRVO
• Visual acuity very low. Often less than 6/60.
• Afferent pupillary defect
• Slightly lower IOP
• More severe field loss
• Fundus: Presence of cotton wool spots
• More hemorrhages
• More than ten disc areas of non perfusion

13. Late Fundus Picture
• Hemorrhages disappear slowly. Some
peripheral hemorrhages may persist even for
years.
• Dilatation and tortuosity of veins reduce.
• Fibrous sheathing of vessels may develop.
• Disc edema will reduce.
• Collaterals may develop near the disc.

14. Late CRVO
• Micro aneurysms may be seen
• Persistent macular edema
• Changes in the macular pigmentation
• Neovascularization of the disc and retina.

15. F.F.A.
• Prolonged arterio venous transit time. If it is
more than 20 sec – ischemia
• Staining of the walls of the vein – ischemia
• Presence of capillary non perfusion areas
may not be seen due to the hemorrhages.
• If non perfusion is seen close to the fovea –
poor prognosis

16. • Ischemia causes increase in permeability of
vessels – edema – diffuse or petalloid pattern
of macular edema.
• Decrease in perifoveal blood flow,
enlargement of capillary avascular zone.
• Increase in peri foveal inter capillary area.

17. O.C.T.A
• Abnormalities are seen both in superficial
and deep retinal capillary network. This is
more in deep vessels
• Decrease in vascular perfusion
• Mean foveal avascular zone will be larger.
• Inter capillary areas are larger in the
perifoveal capillaries

18. E.R.G.
• Reduced B wave amplitude
• Reduced b/a wave ratio
• Prolonged b wave implicit time.

19. Complications
• Major cause of visual loss is macular edema
• Can be mild or severe
• Due to hydrostatic stress and ischemia
• May be transient or persistent

20. Hemorrhage
• Will definitely be present but number will
vary
• If present in the fovea – severe loss of vision
• If lots of hemorrhagic spots are seen it is
called “tomato ketchup” appearance
• Very rarely vitreous hemorrhage may be
present in acute case. If it occurs in late stage
it will be due to neovascularization.

21. Ischemia
• If large number of (more than 10 disc
diopters) capillary avascular zones are
present ischemia should be suspected.
• If ischemia is close to the fovea – severe loss
of vision
• Will lead on to neovascularization

22. Neovascularization
• Seen on the disc, elsewhere in the retina, iris
or in the angle of anterior chamber.
• Neovascularization of the iris is more
common than that of the retina.
• Once neovascularization of iris occurs it will
progress fast. Hence this must be watched
diligently.
• Rarely can occur in non-ischemic cases also

23. Other complications
• Rhegmatogenous and exudative retinal
detachment can occur
• Micro aneurysms
• Large aneurysms which appear similar to
macroaneurysms arise from the capillaries
• Collaterals seen as tortuous vessels near the
disc

24. • Choroidal arteries may be affected
• If cilio retinal artery is present it may get
occluded as this artery has a lower perfusion
pressure compared to retinal artery. This will
gross loss of vision.
• Cotton wool spots
• Rarely hard exudates may be seen. This
indicates severe ischemia and increased
triglyceride levels.

25. D.D
• Early CRVO – AION – no haemorrhage,
altitudinal defect
• Papilledema – no loss of vision
• Hypertension – younger age, bilateral
• Hyper viscosity – bilateral
• Anemia – bilateral
• Diabetes – bilateral, hard exudates, micro
aneurysms

26. D.D
• Early CRVO – AION – no haemorrhage,
altitudinal defect
• Papilledema – no loss of vision
• Hypertension – younger age, bilateral
• Hyper viscosity – bilateral
• Anemia – bilateral
• Diabetes – bilateral, hard exudates, micro
aneurysms

27. BLOOD DYSCRASIAS
Roth’ s spots
ANEMIC RETINOPATHY –see the clear cut hemorrhages
And Roth spots

28. Treatment
• Various studies have been done to find out
the best treatment for CRVO
• Cruise study found that Ranibizumab is
better than sham
• Bevacizumab also was found to be better
than sham
• COPERNICUS study found aflibercept was
better than shams

29. • GALILEO study found aflibercept was better
than sham
• SCORE study compared 1 g and 4 mg intra
vitreal triamcinolone versus standard care
(just observation). Adverse events like
cataract and glaucoma were more in 4 mg
group. Results showed that IVTA is not
favourable.

30. • In GENEVA study micronized dexamethasone
implant (ozurdex) with either 0.3, 0.7 mg or
sham was used
• Decrease in foveal thickness was seen with
ozurdex.
• Cataract and glaucoma were more in 0.7 mg
group
• Ozurdex helps in refractory cases also

31. • TANZANITE study :- here aflibercept alone or
along with supra choroidal injection of
triamcinolone was used.
• It was found that combination resulted in
better visual acuity, more reduction in
edema, and for more than 9 months
additional injections were not needed.

32. • Newer anti VEGF drugs are being tried like
conbercept, brolucizumab.
• Nano particles and liposomes are tried to
deliver the drugs in a better manner.
• Special devices are being tried to deliver the
drugs like tPA in to the vein itself.

33. Laser treatment
• CVO study showed that there is no role for
grid laser in macular edema due to CRVO
• Pan retinal photocoagulation was shown to
be beneficial in eyes which already have 2
clock hours of NVI or NVA.
• Photocoagulation before the appearance of
new vessels is not useful. Hence the need for
frequent follow up to look for iris and angle
new vessels.

34. • In RELATE trial ranibizumab was used for 6
months and the either ranibizumab alone or
along with laser was tried.
• It was found that addition of laser was of no
use.
• Recurrence of edema was more in old age, if
central 1 mm was involved or when initial
edema was >570, late treatment, larger areas of
non perfusion (75 – 150 seen with wide angle
ffa)

35. Inferior Hemiretinal venous occlusion

36. Branch retinal vein occlusion
• In this lesion also hemorrhages will be seen
but restricted to the area drained by that
vein.
• Usually the upper temporal branch is
involved as there are more arterio venous
crossings.
• If the vein is occluded very close to the disc
affected area will naturally be large with
more complications.

37. • Infero temporal branch is the next commonly
affected
• Nasal branches are rarely affected
• When nasal branches are affected visual
deprivation is less. Hence not reported by
affected individuals immediately.

38. • The occluded vein will be tortuous and
dilated due to banking of blood.
• Superficial and deep hemorrhages will be
seen along the affected vessel.
• Cotton wool spots may be seen.
• Retinal edema
• Arterio venous crossing changes must be
looked for in the other eye also

39. • Common in males
• Hypertensives
• Hyperops
• Diabetics
• Open angle glaucoma should be looked for

40. Eye Disease Case Control study
• Predisposing factors are similar to CRVO.
• Cardio vascular diseases more in BRVO
• Obesity and higher serum levels of alpha 2
globulin
• Alcohol consumption and normal levels of
high density proteins reduces BRVO.

41. • Vision will often be affected due to
involvement of the macula by hemorrhages,
edema and ischemia.
• Vitreous hemorrhage and retinal detachment
also can rarely occur affecting vision.

42. BRV0

43. Fundus picture
• The previous slide shows the typical fundus
picture
• Hemorrhages along the involved vein.
• Cotton wool spots may be present
• In late cases intra retinal collateral going
across the median raphe
• If ischemia was there sheathing may be seen

44. F.F.A.
• As expected delay in venous filling in the
involved vein will be seen.
• Retinal edema along the involved vein.
• Macular edema and ischemia may be seen –
this will cause decrease in vision.
• Retinal and disc neovascularisation is rare
and if present will be at the junction of
perfused and non perfused area.

45. • In BRVO study new vessel formation was
seen in 22% of eyes.
• If more than 5 disc diameters of capillary non
perfusion was seen neovascularisation is
likely to occur.
• Neovascularisation can lead on to vitreous
hemorrhage.
• Micro aneurysms and hard exudates may
develop later.

46. Complications
• Rhegmatogenous Retinal detachment can
rarely occur posterior to the equator.
• Fibro vascular proliferations can cause
traction and tears in the retina.
• Ischemia also can cause retinal hole and lead
on to detachment.
• Exudative detachment can occur in the region
of the involved vein if ischemia is present.

47. • Epiretinal membrane
• Irregularities in the retinal pigment
epithelium
• Sub retinal scar
• Macular hole
• Are other complications
• Prognosis will be poor if the occlusion is very
close to the disc.

48. Look for
• Toxoplasmosis
• Eales’
• Behcet’s
• Sarcoidosis
• Coat’s
• Optic nerve drusen
• Retinal macro aneurysm or hemangioma

49. Treatment
• SCORE study :- intra vitreal steroids are
helpful
• VIBRANT study:- Aflibercept is better than
laser.
• GENEVA study found ozurdex to be useful
• Bevazizumab was found to be better than
laser
• MARVEL - Ranibizumab was seen to be better
than Bevazizumab

50. Laser
• Branch vein occlusion study – laser covering
the entire area of involved retina except
within 2 dd of the fovea reduced the risk of
neovascularisation in eyes with >5 dd of non
perfused retina. When new vessels were
already present incidence of vitreous
hemorrhage was also less.
• After the use of anti VEGF laser is used less.

51. THANK YOU