CRVO, BRVO, Hemiretinal vein occlusion

1. Retinal vein occlusion
SHREEJI SHRESTHA

2. Classification
Branch retinal vein occlusion
Central retinal vein occlusion
(hemicentral retinal vein occlusion)

3. Risk factors and Associations:
• HTN
• Arteriosclerosis
• DM
• Smoking
• Hyperlipidemia
• Glaucoma
• Ocular inflammatory disease
• Antiphospholipid antibodies
• Elevated homocysteine levels
• Low serum folate levels
• Shorter axial length
• High HDL
• Light to moderate alcohol
consumption
• increasing age

4. Pathogenesis:
• Lumen of the vein may be compressed up to 33% at the crossing site

5. Some have postulated:
Turbulent blood flow at crossing site
Focal swelling of endothelium and deeper vein wall tissue
Venous obstruction
Actual venous thrombus formation at the point of occlusion
75%- artery cross over vein. (BRVO seen)

6. Venous obstruction
Elevation of venous pressure
Overload the collateral draining capacity
Macular edema and ischemia
Unrelieved venous pressure can result in rupture of vein wall with
intraretinal hemorrhage

7. Vision loss from RVO is due to:
• Macular ischemia
• Macular edema
• Complications from neovascular disease, ERM, Vitreous hemorrahge,
tractional RD

8. Clinical features
Symptoms:
• Sudden painless loss of vision
• Visual field defect
• Subclinical presentation may occur if tributaries distal to macula or
nasal vein involved
• Sometimes floaters- from a vitreous hemorrhage

9. Signs:
BRVOS defined ischemic BRVO as those with greater than a total of 5
disc diameters of non perfused on FA.

10. Location of venous blockage determines the distribution of the
intraretinal hemorrhage
• If the venous obstruction at optic disc – 2 quadrants of fundus
involved
• If the obstruction is peripheral to disc – 1 quadrant or less may be
involved
• If the venous blockage is peripheral to tributary veins draining macula
– there may be no macular involvement and no decrease in vision

11. • The most common location for BRVO is in the superotemporal
quadrant (62%), infertemporal 38%
• Over time the intraretinal hemorrhage may completely resolve.
• In chronic phase of the disease, capillary non perfusion, dilatation of
capillaries, micro-aneurysms, telangiectatic vessels and collateral
vessel formation.

12. • BRVOS – 31-41% pt with ischemic BRVO developed
neovascularization compared to 11% of pt with non ischemic.
• Among those 31-41%, 60% developed periodic vitreous hemorrhage
• Retinal neovascularization typically develops at 6-12 months but may
occur later
• NVI/ NVA develops in 1% eyes in BRVO.

13. Clinical evaluation
1. Clinical examination
2. FA:
• To help verify the diagnosis and evaluate for complications
• Only technique that will accurately define the capillary abnormalities
in BRVO
3. wide field angiography
4. OCT: most important imaging modality in the treatment of patient
with BRVO and macular edema

14. Characteristic findings in FA:
• Varying amount of capillary nonperfusion, blockage from intraretinal
hemorrhage, microaneurysms, dilatation of capillaries, telangiectatic
vessels and collateral vessel formation are encountered.
• In chronic cases, only FA can determine old BRVO

15. Prognosis
• presence or absence of macula or fovea = visual prognosis
• IF FA demonstrates – macular leakage and edema with cystoid
involvement of fovea but no capillary nonperfusion – then 1/3rd
resolve vision and if duration > 1 year then decrease chance of regain
of vision.
• When macular edema is present within 6 months of BRVO no or little
leakage in FA – vision regains normally

16. Work up
Diagnostic workup should be done in young patient for:
• HTN
• DM
• H/O contraception use
• H/O drug use that promote hypercoaguloble state
• Infectious disease: lyme, HIV, syphilis
• Inflammatory disease

17. In suspected inflammatory or coagulopathy
• CBC
• PT/INR
• Lipid profile
• S. homocysteine
• Anticardiolipin
• Antinuclear antibodies
• In B/L or numerous BRVO – look for infections or inflammations or
hypercoagulopathy

18. ultra wide field angiography

19. 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

20. • 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.

21. General guidelines from BRVOS for macular
edema
• 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 FA and
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.

22. BRVOS for neovascularization
• 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%

23. Steroid treatment
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

24. GENEVA study (Global evaluation of implantable dexamethasone in
retinal vein occlusion with macular edema in BRVO and CRVO).
• Dexa 0.7mg implant is an alternative treatment to macular grid laser
in the appropriate patient (i.e. no glaucoma and pseudophakic)

25. Anti VEGF
• In patient of BRVO, retinal ischemia leads to secretion of VEGF which
leads to 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

26. 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)

27. Experimental treatment
FAVOR study
• Intravitreal implant of fluocinolone acetonide

28. 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

29. Central retinal vein occlusion
(CRVO)

30. Pathogenesis
• Pathophysiology not clearly understood
• external compression - compression by atherosclerotic artery,
retrobulbar injection, head trauma
• primary disease of vein - vasculitis
• thrombosis of vein(primary event)-
dec blood flow
inc blood viscosity altered lumen wall

31. in retrolaminar portion of optic nerve
Central retinal artery and vein are aligned parallel in common tissue
sheath
CRA and vein are naturally compressed as they cross the rigid shieve
like openings in the lamina cribrosa
vessels compress from mechanical stretching of lamina as with
increase IOP ----cause a post bowing of the lamina--- impingement on
the vein
• Neovascularization and macular edema are modulated by growth
factors VEGF released from ischemic retina

33. clinical features
VA- normal - HM, Sudden painless loss of vision
gonioscopy- NVA or angle closure from PAS
iris - NVI
Afferent pupillary defect- ischemic CRVO
IOP= glaucoma and inc IOP are risk factors. Acute (decrease)
Visual field- central and peripheral field abnormality

34. Clinical features
cotton wool spots
dilated and tortous veins
disc swelling pallor and collatera
flame shaped and blot hemorrhage
blood and thunder appearance

35. complications
macula edema- leakage of perifoveal vessels persist later ERM
neovascularization- 24% ischemic CRVO
fibrovascular proliferation from NVD or NVE - VH and TRD

36. CVOS
• VA at initial presentation was variable but an important prognostic
indicator of final outcome
• 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%.

37. Perfusion status
• CVOS classified perfusion status of CRVO – perfused, non
perfused or indeterminate based on FA characters
Perfused CRVO (non
ischemic/incomplete/partial/threanened or impending
vein occlusion) 75-80%
• Demonstrates less than 10 disc areas of retinal capillary
nonperfusion on FA
• less intraretinal hemorrhage and better initial VA
• occlusion of CRV at a site further posterior - normal
collateral for drainage, simple occlusion of vein
• cotton wool spots rare

39. Non perfused CRVO
(ischemic/hemorrhagic/complete/total vein
occlusion) 20-25%
• Demonstrates 10 or more disc areas of retinal
capillary nonperfusion on FA
• more intraretinal hemorrhage, macular and disc
edema and worse VA at onset
• occlusion prior to branching of collateral from
main trunk, combined vein and artery occlusion
• cotton wool spots and Visual ield defect more

41. • Electro-retinography - reduced b amplitude
• perimetry

42. Treatment
• Treatment of CRVO is directed at treating the sequelae of CRVO
particularly macular edema and neovascularization
Treatment of systemic medical conditions if any:
Medical therapy
• Topical/systemic anti glaucoma agents to reduce IOP
• Topical steroids to reduce inflammation
• Cycloplegics to prevent from posterior synechiae
• oral pentoxifylline

43. Treatment of macular edema
• 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

44. Score(standard care Vs corticosteroid for RVO)
• Showed significant improvement in VA with intravitreal triamcinolone
compared to observation
• 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

45. Intra vitreal Anti VEGF therapy
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.

46. Treatment of ocular neovascularization
⮚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.
• Patient with NVD/NVE without NVI/NVA should be treated with PRP to
prevent anterior segment neovascularization

47. Alternative treatment
Chorioretinal venous anastomosis:
• 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

48. 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
• extensive anterior segment NVIand NVA, PPV and endolaser may be
combined with pars plana placement of a glaucoma drainage device
to avoid anterior chamber hemorrhage

49. 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

50. General guideline 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

51. Hemicentral retinal vein occlusion
in some eyes, Superior and inferior vein doesnt merge to CRV(1 in 5
eyes)
CRVO affect only 1half of eye (superior or inferior)
scatter PRP

52. References
• Ryan’s 5th edition
• Myron yanoff 4th edition
• American academy of Ophthalmology-sec 12, 2013,2014
• jakobiecs