This document discusses branch retinal vein occlusion (BRVO), including its pathogenesis, risk factors, clinical features, investigations, and management approaches. Some key points: - BRVO is the second most common cause of vision loss due to retinal vascular disease, after diabetic retinopathy. It occurs most often in patients in their 50s-60s and is caused by obstruction of a branch retinal vein. - Risk factors include hypertension, diabetes, hyperlipidemia, glaucoma, smoking, and age-related atherosclerosis. Laser treatment can help manage macular edema and neovascularization complications. - Treatment aims to address modifiable risk factors and manage sight-threatening complications like macular edema,

1. Dr. Shah-Noor Hassan FCPS,FRCS
Consultant, Vitreo-Retina
Bangladesh Eye Hospital & Institute

2. INTRODUCTION
 First described by LEBER in 1877.
 KOYANAGI first described more
incidence in UT branch.
 2nd most common cause of vision d/t
retinal vascular disease (after diabetic
retinopathy)
 BRVO accounts for 69.5% of total RVO.

3. Demography
• Age: 5th – 6th decade
• Sex: males = females
• Incidence : 0.7% between 50 – 60
4.6% after 80 yrs

4. Risk factors
 Systemic hypertension
 Diabetes
 Hyperlipidemia
 Glaucoma
 Smoking
 Age related atherosclerosis

5. Others risk factors–
• Eyes with shorter axial lengths
• Anti-phospholipid antibody syndrome
• Elevated plasma homocysteine levels
• Low serum folate levels
• Inflammatory disease( Sarcoidosis, Bechet’s
disease)
• Acquired & inherited thrombophilic conditions
• Hyper viscosity state ( polycythemia, myeloma,
etc.)

6. Protective factors
 Higher serum HDL
 Moderate alcohol consumption

7. Pathogenesis
• Almost always occurs at AV crossings
• Retinal artery and vein share a common
adventitial sheath & in some cases a
common medium
• Artery located anterior to the vein at the
obstructed site; lumen of the vein
compressed upto 33 % at the obstruction
site
• Role of vitreous – eyes with decreased
axial length and and higher likelihood of
vitreomacular attachment at AV crossings

8.  Turbulent flow at
the crossing site
causes focal
swelling of the
endothelium and
deeper vein wall
leading to venous
obstruction
 Actual venous
thrombus at the
point of occlusion

9. Venous occlusion
stagnation
hypoxia
Edema & hemorrhage
Increased tissue
pressure
perfusion pressure =
art. pres.-vein. pres.
Venous obstruction
Venous pressure
Overloading of collateral
drainage capacity
Macular edema & ischemia
Unrelieved venous pressure
Rupture of vein wall
& intraretinal hemorrhage

10. CLASSIFICATION
1) Major BRVO :
-occlusion of 1st order
temporal branch at disc.
-occlusion of 1st order
temporal branch away from
disc, but involving branch
to macula.
2 ) Minor macular BRVO –
involving only a macular
branch
3 ) Peripheral BRVO – not
involving the macular
circulation

11. INCIDENCE OF TYPES
• Upper temporal quadrant :
49 - 63 %
• Lower temporal quadrant :
29 – 51 %
• Macular : 24 %
• Nasal : 0.5 – 2.6 %

12. CLINICAL FEATURES
PRESENTATION
*macular involvement : sudden
blurred vn,metamorphopsia
,relative V F defect.
*peripheral involvement :
asymptomatic.
VISUAL ACUITY
-depends on macular involvement
-Orth & Patz : farther the site of
occlusion from disc better is
prognosis.

13. EYES VISION
 50 % 6/12 or better
 25 % 6/60 or worse

14. Fundus examination
EARLY STAGE :
Dilatation and tortuosity of the venous segment distal to the
site of occlusion and attenuation proximally
Flame shaped and dot-blot hemorrhages, retinal oedema and
cotton wool spots : usually in triangular pattern, apex of
which lies towards the site of obstruction.

15. Macular edema
 5 – 15 % of eyes over 1 year period
 18 % resolve by 4.5 months, 41% by 7.5
months

16. Course
• Resolve within 6 –
12 months
• Segmental
distribution of retinal
vascular
abnormalities pers
• Hard exudates,
venous sheathing
and sclerosis
peripheral to the site
of obstruction

17. Apparent on FA
• Capillary non-perfusion
• Microaneurysms
• Collateral vessel formation

18. Neovascularization
NVD – 10 %
NVE – 25 %
in cases with extensive
ischemia, >1/3 fundus
Serious complication – leads
to recurent pre-retinal and
vitreous hemorrhage

19. Fellow eye involvement
 Bilateral involvement 4.5 - 6.5 %

20. OCT

21. Fluorescein angiography
• Delayed venous filling
• Blockage by blood
• Hyperfluorescence due to leakage

22. In late cases :in addition to
• nonfilling of the segment (CNP)
• collaterals (non-leaking) may be seen or NV (leaking)
 Fluorescein column is narrowed at site of obstruction.
 Clemette’s sign of focal hyperfluorescence at AV
crossing present from 6th to 12th week.

23. COMPLICATIONS
MACULAR CHANGES
1) Chronic macular
oedema: 48% cases
1/3 rd edema regresses
spontaneously
2) Macular non-perfusion
: vision is unlikely to
improve.

24. 3) Epiretinal membrane
4) Hard Exudates, pigment clumping at
macula

25. NEOVASCULARIZATION :
• In major brvo: NVD 10%,NVE 36% (if CNP areas > 5DD)
• develops at border of ischemic & non-ischemic retina.
• occurs max. upto 6-12 months, may occur upto 3 years.
• NV doesn't develop in macular brvo

26.  VITREOUS & PRE-
RETINAL H’GES:60
%
(22-36% develop
NVE if CNP areas
>5DD, of them 40%
develop VH)

27. Tractional RD
Rhegmatogenous RD
-Ischemia leads to atrophic hole formation.
-secondary to tear formed due to fibrovascular traction
Retinal detachment

28. ANT. SEGMENT NV : 1.6 %

29. INVESTIGATIONS
BP, ECG
CBC, ESR
Fasting blood glucose & lipids
In young patients
• Autoantibodies
• ACE
• Homocysteine
• Thrombophilia screen
• Plasma protein electrophoresis

30. Management
2 main objectives
1. Identification of modifiable risk factors
(example HT, DM, CVS) and their
management – for other eye
2. Recognition and management of sight-
threatening complications

31. Anticoagulant therapy
 Not beneficial in either prevention or
management
 Associated with systemic complications
 Theoretically, severity of intraretinal
hemorrhage in acute phase

32. BRVO with perfused periphery
& normal VA
 Favourable prognosis
 No therapy
 Monitored monthly for 1st 3 months, then
every 2 months for the 1st year

33. BRVO with peripheral
nonperfusion
 Laser treatment

34. Macular BRVO
 Involves a small vein draining a sector of
the macular region
 Favourable natural course

35. Laser photocoagulation
BVOS eligibility criteria
Grid laser recommended in eyes with
1. VA of 20/40 or less
2. Persistent macular edema > 4 mths
3. Resorption of macular hemorrhages

36. BVOS
TREATED
 Gain of 2 or more
lines-65%
 V/A of 6/12 or better-
60%
 Mean gain of lines-
1.33
UNTREATED
 37%
 34%
 0.23
MACULAR GRID LASER:

37. SCORE study
 Recommended grid photocoagulation
for vision loss with macular edema
secondary to BRVO
 However, leads to paracentral visual
field defects

38. Ozurdex
 Sustained release
biodegradable
implant
 0.7 mg
Dexamethasone
 Received FDA & EU
approval for
treatment of
macular edema
secondary to RVO

39. Neovascularization
According to BRVO study group:
Scatter laser - if NVE is present (reduces chances of VH to
20%)
may not treat all cases with CNP areas as 78% may not
develop NVE & VH

40. BVOS
TREATED
 VH incidence – 29%
 NVE incidence –
12%(CNP > 5DD)
UNTREATED
 61%
 22%
Thus 78% cases do not progress
to NVE, hence laser not
recommended till NVE develops.
SECTORAL LASER

41. SURGICAL
INTERVENTIONS
 Isovolaemic haemodilution
 tPA( tissue plasminogen activator)
 Chorio-retinal anastomosis
 Sheathotomy
 PVD Induction
 Steroids
 Anti-VEGF

42. LASER CHORIO-RETINAL
ANASTOMOSIS
 Argon green(2.5-
3.5W)
 Low success rate(30-
40%)
 Complications :
-VH
-SRNVM
-R.D
-ERM

43. Surgical management
SHEATHOTOMY
 OSTERLOH and CHARLES – 1988
Relieves the compression of artery on vein
OPREMCAK and BRUCE – 1999, 85% had
either same / improved V/A, 67 % improved
Mester,Dillinger et al –ILM peeling gives better
results
Shah et al – 2000

44. BMV with PVD induction
(+/- Sheathotomy)
 Proposed mechanisms :
-removal of vitreo-macular traction
-removal of cytokines that increase
vascular permeability
-improvement of oxygen tension in
posterior retina
-faster development of collaterals- 6
months (normally 6-24 months)

45.  Pre-op Post-op

46. BMV+PVD(+/-
Sheathotomy???) No significant difference
in improvement in VA in
eyes with reperfusion of
occluded vein and those
without - indicating that
the reopening of
occluded vein is not
essential for visual
recovery.
 Improvement in macular
oedema but no effect on
macular function
Yamamoto et al AJO 2004

47. Venous occlusion
Retinal circulatory impedence Retinal oedema
Cellular hypoxia Increased capillary
permeability
Angiogenic factor, VEGF Breakdown of inner
blood retinal
barrier
Anti-VEGF

48. anti-VEGF
 Safe and efficacious.
 Unsustainad effect in some cases.
 Does not alter the perfusion status
which determines the end result.

49.  The benefit of any treatment has to be
compared with the natural course of the
disease.
 50-60% maintain maintain initial V/A of
6/12 at 1-3 yrs followup. Thereafter natural
course remains relatively stable.
 Conversely natural course of V/A<6/12 is
unfavourable without treatment.
( at 3 yrs 23% had V/A of 6/60 or worse &
only 37% gained 2 or more lines)

50. Treatment
 Focused on management of vision-
limiting complications
 Macular edema
 Macular non-perfusion
 Vitreous hemorrhage from
neovascularization

51. Treatment algorithm

52. Prognosis
 33 – 50% regain 6/12 or better VA
spontaneously.

54. • More similarities than dis-similarities in the risk
factor profiles for BRVO, CRVO and HRVO
• Testing for patients with HT, DM and open-angle
glaucoma should be part of the evaluation of
patients with retinal vein occlusion

56.  Favorable safety and tolerability profile over 12
months of follow-up.
 can be repeated with no new safety concerns after
the second treatment with regard to IOP
increases, although cataract progression does
seem to increase

57. Edaravone (MCI-186) is effective as a free
radical scavenger following arteriovenous
sheathotomy for treatment of macular
oedema associated with branch retinal vein
occlusion
T Maeno1,2, R Tano1, H Takenaka1, T Mano1
+Author Affiliations
1Tane Memorial Eye Hospital, Osaka, Japan
2Department of Ophthalmology, Osaka Medical
College, Takatsuki, Japan

58. •Stabilization and increase in visual acuity after laser
treatment did not correlate with an overall decrease in
scotoma size.
• Improved central visual function seen in 25% of treated
eyes appeared to be due to
•withdrawal of scotoma from the fovea.

60. Sheathotomy
Principle steps
• Pars plana vitrectomy
• Overlying artery is separated from the
vein by creating an incision in the
adventitial sheath adjacent to the
arteriovenous crossing and then
separating the adhesions.

61. Although the study by Mason et al reported a benefi
cial effect on VA in those patients undergoing
surgery compared with those receiving laser or no
treatment, the
study was not randomized and was partly
retrospective, introducing sources of potential
bias. There is currently no evidence from RCTs
supporting the routine use of adventitial
sheathotomy to improve VA in eyes with BRVO

62. Plasminogen
Activator to Treat Macular
Edema
Associated With Branch
Retinal
Vein Occlusion
(Am J Ophthalmol 2006;142: 318–320
• After topical anesthesia was applied and a
paracentesis created
• tPA (40 k international units [IU]) injected into the
vitreous
• bedrest in the supine position for four hours
following treatment
 Mechanisms - PVD induction & development of
collateral vessels

63. Multifocal ERG
Responses from multifocal
electroretinography demonstrate retinal
dysfunction in branch retinal vein
occlusion

64. Moreover, if repeat injections are required,
the use of a sustained release steroid
implant would obviate the need for
multiple injections, but also magnify the
risk of steroid related complications.

65. Although steroids have antiangiogenic, antifibrotic, and
antipermeability properties, the principal effects of
steroids
are stabilization of the blood-retinal barrier, resorption of
exudation, and down regulation of inflammatory stimuli.
Whereas it is clear that there is a break-down in the
blood
retinal barrier in BVO, studies have shown that there
may
also be an inflammatory component that would respond
to
steroids.

66. Endophthalmitis, sterile endophthalmitis,
pseudo-hypopyon, cataract, retinal
tears, retinal detachment, and vitreous
hemorrhage have all been described
after intravitreal steroid injections.
Additionally, steroid related complications
including cataract and increased
intraocular pressure (IOP) can occur.
Increased IOP was seen in 33% of
patients in the intravitreal injection group