This document provides an overview of branched retinal vein occlusion (BRVO). It discusses the classification, epidemiology, risk factors, pathogenesis, signs and symptoms, diagnostic evaluation, and management of BRVO. Key points include that BRVO is the most common type of retinal vein occlusion and risk factors include hypertension, glaucoma, hyperlipidemia, and advancing age. Diagnostic testing includes fluorescein angiography and OCT to evaluate for macular edema, capillary nonperfusion, and neovascularization. Laser photocoagulation and anti-VEGF injections are common treatment approaches for complications such as macular edema.

1. BRANCHED RETINAL VEIN OCCLUSION
BY
DR ANJALI MAHESHWARI

2. INTRODUCTION
 Segmental retinal involvement in distribution of
involved occluded vein.
 Involved area: wedge shaped with apex near site of
occlusion and extending to periphery.

3. CLASSIFICATION
 BRVO can be classified depending on the anatomical
location :
 Major BRVO - refers to an occlusion of a retinal
vein that drains one of the quadrants
 Macular BRVO- refers to an occlusion of a venule
within the macula.

4.  BRVO is further classified into:
 Perfused (non-ischemic)
 Nonperfused (ischemic)- defined as > 5 disc
diameters of nonperfusion on fluorescein
angiography (FA)

5. EPIDEMIOLOGY
 BRVO is the most common RVO with an incidence of
0.44%-1.6%.
 The beaver dam eye study - The prevalence and 5-year
incidence of retinal branch vein occlusion were each
0.6%
 The blue mountain eye study- determine the prevalence
and associations of retinal vein occlusion (RVO) in a
defined older Australian population : age-specific
prevelance : 0.7%, younger than 60 years; 1.2%, 60 to
69 years; 2.1%, 70 to 79 years; and 4.6%, 80 years or
older

6.  Affects males and females equally and occurs most
frequently between the ages of 60 and 70.
 Prevalence of any RVO and BRVO in increasing order by
ethnicity was: whites, blacks, Asians, and then
Hispanics.

7. RISK FACTORS
 Age
 Significant association of advancing age with BRVO,
and the incidence of BRVO increases with age.
 The prevalence of BRVO is 0.157 per 100 in 40-49
year olds, 0.458 per 100 in 50-59 year olds, 1.11 per
100 in 60-69 year olds, and 1.276 per 100 in 70-79
year olds

8.  Hypertension and atherosclerosis
 After adjusting for age The Beaver Dam Eye Study
showed that BRVO was associated with:
 Hypertension
 Elevated systolic and diastolic pressure
 Pulse pressure
 Ocular perfusion
 Focal arteriolar narrowing
 Arteriovenous nicking.

9.  Ocular hypertension/glaucoma
 In the Eye Disease Case- Control Study (EDCC), a
history of glaucoma was found to increase a patient’s
risk of CRVO by a factor of 5.3, and of BRVO by a
factor of 2.5
 Hyperlipidemia
 Large meta-analysis by O’Mahoney et al, showed a
significant association of hypertension and
hyperlipidemia with BRVO

10.  Diabetes
 Diabetes mellitus was not a major in dependent risk
factor in the EDCC, although 10%–12% of patients
with RVO have the disease.

11. OTHER POSTULATED RISK FACTORS
 Hyperhomocysteinemia
 Anti-cardiolipin antibodies
 Various meta-analysis studies have examined
prevalence and association of thrombophilic risk
factors and BRVO.
 The only significant associations are
hyperhomocysteinemia and anti-cardiolipin
antibodies with BRVO

12.  Body mass index
 BRVO is uncommon in patients younger than 50 years
and there is a significant association of BMI with
BRVO in patients younger than 50 years.
 Smoking

13.  Low serum folate levels
 Cahill MT et al- Meta-analysis of plasma
homocysteine, serum folate, serum vitamin B12, and
thermolabile MTHFR genotype as risk factors for
retinal vascular occlusive disease. Am J Ophthalmol
2003

14.  Shorter axial lengths
 Ariturk N et al .Relation between retinal vein
occlusions and axial length. Br J Ophthalmol
 Simons BD et al . Branch retinal vein occlusion: axial
length and other risk factors. Retina
 Timmerman EA et al. Axial length as a risk factor to
branch retinal vein occlusion. Retina

15. PROTECTIVE FACTORS
 A decreased risk is present in those with :
 Higher serum levels of high density lipoprotein (HDL)
 Greater alcohol consumption.
(Eye Disease Case–Control Study Group. Risk factors for
branch retinal vein occlusion. Am J Ophthalmol)

16. PATHOGENESIS
 Multifactorial in origin and not completely defined.
 Possible mechanisms include a combination of:
 Mechanical compression
 Degenerative changes in vessel wall
 Hypercoagulable factors.

17.  The arteriosclerotic changes (specifically arteriovenous
crossing) are believed to result in venule occlusion
through endothelial cell damage and thrombosis.
 Another hypothesis is that arteriosclerosis results in
arteriolar insufficiency leading to BRVO.

18.  In almost all cases of BRVO (97.6-100%) thick-walled
artery is found anterior to the thin-walled vein.
 The artery and vein also share a common adventitial
sheath at these crossings, predispose vein occlusion at
these crossings.

20.  Arteriolar sclerosis increases the rigidity of the artery
and provides support for the mechanical basis of BRVO
at arteriovenous crossings .
 Mechanical obstruction of the vein by the rigid artery
results in turbulent blood flow at arteriovenous
crossings, resulting in venous intima, media and
endothelial damage which leads to vein occlusion.

21.  It is thought to follow the principle of Virchow's triad for
intravascular thrombus formation:
 Endothelial damage
 Hemodynamic changes in blood flow
 Hypercoagulability.

22.  Histological studies of BRVO:
 Endothelium and intima media are found to be
thickened and altered at the arteriovenous crossings
 With no blood thrombus obliterating the venous
lumen at the arteriovenous crossing
 Suggesting a compression as a major factor in the
pathogenesis of BRVO

23.  Greater number of AV crossings are present in the
superotemporal region
 Approximately two thirds of major BRVO occur in the
superotemporal quadrant(63%), followed by the
inferotemporal quadrant and less commonly in the nasal
quadrants

24.  When the occlusion does not occur at an arteriovenous
crossing, the possibility of an underlying
retinochoroiditis or retinal vasculitis should be
considered.

25. SYMPTOMS
 Typically, patients present with sudden painless vision
loss or visual field defect.
 Rarely, patients present with floaters from vitreous
hemorrhage if the initial vein occlusion was
asymptomatic and retinal neovascularization had
developed.

26.  Patients with macular BRVO presents with a central field
defect, while major BRVO present with a peripheral field
defect corresponding to the retinal quadrant that is
affected.
 The field defects are relative in cases of capillary
nonperfusion and can become absolute scotomas in
long-standing occlusions

27. SIGNS
 Typical funduscopic examination consists of:
 Flame hemorrhages
 Dot and blot hemorrhages
 Cotton wool spots
 Hard exudates
 Retinal edema
 Dilated tortuous veins

28.  Classically there is a wedge-shaped distribution of
intraretinal hemorrhage that is more extensive if the
occlusion is ischemic compared to a non-ischemic BRVO.
 A hemorrhage can be present at the arteriovenous
crossing, which is called the Bonet sign.

29.  Location of the venous block determines the
distribution of the intraretinal hemorrhage
 If the venous obstruction is at the optic nerve head, two
quadrants of the fundus may be involved.
 If the occlusion is peripheral to the disc, one quadrant
or less may be involved with the intraretinal
hemorrhage.
 If the venous blockage is peripheral to tributary veins
draining the macula, there may be no macular
involvement and no decrease in visual acuity.

30.  In patients with chronic BRVO, the intraretinal
hemorrhages are absorbed and subsequent retinal
vascular abnormalities develop in the distribution of the
BRVO.
 The resulting changes include:
 Capillary nonperfusion
 Collateral formation
 Microaneuryms
 Sclerosed veins
 Telangectatic vessels

32.  In patients with BRVO, neovascularization most
commonly occurs in the healthy retina at the border of
the affected, ischemic retina > less commonly, at the
optic nerve head > rare in the anterior segment.

33. CAUSE OF VISUAL DECLINE IN BRVO
 Macular edema
 Macular ischemia
 Hemorrhage over the fovea
 Vitreous hemorrhage from neovascularizations of
the retina or the optic disc
 Epiretinal membrane/vitreomacular traction
 Tractional retinal detachment/combined tractional
and rhegmatogenous retinal detachment.

34. DIAGNOSTIC PROCEDURES
 Fluorescein angiography
 OCT

35. FLUORESCEIN ANGIOGRAPHY
 In patients with BRVO, FA helps to characterize retinal
vasculature including the extent of nonperfusion,
macular ischemia, macular edema and leakage.
 The characteristic FA for BRVO is delayed filling of the
occluded retinal vein with varying degrees of capillary
nonperfusion.

36.  Intraretinal hemorrhages will result in blockage
 Macular edema or retinal neovascularization will results
in dye extravasation

37.  Chronic branch retinal vein occlusion with sclerotic
superotemporal arcade vessel (arrow).
 The small collateral vessels (black arrowhead) can be
confused with neovascularization but do not leak on FA.
 There is also significant surrounding capillary nonperfusion
and areas of neovascularization with leakage (open arrows)

39. OPTICAL COHERENCE TOMOGRAPHY (OCT)
 OCT allows for rapid, non-invasive, and quantitative
analysis of the macula and has become an important
imaging modality in the assessment and treatment of
BRVO.
 Characteristic findings of BRVO on OCT are:
 Cystoid macular edema
 Intraretinal hyperreflectivity from hemorrhages
 Shadowing from edema
 Hemorrhages
 Occasionally subretinal fluid

40.  Spectral-domain optical coherence tomography of an
eye with a branch retinal vein occlusion (BRVO).
 Scan reveals cystoid macular edema with intraretinal
fluid, and subretinal fluid (open arrow).
 Intraretinal h’ge (arrow) appears hyperreflective with a
shadow.

41.  The third high reflectance band in the parafoveal
area corresponds to the junction between inner
segments (IS) and outer segments of
photoreceptors.
 This band (also called the ellipsoid zone) has
prognostic significance on visual acuity.
 Disruption or absence of the third reflectance band
after macular edema resolution is an indication of
photoreceptor cell death or disarrangement, which
results in poor visual outcome.

42.  Optical coherence tomography image of horizontal sections
of the fovea with mostly resolved macular edema.
 The third high reflectance band (red arrow) is continuous in
the parafoveal region and discontinuous in the fovea (blue
arrow).

43. LABORATORY TEST
 The diagnosis of BRVO is based on clinical examination.
 Typical patients will present with history of known risk
factors (hypertension, hyperlipidemia, or glaucoma).
 Initial work-up includes a detailed history to define risk-
factors.

44.  Initial laboratory work-up consists of:
 Comprehensive metabolic panel
 Complete blood count
 Lipid panel

45.  In patients younger than 50 years old, bilateral BRVO at
presentation, or history of numerous BRVOs search for:
 Infectious
 Inflammatory
 Hypercoagulable

46.  Initial work-up includes :
 Detailed history with attention to other risk factors
that might predispose to a hypercoagulable state,
including medications (such as oral contraceptives).
 The work-up should be performed in consultation
with the primary care doctor.

47.  Laboratory work up include:
 Complete metabolic panel
 Complete blood count
 Folate levels
 Vitamin B 12
 homocysteine level
( Cahill MT et al Meta-analysis of plasma homocysteine,
serum folate, serum vitamin B12, and thermolabile
MTHFR genotype as risk factors for retinal vascular
occlusive disease. Am J Ophthalmol)

48.  Anti-phospholipid antibodies
 Anti cardiolipin antibody - found in anti-phospholipid
syndrome, systemic lupus erythematosus, and Behcet
disease
 Activated protein C resistance (factor V Leiden).

49.  Inflammatory BRVO is clinically identified with evidence
of vasculitis and intraocular inflammation (paravascular
infiltrates, vitritis, snow balls).
 The blockage of the vein in such cases do not necessarily
correspond to the arteriovenous crossing.
 These BRVOs are usually peripheral and multiple and
the vasculitis may be in different stages
(active/healing/or healed) in the same eye.

50. STUDIES IN BRVO

51. BRANCH VEIN OCCLUSION STUDY (BVOS)
 Purpose
 To determine whether scatter argon laser
photocoagulation can prevent the development of
neovascularization.
 To determine whether peripheral scatter argon laser
photocoagulation can prevent vitreous hemorrhage.
 To determine whether macular argon laser
photocoagulation can improve visual acuity in eyes
with macular edema reducing vision to 20/40 or
worse.

52.  Inclusion criteria- Patients with three types of diagnoses
were accepted:
 Major BRVO without neovascularization.
 Major BRVO with neovascularization.
 BRVO with macular edema and reduced vision.

53.  Conclusion
 Scatter argon photocoagulation prevents the
development of NV and vitreous hemorrhage but
should be applied after the development of NV.
 Argon laser improved visual outcome in eyes with
BRVO and visual acuity reduced from macular edema
to 6/12 or worse.

54. STANDARD CARE VS. CORTICOSTEROID FOR
RETINAL VEIN OCCLUSION STUDY- SCORE (2004)
 Purpose
 Standard care vs intravitreal injection(s) of
Triamcinolone Acetonide for macular edema of CRVO
and BRVO
 Inclusion criteria
 Centre-involving macular edema secondary to either
CRVO or BRVO
 Retinal thickness >250 microns in the central subfield

55.  Conclusion
 Intravitreal triamcinolone is superior to observation
for treating vision loss associated with macular
edema secondary to CRVO but not in BRVO.
 1-mg dose has a safety profile superior to that of the
4-mg dose

56. RANIBIZUMAB FOR THE TREATMENT OF MACULAR
EDEMA FOLLOWING BRANCHRETINAL VEIN
OCCLUSION: EVALUATION OF EFFICACY AND
SAFETY- BRAVO (2007)
 Purpose
 Intravitreal Ranibizumab vs sham injections in
patients with macular edema due to BRVO
 Inclusion criteria
 Macular edema involving foveal center due to BRVO,
 CFT ≥ 250 µm on OCT
 BCVA of 20/40 to 20/400

57.  Conclusion
 Ranibizumab provided rapid and effective treatment
for macular edema following BRVO with low rates of
ocular and non-ocular safety events .

58. GLOBAL EVALUATION OF IMPLANTABLE
DEXAMETHASONE IN RETINAL VEIN OCCLUSION
WITH MACULAR EDEMA -GENEVA (2004)
 Purpose
 Dexamethasone intravitreal implant vs sham in vision
loss due to macular edema due to BRVO or CRVO
 Inclusion criteria
 Decreased VA due to ME associated with either CRVO
or BRVO
 BCVA of between 34 and 68 letters
 Central subfield ≥ 300 µm on OCT

59.  Conclusion
 Dexamethasone intravitreal implant can both reduce
the risk of vision loss and improve the speed and
incidence of visual improvement in eyes with ME
secondary to BRVO or CRVO

60. VISION-LIMITING COMPLICATIONS

61. NEOVASCULARIZATION AND VITREOUS HEMORRHAGE
 Only eyes with the type of branch vein occlusion that
shows large areas (greater than five disc diameters in
diameter) of retinal capillary nonperfusion are at risk for
developing neovascularization.
 About 40% of these eyes develop neovascularization,
and of this 40%, about 60% will experience periodic
vitreous hemorrhage.

62.  Retinal or disc neovascularization, or both, may develop
at any time within the first 3 years after an occlusion but
are most likely to appear within the first 6 to 12 months
after the occlusion.
 If peripheral scatter laser photocoagulation is applied in
eyes with large areas of nonperfusion, the incidence of
neovascularization can be reduced from about 40% to
20%.

63.  Iris neovascularization is a rare complication of BRVO;
diabetes (with or without retinopathy) may increase this
risk.
 Retinal neovascularization is particularly difficult to
recognize in BRVO because collaterals that develop
frequently may mimic neovascularization

64.  Collaterals occur as vein-to-vein channels around the
blockage site, across the temporal raphe, and in other
locations to bypass the blocked retinal segment.
 These collaterals frequently become quite tortuous,
mimicking the appearance of neovascularization if they
are evaluated by ophthalmoscopy alone.

65.  Diffrentiated by fluorescein angiogram because
leakage from neovascularization is more
prominent than from collateral vessels.

66.  When neovascularization is confirmed by fluorescein
angiography, peripheral scatter laser photocoagulation
can reduce from about 60% to 30% the likelihood of
vitreous hemorrhage.
 The scatter laser photocoagulation is applied with
argon blue-green laser photocoagulation applied to
achieve “medium” white burns (200 to 500 microns in
diameter) spaced one burn width apart .

67.  Covers the entire area of capillary nonperfusion, as
defined by fluorescein angiography, but extending no
closer than two disc diameters from the center of the
fovea and extending peripherally at least to the equator.

68. MACULAR EDEMA
 Most common cause of decreased vision in BRVO is
macular edema.
 Reduced blood flow to the macula results in increased
upregulation of endothelin-1, inflammatory cytokines,
and VEGF.
 Which results in increased endothelial permeability
leading to macular edema and exudates.

69.  In the acute phase of the disease, when there is
substantial intraretinal hemorrhage, it may be
impossible to evaluate potential vision
 Patient should be followed every 2 to 3 months until
there is sufficient clearing of hemorrhage to allow
evaluation by fluorescein angiography.

70.  After the acute phase of the BRVO has passed and
intraretinal hemorrhage has mostly reabsorbed (3 to 6
months) fluorescein angiography should be obtained .
 Retinal vascular characteristics that may have prognostic
significance:
 Macular edema
 Macular non-perfusion
 Large segments of capillary non-perfusion
Fluorescein angiography is the only technique that will
accurately define the capillary abnormalities in BRVO.

71.  Fluorescein angiogram, transit phase, demonstrating
perifoveal capillary dilation with adjacent capillary
nonperfusion.
 Fluorescein angiogram, late phase, demonstrating
cystoid edema with foveal involvement .
 Immediate post treatment fundus photograph showing
grid pattern of laser photocoagulation

72.  When fluorescein angiography demonstrates macular
edema with cystoid involvement of the fovea, but no
capillary nonperfusion- macular edema is the cause of
vision loss , and about 1/3rd regain vision spontaneously.
 Patients who had decreased vision for over 1 year as a
result of macular edema are less likely to regain vision
spontaneously.

73.  When macular edema is present ophthalmoscopically
within the first 6 months after a BRVO and there is little
or no leakage on fluorescein angiography, macular
ischemia may be the cause of the macular edema.
 In such circumstances, the edema almost always
spontaneously resorbs in the first year after the
occlusion, often with return of vision.

74. MANAGEMENT
 The treatment for BRVO is aimed at
treatment/prevention of the complications that cause
vision loss including macular edema, macular ischemia
and neovascularization.
 The systemic risk factors should be optimized in
consultation the primary care doctor.
 Anticoagulation have no proven benefit in the
management of BRVO associated with a
hypercoagulopathy.

75. LASER PHOTOCOAGULATION
 Prior to the advent of anti-VEGF agents, laser
photocoagulation was considered the gold standard for
the treatment of BRVO as established by the BVOS.
 Photocoagulation can be considered in patients with
perfused macular edema with VA ≤ 20/40 without
improvement in visual acuity for at least 3 months.

76.  Before application of laser photocoagulation, an FA of
the macula is obtained to demonstrate absence of a
large area of capillary nonperfusion adjacent to the
capillary free zone that could explain the vision loss.

77.  The recommended parameters for grid laser include:
 Duration of 0.1 seconds
 100 µm diameter spot size
 Power to produce a medium white burn.
 FA is repeated in 2-4 months to assess the need for
additional laser and resolution of macular edema.

79.  Laser photocoagulation is applied in a grid pattern
throughout a leaking area, but not involving the edge of
the capillary-free zone or beyond the major vascular
arcades peripherally.
 Mechanism of action :
 Destruction of nearby capillary beds
 Reducing input of arterial blood supply
 Allows remaining capillaries to drain into less
congested intact capillary bed

80.  Laser photocoagulation should never be placed over
extensive intraretinal hemorrhage in the acute phase of
branch vein occlusion
 Laser energy will be absorbed by the intraretinal
hemorrhage rather than at the level of the pigment
epithelium, probably damaging the nerve fiber layer and
possibly producing preretinal fibrosis.

81.  Laser photocoagulation is also used to prevent vitreous
hemorrhage.
 According to results of the BVOS Group, patients with
BRVO and > 5 disc diameters of retinal capillary
nonperfusion should undergo scattered laser
photocoagulation only once neovascularization has
developed.
 BVOS data showed that scatter photocoagulation after
neovascularization develops is as effective as before
neovascularization in preventing vitreous hemorrhage.

82.  The recommended parameters for scatter laser include:
 Duration of 0.2 seconds
 200-500 µm diameter spot size
 Power to produce a medium white burn.

83. ANTI-VASCULAR ENDOTHELIAL GROWTH FACTOR (VEGF)
 In patients with BRVO, retinal ischemia results in
elevated secretion of VEGF leading to increased vascular
permeability and vasodilation
 There are several anti-VEGF agents available to treat
macular edema due to BRVO :
 Ranibizumab (Lucentis)
 Bevacizumab (Avastin)
 Alfibercept (Eylea).

84.  Both ranibizumab and aflibercept are FDA approved for
the treatment of macular edema following RVO.
 Ranibizumab is a recombinant humanized monoclonal
antibody fragment (Fab) that binds all VEGF-A isoforms
at higher affinity than bevacizumab.
 Bevacizumab is a full length, humanized monoclonal
antibody that binds all VEGF-A isoforms and is used off
label in the eye.

85.  Aflibercept (VEGF-trap) is a recombinant fusion protein
that consists of human VEGF receptor 1 and 2
extracellular domains fused to Fc portion of human
IgG1.
 Aflibercept binds to all forms of VEGF-A with higher
affinity than bevacizumab and ranibizumab.

86. RANIBIZUMAB
 In the BRAVO study patients with macular edema due to
BRVO were randomized to 0.5mg ranibizumab, 0.3mg
ranibizumab and sham injections for monthly injections
for the first six months (treatment period).
 At the 6 month time point there was 16.6 and 18.3
letter gain in the 0.3mg and 0.5mg ranibizumab groups,
respectively.
 There was a 7.3 letter gain in the sham group with
54.5% of the sham group requiring rescue laser.
 Only 18.7% and 19.8% of the 0.3mg and 0.5mg
ranibizumab groups, respectively, required rescue laser.

87.  After the first six months all groups were allowed as
needed (PRN) of ranibizumab (observation period).
 The qualification for PRN ranibizumab was vision:
 ≤ 20/40 or mean central subfield thickness ≥ 250 µm
 The BRAVO study showed that ranibizumab is superior
to traditional grid laser for macular edema from BRVO.
 The study also showed that PRN treatment was able to
maintain gains in vision after 5 monthly injections.
 The study did not evaluate when to switch to PRN
schedule.

88.  The HORIZON trial was a 12 month extension of the
BRAVO and CRUISE trials and followed patients every 3
months for 12 months.
 Patients were given PRN ranibizumab 0.5mg based on
the criteria in the BRAVO study.
 HORIZON concluded that PRN use of ranibizumab after
an intensive year of treatment was able to maintain
visual acuity gains.

89. ALFIBERCEPT
 The VIBRANT study- compared intravitreal aflibercept
2.0mg to grid laser.
 Inclusion criteria - Patients with macular edema due to
BRVO that occurred within 12 months with BCVA 20/40
to 20/320.
 Patients were randomized to aflibercept drug injections
every 4 weeks for the first 20 weeks or grid laser at
baseline followed by a single rescue grid laser from
weeks 12 through 20.
 After 24 weeks, the drug injection group received
alfibercept every 8 weeks, while the grid laser group
received sham injections.

90.  Patient in the grid laser group that qualified for rescue
laser were given 3 monthly drug injections followed by
drug injections every 8 weeks.
 Rescue treatment criteria included:
 > 50µm increase in central subfield thickness
compared with lowest previous measurements
 Loss of ≥ 5 letters compared with best previous
measurement in conjunction with any increase in
central subfield thickness
 Presence of new or persistent cystic retinal changes,
subretinal fluid or persistent diffuse edema.

91.  At 24 weeks the mean change of BCVA was 17.0 in drug
injections group compared to 6.9 in grid laser group.
 At 52 weeks the mean change of BCVA was 17.1 in drug
injection group compared to 12.2 in grid laser group.
 Rescue treatment was required in 10% of drug group
and in 80% eyes in the laser/drug group.

92.  Result- Aflibercept is more effective than gird laser in
treatment of macular edema from BRVO, and the vision
gains established after monthly injections can be
maintained by extending out treatment.

93.  The VIBRANT study included patient with perfused and
nonperfused BRVO, unlike BRAVO study which only
included perfused BRVO.
 The VIBRANT study evaluated retinal perfusion at baseline,
24 weeks and 52 weeks.
 They showed an improvement in retinal perfusion and
reversal of nonperfusion after treatment with intravitreal
aflibercept.
 This effect was also noted in the laser/drug group at 52
weeks after they received drug from weeks 24 to 52, but
not during the laser only duration of the study.

94. BEVACIZUMAB
 One of the studies by Russo et al assigned 30 eyes were
to either grid laser or intravitreal bevacizumab.
 Bevacizumab was given at 1, 3, 6 and 12 months.
 Grid laser was applied at baseline and reassessed at 3
months for possible retreatment.
 At 12 months the mean gain in BCVA was 0.31 logMAR
(15 letters) in the bevacizumab group compared with
0.20 logMAR (10 letters) in the grid laser group

95.  The mean gain in this study is similar to mean gains in
the BRAVO/HORIZON and VIBRANT studies.
 The mean BCVA gain at 6 months was 5.1 lines and 4.5
lines in the 1.25mg group and 2.5mg group,
respectively.
 There was no statistically significant difference between
the two doses on BCVA and central subfield thickness.

96.  The BERVOLT study, a retrospective study, looked at the
efficacy and safety of bevacizumab in macular edema
due to BRVO and CRVO.
 They concluded that the overall mean change in BCVA in
the BRVO group treated with bevacizumab 1.25mg was
0.25 logMAR (13 letters) with no significant adverse
events.

97. STEROID TREATMENT
 The SCORE-BRVO study is the largest trial that evaluated
the safety and efficacy of intravitreal triamcinolone
compared to grid laser in the treatment of macular
edema
 At 12 months, the study concluded that there is no
difference in visual acuity gained between the two
triamcinolone groups and grid laser group.
 Significant cataract formation and elevation of
intraocular pressure in the intravitreal triamcinolone
groups.

98.  Three year results showed a significant increase in vision
in the laser group compared to the intravitreal
triamcinolone groups.
 From the results of this study, intravitreal triamcinolone
is not recommended as a first-line therapy for macular
edema due to BRVO.
 It is utilized as an adjunct to laser or anti-VEGF agents
or as second line agent

99.  Ozurdex, a dexamethasone implant has been evaluated
in the GENEVA study for macular edema in CRVO and
BRVO.
 The implant is injected using a 22-guage custom injector
and gradually releases dexamethasone over several
months (1-3 months), with peak response at 60 days.

101.  The study found that the Ozurdex implant group had
higher percentage of patients with gain ≥ 15 letters at
the 90 day period compared to sham group and also a
lower percentage of patients with losses of ≥ 15 letters.
 Limited by the absence of comparison of standard
treatment that is rescue treatment for the sham group.

102. SURGICALMANAGEMENT
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

103.  Vitrectomy with separation of the posterior hyaloid
results in reduced macular edema.
 Reasons:
 Removal of vitreous traction
 Increased oxygenation of the macula
 Tamponade of the macula by intraocular gas.

104. ISOVOLEMIC HEMODILUTION
 There have been studies evaluating various agents for
hemodilution and there has been a consistent VA
improvement of 2 lines.
 Many reported systemic complications due to
hemodilution including headaches, exertional dyspnea,
fatigue, deep vein thrombosis and hypotension.
 Due to the systemic invasiveness of the treatment and
the many systemic complications from isovolemic
hemodilution it is not generally accepted to treat BRVO.

107. MEDICAL FOLLOW UP
 The typical follow up should be tailored on an individual
basis to monitor for the development of complications.
 After initial presentation, typical follow up - every
month or two months to monitor the development of
macular edema and/or neovascularization.
 If macular edema develops, initiate treatment with anti-
VEGF therapy with/without laser and monitor for
resolution.

108.  Once edema has resolved or stabilized, follow up
interval can be extended to three to six months or
longer for stable chronic cases.
 Patients with nonperfused BRVO (> 5 disc diameters),
that has not been treated with laser should be
monitored every three months due to increased risk of
neovascularization.

109. DIFFRENTIAL DIAGNOSIS
 Hypertensive retinopathy
 Diabetic retinopathy
 Radiation retinopathy
 Macular telangiectasia
 Retinal angiomatous proliferation
 Age-related macular degeneration or variants such as
retinal angiomatous proliferation
 Ocular contusion or retinal trauma

110. THANK YOU