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BRANCH RETINAL VEIN OCCLUSION


Epidemiology, Pathogenesis, Risk Factors,
Clinical Features, Diagnosis, and
Complications. An Update of the Literature
ARTICLE in RETINA (PHILADELPHIA, PA.) MAY 2013
Impact Factor: 3.24 DOI: 10.1097/IAE.0b013e3182870c15 Source: PubMed

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Irini Chatziralli
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Review
BRANCH RETINAL VEIN OCCLUSION
Epidemiology, Pathogenesis, Risk Factors, Clinical
Features, Diagnosis, and Complications. An
Update of the Literature
ADIL JAULIM, MS,* BADIA AHMED, MS,* TINA KHANAM, MBBS, MSC, IRINI P. CHATZIRALLI, MD
Background/Purpose: Retinal vein occlusion is the second most common retinal
vascular disorder after diabetic retinopathy and is considered to be an important cause of
visual loss. In this review, the purpose is to make an update of the literature about the
classication, epidemiology, pathogenesis, risk factors, clinical features, and complications
of branch retinal vein occlusion (BRVO).
Methods: Eligible articles were identied using a comprehensive literature search of
MEDLINE, using the terms branch retinal vein occlusion, pathogenesis, epidemiology,
risk factors, clinical features, diagnosis, and complications. Additional articles were
also selected from reference lists of articles identied by the electronic database search.
Results: Classication, epidemiology, pathogenesis, risk factors, clinical features, and
complications are analyzed.
Conclusions: Branch retinal vein occlusion has an incidence of 0.5% to 1.2%. Several
risk factors, such as hypertension, hyperlipidemia, diabetes mellitus, thrombophilia and
hypercoagulation, systemic and inammatory diseases, medications, and ocular conditions, have found to be associated with BRVO. The symptoms depended on the site and
severity of the occlusion. The average reduction in visual acuity for ischemic BRVO is 20/50
and for nonischemic BRVO is 20/60. Acute BRVO can be detected by fundoscopy, where
ame hemorrhages, dot and blot hemorrhages, cotton wool spots, hard exudates, retinal
edema, and dilated tortuous veins can be observed. Chronic BRVO would be more subtle
and characterized by the appearance of venous collateral formation and vascular
sheathing, in addition to complications previously mentioned. Areas of ischemia can be
evaluated using uorescein angiography. The extent of macular edema and the presence of
retinal detachment can be detected by fundoscopic examination or uorescein angiography, although optical coherence tomography is considered to be the best method. As far as
complications, the most common is macular edema, followed by retinal neovascularization,
vitreous hemorrhage, or retinal detachment.
RETINA 33:901910, 2013

etinal vein occlusion (RVO) is the second most


common retinal vascular disorder after diabetic ret-

inopathy and is considered to be an important cause of


visual loss.1,2 Retinal vein occlusions are divided into
central (CRVO), hemi-, and branch retinal vein occlusions (BRVO).36 Central RVO is an obstruction occurring within the central retinal vein, which is virtually the
sole venous drainage source of the retina, whereas
BRVO can be thought as venous occlusion that occurs
in any of the branches of the central retinal vein.3,4 In
addition, hemi-RVO, which involves the anterior part of

From the *Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, United
Kingdom; Department of Ophthalmology, Barts and the London
NHS Trust, London, United Kingdom.
The authors have no conict of interest to disclose.
Reprint requests: Irini P. Chatziralli, MD, MSc, 28, Papanastasiou
street, Agios Dimitrios, 17342, Athens, Greece; e-mail: eirchat@
gmail.com

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RETINA, THE JOURNAL OF RETINAL AND VITREOUS DISEASES  2013  VOLUME 33  NUMBER 5

a trunk of the central retinal vein, can be considered as


a subtype either of CRVO or BRVO, although it is better
to consider hemi-RVO as a separate entity.7 Interestingly,
some authors differentiate hemicentral and hemispheric
RVO.8 This topic is outside the scope of our review, but
sometimes it is important to make this differentiation, as
the two clinical entities are quite different concerning
pathogenesis, clinical evolution, and visual outcome.8
In this review, our purpose is to make an update of
the literature about the classication, epidemiology,
pathogenesis, risk factors, clinical features, and complications of BRVO, although it must be noted that many
studies group RVOs together. Eligible articles were
identied using a comprehensive literature search of
MEDLINE (PubMed), using the terms branch retinal
vein occlusion, risk factors, pathogenesis, epidemiology, clinical features, diagnosis, and complications. Additional articles were also selected from
reference lists of articles identied by the electronic
database search. There were no language restrictions.

Classication
The rst case of BRVO was described by Leber in
1877.9 Brain RVOs are classied according to their
anatomical location either as major, when one of the
major branch veins draining one of the retinal quadrants is involved, or as macular, when one of the smaller venules within the macula is occluded, although
often groups of quadrants can be considered together.10
Particular attention can be given to the superotemporal
quadrant, because of increased incidence of BRVOs in
that quadrant, thought to be because of a tendency of
increased arteriovenous (AV) crossing at the site.11
Interestingly, a recent Nepal hospital-based study
showed that of 155 BRVOs, 99 were superotemporal,
in line with Lang and Freissler,11 who found that, in
66% of BRVO eyes, there was a major occlusion in the
superotemporal quadrant.12 Nasal BRVOs appear on
the whole to give rise to a lesser degree of decreased
visual acuity and a lower complication rate.11 Therefore, absence of subjective symptoms may lead to them
being underdetected, and they are commonly diagnosed, when a complication occurs.10 Moreover, studies can also occasionally divide BRVOs into ischemic
and nonischemic types.11 However, this subclassication is usually reserved for CRVOs and hemi-RVOs.

Epidemiology
Branch retinal vein occlusion is considered to be the
most common among RVOs with an incidence of 0.5

to 1.2 per 100.2,1017 A recent meta-analysis by Rogers


et al13 analyzed data from 11 studies with 49,869 participants pooled from various ethnicities to yield a total
RVO prevalence of 0.52 per 100, supporting also the
fact that BRVOs are the most common RVOs with
a prevalence of 0.44 per 100.
The Beaver Dam Eye Study examined 4,926 participants with a 5-year follow up in the United States.1
The overall prevalence of BRVOs was 0.6% (95% condence interval [CI]: 0.40.9) with a 5-year incidence
of 0.6%. Central RVOs were less frequent at 0.1% to
0.2%, respectively,1 whereas another study in the
United States found a prevalence of 1.1% RVOs, with
0.9% BRVOs among 6,147 participants.14 The Australian Blue Mountains Eye Study found an overall prevalence of RVOs at 1.6% (95% CI: 1.31.9) in 3,654
participants, with 69.5% of these cases being BRVOs.15
In Israel, a study found an incidence over a 4-year of
period of 0.21 RVOs per 100 in those aged older than
40 years, with a BRVO:CRVO ratio of 3.2:1 in
participants without glaucoma.16 Finally, the Singapore Malay Eye Study found 0.7% RVOs in 3,280
participants, with 0.55% BRVOs at a BRVO:CRVO
ratio of 3.6:1.17
Furthermore, there was thought to be little variation
between ethnicities and gender for incidence of
BRVO.14,15,17,18 The recent meta-analysis by Rogers
et al13 conrmed no gender differences but showed
that there is ethnic variation with higher incidences
found in Asians (5.7 per 1000; 95% CI: 4.56.8) and
Hispanics (6.9 per 1000; 95% CI: 5.78.3). Ethnic
variation may be attributed to increased risk factors
for RVO in these populations.
As far as age is concerned, advancing age is a very
important risk factor for RVO. The meta-analysis by
Rogers et al13 showed a 1.57 per 1,000 prevalence of
BRVOs in 40 to 49 year olds, 4.58 per 1,000 in 50 to
59 year olds, 11.11 per 1,000 in 60 to 69 year olds,
12.76 per 1,000 in 70 to 79 year olds, and 10.32 per
1,000 in those older than 80 years.

Pathogenesis
In the majority of cases, arterial disease is a predominant pathogenetic mechanism for RVO. In
CRVOs, this is thought to be because of the presence
of central retinal veins and arteries within the same
adventitial sheath within the lamina cribrosa, thus
arterial stiffness affecting neighboring veins. In
BRVOs, it is thought that a combination of compression of veins at AV crossings, degenerative changes
within venous walls, and hypercoagulability may be
causative. Brain RVOs occur almost invariably at AV

RISK FACTORS AND CLINICAL FEATURES IN BRVO  JAULIM ET AL

crossings, where again, as in CRVOs, an adventitial


sheath is shared.19,20 Thus, arterial pathology can play
a role with the relatively thick-walled artery compressing the thin-walled vein. Jefferies et al20 found that at
AV crossings, there was focal thickening of the
venous basement membrane and hyperplasia of extracellular matrix and adventitia at AV crossings, possibly because of increased hemodynamic stress at the
AV crossing where the vein changes direction, which
results in venous endothelial injury. The fact that
BRVO occurs when retinal arteries cross anterior to
the vein supports the mechanical compression hypothesis.2124 However, it has recently been postulated that
an additional pathogenetic mechanism for venous
occlusion may occur. Atherosclerotic arteries may be
producing increased endothelin-1, which may diffuse
across to the neighboring vein, stimulating venous
vasoconstriction.25 Brain RVOs can induce hypoxia
and capillary nonperfusion in the area affected, with
arteriolar constriction. Using a pig model, it has been
found that this is caused by a decrease in nitric
oxide.26

Risk Factors
Various cardiovascular, thrombophilic, systemic,
and ocular conditions have been considered to predispose to the development of RVOs and are depicted
on Table 1. It is difcult to tease out which risk factors, if any, are specic to BRVO, as RVOs are often
grouped together in the literature.
There are interesting studies attributing a group of
classic risk factors as more strongly correlated with

903

the development of BRVO than CRVO, especially in


patients younger than 50 years.2432 Classic risk factors include hypertension, hyperlipidemia, and diabetes mellitus.12,14,15,18,2832 However, a meta-analysis
showed that, in BRVO, the odds ratio for hypertension
is 3.0 (95% CI: 2.04.4), for hyperlipidemia 2.3 (95%
CI: 1.53.5), and for diabetes mellitus 1.1 (95% CI:
0.81.5).91 Of note, diabetes mellitus was shown to be
not signicantly associated with BRVO but with
CRVO.91 In addition, Kaderli et al92 found that arterial
stiffness as measured by pulse wave velocity and aortic distensibility was abnormal in BRVO patients, in
comparison with both healthy and hypertensive controls. In younger patients, a retrospective casecontrol
study of 60 patients aged younger than 50 years indicated that hypertension, hyperlipidemia, and body
mass index were important risk factors in this patient
group.34 Overall, cardiovascular risk factors appear to
be important in developing BRVO.
As far as thrombophilic risk factors are concerned, it
has been difcult to determine to what extent thrombophilias play a role in BRVO. A meta-analysis of
RVOs examined the prevalence of hyperhomocysteinemia, methylenetetrahydrofolate reductase gene
mutation, factor V Leiden mutation, protein C and S
deciency, antithrombin deciency, prothrombin gene
mutation, anticardiolipin antibodies, and lupus anticoagulant.59 Only hyperhomocysteinemia and anticardiolipin antibodies had major effects at odds ratios
of 8.9 (95% CI: 5.713.7) and 3.9 (95% CI: 2.3
6.7), respectively.50 Thrombin activatable brinolysis
inhibitor was evaluated in another study and appeared
to have no effect on BRVO development.93 Moreover,
thrombophilic gene polymorphisms examined in 294

Table 1. Risk Factors for BRVO


Cardiovascular Disease and Risk Factors
Hypertension,1,12,14,17,2730 widened pulse pressure,1 diabetes mellitus,1,12,29,30 renal function,14 hypercholesterolemia,17
hypertriglyceridemia,14,31 elevated LDL,17 increased lipoprotein A,30 hyperhomocysteinemia,32 hyperuricemia,33
angina,17 previous myocardial infarction17
Coagulation Disorders
Increased hematocrit,32 factor V-Leiden mutation,3439 protein C/protein S/antithrombin III deciency,40 prothrombin
(factor II) gene mutation,39,40 antiphospholipid antibodies,4143 genetic predispositions to BRVO and thrombophilia,4446
HPA-2 platelet membrane glycoprotein polymorphism,47 sickling hemoglobinopathies,48 acute intermittent porphyria,49
polycytemia rubra vera,50 multiple myeloma,50 leukemia and lymphoma50
Systemic Disorders
Mediteranean fever,51,52 HIV/CMV retinitis,5355 tuberculosis,56 Churg-Strauss syndrome,57,58 systemic lupus
erythematosus,29,59,60 sarcoid,6163 syphilis,64,65 Behet disease,66 high sensitive C-reactive protein,67 Takayasu
arteritis68
Ocular Disorders
Glaucoma,12,14,27,6971 optic nerve drusen,72 previous RVO,3,73 retrobulbar external compression from Grave disease or
orbital tumor,50 arteriovenous nicking,1,14 foveal arteriolar narrowing,1,14 increased intraocular pressure,1,17,74
hypermetropia,7577 short axial length30,76,7884
Medications and Other Causes
Oral contraceptive pill,85 anabolic steroid abuse,86 robecoxib/cox-2 inhibitor,87 interferon therapy in hepatitis patients,88,89
dehydration,90 decreased educational level,14 smoking,1,27,32 increased body mass index34

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patients seemed to have no effect as well.94 In addition, a recent casecontrol study of 117 patients found
no effect of hyperhomocysteinemia and anticardiolipin
antibodies.29
Several studies postulate that thrombophilic risk
factors may be more prevalent in younger patients,34,38,9597 and it may be more prudent to screened
patient groups for thrombophilias who have no systemic risk factors or who have bilateral RVOs.50,97
By and large, it appears that arteriopathic risk factors
are more important in RVOs and special hematological
abnormalities should not be routinely investigated.33
Branch retinal vein occlusion can also occur as
a complication of a local or systemic vasculitis. It has
been reported as a complication of retinal vasculitis in
cases of both familial and spotted Mediterranean
fever.51,52 Brain RVOs have also been described in
patients infected with human immunodeciency virus,53
as a noninfective consequence of retinopathy associated
with severity of the immunodeciency syndrome54 or
as a consequence of opportunistic cytomegalovirus
retinitis.55 Moreover, BRVO is a presenting feature of
Takayasu arteritis68 and Churg-Strauss syndrome.57,58
A meta-analysis found that anticardiolipin antibodies
are associated with RVOs: these can be found in antiphospholipid syndrome, systemic lupus erythematosus,
and Behet disease.59 Brain RVOs have been reported
in roughly 6% of patients with ocular Behet disease in
a Turkish study.66
Furthermore, BRVO can be a result of direct
inltration of the eye leading to venous obstruction.
Sarcoidosis,6163 ocular tuberculosis,56 or neoplastic
diseases, such as in a case of non-Hodgkin lymphoma,98 could also be considered as systemic risk
factors for the development of RVO. Conversely,
inammation seems to play an important role in
BRVO. A small pilot study evaluating levels of highly
sensitive C-reactive protein in 11 patients showed
some indication that RVOs may be associated with
an elevated highly sensitive C-reactive protein, but
was limited by its size.67 This may be an underlying
factor in case reports of RVOs, such as in one report of
a CRVO in a young patient with syphilis.64
Ocular conditions related to BRVO should be taken
into account when identifying a patient with BRVO. In
a Japanese study, patients with glaucoma had an
incidence of BRVO of 8.1% as opposed to an
incidence of 0.59% in those attending general outpatient clinics.65 They were also more likely to
develop CRVOs proportionally; the ratio of BRVO
to CRVO is 1:1, whereas in the general outpatient
population, it was 4.3:1.69 An Israeli study also found
similar 1:1 results, with a ratio of 3.2:1 in the general
population.16 Patients with glaucoma had equal chance

of developing BRVO or CRVO. Incidence of retinal


vein occlusions in the Israeli study over 4 years was
1.85 per 1,000 in the general population and 17.3 in
glaucoma patients.16 A U.S. study postulates that this
apparent increase in incidence in glaucoma populations may disappear once adjustments are made for
age.14 Glaucoma and raised intraocular pressure may
predispose to RVO because of the increased ocular
pressure leading to venous stasis in blood ow50,99
but are not considered as important risk factors for
BRVO.11
In addition, it has been found that developing RVO
in one eye predisposes to development in the other.
The Branch Vein Occlusion Study found that a BRVO
in one eye predisposes to development of any RVO in
the other eye by 10%,73 in line with Hayreh et al, who
found that, for RVOs, there was a 7% chance of developing an RVO in the other eye within 3 years.3
Moreover, medications can play a signicant role in
BRVO. The presumptive mechanism for the oral
contraceptive pill85 and other medication regimens8789
resulting in reports of increased risk for BRVO lies
primarily in hypercoagulability. However, the mechanism in anabolic steroid abuse in particular appears to
be more complex encompassing cardiovascular risk factors.86 Retinal artery hypertension, vessel wall dysfunction, and hyperviscosity may all play a role in BRVO
development with anabolic steroid users.86
It is also worthy to mention that Alghadyan
postulated a link between RVO and dehydration based
on the observation of increased presentations of RVOs
to clinic when patients were in a fasting state during
the Muslim holy month of Ramadan. Dehydration may
function as a trigger in those with predisposition to
RVO development.90

Clinical FeaturesDiagnosis
Branch retinal vein occlusion symptoms depend on
the site and severity of the occlusion. BRVO may be
asymptomatic. The average reduction in visual acuity
for ischemic BRVO is 20/50 and for nonischemic
BRVO is 20/60.12 Macular BRVO presents with a central visual eld defect, whereas major BRVO presents
with a peripheral visual eld defect corresponding to the
retinal quadrant that the affected vein drains.100 Longstanding occlusion results in absolute scotomas, wheresd
short-term occlusion causes relative scotomas in areas of
capillary nonperfusion.101 Visual eld defects, such as
central scotomas, paracentral scotomas, nerve ber bundle scotomas, and segmental peripheral constriction patterns can be also observed.102 Some authors have
suggested that it is imperative to test visual elds using

RISK FACTORS AND CLINICAL FEATURES IN BRVO  JAULIM ET AL

manual kinetic or automated perimetry, along with


visual acuity testing, because visual elds defects are
a component of vision loss in patients with RVOs.10
Noticeably, symptoms tend to occur more frequently
in the morning.103 Overall, symptoms result from any
combination of retinal ischemia, retinal exudates, macular edema, and/or intraretinal haemorrhages.35,104
Acute BRVO can be detected by fundoscopy, where
ame hemorrhages, dot and blot hemorrhages, cotton
wool spots, hard exudates, retinal edema, and dilated
tortuous veins can be observed.2 Interestingly enough,
the Bonnet signhemorrhage at an AV crossing
may be present.35,105 Chronic BRVO would be more
subtle and characterized by the appearance of venous
collateral formation20 and vascular sheathing,2 in addition to complications previously mentioned.106
Areas of ischemia can be evaluated using uorescein angiography.107 The extent of macular edema and
the presence of retinal detachment can be detected by
fundoscopic examination or uorescein angiography,
although they appear to be underdetected using these
methods; optical coherence tomography is considered
to be the best method.108,109 Indeed, optical coherence
tomography is widely used to measure quantitatively
the retinal thickness so as to monitor the effectiveness
of various treatment modalities and to conrm the
resolution of macular edema, giving an explanation
in pathogenesis of BRVO as well.110,111 Specically,
the third high reectance band in the parafoveal area,
showing reection derived from the junction between
the inner and outer segments of the photoreceptors,
visualized by optical coherence tomography can be
signicant for visual prognosis.110 Ota et al110 have
found that, although macular edema had resolved
and there had been a decrease in foveal thickness,
visual acuity remained poor in eyes with an incomplete or no third high reectance band. A possible
cause for lack of the third high reectance band pertains to the fact that severe ischemia or severe swelling
during acute or chronic BRVO could lead to photoreceptor cell death or disarrangement of the photoreceptor cells.110
Another useful measurement can be made, using the
Micro Perimeter-1 system, which combines digital
imagining and automated microperimetry, so as to
measure perimetric retinal sensitivity; there has been
evidence that retinal sensitivity correlates with the
extent of macular edema,112,113 although the strength
of the evidence has been questioned.114 Doppler imaging and spectral analysis reveals a lower resistance
index in BRVOs as opposed to CRVOs, with no difference in blood ow velocities between affected and
unaffected eyes in BRVOs, whereas CRVOs show
decreased venous and mean diastolic arterial blood

905

ow velocities in the affected eye.115,116 Furthermore,


patients with BRVO have been shown to have reduced
electroretinogram transient and steady-state patterns
and reduced visual evoked potential amplitudes and
delayed peak times.117

Complications of BRVO
Complications of BRVO include macular edema,118
ischemic maculopathy,11 retinal neovascularization,119
macroaneurysmal formation,120,121 retinal telangiectasia,122
retinal detachment,123 and vitreous hemorrhage.124,125
Cystoid macular edema is a common sight-threatening complication of BRVO. In a study of 109
BRVO cases, 90% of those with major BRVO and
97% of those with macular BRVO had cystoid
macular edema.126 Although BRVO and macular
edema can resolve spontaneously within a year in perhaps 50% of cases,127 prolonged hypoxia associated
with the edema can result in irreversible reduction of
visual acuity. The extent of macular edema may be
quickly assessed with a retinal thickness analyzer.128
Macular capillary blood ow is found to be reduced
in BRVO.129 Atherosclerosis induces hypoxia and hypoxic tissues activate the hypoxia-inducible factor-1a
cascade.25 This factor upregulates endothilin-1 and vascular endothelial growth factor (VEGF), which increase
endothelial permeability and contribute to the breakdown of the bloodretinal barrier, leading to macular
edema and exudate formation.25 Increased levels of
VEGF and interleukin-6 have been found to be positively correlated with the severity of macular edema in
BRVO and the size of the area of nonperfusion.130,131
The VEGF mRNA was found to be upregulated in cells
of the neuroretina up to 3 days post-BRVO in a rat
model and in day 7 in a mouse model.132 This was
followed by delayed upregulation of pigment-epithelium
derived factor.132 Various proinammatory factors,
such as interleukin-8 and monocyte chemoattractant
protein-1, have also found to be elevated within the
vitreous uid, which may result in vessel wall breakdown and increased endothelial permeability of the
retinalblood barrier and thus edema.133,134
Reduced uid clearance may also contribute to
macular edema. Clearance is carried out by Mller
glial cells and retinal pigment epithelium cells.135 In
a rat model of BRVO, Mller cells became dysfunctional. They displayed a gliosis reaction resulting in
inactivation of potassium channels, leading to interstitial potassium ion accumulation and uncoupling of
aquaporin-4 water transport from potassium currents,
thus reduced uid uptake via aquaporin-4 channels in
Mller cells.132 Another pathogenetic mechanism for

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RETINA, THE JOURNAL OF RETINAL AND VITREOUS DISEASES  2013  VOLUME 33  NUMBER 5

macular edema seems to occur because of Starling


law, which postulates that uid will leak out from
the vessels because of increased net ltration pressure
when once hydrostatic pressure is increased in venules
because of occlusions.136
Finkelstein137 divided macular edema into perfused
and incompletely perfused, suggesting better visual
acuity prognosis in nonperfused (ischemic) macular
edema. In addition, Noma et al138 found that vitreous
levels of VEGF and soluble VEGF-2, which are associated with vascular permeability, were elevated in
macular edema and correlated that with its severity.
A common cause for reduced visual acuity, secondary to chronic macular edema, is vitreous hemorrhage
caused by new vessel formation.127 Increased VEGF
levels will stimulate neovascularization.139 A South
Korean study found that 3.9% of 308 patients developed neovascularization, which occurred more frequently in BRVO patients with a lling defect within
a major branch artery; 21.4% of this group displayed
neovascularization.140 Disk hemorrhages have been
noted in BRVO, which may be more common in patients suffering from normal tension glaucoma.141 It is
important to note that, in BRVO, neovascular glaucoma occurs infrequently.127
Furthermore, retinal neovascularization may lead
to vitreous traction and retinal tears.142 Evidence of
extrafoveal vitreous traction and vitreous traction at
the occlusion site can be also found in cases of
BRVO.143,144 In a study of 109 patients, serous retinal
detachment was more common in major BRVO than
macular BRVO with 44 of 70 cases (63%) in major
BRVO compared with 8 of 39 cases (21%) in macular
BRVO.126 Another retrospective study of 111 patients
showed 20% serous retinal detachment incidence.145
Increased VEGF levels have been found to be associated with the likelihood of serous retinal detachment.139 Rhegmatogenous retinal detachment occurs
less commonly than serous retinal detachment, with
one retrospective study reporting an incidence of
1.3% rhegmatogenous retinal detachment of a total
incidence 3% of retinal breaks in 230 eyes of 214
BRVO patients.146
Conclusions
In conclusion, BRVO is considered to be the most
common among RVOs with an incidence of 0.5% to
1.2%. In the majority of cases, it is thought that
a combination of compression of veins at AV crossings, degenerative changes within venous walls, and
hypercoagulability may be the pathogenetic mechanism. Several risk factors, such as hypertension,
hyperlipidemia, diabetes mellitus, thrombophilia and

hypercoagulation, systemic and inammatory diseases, medications, and ocular conditions, have found
to be associated with the development of BRVO. The
symptoms are variable and depend on the site and
severity of the occlusion. The average reduction in
visual acuity for ischemic BRVO is 20/50 and for
nonischemic BRVO is 20/60. Acute BRVO can be
detected by fundoscopy, where ame hemorrhages,
dot and blot hemorrhages, cotton wool spots, hard
exudates, retinal edema, and dilated tortuous veins can
be observed. Chronic BRVO would be more subtle
and characterized by the appearance of venous collateral formation and vascular sheathing, in addition to
complications previously mentioned. Areas of ischemia can be evaluated using uorescein angiography.
The extent of macular edema and the presence of
retinal detachment can be detected by fundoscopic
examination or uorescein angiography, although
optical coherence tomography is considered to be the
best method. As far as complications, macular edema
is the most common, followed by retinal neovascularization, vitreous hemorrhage, and retinal detachment.
Key words: BRVO, clinical features, complications, diagnosis, epidemiology, pathogenesis, retinal
vein occlusion, risk factors.
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