Branch Retinal Vein Occlusion
Dr. Atul Mishra MS. Fellow Retina Foundation Ahmedabad.
(Rajendra Eye Hospital. Jabalpur. M.P.)
J.D.O.S Clinical meeting for the month of June 2005, held at Hotel
Satya Ashoka, dinner meeting sponsored by ENTOD pharma.
Retinal Blood Supply

When we talk about the Branch Vein occlusion of retina , we might
as well devote a couple minutes on the blood supply by the arterial
system and the drainage by the venous system
The central retinal artery enters the globe from the center of the
optic nerve, immediately adjacent and parallel to the exiting central
retinal vein.
The blood supply to the inner layers of the retina is exclusively
from the central retinal artery except in 15% to 30% where cilioretinal
artery is present. The outer retina is supplied by the choroidal circulation.
After the first or second bifurcation, the so called retinal arteries
and veins are actually arterioles and venules due to loss of elastic
lamina and a continuous smooth muscle layer,
Occlusion of the venous drainage system.
Occlusion of the Central venous drainage system has a peak incidence
in individuals of 60 years plus, and predominantly men.
Close proximity of the central retinal artery and vein in the region
of the lamina and their common adventitial sheath are critical anatomic
factors.
The venous occlusion may effect by a common pathology-- The central
retinal vein, the dual trunk of central retinal vein (seen in about
20% individuals) and a branch vein. Names are given accordingly. CRVO
,Hemispheric Retinal vein occlusion,(HRVO) and BRVO
BRVO
Branch Retinal vein occlusion


A relatively common cause of ret. vascular disease. Incidence - male
and females -equal. Age incidence - 60 plus. Site of occlusion is
rarely other than at A-V crossing. Frequently a unilateral condition.
Cause
Compression of the vein by the sclerotic artery, leading to turbulent
blood flow, endothelial damage, and thrombus formation is the postulated
etiology
Risk Factors
History of systemic hypertension, cardiovascular disease, glaucoma,
increased body mass index at 20 yrs. old, higher serum levels of alpha-2.
and shorter axial lengths of the eye.
Clinical Features
1. Branch retinal vein occlusion has many similarities to diabetic
retinopathy, including edema, capillary nonperfusion, neovascularization,
and vitreous hemorrhage.
2.Diabetic retinopathy is a continued progressive abnormality of
the microcirculation that may involve the entire fundus, whereas in
branch vein occlusion the abnormalities are caused by a single acute
event.
3.Almost always of sudden on set of blurred vision or field defect,
segmentally distributed intraretinal hemorrhage. ,Intraretinal hemorrhage
is less marked in nonischemic occlusion and much more marked if occlusion
is ischemic
4.The location of obstruction determines the distribution of the
intraretinal hemorrhage; obstruction at the optic nerve head, will
involve two quadrants of the fundus whereas occlusion at peripheral
to the disc, one quadrant or less may be involved.
5.If the venous blockage is peripheral to tributary veins draining
the macula, there may be no macular involvement and no decrease in
visual acuity. An incomplete block at the A/V crossing may progress
to more complete occlusion and hemorrhage becomes more extensive in
succeeding weeks to months.
6.After an year or so the, fundus picture may become more benign
and the intra retinal hemorrhages may be absorbed but the venous abnormalities
that occurred may persist including capillary non perfusion, dilation
of capillaries and collateral vessel formation.
Vision Limiting Complications
1. Macular edema.
2. Macular non perfusion.
3. Vitreous hemorrhage from neovascularization.
In the acute phase of the disease with a 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.
Although it may be difficult to provide a prognosis in the acute
phase, it is helpful to recognize that about one third to one half
of patients with BRVO have a return of vision to 20/40 or better without
therapy
Fluorescein Angiography and its prognostic value
After the acute phase of the BRVO has passed and intra retinal hemorrhage
has mostly absorbed, which usually takes 3 to 6 months, Fluorescein
angiography should be obtained
Fluorescein angiography is the only technique that will accurately
define the capillary abnormalities in BRVO; it is therefore particularly
important that high-quality angiography be obtained.

When Fluorescein angiography demonstrates macular edema with cystoid
involvement of the fovea, but no capillary nonperfusion, it is presumed
that the macular edema is the cause of vision loss and about one third
of patients will spontaneously regain some vision.
Foveal leak
However, patients who have had decreased vision for over 1 year as
a result of macular edema are much less likely to regain vision spontaneously.

When macular edema is present ophthalmoscopically in the first 6
months after a BRVO and there is little or no leakage on F.A, macular
ischemia may be the cause of the macular edema. In these cases, edema
absorbs almost always spontaneously in the first year after the occlusion
and often with return of vision.
Complications of BRVO
Retinal neovascularization may develop when the capillary non-perfusion
area is more than five disc diameters as visualized by Fluorescein
angiography.
Of large branch vein occlusions (involving a quadrant or more), about
50% are associated with a large area of capillary non-perfusion; of
this 50% about 40% will develop neovascularization.
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.
Those who develop neovascularization, about 60% of them experience
episodes of vitreous hemorrhage .If neo-vascularization left untreated
it can lead to prolonged visual disability in the affected eye
Iris neovascularization is a rare complication of BRVO; diabetes
may increase this risk. Retinal neovascularization is particularly
difficult to recognize in BRVO because the collaterals that develop
frequently may mimic neovascularization.
In BRVO Neovascularization on the retina frequently mimics the collaterals
on the retina.
F.F.A differentiates between the collaterals and neovascularization
Ret. Neo Vascularization

TREATMENT of BRVO
(a). Medical
(b) LASER
(c). Surgical
Medical: -Control of provocative factors like hypertension,
Diabetes, Cardiovascular diseases and blood cholesterol have been
recommended. Anticoagulant therapy has not shown to be beneficial
in either the prevention or the management of BRVO
Laser therapy in BRVO -
Familiarity with the laser treatment technique is required.
Important variables, such as residual intraretinal hemorrhage, thickness
and extent of retinal edema, location of neovascularization and presence
of retinal traction they all influence the exact mode of therapy.
High quality FFA is essential before any planning for Laser therapy.
Laser therapy is indicated only where the following criteria are met
Eligibility Criteria for Laser therapy
1.Fluorescein proven per fused macular edema involving the foveal
center,
2.Absorption of intraretinal hemorrhage from the foveal center,
3.Branch retinal vein occlusion of 3 to 18 months' duration.
4. No diabetic retinopathy,
5.Vision reduced to 20/40 or worse after best refraction.
Treatment of Macular Edema
Grid laser applied through out the leaking area. Extending from major
vascular arcade to the Edge of FAZ
In grid laser, energy absorption occurs at R.P.E level
In grid P.C laser is not applied directly and immediately close to
leaking and dilated capillary vasculature.
Grid Laser PC FA Transient Face

Laser Parameter for Grid.
1.Duration 0.1 sec.
2.Spot Size 100 micron
3.Power Medium white burn
Mechanism of Grid Laser in macular edema
How laser P.C. reduces edema is not clear. Probable mechanisms are:
-
1. Laser tickles and activates R P E pump to reduce edema.
2. Laser produces thinning of retina and Choroidal vasculature helps
in reducing edema by auto regulatoryconstriction of retinal vasculature
in the leaking area.
Treatment of Neovasularization in B.R.V.O study
Prophylactic scatter laser P.C. can lessen subsequent neovascularization
and, if neovascularization already exists, then peripheral scatter
laser P.C. can reduce subsequent vitreous hemorrhage.
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%.
In prophylactic treatment view many eyes (60%) that would never develop
neovascularization would receive peripheral scatter laser. For this
reason, it is recommended that laser P.C. be applied only after neovascularization
is clearly documented by F.F.A.
In confirmed neovascularization by FFA, peripheral scatter laser
P.C. can reduce the likelihood of vitreous hemorrhage from 60% to
30%.
Scatter Photocoagulation

Laser setting for Scatter photo coagulation
1.Spot size 200-500
2.Duration 0.1 second
3.Intensity Medium white color
4.Placement - one burn apart at the entire Capillary non-perfusion
area
Caution-complications and side effects
Careful consideration and discussion with the patient before initiation
of treatment is required.
With proper attention to detail, complications are infrequent. Side
effects of treatment, include scotoma production .On average, vision
will improve from 20/70 to 20/40.
It is particularly important to recognize that laser photocoagulation
should never be placed over extensive intraretinal hemorrhage in the
acute phase of branch vein occlusion As it can produce preretinal
fibrosis.
Wait period
Branch Vein Occlusion Study emphasize waiting at least 3 to 6 months
before considering laser therapy after the BRVO
Surgical Treatment of BRVO
A recent study by Kumar and associates postulated that removal of
the compressive factor by sectioning the adventitial sheath (sheathotomy)
might be an effective treatment for BRVO. This is still a very specialized
arena.
Conclusion
BRVO is a common cause of visual loss in Pts. over the age of 60
yrs. through neovascularization ,macular edema and macular ischemia
Adequate and timely treatment of such conditions like Hypertension
, Diabetes mellitus, raised blood cholesterol and retinal inflammation
are the precautions to be advised to the patient.