Management of Retinal Vein Occlusions –An Overview

Introduction
Retinal vein occlusion (RVO) is an obstruction of the retinal venous system and is the
second commonest cause of reduced vision due to retinal vascular disease4,5(1st being
Diabetic retinopathy)with BRVO occurring 2-3 times as common as CRVO.6,7. Even
today, the understanding of the disease and its treatment is still evolving. This article
attempts to give some broad guidelines in the management of these set of conditions.

Classification.
1. Branch Retina Vein Occlusion(BRVO)
2. Central Retinal Vein Occlusion(CRVO)
a. Non Ischemic
b. Ischemic
3. Hemiretinal Vein Occlusion

Pathogenesis

Central retinal artery and vein share a common adventitial sheath, as they exit
the optic nerve head and pass through narrow opening in the lamina cribrosa.
Because of this narrow entry in the lamina cribrosa, vessels are in a tight
compartment with limited space for displacement. This anatomical position
predisposes to formation of thrombus in the central retinal vein by various
factors, including slowing of blood stream, changes in the vessel wall, and
changes in the blood. Similarly in the areas of arteriovenous crossings in the
Retina, a retinal arteriole and its corresponding vein share a common adventitial
sheath and hence is predisposed to thrombus formation resulting in BRVO.
Arteriosclerotic thickening of the arterial wall and consequent compression of the
vein/venule is the commonest cause that leads to the formation of a thrombus.

Whatever the mechanism of the occlusion it leads to backup of blood in the

retinal venous system and increased resistance to venous blood flow. This
increased resistance causes stagnation of blood and ischemia of inner retinal
layers in the affected areas.This results in damage to the capillary endothelial
cells and leakage of blood constituents .The tissue pressure is increased causing
further stagnation of the circulation and hypoxia and this sets up a vicious cycle.

The ischemic damage to the Retina is supposed to give rise to angiogenic factors
which stimulates abnormal vascularization of the posterior and anterior segment.
In addition, increased blood pressure in the venous system causes break down
of inner retinal barrier at the retinal capillary endothelium, leading to abnormal
leakage of fluid in the retinal layers causing macular edema
Aetiology and Risk factors
Retinal vein occlusion is due to thrombosis of retinal veins (central,
hemi or branch) The predominant medical associations for both
central and branch vein occlusions are summarised below in the
order of their importance

1. Hypertension
This is the predominant risk factor with up to 64% of patients
having hypertension in the older age group (more than 50
years).10 This is more prevalent in BRVO than CRVO. A new
diagnosis or uncontrolled hypertension is a common finding.
Inadequately controlled hypertension is associated with
recurrence of RVO in the same eye or fellow eye involvement.
2. Hyperlipidaemia
Hyperlipidaemia (cholesterol > 6.5 mmol/l) is the predominant
association in the younger age group (< 50 years) of patients
with retinal vein occlusion and is associated in up to 50% of
older patients.11
3. Diabetes mellitus
Diabetes mellitus is associated with retinal vein occlusion. This
may be due to an increase of other cardiovascular risk factors
(e.g. 70% of type II diabetics are hypertensive).10,12,13
4. Glaucoma
Current evidence suggests an association between central
retinal vein occlusion and glaucoma.7,14 One study suggests
that BRVO is associated with glaucoma 12
5. Thrombophilia
Factor V Leiden and other such abnormalities have been
implicated in RVO but their aetiology is unclear. Deficiency or
abnormal activity of various factors have been identified in
patients with RVO including protein S,C, anti-thrombin 3,
activated protein C resistance, hyperhomocysteinaemia and
the presence of lupus anticoagulant or anti-cardiolipin
antibody deficiency.15 Thombophilia and the other rarer
associations e.g. oral contraceptive pill, and optic
disc vasculitis assume more importance in the younger
patients (<50 years).16,17
6. Myeloproliferative disorders occur in 1% of patients presenting
with retinal
vein occlusion.9 7 C B C C D
7. Other rare associations with retinal vein occlusion include
a. Inflammatory disease that cause or are associated with
retinal vasculitis –Behçets disease, polyarteritis nodosa,
 sarcoidoisis, Wegener’s Granulomatosis,Goodpasture’s
Syndrome.
b. Chronic renal failure and other secondary causes of
hypertension and diabetes e.g. acromegaly, Cushing’s
syndrome.
c. Secondary causes of hypercholesterolaemia eg
hypothyroidism.
D

Clinical Features
Clinically, patients with CRVO typically present with sudden loss of central vision.
Transient obscurations of vision can also occur, but are less common. In the acute phase
all four quadrants show venous dilation and tortuosity, superficial and deep intraretinal
hemorrhages, and/or cotton wool spots. There is usually disc edema and there may be
macular edema and/or serous detachment . The characteristic fluorescein angiographic
findings in CRVO include delayed venous filling and capillary non-perfusion which may
be obscured by the retinal hemorrhages. If the retinal hemorrhages are primarily in the
peripheral retina and predominantly blot shaped, carotid insufficiency should be ruled out

In BRVO similar fundus findings are seen except that these are confined to a portion of
the Retina. Vision loss at presentation is related to the extent of macular damage from
intraretinal edema (most common), hemorrhage or capillary non-perfusion and can range
from severe blurring to completely asymptomatic (as in nasal occlusions).

Management
Can be considered under 2 headings
1. The identification of modifiable risk factors and their medical
management
2. Recognition and management of sight-threatening
complications.

The former is similar for all types of Vein occlusions and hence will
be considered together.However the ophthalmological management
of branch and central retinal vein occlusion differs and will be dealt
with separately.

1.OPHTHALMOLOGICAL MANAGEMENT

Central retinal vein occlusion

Management of CRVO still remains uncertain and controversial.Writing about the
treatment of CRVO one tends to remember the old adage-“a disease which has no
treatment has many treatments”. However the present guidelines are generally formulated
based on the landmark “Central Retinal Vein Occlusion Study(CVOS)”

Fact of the matter is there is no proven early treatment that will

alter the visual prognosis in established central retinal vein
occlusion.
The first all importrant step in the management is to differentiate
ischaemic from non-ischaemic central retinal vein occlusion.
Patients with ischaemic CRVO are at risk of neovascular glaucoma
for which
laser photocoagulation may be beneficial. This risk of iris
neovascularisation is
higher if the area of retinal ischaemia (retinal non-perfusion as
determined by
FFA) is >10 disc diameters (CVOS).18
Ischaemic central retinal vein occlusion is
associated with one or more of the following characteristics:-
1. Poor visual acuity (44% of eyes with vision of <6/60 develop
rubeosis
[CVOS])18
2. Relative afferent pupillary defect
3. Presence of multiple dark deep intra-retinal haemorrhages
4. Presence of multiple cotton wool spots
5. Fluorescein angiography showing greater than 10 disc areas of
retinal
capillary non-perfusion (CVOS)18
6. Electrodiagnostic tests (ERG): reduced b wave amplitude,
reduced b:a ratio
and prolonged b-wave implicit time19-23
There is no evidence as to which combination of the above
characteristics best defines
ischaemic CRVO.Also authors like Hayreh cautions against the use
of Ophthalmoscopy and FFA especially in the acute stages for this
differentiation.The argument against FFA being that a good quality
ffa may not be possible in the early stages and that capillary non
perfusion might still be evolving. But there is no doubt that a good
quality FFA obtained at 1-2 months time after absorption of
hemorrhages and taking care to include the pe
ripheral zones is extremely useful to settle the issue and plan
management. But in the acute stage 1,2 and 6 of the above is
supposed to be the most useful. Hayreh has also demonstrated the
efficiency of Peripheral Visual field charting using Goldman
Perimetry in differentiating the 2 types of CRVO
But one confounding factor in this assessment is that up to 30% of
patients with initially nonischaemic central retinal vein occlusion will
convert to Ischemic type.24- 27
This is usually heralded by further rapid visual deterioration and
requires further
assessment. CRVO especially of the non-ischaemic type needs to be
differentiated
from the ocular ischaemic syndrome and other simulating
retinopathies.

Management of ischaemic central retinal vein occlusion and anterior

segment neovascularisation
An initial evaluation of risk factors and the appropriate treatment of the present risks
must proceed alongside management of the ocular findings.

The evidence collected supports the use of laser pan-retinal photocoagulation when iris
new vessels (INV) or angle new vessels (ANV) are visible. The others have to be
followed up monthly for six months and the examination should
include undilated pupil examination and gonioscopy. PRP should be applied at the
earliest sign of INV and or ANV.
However in circumstances when regular follow-up is impractical, many authors would
consider prophylactic PRP.

Posterior segment neovascularisation

This alone is unusual in Ischemic CRVO and there is no conclusive evidence to suggest
that PRP is required.

Pan-retinal Photocoagulation Technique

Pan-retinal photocoagulation for CRVO with INV or ANV requires 1500 - 2000
of 500-micron burns at the retina. This is best applied with 0.05-0.1 seconds
applications one burn width apart with sufficient energy to produce a pale burn
in the retina. Treatment is usually placed outside the posterior pole avoiding areas of
retinal haemorrhage. Some cases require further treatment if the iris
neovascularisation fails to regress.18

However Hayreh et al is of the view that rubeosis does not

inevitably lead to glaucoma and therefore laser photocoagulation
should be withheld because this treatment leads to further
contraction of the visual field.30 But the
weight of evidence supports the CVOS guidelines
If ocular media is hazy for laser to be applied, cryoablation of the peripheral
fundus is an option. About 16-32 transscleral cryo spots are applied from ora
serrata posteriorly.

Management in NVG stage

If there is visual potential then intraocular pressure should be controlled with
topical pressure-lowering agents or cyclo-ablative procedures. Drainage
procedures are of limited value.
The aim in other cases ie a blind eye is to keep the eye pain
free. This is usually achieved by topical steroids and atropine.

Macular oedema

This is a real problem area in CRVO and Nothing really seems to be

working here. Macular edema: CVOS evaluated the efficacy of macular grid
photocoagulation in preserving or improving central visual acuity in eyes with
macular edema due to central vein occlusion (CVO) and best-corrected visual
acuity of 20/50 or poorer. Macular grid photocoagulation was effective in
reducing angiographic evidence of macular edema, but it did not improve visual
acuity in eyes with reduced vision due to macular edema from CVO. At present,
the results of this study do not support a recommendation for macular grid
photocoagulation for macular edema.

Follow up
Follow up for 1st 6 mnths for Ischemic CRVO already described. Follow-up after 6
months for ischaemia (> 10DD non-perfusion) should be
every 3 months for 1 year. Non ischaemic eyes should have initial
follow up
every 3 months for 6 months. Subsequent follow-up for all patients
will
depend upon laser treatment and complications but will not
normally be
required after 2 years in uncomplicated cases. With the
development of disc
collaterals +/- resolution of the CRVO the need for further clinical
supervision may not be there..

Experimental Treatments
Numerous surgical techniques with varying degrees of success are being advocated for
the treatment of CRVO. But all of these newer techniques and therapies need more
extensive trials before they can be routinely performed and hence cannot be
recommended at present except as part of clinical trials..Some of these are briefly
mentioned
1.Laser induced Chorio Retinal Anastomosis between a retinal vein and the choroid is a
procedure that seeks to bypass the central retinal vein outflow. Argon laser is used to
disrupt the wall of the vein as well as the underlying Bruch’s membrane. Limitations of
this technique include a low success rate (30 to 50 percent) and complications such as
vitreous hemorrhage, choroidal neovascularization, preretinal fibrosis and traction retinal
detachment.
2.Radial optic neurotomy is a procedure that attempts to decompress the central retinal
vein at the lamina cribrosa. A radial incision of the lamina and sclera is made at the nasal
edge of the optic disc. Concerns with this technique include damage to the nerve fiber
layer, the arterial circle of Zinn, and the central retinal artery. In addition, it is not known
if the reported beneficial effects are secondary to the incision or to the vitrectomy alone.

3.Intravitreous triamcinolone acetonide administration has been used to treat macular

edema in both ischemic and non-ischemic CRVO.Reduction in macular thickness with
improved visual acuity can last three to six months; however, improvement is unlikely in
eyes with chronic macular edema and secondary macular changes. Furthermore,
especially in the ischemic group, visual acuity may not improve despite resolution of
macular edema.
4.Thrombolytic therapies
Currently, there is no definitive data to support the use of systemic anticoagulation for
prophylaxis or treatment of CRVO. Thrombolytic agents such as t-PA have been used via
the systemic, intravitreous, and retinal venous route. Systemic administration is
associated with the risk of systemic and intraocular bleeding. Intravitreous administration
of t-PA shows outcomes that are similar to the natural history of CRVO. Cannulation and
injection of t-PA into a peripapillary branch retinal vein specifically targets the thrombus
at the lamina cribrosa, but it is not clear if the reported beneficial effects are from lysis of
the thrombus or from mechanical dilation of the central retinal vein. Logically, this
technique should be used in the acute stage before the thrombus is organized.

Branch retinal vein occlusion

The diagnosis of branch retinal vein occlusion is clinical, as described before. In
doubtful cases, especially small BRVO, fluorescein angiography may be indicated to
confirm the diagnosis. Fluorescein angiography is particularly useful in determining
the extent of macular oedema and ischaemia. Approximately 50% of untreated eyes
with BRVO retain vision of 6/12 or better whilst 25% will have vision of <6/60.
Macular oedema and neovascularisation of the retina or disc are the two major
complications which may require therapy. Retinal neovascularisation occurs in 36% of
eyes with >5 DD and 62% with >4DD area of non-perfusion.the treatment guidelines are
based mainly on the recommendations of the BRVO study.

Treatment of neovascularisation
New vessels occur only when there is at least a quadrant of capillary
closure and commonly after six months following the occlusion.
Follow up visits at 3- 4 monthly intervals are recommended in
patients with one quadrant or more retinal ischaemia. It is
recommended that sector laser photocoagulation is applied once
retinal or optic
disc neovascularisation occur. Fluorescein angiography is not
usually necessary
prior to laser because the area of ischaemia is visible clinically.
The BVOS demonstrated that sector panretinal photocoagulation reduced the risk of
retinal neovascularization from 22 percent to 12 percent (average follow up 3.7 years),
and it reduced the risk of vitreous hemorrhage in eyes with neovascularization from 60
percent to 30 percent (average follow up 2.8 years). BVOS data also suggest that there
may be no advantage to treating prior to the development of neovascularization, and
therefore, the BVOS recommends that nonperfused eyes with BRVO should be treated
only if neovascularization develops, or if the patient is unable to follow up on a regular
basis.

Technique
Photocoagulation for neovascularisation is applied to the sector of
retinal
capillary closure. 500-micron burns at the retina are used and are
applied in a
scatter pattern to the affected sector, one burn width apart are
appropriate with
sufficient energy to create a gentle burn. A quadrant usually
requires 400-500
burns.

Treatment of macular oedema

The BVOS recommends an observation period of three months to allow for spontaneous
improvement of macular edema and hemorrhage. If resolution does not occur, fluorescein
angiography is used to assess the extent of macular edema, foveal hemorrhage, and
perifoveal capillary drop out. Eyes with visual acuity of 20/40 (6/12)or worse, persistent
macular edema, absence of foveal hemorrhage and an intact perifoveal capillary network
should undergo argon laser grid photocoagulation to the area of macular capillary
leakage.
Eyes with severe visual loss (less than 6/60 vision) and those in
whom symptoms have been present for more than one year are
unlikely to benefit from photocoagulation.

Technique
Laser photocoagulation for macular oedema requires gentle burns
of 100-200
microns. About 20 to 100 applications (depending on the area of
vascular leakage) are given in a grid pattern to the areas of vascular
leakage but avoiding the foveal
avascular zone (i.e the burns must not approach the foveal centre
by less than
1/2 DD). Collaterals should be avoided.

Follow-up
Initial follow-up in all patients should be at three months following
the occlusion.
Subsequent follow-up at three to six monthly intervals will depend
on complications
and laser treatment, and will not normally be required after two
years in
uncomplicated cases.

New treatments
1. Intravitreous triamcinolone acetonide is being increasingly used for the treatment
of macular edema unresponsive to laser. Potential complications include
infectious, sterile, or pseudo-endophthalmitis, elevated intraocular pressure,
cataract formation, retinal detachment, and intraocular hemorrhage. Recurrence of
retinal edema occurs commonly, often requiring repeated injections.
2. Vitrectomy and sheathotomy to separate the artery and vein at the AV crossing.as
treatment for BRVO are currently under evaluation. A number of non-randomized
studies have shown that AV sheathotomy may be associated with improvement in
visual acuity, macular edema, macular hemorrhage, and even retinal perfusion.
Theoretically, relieving the pressure on the retinal vein from the relatively rigid
arterial wall may restore venous flow, presumably following recanalization of the
thrombus.
However prospective, randomized, controlled, multicenter clinical trials are required
to accurately assess these results and No recommendations on these new treatments
are possible at present.

Hemisphere vein occlusion

Hemi-retinal vein occlusions are variants of central retinal vein occlusions that involve
the superior or inferior half of the retina. This pattern develops due to an anatomic
variation at the optic nerve head.. The pathophysiology of HRVO mimics CRVO, but the
clinical findings and complications are intermediate between CRVO and BRVO.
The risk of rubeosis in ischaemic hemi-central vein occlusion is
greater than that of
BRVO but less than that of CRVO.The risk of disc neovascularisation
appears
greater for hemispheric vein occlusion than either ischaemic CRVO
or BRVO. The
management of hemispheric vein occlusion is similar to that
described for branch
retinal vein occlusion, the guidelines for laser treatment being those
described above
for retinal branch vein occlusion.

Medical Management of Retinal Venous Occlusions

It is binding on the Ophthalmologist to undertake the necessary investigations and
referral to the concerned specialist to ensure identification and treatment of the
underlying risk factors which has directly or indirectly led to the venous occlusion .This
is important to prevent further non-ocular target organ damage, as well as to prevent
recurrence of venous occlusion particularly in the fellow eye. Few long-term followup
studies of patients with retinal vascular disease (retinal vein occlusion and retinal
arterial occlusion) have demonstrated excess cardiovascular morbidity, mortality from
stroke,and myocardial infarction over a ten-year period.41,42
Therefore, medical management should be targeted at three areas:
1. Reverse retinal vein occlusion
2. Ameliorate cardiovascular morbidity and mortality associated with retinal vein
occlusion.
3. To prevent the recurrence of retinal vein occlusion(Incidence of this in the same
or fellow eye can occur in 9-15% cases)

1.Reversing Retinal Vein Occlusion

Few of the Retinal vein occlusion cases may present at a very early
stage –impending or incipient occlusions-
consisting of the presence of dilated retinal veins and few
widely scattered haemorrhages without any macular oedema in patients who
are either asymptomatic or have transient episodes of blurring in the affected
eye and may have slight increase in retinal circulation time on fluorescein
angiography
In these cases there might be potential to prevent progression,
or to reverse the existing occlusion .Hence they need urgent medical investigations for
underlying systemic risk factors and treatment .Anti-platelet agents may be of benefit.
The medical therapies explored to improve retinal venous flow include
1.Anti-coagulants, heparin
Fibrinolytic agents: streptokinase, tissue plasminogen activator (intravitreal or
systemic)
Anti-platelet drugs: aspirin, prostacyclin, ticlopidine
These would seem to be logical treatments, but results from trials using
heparin, streptokinase and warfarin have been disappointing with limited
evidence of benefit owing to adverse effects of retinal and vitreous
haemorrhage.
Haemodilution
The effects of haemodilution have been inconsistent in completed control trials
in RVO although results from further trials are awaited.

2.As far as the other 2 areas are concerned the following steps are to be taken
 i. Proper management of Cardiovascular risk factors identified
in these patients by the concerned specialists.
It is now proven that drug treatment of hypertension reduces
the severity of its complications, and additional therapy of
aspirin in well controlled hypertensive subjects given as a
primary prevention reduces cardiovascular event rate.
Recent trials of cholesterol lowering using statins have
confirmed the beneficial effect of this therapy with reduction
of cardiovascular morbidity and mortality.
ii. Patients with rarer underlying conditions such as myeloma
and inflammatory disorders should be referred and managed
by appropriate specialists.
iii. Good control of intraocular pressure in patients known to have glaucoma
may prevent CRVO

Management of younger patients (less than 50 years of age)

Risk factors like Hypertension and Hyperlipidemia to be looked for

and managed in this group also. But many of these patients will
have no identifiable underlying cause despite extensive
investigation including the specialised investigations listed in Table
2. In females the contraceptive pill is the most common underlying
association, and is contraindicated in patients with retinal vein
occlusion. There is debate as to the exact prevalence of
thrombophilic disorders in this patient group as well as appropriate
therapy. Identified inflammatory disease should be treated as
appropriate to the condition and referred for specialist medical
advice.

Initial Medical Investigations for Patients Presenting with Retinal

Vein Occlusion
ALL PATIENTS
Full blood count and ESR or plasma viscosity
Urea, electrolytes, creatinine
Random blood glucose
Random cholesterol and HDL cholesterol
Plasma protein electrophoresis
ECG
Thyroid function
MORE SPECIALISED TESTS ACCORDING TO CLINICAL INDICATION
Thrombophilia screen
Anti-cardiolipin antibody, lupus anticoagulant
C-reactive protein
Serum ACE
Auto-antibodies - rheumatoid factor / anti-nuclear / anti DNA / ANCA
Chest X-ray
Fasting homocystine level

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RETINAL VEIN OCCLUSION GUIDELINES