ARTERIAL

&
VENOUS
OCCLUSIVE DISEASE OF RETINA

MODERATOR-- DR.(PROF) V. BHAISARE

PRESENTOR-- DR. ANKITA
 "Research into retinal ischemic disease is
fraught with challenges, from accurate disease
classification to its treatment; even the most
prestigious trials have become controversial."
VASCULAR SUPPLY OF RETINA
INTERNAL CAROTID ARTERY

OPHTHALMIC ARTERY

CENTRAL RETINAL ARTERY 20 SHORT POSTERIOR CILIARY ARTERY

(penetrates 13 mm posterior to the globe) ( penetrate the sclera in a ring around the optic nerve)

I. DEEP OPTIC NERVE I. CHOROID

by intraneuron branch, recurrent pial branch
II. NERVE FIBRE AND GANGLION CELL LAYER II. OUTER RETINA
by larger branches of cra
III.CILIORETINAL ARTERY
- present in 30% of eyes and 50% population

- 15%-supplies macular circulation

.
Retinal circulation is generally end arterial in nature

BUT....
in the capillary beds of the
optic nervehead.
superficial capillaries derived from the CRA lie adjacent to
those capillaries that penetrate the deeper regions of the
2 anastomoses prelaminar and lamina cribrosa, that originate from posterior
ciliary circulation

within dural sheath of the

optic nerve
intraneuronal branches of the central retinal artery
communicate with recurrent pial branches.
 Let’s begin with

RETINAL ARTEY OCCLUSION

RETINAL VEIN OCCLUSION
RAO
 HISTOPATHOLOGY OF OCCLUSION
Retina has a high oxidative capacity and a high level of glycolytic activity.
Decrease/ absence of perfusion leads to

Decreased delivery of glucose and more importantly oxygen to the tissues of the retina.

Ischemia + edema[ as neuron cellular membranes burst,]

funduscopic whitening of the retina caused by opacification of the ganglion cell layer.
• Opacification most prominent = macular region where the multiple layers of ganglion
cells reside. Retinal opacification generally decreases toward the periphery as the
ganglion cell population diminishes
• Absent from the avascular zone of the foveola where ganglion cells are absent.
• The classic ‘cherry red spot’ is a result of the visible red reflex of the perfused choroid
at this location.
• Dendritic lysis = 3.5 h
• Extensive cellular loss =16 h
• Retina could tolerate 97–98 min of total occlusion
• Half of eyes occluded for 102 min recovered vision.
• All eyes >105 min = irrecoverable ischemia
 MECHANISMS OF OCCLUSION
Principal mechanisms
 embolic > 50 year pt m/c/c
 thrombotic younger pt m/c/c
 vaso spastic,
 extravascular compression,
 vasculitic-giant cell arteritis - thrombosis being the ultimate occlusive event.

Other mechanisms
 radiation
 elevated intraocular pressure
 EMBOLI
I. Endogenous II. Exogenous
A. Carotid atheroma A. Injected steroids
• m/c source of retinal emboli
• > 80% being a/w carotid artery disease B. Catheter tips
B. Cardiac valvular disease
• Valvular abnormalities, C. Talc
• tumors- atrial myxoma
• thrombus in the LA
• (e.g. AF, right to left shunts- patent foramen ovale) D. Artificial heart valves
C. Fat emboli
D. Leukoemboli
E. Amniotic fluid emboli
F. Septic emboli
• Visible emboli detected
ophthalmoscopically =evident in 20–
30% of patients with retinal arterial
occlusive disease
• Clinically the most common are
– cholesterol emboli,
– platelet fibrin emboli, and
– calcific emboli

• Cholesterol emboli
 small, glistening yellow in color, and
 typically do not occlude the vessel
distal to the emboli.
• Calcific emboli
 larger,
 gray-white in color
 a/w more severe local obstructions
• Platelet fibrin emboli
 Appear gray-white,
 larger and longer than cholesterol emboli,
 may be seen to pass through the retinal vessels.
 Thrombophilias Associated with Retinal
I. Factor V Leiden
Arterial Occlusions
II. Antithrombin deficiency
III. Protein C deficiency
IV. Protein S deficiency
V. Hyperhomocystinemia
VI. Anti-phospholipid antibodies
VII. Lupus anticoagulant
VIII. Anticardiolipin
IX. MTHFR C677T polymorphism( in methylene tetrahydrofolate reductase)
X. Prothrombin G20210A mutation
XI. Dysfibrogenemia
XII. Elevated factor VIII
XIII. Elevated factor IX
• VASCULITIS AND GIANT CELL ARTERITIS
 The classic vasculitis-related CRAO occurs in giant cell arteritis.
 a/w ocular pain because of the profound ischemia
 patients >55 years - present with CRAO should be questioned for associated
symptoms like headache, scalp tenderness, jaw claudication, malaise,
anorexia, fever, and weight loss
 20% of patients with giant cell arteritis are without systemic symptoms.
 Patients with acute CRAO secondary to giant cell arteritis may have
prodromal transient blurring of vision for weeks to months prior to the
occlusive event.
 ESR and C-reactive protein- raised
 confirmed by temporal artery biopsy.
 Making an accurate diagnosis and initiation of high-dose steroid therapy M/I
because second eye involvement may occur soon following presentation.
Classification
1. Central retinal artery obstruction.
2. Branch retinal artery obstruction.
3. Cilioretinal artery obstruction.
4. Combined central retinal artery and vein obstruction.
CENTRAL RETINAL ARTERY OCCLUSIONS
 painless unilateral profound loss of vision.
 VA >20/400- >90% of eyes at the time of presentation.
 Afferent pupillary defect present.
 Visual fields- depressed in the area of the ischemic retina.
 Retina shows ischemic whitening, and the retinal arterials and veins manifest
boxcarring.
 A cherry red spot - present due to the intact choroidal circulation
 FA-show an intact choroidal flush with absent,incomplete, or delayed filling and
a leading edge of dye in the retinal circulation
 median final visual acuity following resolution of edema in CRAOs is counting
fingers.
 However, in select casaes with intact cilioretinal arteries supplying the fovea,
Snellen visual acuity may improve to 20/20
 Chronic fundus changes in CRAO include optic atrophy, attenuated retinal
arterials and venules, and an atrophic-appearing retina.
 Branch retinal artery occlusion (BRAO)
 pt-acute painless loss of visual field in the distribution of the occluded artery.
 VA 20/20 to 20/400 (on the degree of foveal involvement.)
 An afferent pupillary defect may be present
 Retinal whitening, along the distribution of the artery is usually present, but may
not occur in nasal branch artery occlusions due to the single layer of ganglion
cells present there.
 Emboli are identified in ~30% of cases.
 FA -delayed transit of the dye through the affected vessel, and often retrograde
filling of the vessel can be observed later in the angiogram .
 Pt typically retain excellent visual acuity following the acute event, as long as a
portion of the foveal vasculature maintains normal perfusion.
 VA improves to >20/40 in 80% of these eyes but visual field defect persist.
 The fundus appearance may return to near normal weeks to months following
the event.
CILIORETINAL ARTERY OCCLUSIONS
 35% of eyes and 50% of people have cilioretinal arteries.
 Typical symptoms of patients with cilioretinal artery occlusions are pericentral
scotomas,often subtle, in the distribution of the artery.
 afferent pupillary defects - often not present.
 Cilioretinal artery occlusions occurring in isolation usually have a prognosis as
good as or better than BRAOs, with 90% improving to 20/40 or better visual
acuity.
 MANAGEMENT
considered in three aspects:
(1) management of the acute occlusive event in an attempt to restore visual
function;
(2) workup of the patient looking for potential systemic conditions requiring M/I
treatment; and
(3) management of the remote complications and sequelae of the arterial
occlusive event.
With regards to visual function
• the duration of retinal ischemia is the most important
factor in determining prognosis.
• Therapeutic goals are to restore blood flow as quickly
• ocular treatment be given if a patient with an
acute central retinal artery obstruction is seen
within 24 hours after the onset of visual loss.
 Ocular massage
 can be attempted with an in-and-out movement
 using a Goldmann contact lens or via digital
massage.
 In rare instances, this manipulation can dislodge an
obstructing embolus.
 Repeated manipulations to increase the pressure for
dislodgement of emboli probably secondary to
autoregulation
 The use of an oxygen and carbon dioxide (95%
oxygen, 5% carbon dioxide)- carbogen
 Carbon dioxide, is a vasodilator and can produce
increased retinal blood flow.
 In the absence of a carbon dioxide mixture,rebreathing into
a paper bag can be considered
 Anterior chamber paracentesis
 Hyperbaric oxygen
 Fibrinolytic agents
 delivered through the supraorbital artery in eyes with acute
central retinal artery obstruction.
 the drug travels retrograde into the ophthalmic artery and
allows doses into the central retinal artery that are over 100
times greater than those which would be achieved if a
similar amount of drug was injected intravenously.
 retrobulbar injection or systemic administration of vasodilator such as
papaverine or tolazaline.
 Laser therapy has been suggested as a mechanism of obliterating emboli
 RETINAL VEIN OCCLUSION
the second most common retinal vascular disease
following diabetic retinopathy.
 M=F ,> 65 years.
 Population-based studies report the
prevalence of CVO at 0.1 to 0.4%.
 usually a unilateral disease
 annual risk of development any type of RVO
in the fellow eye is = 1% / year
 usually presents as a sudden painless loss
of vision
 three distinct types of RVO:
– branch retinal vein occlusion(BRVO),
– central retinal vein occlusion (CRVO),
– hemiretinal vein occlusion(HRVO) - Anatomical varient
of crvo
 1.CENTRAL RETINAL VEIN OCCLUSION
 The hemorrhages radiate from the optic
nerve head and are variable in quantity and
may result in the classic “blood and
thunder” appearance .
BLOOD AND THUNDER
APPEARANCE
 Fibrovascular proliferation from NVD or NVE may result in vitreous
hemorrhage or traction retinal detachment.

 Anterior segment -- iris and angle neovascularization (INV/ANV).

 Angle neovascularization is detected during undilated gonioscopy and can
be detected as fine branching vessels bridging the scleral spur.
 Angle neovascularization may develop without any INV in 6–12% of eyes
with CRVO.
 Elevated intraocular pressure associated with INV/ANV is the hallmark of
neovascular glaucoma.
 Longstanding ANV may lead to secondary angle closure from peripheral
anterior synechiae formation.
 PERFUSION STATUS
CVOS classified perfusion status of CRVO
(based on the FA characteristics)
1. perfused/nonischemic/incomplete/partial
 demonstrates less than 10 disc areas in diameter of
retinal capillary nonperfusion on angiography

2.nonperfused/ischemic/hemorrhagic/complete
 demonstrates 10 or more disc areas in diameter of
retinal capillary nonperfusion on angiography

3. indeterminate
 sufficient intraretinal hemorrhage to prevent
angiographic determination of the perfusion status.
 role of FA
very helpful in evaluating the extent and mechanism of retinal dysfunction based
on perfusion characteristics.
• Wideangle FA using a 60° fundus camera is helpful in evaluating peripheral
retinal perfusion.
• The overall arterial perfusion time after injection is normal to slightly delayed in
CRVO
• delay in arteriovenous transit time is typically significant
• A delay >20 seconds a/w a greater risk of iris neovascularization.
• Nonperfused areas- patchy areas of hypofluorescence with ground-glass
appearance .
• Staining of the walls of the retinal veins an indicator of nonperfusion.
• FA shows parafoveal and paramacular capillary leakage- hyperfluorescence that
increases in size and intensity with time, often in a petalloid type pattern.
• The hyperfluorescence persists longer than that of normal retinal tissue.
 PATHOGENESIS
The clinical picture of CVO may be explained by the occlusion of the main trunk of
the central retinal vein
pathophysiology of CVO is not clearly understood.
Histopathologic studies of eyes enucleated for CVO demonstrated a thrombus
occluding the lumen of the central retinal vein at or just proximal to the lamina
cribrosa.
• Within the retrolaminar portion of the optic nerve, the central retinal artery and
vein are aligned parallel to each other in a common tissue sheath.
• The central retinal artery and vein are naturally compressed as they cross lamina
cribrosa
 • anatomic variations at the local factors = compression
by an atherosclerotic central
level of the lamina cribrosa retinal artery or primary
occlusion of the central
retinal vein from
inflammation
Raised IOP
Development of
CRVO
mechanical
stretching of the
lamina.

posterior shift or bowing of the lamina with subsequent

impingement on the central retinal vein.
• Anterior segment neovascularization is modulated by growth factors
Vascular endothelial growth factor (VEGF) has been implicated in the
development of neovascular complications from CVO.
• Aqueous VEGF levels increase prior to the development of NVI and
decrease with the regression of NVI after panretinal laser photocoagulation.
DIFFERENTIALs DIFFERENTIATING FEATURE

DM RETINOPATHY CRVO-U/L
DM-B/L
OIS OIS-veins dilated and irregular never tortous
-H/O amaurosis fugax, transient ischemic attacks, or orbital pain.
Intraocular pressure may be low

PAPILLOEDEMA Disk swelling +

Similar disk hemorrhages may be observed however, the
hemorrhages are generally localized to the optic disk with
papilledema and typically do not involve the peripheral retina

REDIATION RETINOPATHY H/o radiation

HTN RETINOPATHY generalised attenuation of arteries

 CLINICAL EVALUATION
• At the time of initial presentation
• duration and the degree of retinal ischemia-determine treatment options and
the follow-up schedule.
• An ocular history-determine the onset of the occlusion.
• A history of systemic diseases and a personal or family history of thrombosis
.
• The ophthalmic examination ( on both eyes) includes- visual acuity, pupillary
reaction, and intraocular pressure.
• Undilated slit lamp - INV or ANV.
• Undilated gonioscopy - determine the presence of ANV or evidence of angle
closure from peripheral anterior synechiae
• SYSTEMIC WORK UP
• >60 year old- no need of systemic work up
• pt with a prior occlusion in the fellow eye, prior systemic thrombotic disease,
family history of thrombosis, or other symptoms suggestive of a hematologic
or rheumatologic condition- limited systemic work up
• young patient- extensive systemic evaluation to r/o inflammation
• An initial lab inv- an erythrocyte sedimentation rate, anti-nuclear
antibody,antiphospholipid antibody, and fasting plasma homocysteine levels.
 THERAPEUTIC OPTIONS
1.Medical therapy
• Identification and treatment of systemic vascular risk factors,
• The role of systemic anticoagulation in CVO
• is unclear as there is no evidence that agents, such as aspirin or heparin, can
prevent or alter the natural history of CVO
• Prophylactic use of these medications, however, may help prevent non-
ocular thrombotic events, especially in individuals with known systemic
vascular disease.
• Oral pentoxifylline is used in systemic vascular diseases to improve perfusion
to occluded vessels, enhance the development of collateral circulation, and is
a potent vasodilator.
• pentoxiphylline may help to reduce macular edema in CVO
• role of systemic immunosuppression in select cases of CVO-transient
improvement in visual acuity and reduction in macular edema - d/t reduction
of both local and systemic inflammatory disease .
• Medical therapy in sequela of CVO,
( neovascular glaucoma.)
• Topical or systemic anti-glaucoma agents - help to reduce intraocular
pressure typically by
– reducing aqueous humor production and enhancing outflow in sections of the anterior chamber
outflow tract not occluded by anterior synechiae. Topical corticosteroids can reduce anterior
segment inflammation by stabilizing tight junctions in neovascular tissue, thereby reducing vascular
exudation.
• Cycloplegic agents prevent posterior synechiae formation between the iris
and lens.
• Failure of medical therapy to control intraocular pressure may require
surgical intervention (e.g. trabeculectomy or seton placement).
 Laser photocoagulation
1) In ocular neovascularisation
2) In macular edema
3) In chorio-retinal venous anastomosis
 1) In ocular neovascularisation
• PRP- delivered after the development of INV/ANV prophylactically,
 = 90%- regression of INV/ANV < 1–2 months.
 Persistent neovascularization after PRP - follow closely,
 additional PRP - to halt its progression.
 Persons presenting with NVD/NVE without INV/ANV- treated with PRP( to
prevent anterior segment neovascularization).
Prophylactic PRP
 nonperfused CVO risk factors for developing INV/ANV
male gender with
short duration of CVO, caution
extensive retinal non-perfusion,
extensive retinal hemorrhage
 In cases where frequent ophthalmologic follow-up is not possible.
 2)In macular edema

CVOS did not recommend grid laser photocoagulation for CVO-

associated macular edema.
– widespread damage to the perifoveal capillary network is hypothesized to
contribute to the lack of visual recovery.
 FOLLOW UP IN CRVO
VA at presentation Follow up
>20/40 or >6/12 every 1–2 months for 6 months, then annually if stable

20/50-20/200 monthly for the first 6 months if at any time in the follow-up
period the visual acuity drops below the 20/200 level, an
evaluation .with assessment of perfusion status and anterior
segment examination is required, and monthly follow-up for an
additional 6 months is recommended.

<20/200 or <6/60 monthly for the initial 6 months, then bimonthly for the next 6
months, as these eyes have a greater risk of developing INV/ANV

examinations assess visual acuity and include undilated slit lamp examination looking for INV/ANV. Laser
photocoagulation is performed if INV / ANV is detected to prevent neovascular glaucoma
 3)In chorio-retinal venous anastomosis
• bypass the occluded central retinal vein by creating a chorioretinal
anastomosis (CRA) b/w a nasal branch retinal vein with the choroidal
circulation.
• Successful creation of an anastomosis may allow trans-retinal retrograde
flow of venous blood from the eye and prevent the development of retinal
ischemia.
• Visual acuity may improve as a result of the reduction or resolution of
macular edema and/or maintenance of retinal perfusion.
• CRA have been created surgically through a trans-retinal venipuncture
technique m/c laser energy delivered through argon or Nd-YAG systems, is
directed directly at a branch retinal vein to rupture the posterior vein wall and
Bruch’s membrane.
• In successful cases, the treated site along the vein demonstrates a retinal
vessel diving into the choroid with dilation of the proximal portion and
narrowing of the distal portion of the treated vessel.
• Successful CRA creation is reported in 10–54% of perfused CVO with
subsequent conversion to ischemic CVO in 0–8% of eyes
• Complications
– immediate- intraretinal, subretinal or vitreous hemorrhage.
– Long-term complications-nonclearing vitreous hemorrhage, epiretinal avascular
proliferation, fibrovascular proliferation, secondary neovascularization (choroidal,
retinal, choroidovitreal, anterior segment), and traction retinal detachment.
• Visual recovery may be limited in spite of successful anastomosis creation d/t
thrombosis of the treated vein with progressive retinal ischemia and
development of macular pigment abnormalities related to resolution of
chronic macular edema.
• Because of an increased risk of fibrovascular complications in eyes with a
nonperfused CVO, laser chorioretinal anastomosis is not a recommended
treatment option in these eyes.
 SURGICAL OPTIONS
1) Pars plana vitrectomy
2) Radial optic neurotomy
3) Tissue plasminogen activator(intavitreal/endovascular)
4) Corticosteroid therapy(intravitreal)
 1)Pars plana vitrectomy
• to alter the natural course of the disease.
• Eyes with nonclearing vitreous hemorrhage from secondary retinal
neovascularization
• At the time of vitrectomy clearing of the hemorrhage can be combined with
removal of epiretinal membranes and removal of fibrovascular proliferations
• Although this technique may prevent or aid in regression of anterior segment
neovascularization, visual outcomes may be limited due to the extent of
underlying retinal nonperfusion.
 2)Radial optic neurotomy

• proposed combining pars plana vitrectomy with transvitreal incision of the

nasal scleral ring to release pressure on the central retinal vein at the level of
the scleral outlet.
• The procedure addresses the “compartment syndrome” that may exist in
these eyes where the central retinal
• artery, central retinal vein and optic nerve traverse through a 1.5 mm
diameter area.
• RON is performed by pars plana vitrectomy followed by use of a 20-gauge
microvitreoretinal (MVR) blade to incise the lamina cribrosa and adjacent
retina.
 3)Tissue plasminogen activator
rTPA
• PLASMINOGEN PLASMIN Destabilises the clot
• Reduction in clot size may facilitate dislodging of the entire thrombus or
recanalization of the occluded retinal vein.
• administered by several routes:
– systemic-
– intravitreal, a mean improvement
of five lines of acuity
– endovascular cannulation in 42% of individuals
of retinal vessels.
• Administration of r-tPA did not significantly alter final perfusion status,
especially in pre-treatment ischemic eyes.
• Endovascular delivery of r-tPA - cannulation of retinal vessels via
neuroradiologic / vitreoretinal approach, and delivery of minute quantities of r-
tPA directly to the occluded vessel.
 4)Corticosteroid therapy
• to improve visual acuity by reducing macular edema.
• MOA in modulating retinal edema -unknown,
• anti-inflammatory effects modulation of cytokine and GF production stabilization of the
blood–retinal barrier reduction in vascular permeability HYPOYHESIS
• efficacy of oral corticosteroids to treat macular edema from CVO- unknown
• Intravitreal delivery of corticosteroids provides targeted delivery of the drug to
the retinal vessels and macular tissue while limiting potential systemic
toxicity.
• An i/v sustained release fluocinolone acetonide device (Retisert, Bausch and
Lomb) is being implanted, via a pars plana incision- in clinical trials.
• I/v inj of TA to treat macular edema a/w CVO m/p d/t -
reported VA, safe drug, ease administration and low complication
• Potential complications from these intravitreal TA injections include cataract
progression, sterile endophthalmitis, elevated intraocular pressure, and
retinal detachment.
 2)Branch retinal vein occlusion (BRVO)
• M=F
• M/C age grp=60-70
• occurs at a retinal AV intersection- retinal artery crosses a retinal vein
• may rarely occur at a site other than AV crossing- in ocular inflammatory
disease.
• The most common risk factors are systemic HTN, DM, hyperlipidemia,
glaucoma, smoking and age-related atherosclerosis, Antiphospholipid
antibodies, elevated plasma homocysteine levels, and low serum folate levels
• Studies have suggested an increased risk of BRVO in eyes with shorter axial
lengths.
 CLINICAL FEATURES
• almost always of sudden onset.
• presents with blurred vision or a field defect .
• fundus-segmentally distributed intraretinal hemorrhage.
• intraretinal hmg-less marked if occlusion -perfused or and vice versa
• location of the venous block determines the distribution of intraretinal hmg
• venous obstruction-at optic nerve head, 2 quadrants of fundus involved
• venous blockage- peripheral to tributary veins draining the macula, no
macular involvement and no decrease in visual acuity.
• in the chronic phase of the disease, after the intraretinal hemorrhage has
been absorbed, the diagnosis depend on noting a segmental distribution of
retinal vascular abnormalities - include capillary nonperfusion, dilation of
capillaries, microaneurysms, and collateral vessel formation.
 PATHOGENESIS
• Few studies shows that venous obstruction
A. Histopathologically, the retinal artery and
vein share a common adventitial sheath, in
some cases, a common media -lumen of elevation of venous pressure that
vein compress = 33% at the crossing site. may overload the collateral
B. vitreous - role in compression of susceptible drainage capacity and lead to
macular edema and ischemia
av crossing sites as eyes with decreased AL
and higher chance of vitreomacular
attachment at the av crossing are at
increased risk of BRVO.
Unrelieved venous pressure
C. turbulent blood flow at crossing site causes result in rupture of the vein wall
focal swelling of endothelium- leading to with intraretinal hemorrhage
venous obstruction.
D. actual venous thrombus formation at the
point of occlusion.
 DIFFERENTIAL DIAGNOSIS
Differentials Differentiating feature

DIABETIC RETINOPATHY DM-b/l involve all 4 quadrants.

BRVO-- u/l (few exception).
--hemorrhages involve only the sector of retina that is drained by
the occluded vein.

HYPERTENSIVE HTN- b/l narrowed retinal arterioles and hemorrhages that involve the
RETINOPATHY entire fundus.

RADIATION RETINOPATHY H/O of radiation present.

Like BRVO disk swelling, disk hemorrhages, retinal
neovascularization,
and cotton-wool spots present
 MEDICAL TREATMENT
prevention

• Anticoagulant therapy not recommended as no benefit in management

• systemic administration of anticoagulants can be associated with systemic

• complications
and
• anticoagulants( in theory) increase the severity of intraretinal hemorrhage
occurring in the acute phase of disease
• Treatment of BRVO has focused on management of vision-limiting complications.
 Grid pattern photocoagulation
• typically delayed for at least 3 months after the
development of a BRVO to allow for spontaneous
resolution of edema and intraretinal blood.
• Treatment may be considered in patients with a visual
acuity of 20/40 or worse in the absence of capillary
nonperfusion.
 Scatter Laser Photocoagulation
• study concluded that treatment should be reserved until
after the development of retinal neovascularization
 Other T/t modalities
• Conventional Pars Plana Vitrectomy for Complications of
BRVO
• Arteriovenous Adventitial Sheathotomy
• Intraocular Corticosteroids
• Isovolemic Hemodilution-BRVO has been reported to be
associated with hyperviscosity
• Antivascular Endothelial Growth Factor(Anti-VEGF)
 STUDIES
• CVOS
Study Type :Interventional (Clinical Trial)
Allocation :Randomized
Primary Purpose: Treatment
Study Start Date :August 1988
Actual Study Completion Date :February 1994
 1 STUDY=3 QUESTIONS
Q1. Does early panretinal
photocoagulation prevent
anterior segment Q2.Is early panretinal photocoagulation
neovascularization (PRP) more effective than delaying
in eyes with nonperfused CVO? treatment until anterior segment
neovascularization is first seen
Q3. Does macular grid pattern in preventing neovascular glaucoma in
laser photocoagulation improve eyes with nonperfused CVO?
visual acuity in eyes with vision
loss from macular edema?
Eligible patients were divided into four groups:

Group N: Eyes with extensive retinal ischemia (at least 10 disc areas of
nonperfusion) were randomly assigned to receive panretinal photocoagulation
or nontreatment unless iris neovascularization developed.
Group M: Eyes with visual loss ascribable to macular edema were randomly
assigned to receive grid-pattern photocoagulation or nontreatment.
Group P: Eyes with relatively perfused retinas were followed to provide
information about the natural history of the disease.
Group I: Indeterminate eyes in which the retina could not be visualized
accurately because of hemorrhage were followed in a natural history study.

Green argon laser with a slit lamp delivery system was used for all treatments.
 rESULt ShoweD...
• Panretinal photocoagulation should be delivered promptly after
the development of INV/ANV, not prophylactically in eyes with
nonperfused CVO.
• At 36 months, there was no significant difference in mean visual
acuity between treated (20/200) and untreated (20/160) eyes.
Therefore, the CVOS did not recommend grid laser
photocoagulation for CVO-associated macular edema.
• Overall, 34% of initially perfused eyes converted to nonperfused
status after 3 years.
• Eyes (83%) with an indeterminate CVO at baseline were
ultimately determined to be nonperfused.
THANK YOU