This presentation was made from Ryan's Retina 6th edition; going through this presentation will more or less cover your entire Vein Occlusions topic. I have tried to cover all the recent Trials in vein occlusion and recent DNB exam questions.

1. Retinal vein occlusion
Dr.Piyushi Sao
Ophthalmology Resident
Shri BM PATIL MEDICAL COLLEGE , BLDE UNIVERSITY, VIJAYAPURA
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2. Branch retinal vein occlusion
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3. Introduction
• BRVO is a common cause of retinal vascular disease
• RISK FACTORS:
• HYPERTENSION
• AGE (60-70 YR)
• MEN=FEMALE
• PATHOLOGY: interruption of venous flow
• At retinal arteriovenous intersection
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4. Risk factors
• systemic hypertension : retinal arteriolar changes - arteriovenous
nicking and retinal arteriolar narrowing
• Cardiovascular RISK FACTOR:
• diabetes,
• smoking,
• hyperlipidemia,
• atrial fibrillation,
• renal dysfunction, and
• atherosclerosis
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5. Risk factors
• hypercoagulability
• increased prevalence of Factor V Leiden mutation in patients with
RVO
• hyperhomocysteinemia and
• anticardiolipin antibodies
• elevated plasma homocysteine and lower serum folate
• higher serum levels of high-density lipoprotein and light to moderate
alcohol consumption may be protective 1
• Oral contraceptive pills
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6. OCULAR RISK FACTOR
• shorter axial length
• history of glaucoma
• Retinal and systemic vasculitides
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7. PATHOGENESIS
The pathologic
interruption of venous
flow in eyes with BRVO
almost always occurs at an
arteriovenous crossing.
Artery crosses over the
obstructed vein.
This observation coupled
with the strong
association of BRVO with
systemic hypertension and
arteriosclerosis support
the theory that
mechanical compression
plays a role in the
pathogenesis of BRVO
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8. PATHOGENESIS
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9. Acute branch retinal vein occlusion
Intraretinal hemorrhages in a
wedge-shaped pattern
delineating the area drained
by the occluded vein. The
occluded vessel is often seen
passing underneath a retinal
artery (arrowhead).
Cotton-wool spots
dilated and tortuous
occluded vein (arrow)
compared to the normal
retinal vein in the inferior
arcade.
9
PATHOGENESIS
DR. PIYUSHI SAO

10. PATHOGENESIS
• Histopathologically, the retinal artery and vein share a common
adventitial sheath, and in some cases, a common medium
• The lumen of the vein may be compressed up to 33% at a normal
arteriovenous crossing site
• this may be further exacerbated by increased rigidity and thickening
of the arterial wall due to Arteriosclerosis
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11. PATHOGENESIS
vitreous may also play a role in compression of susceptible
arteriovenous crossing sites
eyes with decreased axial length
• And
higher likelihood of vitreomacular
attachment at the arteriovenous crossing
are at increased risk of BRVO
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12. PATHOGENESIS
turbulent blood
flow at the crossing
site
focal swelling
of the
endothelium
thicker vein
wall tissue
venous
obstruction
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13. PATHOGENESIS
• venous thrombus formation at the
point of occlusion- primary pathologic
event
• pathogenesis of BRVO is multifactorial
mechanical
obstruction
degeneration
of the vessel
wall
hematologic
abnormalities
inflammatory
disorders and
thrombophilia
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14. PATHOGENESIS
The resulting
venous obstruction
leads to
elevation of
venous pressure
upstream of the
crossing
overload the
collateral drainage
capacity
intraretinal
hemorrhages,
macular edema,
ischemia
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15. CLINICAL FEATURES
Symptoms
1. Patients with BRVO present with sudden painless loss of vision or a
visual field defect.
2. Subclinical presentations may occur if a tributary distal to the
macula or a nasal retinal vein is involved.
3. Rarely, patients with BRVO will present with floaters from a vitreous
hemorrhage if the initial vein occlusion was unrecognized and
retinal neovascularization has occurred.
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16. Signs
•wedge-shaped distribution of
intraretinal hemorrhage
• less marked if the occlusion is
perfused (or nonischemic),
• and more extensive if the occlusion
is nonperfused (or ischemic)
and associated with retinal capillary
nonperfusion.
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17. Signs
• The Branch Vein Occlusion Study Group (BVOS) defined ischemic
BRVO “as those with greater than a total of five disc diameters of
nonperfusion on fluorescein angiography (FA)”.
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18. Signs
• The location of the venous blockage 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
whereas if the occlusion
is peripheral to the disc,
• one quadrant or less
may be involved
If the venous blockage is
peripheral to tributary
veins draining the macula
• there may be no
macular involvement
and consequently
minimal to no decrease
in visual acuity
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19. Signs
• The most common location for BRVOs is in the superotemporal
quadrant.
• This favored location may be attributed to a larger number of
arteriovenous crossings in the superotemporal quadrant.
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20. Sequelae
• a patient may present initially with very little intraretinal hemorrhage,
which then becomes more extensive in the succeeding weeks to
months.
• Here an incomplete block at the arteriovenous crossing has
progressed to more complete occlusion
• Over time the intraretinal hemorrhage may completely resorb.
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21. • In the chronic phase of the disease, after intraretinal hemorrhage
absorption, the diagnosis may depend on
• detecting a segmental distribution of retinal vascular abnormalities
like
• capillary nonperfusion,
• dilation of capillaries,
• microaneurysms,
• telangiectatic vessels, and
• collateral vessel formation
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22. Inferotemporal branch retinal vein occlusion. (A) Acute – flame-shaped
and blot haemorrhages, cotton wool spots and venous tortuosity 22DR. PIYUSHI SAO

23. 6 months later – venous sheathing, a few exudates and residual
haemorrhages, with collaterals at the temporal macular edge 23DR. PIYUSHI SAO

24. early FA image of
the acute
occlusion
principally showing
capillary non-
perfusion with
some blockage by
blood
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25. later image clearly
demonstrates vessel
wall staining,
pruning and non-
perfusion
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26. FA of chronic BRVO
shows capillary non-
perfusion, with
tortuous superior–
inferior collaterals
temporally
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27. Complications
There are three common vision-limiting complications of BRVO:
(1) macular edema;
(2) macular ischemia; and
(3) sequelae of neovascularization.
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28. During the acute phase,
extensive intraretinal
hemorrhages may block the
view of macular ischemia
and leakage on the FA.
impossible to evaluate the
perfusion status
hemorrhage itself blocks
the view of the vasculature.
the hemorrhage in the
foveal center may reduce
visual acuity independently
of any macular edema or
ischemia
this reduction in visual
acuity may completely
recover if there is no other
cause for the visual loss
observation in these cases
can be considered
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29. Complications:
Ischaemia
iris
neovascula
rization
traction
retinal
detachme
nt
Vitreous
hemorrhag
e
Retinal
neovascula
rization
macular
ischemia
macular
capillary
nonperfusi
on
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30. NATURAL HISTORY OF BRVO
• visual acuity generally improved without treatment
• although improvement beyond 20/40 was uncommon.
• Macular edema developed in 5–15% of eyes over a period of 1 year
• those presenting with macular edema, 18–41% resolved by 1 year
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31. Chronic branch retinal vein occlusion.
(A) Color fundus photograph showing microaneurysms, exudates, and a sclerosed retinal vein (arrowhead) draining into
a sheathed vessel (arrow).
sclerosed retinal vein
sheathed vessel
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32. Corresponding mid- to late-phase fluorescein angiogram shows abundant collaterals (arrowhead) and highlights the
microvascular abnormalities
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33. Neovascularization
• Retinal neovascularization occurs in 8% eyes by 3 years
• Higher risk in eyes with more than 4 disk diameter of non perfusion
area on FA (more than 1/3rd of eye involved)
• NVE is more common than NVD
• NVE develops at border of ischaemic retina drained by occluded vein.
• Secondary to neovascularization: recurrent vitreous hemorrhage
preretinal haemorrhage, and occasionally tractional retinal
detachment.
• Thus, eyes with ischemic BRVO may need to be followed more closely.
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34. Central Retinal Vein Occlusion
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35. INTRODUCTION
• Central retinal vein occlusion (CRVO) is a retinal vascular condition
that may cause significant ocular morbidity.
• It commonly affects men and women equally
• Occurs predominantly in persons over the age of 65 years.
• In this population, there may be associated systemic vascular disease,
including hypertension and diabetes.
• Younger individuals who present with a clinical picture of CRVO may
have an underlying hypercoagulable or inflammatory etiology
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36. Clinical Features
CRVO usually presents with sudden painless loss
of vision
but it may also present with a history of
gradual visual decline
intraretinal hemorrhages (both
superficial flame-shaped and
deep blot type) in all four
quadrants of the fundus
hemorrhages radiate from the
optic nerve head
dilated, tortuous
retinal venous
system
“blood and
thunder”
appearance36DR. PIYUSHI SAO

37. Fundus photograph of a central retinal vein occlusion with extensive intraretinal hemorrhage. Extensive blocking on fluorescein
angiography precludes accurate determination of perfusion status.
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38. Clinical Features
• Optic nerve head swelling,
• splinter hemorrhages,
• cotton-wool spots, and
• macular edema (ME) are present to varying degrees
• Breakthrough vitreous hemorrhage may also be observed.
38DR. PIYUSHI SAO

39. Fundus photograph of a central retinal vein occlusion demonstrating typical
features of venous tortuosity, macular thickening, and intraretinal hemorrhage
in all four quadrants of the fundus. 39DR. PIYUSHI SAO

40. Early-phase angiogram of the fundus depicted in (A), demonstrating an intact
parafoveal capillary network in this perfused central retinal vein occlusion.40DR. PIYUSHI SAO

41. Clinical Features
• A cilioretinal artery occlusion rarely occurs in association with CRVO.
• Rarely, a central retinal arterial occlusion may also accompany a CRVO
whose perfusion
pressure is lower
than the central
retinal artery
inducing relative
occlusion of the
cilioretinal artery
Sudden increase in
the intraluminal
capillary pressure
due to CRVO
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42. Fundus photograph of an eye with central retinal vein occlusion demonstrating scattered
intraretinal hemorrhage, venous engorgement, and cotton-wool spots.
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43. Midphase fluorescein angiogram of the eye shown in (A), demonstrating capillary nonperfusion
involving the foveal center. This eye also had extensive peripheral nonperfusion and is an example
of the nonperfused form of central retinal vein occlusion. 43DR. PIYUSHI SAO

44. Natural History
• With time, the extent of intraretinal hemorrhage may decrease or
resolve completely with variable degrees of secondary retinal
pigment epithelium alterations.
• The time course for resolution of the hemorrhages varies and is
dependent on the amount of hemorrhage produced by the occlusion.
• In the natural history of CRVO, ME often chronically persists despite
resolution of intraretinal hemorrhage.
• An epiretinal membrane and foveal pigmentary alterations may
develop.
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45. Fluorescein angiogram of a chronic central retinal vein occlusion with resolution of intraretinal
hemorrhage but persistence of cystoid macular edema demonstrated by petaloid leakage
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46. 46DR. PIYUSHI SAO

47. • Optociliary “shunt” vessels can form on the optic nerve head, a sign
of newly formed collateral channels with the choroidal circulation .
Fundus photograph demonstrating
optociliary shunt vessels (aka
collaterals) at the inferior border of the
optic nerve head in this patient with a
chronic central retinal vein occlusion.
These vessels do not leak on
fluorescein angiography. 47DR. PIYUSHI SAO

48. Paracentral Acute Middle Maculopathy
• Paracentral acute middle maculopathy (PAMM) refers to acute
ischemic events that affect the deep macular capillary layers.
• It is best visualized as hyperreflective bands on SD-OCT.
• There are 2 variants:
• type 1 affects the superficial capillary plexus in the outer plexiform layer
(OPL)/inner nuclear layer (INL) region, and
• type 2 affects the deep capillary plexus in the OPL/outer nuclear layer (ONL)
region. Visual consequences vary; upon resolution,
• type 1 lesions produce INL thinning, and
• type 2 lesions cause disturbance of the ellipsoid or inner segment and outer
segment line.
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49. Neovascularization of the optic disc (NVD) or retinal
neovascularization elsewhere (NVE) may develop as a response to
secondary retinal ischemia.
The vessels that comprise NVD are typically of
smaller caliber than optociliary shunt vessels
Fibrovascular
proliferation from NV may
result in
vitreous
hemorrhage
branch into a vascular
network resembling a
net, and leak on
fluorescein angiography
traction retinal
detachment
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50. Anterior segment findings
• Iris and/or angle neovascularization (NVI/NVA).
• NVI typically begins at the pupillary border but may extend across the
iris surface.
• NVA is detected during undilated gonioscopy as fine branching
vessels bridging the scleral spur and may develop without any NVI in
6–12% of eyes with ischemic CRVO
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51. Rubeosis iridis at the pupillary border
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52. neovascularization of an open angle
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53. Anterior segment findings
• Longstanding NVA may lead to secondary angle closure from
peripheral anterior synechiae formation.
• Elevated intraocular pressure associated with NVI/NVA is the hallmark
of neovascular glaucoma.
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54. PERFUSION STATUS
• The CVOS classified the perfusion status of a CRVO as
• perfused,
• nonperfused, or
• indeterminate
based on fluorescein angiographic characteristics.
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55. • A Perfused CRVO (aka nonischemic, incomplete, or partial) demonstrates
<10 disc areas of retinal capillary nonperfusion on angiography
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56. Perfused CRVO
• These eyes typically have a lesser degree of intraretinal hemorrhage
on presentation.
• Generally, eyes with perfused CRVO have better initial and final visual
acuity.
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57. • A Nonperfused CRVO (aka ischemic, hemorrhagic, or complete)
demonstrates ≥10 disc areas of retinal capillary nonperfusion on
angiography
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58. Nonperfused CRVO
• Acutely, these eyes often demonstrate a greater degree of
intraretinal hemorrhage, macular and disc edema, and capillary
nonperfusion than eyes with perfused CRVO.
• risk for ocular neovascularization is much greater in ischemic than in
perfused CRVO and greatest within the first 6 months of onset.
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59. Indeterminate CRVO
• A CRVO is categorized as indeterminate when there is sufficient
intraretinal hemorrhage to prevent angiographic determination of the
perfusion status.
• Other examination features that may help in determining the
perfusion status include
• baseline visual acuity,
• presence of an afferent pupillary defect,
• electroretinography (a negative waveform may be seen), and
• Goldmann perimetry
59DR. PIYUSHI SAO

60. PATHOGENESIS OF CRVO
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
they are
naturally
compressed
as they cross
through the
rigid sieve-like
openings in
the lamina
cribrosa
compression
from
mechanical
stretching of
the lamina
posterior
bowing of the
lamina and
subsequent
impingement
on the central
retinal vein.
compression
by an
atheroscleroti
central retinal
artery
primary
occlusion of
the central
retinal vein
from
inflammation 60DR. PIYUSHI SAO

61. • Hemodynamic alterations
may produce stagnant flow
and subsequent thrombus
formation in the central
retinal vein
• concurrent retinal artery
insufficiency or occlusion may
play a role in an ischemic
CRVO
altered
lumen
wall
Endothel
ial injury
(Virchow
triad)
increase
d blood
viscosity,
61DR. PIYUSHI SAO

62. • In acute occlusions, a thrombus at the level of the lamina cribrosa
was adherent to a portion of the vein wall devoid of an endothelial
lining.
• there was endothelial cell proliferation within the vein and secondary
inflammatory cell infiltrates.
• Recanalization of the thrombus was demonstrated in eyes 1–5 years
after the documented occlusion.
• intraretinal vascular endothelial growth factor (VEGF) production
occurs from areas of ischemic retina.
• Intraocular VEGF levels correlate with severity of ocular findings
62DR. PIYUSHI SAO

63. 63DR. PIYUSHI SAO

64. Hemiretinal vein occlusion
• A hemispheric occlusion blocks a major branch Of the CRV at or
near the optic disc.
• The less common hemicentral occlusion involves onetrunk of a
dual-trunked CRV that has persisted in the anterior part
of the optic nerve head as a congenital variant.
• Symptoms. A sudden onset altitudinal visual field defect
64DR. PIYUSHI SAO

65. 65DR. PIYUSHI SAO

66. 66DR. PIYUSHI SAO

67. CLINICAL EVALUATION
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68. CLINICAL EVALUATION
• Complete ophthalmic examination should be performed
• history of glaucoma
• signs of intraocular inflammation
• examination of the iris and angle
• early signs of rubeosis or
• neovascular glaucoma
68DR. PIYUSHI SAO

69. Fluorescein Angiography:BRVO
• FA should be obtained to delineate the retinal vascular
characteristics:
• macular leakage and edema,
• macular ischemia, and
• large segments of capillary nonperfusion
• neovascularization
• capillary abnormalities in BRVO
69DR. PIYUSHI SAO

70. Characteristic finding on FA :BRVO
• delayed filling of the occluded retinal vein.
• Varying amounts of capillary nonperfusion,
• blockage from intraretinal hemorrhages,
• microaneurysms,
• telangiectatic collateral vessels, and
• dye extravasation from macular edema or
• retinal neovascularization
70DR. PIYUSHI SAO

71. • Fluorescein angiogram of
branch retinal vein occlusion.
(A) Blocked fluorescence
from intraretinal hemorrhage
is common in acute branch
retinal vein occlusion.
• Note the telangiectatic
vessels forming collaterals
across the horizontal raphe.
• The hemorrhages obscure
underlying areas of capillary
nonperfusion and edema.
71DR. PIYUSHI SAO

72. • Six months later, the
hemorrhages have
cleared, revealing small
patches of nonperfusion
and macular edema.
72DR. PIYUSHI SAO

73. Wide-Field
Angiography
• To delineate areas of
peripheral nonperfusion and
help categorize a patient
based on perfusion status.
73DR. PIYUSHI SAO

74. OCT B-scans
• The characteristic findings of BRVO on are
• cystoid macular edema, intraretinal hyperreflectivity from
hemorrhages or exudates, shadowing from edema and hemorrhages,
and occasionally subretinal fluid
74DR. PIYUSHI SAO

75. • Macular edema can be detected by optical coherence tomography
(OCT).
• The presence of
• intraretinal fluid,
• subretinal fluid, or
• cystoid macular edema
• is visible on OCT
• retinal thickness maps can reveal areas of localized increased retinal
thickening.
75DR. PIYUSHI SAO

76. ERG
• Differentiate ischaemic from non ischaemic CRVO
• Ischaemic CRVO: reduced b wave amplitude
• Reduced b:a ratio
• Prolonged b wave implicit time
76DR. PIYUSHI SAO

77. Young Patient Workup
• Younger patients with BRVO may have a higher prevalence of
cardiovascular risk factors than their age-matched counterparts,
including
• hypertension,
• hyperlipidemia, and an
• increased body mass index
• higher risk of thrombophilic disorders, such as Factor V Leiden
mutation
77DR. PIYUSHI SAO

78. Young Patient Workup
• In young patients without cardiovascular risk factors or with systemic
symptoms suggestive of a coagulopathy, workup should include
• complete blood count,
• prothrombin time/ partial thromboplastin time/international normalized ratio,
• lipid panel,
• serum homocysteine,
• anticardiolipin antibodies,
• antinuclear antibodies with lupus anticoagulant,
• protein C/S,
• antithrombin III,
• activated protein C resistance, and
• factor V Leiden
78DR. PIYUSHI SAO

79. In bilateral cases and cases with a history of multiple BRVOs
• infectious or
• inflammatory disorder or
• hypercoagulopathy
• systemic hypertension
79DR. PIYUSHI SAO

80. Treatment of Underlying Etiology
• Systemic Anticoagulation
• In cases where a hypercoagulopathy has been identified,
anticoagulation may be considered in consultation
• systemic administration of anticoagulants can be associated with
systemic complications, and could, in theory, increase the severity of
intraretinal hemorrhage occurring in the acute phase
80DR. PIYUSHI SAO

81. Vitrectomy With Sheathotomy
• The majority of the venous lesions in BRVO occur downstream
from the arteriovenous crossing site.
• Removal of the compressive factor by sectioning the adventitial
sheath (sheathotomy)
• significant visual improvement
• gain of four lines of vision
• marked resolution of the intraretinal hemorrhage and edema
81DR. PIYUSHI SAO

82. • removal of the internal limiting
membrane in the area of the
arteriovenous crossing
• unable to separate the artery from the
vein
82DR. PIYUSHI SAO

83. • complications of the
procedure:
• including retinal tear,
• retinal detachment,
• vascular bleeding,
• nerve fiber layer defects with
associated scotoma
• vitreous hemorrhage, and
• postoperative cataract,
• vitrectomy with sheathotomy
is currently not employed as
first-line therapy.
83DR. PIYUSHI SAO

84. Treatment of Vision-Limiting Complications
Treatment of Neovascularization and
Vitreous Hemorrhage
• BRVO to receive Panretinal Scatter
Photocoagulation to prevent
neovascular complications
• photocoagulation be applied only
after neovascularization is observed.
84DR. PIYUSHI SAO

85. • Fluorescein Angiography
to differentiate
• leakage from
neovascularization is more
prominent than from
collateral vessels.
85DR. PIYUSHI SAO

86. peripheral scatter laser photocoagulation
86
• can reduce the likelihood of vitreous
hemorrhage from about 60% to 30%
• scatter laser photocoagulation can be
applied with argon blue–green laser to
achieve “medium” white burns (200–
500 µm in diameter)
• spaced one burn width apart
• covering the entire area of capillary
nonperfusion
• extending no closer than two disc
diameters from the center of the fovea
• extending peripherally at least to the
equator
DR. PIYUSHI SAO

87. • laser energy will be absorbed
by the intraretinal hemorrhage
rather than at the level of the
pigment epithelium
• damaging the nerve fiber layer
• development of preretinal
fibrosis.
laser
photocoagulation
should never be
placed over extensive
intraretinal
hemorrhage in the
acute phase of branch
vein occlusion
87DR. PIYUSHI SAO

88. vitreous hemorrhage
• Of patients who develop neovascularization, approximately 60%
experience episodes of vitreous hemorrhage if the condition is left
untreated.
• a pars plana vitrectomy with sector endolaser photocoagulation
• may clear spontaneously without causing permanent visual
impairment
• When the hemorrhage is dense, B-scan ultrasonography may help
rule out an associated traction retinal detachment
88DR. PIYUSHI SAO

89. Treatment of Macular Edema
Laser Treatment
89
Grid macular laser for macular edema. (A)
Fluorescein angiogram, late phase, demonstrating
macular edema with foveal involvement.
DR. PIYUSHI SAO

90. • Argon laser photocoagulation was
applied in a grid pattern throughout
the leaking area demonstrated by FA
• Laser treatment extended no closer
to the fovea than the edge of the
capillary free zone and no further into
the periphery than the major vascular
arcade
90
(B) Immediate posttreatment fundus
photograph showing grid pattern of laser
photocoagulation.
DR. PIYUSHI SAO

91. • Before laser photocoagulation is
performed, it is important to obtain
high-quality FAs of the macula
• FA must demonstrate that the
macular edema involves the center
of the fovea and that there is not a
large amount of capillary
nonperfusion adjacent to the
capillary-free zone that could
explain the visual loss.
91DR. PIYUSHI SAO

92. • grid pattern photocoagulation is that it results in a thinning of the
retina (in particular the outer retina),
• reducing oxygen consumption and increasing choroidal delivery of
oxygen to the inner retina,
• producing a consequent autoregulatory constriction of the retinal
vasculature in the leaking area and thereby decreasing the edema.
92DR. PIYUSHI SAO

93. grid photocoagulation:
• laser absorption occurs at the level of the pigment epithelium
• photocoagulation is not applied to close the leaking and dilated
capillary vasculature directly and immediately.
93DR. PIYUSHI SAO

94. Steroid Treatment
• Macular edema in BRVO results from increased vascular permeability
mediated at least in part by upregulation of VEGF.
• Intravitreal steroids have been shown in animal models to inhibit the
expression of VEGF and thus reduce macular edema in retinal
vascular disease
94DR. PIYUSHI SAO

95. Triamcinolone. (SCORE) BRVO study
• In the Standard Care vs. Corticosteroid for Retinal Vein Occlusion
(SCORE) BRVO study, the effectiveness and safety of intravitreal
triamcinolone acetate (IVTA) for the treatment of macular edema
from BRVO were evaluated
• In this multicenter, randomized controlled study, 411 patients were
randomized to receive macular grid laser, 1 mg IVTA, or 4 mg IVTA.
• Three-year results from 128 patients suggested that the laser group
maintained a significantly greater average increase in vision (12.9
letters) compared with the two IVTA groups (4.4 letters, 1-mg and 8.0
letters, 4-mg).
95DR. PIYUSHI SAO

96. Dexamethasone Implant.
• The Global Evaluation of Implantable
Dexamethasone in Retinal Vein
Occlusion with Macular Edema
(GENEVA) study evaluated a
sustained-release, biodegradable,
dexamethasone intravitreal implant
(Ozurdex, Allergan, Irvine, CA) for the
treatment of macular edema in
central retinal vein occlusion (CRVO)
and BRVO patients.
96DR. PIYUSHI SAO

97. Dexamethasone Implant
• The only complications that were significantly greater in the Ozurdex
groups compared with sham were elevated IOP and anterior-chamber
cell
• no increase in the risk of serious adverse effects, including IOP rise,
with a second treatment;
• significant increase in the development of cataract with repeated
injection
• The GENEVA study showed that the dexamethasone implant is an
alternative treatment to macular grid laser in the appropriate patient
population (i.e., no glaucoma, pseudophakic) and is approved by the
Food and Drug Administration (FDA) for this indication.
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98. Posurdex dexamethasone implant
• In the study, 172 patients with diabetic macular edema, 103 patients with branch retinal vein
occlusion or central retinal vein occlusion, 27 patients with Irvine-Glass syndrome and 14 patients
with uveitic macular edema were randomized to one of two dosages of the Posurdex
dexamethasone implant.
• The implants were inserted directly into the posterior segment.
• They continuously released dexamethasone for 35 days before biodegrading in the eye.
• Improvement in macular edema was marked by significant decreases
in retinal thickness and fluorescein leakage
• visual acuity improvement
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99. Anti-VEGF Treatment
• In patients with BRVO, retinal ischemia leads to the secretion of VEGF,
which leads to increased vascular permeability, vasodilation,
migration of endothelial cells, and neovascularization.
• Increased vascular permeability and perhaps vasodilation lead to
retinal edema.
• Thus, inhibition of VEGF is an attractive treatment for macular edema
from BRVO.
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100. Anti-VEGF Treatment
• Ranibizumab (lucentis) : branch retinal vein occlusion (BRAVO) study
To evaluate the efficacy and safety of ranibizumab in the treatment of macular edema from BRVO
Central retinal vein occlusion (CRUISE) trial prospectively compared monthly intravitreal injections
of 0.3 mg or 0.5 mg ranibizumab to sham-injected controls in the treatment of 392 patients with
CRVO and ME
• Aflibercept (eylea): VIBRANT study
Aflibercept Two double-masked, randomized, prospective phase III trials named COPERNICUS and
GALILEO were carried out to investigate intravitreal aflibercept for CRVO-associated ME
• Bevacizumab (avastin): MARVEL study
SCORE2 trial is currently evaluating whether bevacizumab is noninferior to aflibercept
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101. Anti-VEGF Treatment
• Ranibizumab is an affinity-matured, humanized
monoclonal antibody fragment (Fab) that binds
all VEGF-A isoforms
• Aflibercept is a fusion protein composed of key
binding domains from VEGF receptors 1 and 2
fused to the Fc portion of human
immunoglobulin G that binds all isoforms of
VEGF-A, VEGF-B, VEGF-C, and placental growth
factor (PlGF).
• Bevacizumab is a full-length, humanized
monoclonal antibody that binds all VEGF-A
isoforms and is FDA-approved for colorectal
cancer, but is used off-label in the eye.
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102. 102
Anti-VEGF Treatment
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103. Pegaptanib
• Pegaptanib (Macugen) is currently the
third FDA-approved intravitreal anti-VEGF
agent, which received approval for the
treatment of neovascular age-related
macular degeneration, but not for CRVO.
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104. Neovascularization During Anti-VEGF Therapy
• While anti-VEGF treatment alters the natural history of CRVO,
neovascular events are reduced but not eliminated.
• Even under clinical study conditions among CRUISE, COPERNICUS,
and GALILEO patients, neovascularization occurred
• Brown and coworkers : neovascular complications during concurrent
treatment with ranibizumab after a mean follow-up of 24 months
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105. Definitive Treatment of Ocular
Neovascularization
Laser Photocoagulation
Persons presenting with NVD/NVE without NVI/NVA should be treated with PRP, as
performed in eyes with proliferative diabetic retinopathy or branch retinal vein
occlusion, to prevent anterior segment neovascularization
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106. Medical Therapy
• Topical or systemic antiglaucoma agents may be required to reduce
elevated intraocular pressure due to NVA.
• 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.
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107. Treatment of Systemic Medical Conditions
• Oral pentoxifylline is a vasodilator and enhancer of red blood cell
deformability used in systemic vascular diseases
• 10% mean reduction in macular thickening by volumetric OCT
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108. Alternative Treatments Aimed at Underlying
Etiology
• Chorioretinal Venous Anastomosis
• In eyes with perfused CRVO, investigators have bypassed the
occluded central retinal vein by creating a chorioretinal anastomosis
(CRA) between a nasal branch retinal vein and the choroidal
circulation.
• Successful creation of an anastomosis may allow transretinal
retrograde flow of venous blood from the eye and prevent the
development of retinal ischemia or allow reduction of ME.
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109. Chorioretinal Venous Anastomosis
• CRAs have been created through a surgical transretinal venipuncture
technique
• argon or Nd-YAG laser delivery directly at a branch retinal vein to
rupture the posterior vein wall and Bruch’s membrane.
• Visual recovery may be limited in spite of successful anastomosis
creation due to thrombosis of the treated vein with progressive distal
retinal ischemia.
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110. Tissue Plasminogen Activator
• Thrombolytic agents have been proposed as a treatment of a suspected
thrombus in the central retinal vein.
• If a thrombus is indeed etiologic, lysis is recommended within 21 days of its
formation.
• Recombinant tissue plasminogen activator (r-tPA) is a synthetic fibrinolytic
agent that converts plasminogen to plasmin and destabilizes intravascular
thrombi.
• Reduction in clot size may facilitate dislodging of the entire thrombus or
recanalization of the occluded retinal vein.
• Recombinant tissue plasminogen activator has been administered by
several routes: systemic, intravitreal, and by endovascular cannulation of
retinal vessels.
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111. VITRECTOMY
• Eyes with nonclearing vitreous hemorrhage from secondary retinal
neovascularization may benefit from surgical evacuation.
• At the time of vitrectomy, clearing of the hemorrhage can be
combined with removal of epiretinal membranes and removal of
fibrovascular proliferations.
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112. Radial Optic Neurotomy
• Opremcak and colleagues first reported combining vitrectomy with
radial optic neurotomy (RON)
• Involves transvitreal incision of the nasal scleral ring to release
pressure on the central retinal vein at the level of the scleral outlet
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113. Radial Optic Neurotomy
• RON has been associated with significant risks, including
postoperative visual field defects, laceration of central retinal vessels,
globe perforation, choroidal neovascularization, subretinal
hemorrhage, and retinal detachment.
• LIMITED efficacy
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114. Conclusion BRVO
• The BRAVO and VIBRANT trials established that intravitreal anti-VEGF
therapy results in better visual and anatomical outcomes than
macular grid laser, which had been the standard of care for macular
edema associated with BRVO for over 25 years
• several studies showing similar efficacy between ranibizumab and
bevacizumab
• SCORE2 is evaluating aflibercept and bevacizumab head to head
• In both the VIBRANT and BRAVO trials, patients received monthly
injections for the first 6 months
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115. Conclusion BRVO
• he SHORE study randomized patients with macular edema from
BRVO to monthly versus PRN ranibizumab after receiving monthly
injections for 7 months.
• Currently, steroid injections are second-line therapy owing to side-
effects including increased IOP and cataract.
• pilot studies suggest that combination therapy may have a synergistic
treatment effect as well as reduce treatment burden.
• combination of intravitreal bevacizumab and dexamethasone
resulted in fewer injections and better anatomic outcomes than
bevacizumab alone
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116. Conclusion BRVO
• Another group found that dexamethasone implant and grid laser
resulted in better anatomic and visual outcomes than dexamethasone
alone
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117. Conclusion : CRVO
• Central Vein Occlusion Study, which recommended observation of
ME and retinal ischemia with management of neovascular sequelae
using PRP.
• In the absence of robust treatment options for CRVO, other
approaches including the
• administration of r-tPA,
• creation of chorioretinal anastomosis, and
• various surgical interventions had been reported with variable
success and often unacceptable side effects
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118. Conclusion : CRVO
• intravitreal corticosteroids and then anti-VEGF agents have
demonstrated improvements in ME, visual acuity, and even
neovascular complications with a favorable side effect profile.
• The use of ranibizumab (Lucentis), aflibercept (Eylea), and a
sustained-release dexamethasone implant (Ozurdex) have been FDA-
approved for the treatment of CRVO.
• Intravitreal pharmacotherapy has now replaced observation as the
standard of care for the management of CRVO.
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119. REFERENCES
1. RYAN’S RETINA ; SIXTH EDITION VOLUME 2
2. Kanski Ophthalmology 8th edition
3. Ophthalmology Clinics for Post Graduates -1 Prafulla
4. Retina, Choroid and Vitreous: DOS TIMES COMPILATION-Krati Gupta
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120. 120DR. PIYUSHI SAO

121. DNB QUESTIONS
• 34. Clinical features, diagnosis and management of retinal vein
occlusions. (2+3+5) D2016
• 35. Management of macular edema following retinal vein occlusion.
(10) D2015
• 36. What is the role of intraocular corticosteroids in retinal vein
occlusions? Discuss the findings of SCORE and Posurdex trial in
venous occlusions. [4+(3+3)] D2013
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122. CRVO
• 37. Etiopathogenesis, clinical features, investigation and management
of central retinal vein occlusion. (2+2+2+4) J2017
• 38. Write down management and complications of ischemic central
retinal vein occlusion. J2009 39. CRVO- Changing trends in
management. (2005)
• 40. Discuss the management of central retinal vein occlusion (CRVO).
(1999)
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123. BRVO
• 41. a) CF of early & late branch vein occlusion b) Results of important
trials in management of BRVO 4+(3+3) J2018
• 42. Describe clinical features, etiology, investigations and various
modalities of management in branch retinal vein occlusion. J2012
• 43. Clinical signs and management of branch vein occlusions. D2010
• 44. Management of branch retinal vein occlusion. D2009,2005
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