Transcript Central Retinal Vein Occlusion (Powerpoint)

CASE V
CENTRAL RETINAL VEIN
OCCLUSION
Patient History; 52yo female
Cc: Colorless, gray spot interfering with
vision, OS. Began this morning, comes and
goes.
Pt reports no loss of vision, or flashing
lights, OU.
Pt being followed by PCP for fatigue,
‘loopiness’. Possible DM. Blood work
ordered.
Examination Results, I
VA- 20/20 OU.
PERRL (-)APD.
Slit Lamp Exam
 Unremarkable.
Dilated Fundus Exam
OD, Unremarkable.
Temporal swelling of optic disc, OS.
Dilated retinal veins, OS.
Mid-peripheral dot and blot hemes, OS.
Fundus View, OD
Fundus View, OS
Symptoms of CRVO
50+ years of age
The patient may be asymptomatic, but often will
complain of sudden painless unilateral loss of
vision and/or visual field
May complain of a sudden onset of floating spots
or flashing lights.
Acuity may range anywhere from 20/20 to finger
counting.
If vision loss is severe, there may be an APD.
Signs
Retinal edema.
Superficial hemorrhages.
Disc swelling.
Cotton wool spots.
Tortuous and dilated retinal veins.
Predisposing Factors
Glaucoma
Papilledema
Optic N. hemorrhage
Optic N. drusen
Vascular disease (DM, HTN)
SLE
Trauma
Leukemia
CRVO and Systemic Disease
Carotid Artery Disease
Antithrombin Deficiency
Hypercholesteremia
Hyperlipidemia
Mitral Valve Prolapse
Hypercoagulopathies
CRVO and Age
Under 50 years
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Head injury.
Hyperlipidemia.
Estrogen preparations.
Over 50 years
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Hypertension.
Hyperlipidemia.
Abnormal glucose tolerance test.
Hyperviscosity syndrome.
Pathophysiology
The exact pathogenesis of the thrombotic
occlusion of the central retinal vein is not
known.
Various local and systemic factors play a
role in the pathological closure of the
central retinal vein.
Pathogenesis of CRVO
CRV/CRA anatomy.
Compression induced changes in the vein;
turbulence, endothelial cell damage,
thrombosis.
Anatomy Review
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.
Arterial Disease and CRVO
Arteriosclerotic changes in the central
retinal artery.
Becomes rigid and impinges upon the
thinner vein, causing hemodynamic
disturbances, endothelial damage, and
thrombus formation.
Expect associated arterial disease with
CRVO. However, this association has not
been proven consistently.
Causes of Thrombotic Occlusion
Compression of the vein (mechanical pressure due
to structural changes in lamina cribrosa,
glaucomatous cupping, inflammatory swelling in
optic nerve, orbital disorders).
Changes in blood (deficiency of thrombolytic
factors, increase in clotting factors).
Hemodynamic disturbances (hyperdynamic or
sluggish circulation); vessel wall changes.
More Pathophysiology…
Occlusion leads to backup of blood in the retinal
venous system and increased resistance to venous
blood flow and stagnation of blood resulting in
ischemia of inner retinal layers.
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.
Ischemic damage to the retina produces
angiogenic factors, stimulates neovascularization.
Neovascularization
Neovascularization will form most typically the
posterior iris.
This can lead to rubeosis irides and neovascular
glaucoma.
Anterior segment neovascularization with
associated neovascular glaucoma develops in more
than 60% of ischemic cases, 20% for nonischemic.
Occurs within a few weeks and up to 1-2 years
afterward.
Ischemic v. Non-ischemic
Primary difference involves presence of
retinal hypoxia of ischemia.
Ischemic characterized by at least 10DD of
retinal capillary non-perfusion.
Determined by fluorescein angiogram.
10 DD Capillary Obliteration
Studies have shown that this may be an invalid
criterion for diagnosis of ischemic CRVO by
fluorescein angiography.
Study results shows that eyes with less than 30
disc diameters of retinal capillary nonperfusion
and no other risk factor are at low risk for
developing iris/angle NV, “whereas eyes with 75
disc diameters or more are at highest risk”.
Normal FA
Non-Ischemic CRVO
Ischemic CRVO
Ischemic v. Non-ischemic
Ischemic CRVO
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Severe.
Usually presents with
severe visual loss
Extensive retinal
hemorrhages and
cotton-wool spots.
(+) APD
Poor perfusion to
retina.
Non-Ischemic CRVO
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Milder.
It may present with
good vision.
Few retinal
hemorrhages and
cotton-wool spots.
(-) APD
Good perfusion to the
retina.
Management, Ischemic
Find underlying cause.
Rule out glaucoma.
Possible use of IOP-lowering agents.
Possible need for anti-coagulation.
Retinal consult, fluorescein angiography.
Follow every 3-4 weeks for 6 months for
development of NVG.
Management, Non-ischemic
Find underlying cause.
Rule out glaucoma.
Possible use of IOP-lowering agents.
Possible need for anti-coagulation.
Retinal consult, fluorescein angiography.
Follow every 4 weeks for 6 months for
conversion to ischemia.
Finding Underlying Cause
Blood pressure and pulse evaluation.
Fasting blood glucose.
Complete blood count with differentials and
platelets.
FTA-ABS
Antinuclear antibodies
Carotid palpitation and auscultation.
Medical Care
No known effective medical treatment is
available for either prevention or the
treatment of CRVO.
Possibilities include; Aspirin, Systemic
anticoagulation with warfarin and heparin,
Fibrinolytic agents, Systemic
corticosteroids, Anti-inflammatory agents,
Isovolumic hemodilution, Plasmapheresis.
Definitions:
Plasmapheresis
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Selective removal of certain proteins or
antibodies from the blood,followed by
reinjection of the blood.
Isovolumic hemodilution
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Removal of certain volume of blood replaced
by same volume of saline.
Surgical Care
Neovascularization: CVOS evaluated the efficacy
of prophylactic PRP in ischemic eyes, in
preventing development of 2 clock hours of iris
neovascularization or any angle
neovascularization.
CVOS concluded that prophylactic PRP did not
prevent the development of iris
neovascularization.
Recommended to wait for the development of
early iris neovascularization and then apply PRP.
Surgical Care, II
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 due to macular edema from CVO.
Surgical Care, III
Chorioretinal venous anastomosis bypasses the
site of venous occlusion in the optic disc, creating
a venous outflow channel to choroidal circulation.
Retinal veins are punctured, either using laser or
by surgery, through the RPE and Bruch’s
membrane into the choroid, developing
anastomotic channels into the choroid.
This reduces macular edema and may improve
vision in non-ischemic CRVO.
Thrombosis Location and
Prognosis
May be relative to risk of ischemia.
Occlusions posterior to lamina may provide
more venous collaterals and improved
perfusion.
Ischemic CRVO Prognosis
More than 90% of patients will have 20/200
or worse vision.
About 60% of patients develop ocular
neovascularization with associated
complications.
About 10% of patients can develop CRVO
or other type of vein occlusions either
within the same eye or fellow eye within 2
years.
Non-Ischemic CRVO Prognosis
Complete recovery with good visual
recovery occurs only in about 10% of cases.
Fifty percent of patients will have 20/200 or
worse vision.
About one third of patients convert to
ischemic CRVO within 3 years; 15%
convert within the first 4 months.
Fellow Eye Studies…
It has been reported that the fellow eye may
develop retinal vein occlusion in about 7%
of cases within 2 years.
The 4-year risk of developing second
venous occlusion is 2.5% in the same eye
and 11.9% in the fellow eye.
Under Investigation
Intravitreal Steroid
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May improve macular edema, visual acuity.
Vitrectomy
Arteriovenous Sheathotomy
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Separate CRA from CRV
Anti-VEGF Antibodies
Under Investigation, II
Radial Optic Neurotomy
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Attempts to decompress pressure at lamina
opening.
Involves an incision through the scleral ring
and cribiform plate.
Fibrotic tissue seems to fill void in early
attempts.
CVOS Summary: Purpose
To determine whether photocoagulation therapy
can help prevent iris neovascularization in eyes
with CVO and evidence of ischemic retina.
To assess whether grid-pattern photocoagulation
therapy will reduce loss of central visual acuity
due to macular edema secondary to CVO.
To develop new data describing the course and
prognosis for eyes with CVO.
CVOS Results
Macular Edema - Macular grid photocoagulation
was effective in reducing angiographic evidence
of macular edema but did not improve visual
acuity.
Indeterminate: Eyes with such extensive
intraretinal hemorrhage that it is not possible to
determine the retinal capillary perfusion status act
as if they are ischemic or nonperfused.
CVOS Results
Non-ischemic CVO - Prophylactic
panretinal photocoagulation did not prevent
the development of iris neovascularization
in eyes with 10 or more disc areas of retinal
capillary nonperfusion. It is safe to wait for
the development of early iris
neovascularization and then apply
panretinal photocoagulation.