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CASE PRESENTATION

Dr Kanav Gupta
29/07/09

1
Mrs Sakunbai Meshram, 45 Year old Female
with H/O…
GPDOV – LE>RE since 1 month

H/O RE Cataract surgery + PCIOL 4 yrs back at Hingna

H/O Redness and eyeache

K/C/O HTN since 15 years under irregular treatment

No H/O ocular trauma / discharge

No H/O spectacles

No H/O any systemic illness

2
Ophthalmic examination

Visual Acuity – RE – 6/60p with pinhole NI


LE – PL+ PR Accurate
SLE
RE LE
Lids WNL Meibomiantis
Conjunctiva WNL Mild congestion, CCC
Cornea Clear Clear
AC ND Slight shallow
Iris CPN Atrophic patch at 7-9o`clock
Pupil NSRTL SD Fixed, posterior synechiae
Lens PCIOL ISC

3
Contd….
Fundus: RE – Media clear LE – No View

O.D : normal margins,circular,slight pale

C:D : 0.3
B.V : mild venous tortuosuty,A.V.
changes present with A.V. ratio of 1:4

Macula : dull with exudates

FR : Not seen
Hemorrhages from 6-9.30 o` clock involving macula

Tonometry: RE – 14.6 mm Hg LE – 46.9mm Hg with 10 gms

Sac Syringing : RE – Patent 4 LE - Patent


SYSTEMIC EXAMINATION
Temperature – Afebrile

BP – 130/80mmHg

Pulse – 80/min

RR – 18/min

7
Lab Investigations
CBC – WNL

Urine R & M – WNL

ECG – T inversion V1-V3

2D ECHO – IHD, Septal Wall hypokinesia, EF-45 – 55%

RBS – 90mg/dl

Conjunctival smear LE – negative

8
TREATMENT
Initially started with - I.V. Mannitol 100cc stat
T.Diamox 250 mg tds
Iotim 0.5% bd in LE

Pressure controlled : added :LE – Predfax E/D Qid


Homide E/D bd

LE cataract surgery

9
Retinal Vein Occlusions
Morphology
CRVO
BRVO
Hemispheric VO
Hemicentral VO
Papillophlebitis
Macular BRVO
CENTRAL RETINAL VEIN
OCCLUSION
Mechanism :

» Conditions producing
a physical blockage
at the level of the
lamina cribrosa.

2. Hemodynamic factors
resulting in an
obstruction to the
flow of blood.

"Blood and thunder" appearance of a central retinal vein occlusion.


CRVO
PATHOLOGY
Histopathologic evaluation of eyes removed
because of a central retinal vein occlusion
demonstrates an occlusion at or just behind the
level of the lamina cribrosa.
At this location, the lumina of the central retinal
artery and central retinal vein are narrower than
they are in the orbital optic nerve, and the
vessels are bound by a common adventitial
sheath.
CRVO ANATOMY
Anatomical Studies
In a study of 29 eyes that were enucleated 6
hours to 10 years after occlusion. It was
hypothesized that the flow of blood through the
central retinal vein becomes increasingly
turbulent as the vein progressively narrows at
the lamina cribrosa, where it also may be further
impinged upon by arteriosclerosis of the
adjacent central retinal artery. This turbulence
damages the endothelium in the retrolaminar
vein, which exposes collagen and initiates
platelet aggregation and thrombosis.
In another study of enucleated eyes with
CVO and NVG, intraretinal VEGF
production from areas of ischemic retina
was demonstrated.
Aqueous VEGF levels increase prior to the
development of NVI and decrease with
regression of NVI after panretinal photo
coagulation
Risk Factors
Increasing Risk : Hypertension (BRVO)
Diabetes Mellitus
Advancing Age
Hyperlipidemia
Raised IOP (increases risk of CRVO)
Increased ESR(females)
Decreasing Risk : Physical Activity
Increased Alcohol Consumption
Exogenous Oestrogens(females)

The Eye Disease Case-Control Study Group: Risk factors for


central retinal vein occlusion.
Arch Ophthalmol 114:545, 1996
UNCOMMON FACTORS
Myeloproliferative disorders: Polycythemia, Abnormal
plasma proteins(myeloma).

Acquired hypercoagulable states:


Hyperhomocysteinemia, Lupus anticoagulant,
Antiphospholipid antibodies.

Inherited hypercoagulable states: Activated protein C


resistance, Protein C,S deficiency, Antithrombin
deficiency,Factor XII deficiency.

Inflammatory disease: Bechet syndrome, Sarcoidosis,


Goodpasture Syndrome.

Misc: CRF, Oral contraceptives, Hyperlipidemia


Classification
CVOS classification based on Fluorescein
angiographic characteristics:

Perfused or Non Ischemic –less than 10


disc areas in diameter of retinal capillary
non perfusion on angiography.
Non Perfused or Ischemic – 10 or more
disc areas in diameter if retinal capillary non
perfusion.
Indeterminate –when there is sufficient
intraretinal hemorrage to prevent
angiographic determination of perfusion
status
Clinical Presentation
Sudden visual impairment.

VA is impaired to moderate to severe degree.

Pain – usually advanced with NVI, NVG and


increased IOP.

Classic clinical picture on dilated examination.


Ischemic Central Retinal Vein
Occlusion
Sudden, painless decrease in visual acuity.
Vision ranges from CF to hand movements.
Afferent Pupillary Defect is marked.
Patients with ischemic occlusion have an average age of 68.5
years.
Fundus : Entire venous tree is tortuous, engorged, dilated, and dark
- Extensive Dot-Blot & Flame Shaped Hemorrhages
involving peripheral retina and posterior pole.
- Severe Disc Oedema and Hyperemia.
- Cotton wool spots may be present
FA : marked delay in AV transit time >20 seconds
central masking by retinal hemorrhages
extensive areas of capillary non perfusion and vessel wall
staining
COURSE & PROGNOSIS
Acute signs resolve within 9-12 months and residual findings like
disc collaterals, macular epiretinal gliosis & pigmentary changes
may remain.

Poor prognosis because of decreased visual acuity and


neovascularization. Visual loss occurs because of macular edema,
capillary nonperfusion, overlying hemorrhage (either retinal or
vitreal), or a combination of all of these. Retinal edema usually
gradually subsides except in the macula, where it may persist for
many months or years. Macular holes or cysts may form.

Rubeosis iridis develop in 50% between 2-4 months which may lead
to NVG.

FOLLOW UP
Monthly for 6 months to detect anterior segment neovascularisation,
angle neovascularisation (for risk of NVG)
Nonischemic Central Retinal
Vein Occlusion
Most common type

Sudden, unilateral blurred vision.

VA impaired to moderate-severe degree.

APD absent or mild.

Fundus : Tortuosity and dilatation


- Dot n Blot & Flame shaped haemorrhages in
all 4 quadrants, most common in periphery
- Cotton Wool spots, Optic Disc and macular edema.

FA : Delayed AV transit time


Good retinal capillary perfusion and late leakage
COURSE & PROGNOSIS
Acute signs resolve within 6-12 months and residual
findings like disc collaterals, macular epiretinal gliosis &
pigmentary changes may remain.
Conversion to ischaemic CRVO occurs in 15% within 4
months and 34% within 3 years.
Cases that do not progresses to ischemic type the
prognosis is good with return of vision to normal or near
normal in 50%.
Main cause for poor vision is chronic macular edema
which may lead to secondary RPE changes.
Standard Investigations
Blood Pressure
ECG
CBC, ESR
Urine Analysis
Protein Electrophoreseis
Random Blood Glucose, Lipid
INVESTIGATIONS <50 YRS
Chest X Ray
Thrombophilia screen :
Clotting screen
Protein C,S defficiency
Elevated factor V
Actviated protein C resistance
Factor V Leiden a major risk factor in females
Dysfibrogenaemia
Prothrombin G20210A
Antiphospholipid antibodies
Autoantibodies: anti cardiolipin, lupus anticoagulant, ANA
General Therapy

Avoid oral contraceptives


Aspirin
Treat hypercholesterolemia and hypertension
Lower IOP
Anticoagulants if required
Oral steroids and non steroidal
immunosuppressive agents

If vision drops consider re-occlusion.


TREATMENT
Ischaemic : Laser PRP in eyes with angle neovascularisation
(1500-3000 burns, spaced one burn apart) avoiding areas of
haemorrhage.
Laser PRP in patients with NVD/NVE without INV/ANV (Ryan).

Non Ischaemic : Laser PRP


Newer Modalities – Cannulation and infusion of tPA
into vein via vitrectomy.
- Intravitreal Triamcinolone
acetonide for CME but its effect
is short lived.
- Optic Nerve Sheathotomy or
Radial optic neurotomy via
PPVitrectomy for
decompressing the
central retinal vein.
Chorioretinal Anastomosis in Non-Ischemic CRVO

McAllister and Constable reported a surgical technique to create a chorioretinal


anastomosis in patients with non ischemic CRVO. Their current technique is to
rupture Bruch's membrane first in an area adjacent to the edge of a vein located at
least three disc diameters from the optic disc with the argon laser; they then use a
YAG laser to create a small opening in the sidewall of the adjacent vein.
In their study there was an average of 2 attempts to create an anastomosis, which
was successful in 42% patients in the first series and 67% of patients in the second
series. In the first series, ischemic central vein occlusion did not develop in any of the
patients in whom a successful anastomosis was produced, but it did develop in 31%
of patients in whom such an anastomosis could not be created. All the patients with a
successful anastomosis had an improvement in final visual acuity compared with
pretreatment visual acuity. In the group of patients with an unsuccessful
anastomosis, 38% had an improvement in visual acuity, 44% had a worse visual
acuity, and 19% had no change.
There were some minor complications, such as vitreous and retinal hemorrhages,
that tended to clear well. However, there were some major complications, including a
major fibrovascular proliferation at the sites where surgery was attempted.This
complication can lead to serious, nonclearing vitreous hemorrhages and/or traction
retinal detachment and may require a vitrectomy for treatment.
Neovascularization
Most serious complication.

NVI and NVG occurs in about 25% cases


of ischemic CRVO`s.
The low incidence of retinal surface
neovascularization in ischemic central
retinal vein occlusion is thought to be due
to the destruction of endothelial cells,
which provide the source for endothelial
proliferation and neovascularization.
BRANCH RETINAL VEIN
OCCLUSION

The clinical picture of BRVO


is the retinal hemorrages that
are segmental in origin
Pathology & Morphology
Leber was probably the first investigator to note the
connection between branch retinal vein occlusion and
the arteriovenous intersection. Koyanagi found that the
majority (77.7%) of his cases of temporal vein occlusion
involved the superior retina and later confirmed this
anatomic observation, noting that branch retinal vein
occlusion always occurs at an arteriovenous intersection.
Histologically, where the vein and artery cross, they
share a common adventitial sheath, and the venous
lumen may be diminished by as much as a third at this
crossing.

Some have postulated that turbulent blood flow at the


crossing site causes focal swelling of the endothelium
and deeper vein wall tissue leading to venous
obstruction and sometimes thrombus formation.
Risk Factors
Systemic hypertension
Diabetes
Hyperlipidemia
Glaucoma
Smoking
Age related atherosclerosis
Antiphospholipid antibodies
Elevated plasma homocysteine levels
Low serum folate
Eyes with shorter axial lengths
CLASSIFICATION
Major BRVO: At the Optic disc
Away from the disc but
involving the branches of macula.

Minor Macular BRVO : involving only macular branch

Peripheral BRVO
Clinical Features
VA depends on extent of macular involvement. Patients with
macular involvement presents with sudden onset of blurred vision
and metamorphopsia or a relative visual field defect.
Fundus: Dilatation and tortuosity of venous segment distal to site of
occlusion and attenuation proximally.
- Flame shaped, dot n blot haemorrhage, retinal
edema and occasionally cotton wool spots.
 FA: Variable delayed venous filling
blockage by blood
Hyperfluorescence due to leakage
Hypofluorescence due to capillary non perfusion
Pruning of vessels in ischaemic areas
COURSE & PROGNOSIS
Acute phase resolves in 6-12 months and may be replaced by the
following:
- Hard exudates, venous sheathing and variable amount of residual
haemorrhage.
- Collateral venous channels characterised by slightly tortuous
vessels between inferior and superior vascular arcades.

Prognosis is good due to formation of collaterals within 6 months in


50% of eyes with return of visual acuity to 6/12.
Management of BRVO
BRVO is often associated with pre-existing vascular disease.

Evaluation for systemic abnormalities, in particular hypertension,


should be performed.

Exclusion of diabetes, hyperlipidaemia, hyperviscosity/coagulation


states, antiphospholipid syndrome, or any other predisposing
condition should be performed and regular review is required until
the haemorrhages clear.

Approximately one third to one half of patients with BRVO have


recovery of visual acuity to 6/12, or better, without therapy.

Thus the treatment of BRVO has focused on management of vision-


limiting complications.
COMPLICATIONS
3 main vision limiting:
- Chronic macular edema
- Macular nonperfusion
- Vitreous hemorrhage from
Neovascularisation
Chronic Macular Edema
Most common cause of persistent poor VA after BRVO.

Treatment:
Grid laser photocoagulation-(100-200 um, 0.1 sec duration
spaced one burn width apart, away from fovea and intraretinal
haemorrhages should be avoided. Follow up should be after 3
months.
Intravitreal Triamcinolone acetonide(a corticosteriod suspension
which reduces breakdown of blood retinal barrier) but its effect lasts
for only 6 months.
Vitrectomy with or without sheathotomy.
Neovascularization
NVD develops in 10% and NVE in about 25% of eyes within 6-12
months usually but may develop at anytime within first 3 years, only
in eyes that shows large area(>5 disc diameters in diameter) of
retinal capillary nonperfusion.

Neovascularisation is a serious complication which can lead to


recurrent vitreous and pan-retinal haemorrhage and tractional retinal
detachment.

Vitreous haemorrhage due to neovascularization occurs in


approximately half of the eyes with neovascularization. Butner and
McPherson found that 11.3% of spontaneous vitreous hemorrhages
were due to a BRVO, an incidence second only to proliferative
diabetic retinopathy as a cause of vitreous haemorrhage.

Treatment : Scatter laser photocoagulation covering the entire


involved sector with PPV if vitreous Hemorrhage Is present. Follow
up should be after 3 weeks
HEMICENTRAL AND
HEMISPHERIC
RETINAL VEIN OCCLUSION
The terms hemicentral retinal vein occlusion and
hemispheric retinal vein occlusion refer to eyes
in which approximately half of the venous outflow
from the retina, either the superior or the inferior,
has been occluded. In approximately 20% of
eyes, the branch retinal veins draining the
superior and inferior halves of the retina enter
the lamina cribrosa separately before joining to
form a single central retinal vein.
Hemicentral retinal vein occlusion is an occlusion
of one of these dual trunks of the central retinal
vein within the nerve. Hemispheric retinal vein
occlusion is an occlusion involving the venous
drainage from approximately half of the retina,
either the superior or the inferior retina
ANATOMY OF HCRVO
Hemispheric retinal vein
occlusions
In some eyes, the nasal retina is not drained by a separate vein, but
by a branch of either the superior or the inferior temporal vein. It is
the occlusion of one of these veins draining both the nasal retina
and the superior or inferior retina near the optic disc that accounts
for the majority of hemispheric retinal vein occlusions.
The treatment and classification are similar to that of branch retinal
vein occlusion.
Fluorescein Angiography HCRVO
MACULAR BRANCH RETINAL
VEIN OCCLUSION
Patients complain of blurring or distortion of vision.
Superior macular vein occlusions are more common than inferior,
and some degree of macular edema is present in approximately
85% of these eyes.
Although small areas of capillary nonperfusion are present in
approximately 20% of eyes, neovascularization is not seen. Joffe
and associates pointed out that clues such as small collateral
channels and microaneurysms often suggest the diagnosis.
Treatment of macular edema in macular vein occlusion by grid laser
photocoagulation.
Macular Oedema- FFA

Fluorescence in the
macula indicates capillary
leakage and acute phase.
PAPILLOPHLEBITIS
In 1961, Lyle and Wybar described six young, healthy patients with
a unilateral, relatively benign condition characterized by mild
blurring of vision, essentially normal visual acuity, dilated and
tortuous retinal vessels, a varying amount of retinal hemorrhage,
optic disc edema and cotton wool spots.

All six patients improved spontaneously, but were left with sheathing
of retinal vessels and the formation of vessels on the optic disc. Lyle
and Wybar called this condition "retinal vasculitis" and believed it to
be due to a central retinal vein occlusion secondary to an
inflammatory vasculitis of the venous system.

Lonn and Hoyt agreed with this aetiology, but felt that
"papillophlebitis" was a more appropriate descriptive term.

Other C/F – enlarged blind spot on perimetry.

FA – mild delay in AV transit time, hyperfluorescence and good


capillary perfusion