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Transcript
OCCLUSIVE VASCULAR
DISORDERS OF THE RETINA
AYESHA S ABDULLAH
27.02.2015
Learning outcomes
By the end of this lecture the students would be able to
 Classify occlusive vascular disorders (OVD) of the
retina.
 Correlate the clinical features of OVD of the retinal
with the underlying pathophysiological changes.
 List treatment modalities for OVD
 List the complications of OVDs
Retinal vein occlusion



Central retinal vein occlusion (CRVO)
Branch retinal vein occlusion (BRVO)
Hemiretinal vein occlusion (HRVO)
BRVO
HRVO
CRVO
Epidemiology



Retinal vein occlusion is the second most
common cause of visual loss due to retinal
vascular disease
BRVO is the most common type
It is a significant cause of severe visual loss in
people over the age of 40 yrs
Pathophysiology

Can you think of some anatomical factors that could
predispose retinal veins to occlusion?
With occlusion of the central retinal vein (CRVO)
increased venous & capillary pressure
stagnation of the blood in the retinal venous system and
increased resistance to venous blood flow
ischemic damage to the retina
increased production of vascular endothelial growth
factor (VEGF)
neovascularization of the posterior and anterior
segment
Neovascular
Glaucoma ,
NVD, NVE,RD
Capillary leakage
Macular
oedema
CRVO

The prognosis depends upon the reestablishment of
patency of the venous system by recanalization,
dissolution of clot, or formation of optociliary shunt
vessels.
Risk factors
Blood
Systemic
Vessel
wall
Risk factors







Age: 50% of these cases occur in patient over 65 years of
age
Systemic diseases like diabetes mellitus, hypertension,
hyperlipidemics states, smoking & obesity
Inflammatory diseases like sarcoidosis, Bechet disease
Hyperviscosity syndromes like polycythemia,
paraproteinemias
Clotting disorders - Activated protein C resistance, lupus
anticoagulant, anticardiolipin antibodies, protein C, protein
S, antithrombin III
Raised Intraocular pressure (IOP)
Oral contraceptive use
CRVO Clinical presentation

Clinical entities
 Non
–ischemic CRVO (about 75% of cases)
 Ischemic CRVO (worse prognosis)

How would you diagnose retinal ischemia?
CRVO Clinical presentation



Asymptomatic
Decreased vision
Visual loss
sudden or gradual,
 over a period of days to weeks.
 ranges from mild to severe.
 Patients can present with transient obscurations of vision
initially, later progressing to constant visual loss.




Photophobia
Redness of eyes
Painful blind eye
Clinical examination
Patients should undergo a complete eye examination,
including
 visual acuity,
 pupillary reactions,
 slit lamp examination of the anterior and posterior
segments,
 undilated examination of the iris….Why?
 gonioscopy,
 Dilated fundus examination
Signs






Visual acuity: (Best-corrected vision acuity) It is one of the
important indicators of the final visual prognosis.
Pupillary reactions: normal/ relative afferent pupillary reflex.
If the iris has abnormal blood vessels, the pupil may not react.
Conjunctiva: Advanced stages may show congestion on
conjunctival and ciliary vessels.
Cornea: Advanced stages may show diffuse corneal edema
obscuring the visibility of internal structures.
Iris: normal/ neovascularization
The anterior chamber angle: it may show neovascularization
with open angles and later show total peripheral anterior
synechia and closed angles.
Signs

Fundus examination:
 Retinal
hemorrhages
 Dilated tortuous veins
 Optic disc edema
 Cotton-wool spots
 Macular oedema
 Late signs: Neovascularization (NVD, NVE), optic disce
cupping, optociliary shunt vessels at the disc (a
prognostic sign), pigmentary changes in the macula
Rubeosis – 100 day glaucoma
Investigations



Risk factors screening (Lab tests)
FFA
Electro-retinogram (ERG)- amplitude of the b-wave
is decreased relative to the a-wave
TREATMENT


Depends on the type & stage of CRVO
Principles of treatment are
 Treat
the underlying cause
 Monitor
 Treatment modalities
 Intravitreal
corticosteroid and anti-VEGF injections
 Dexamethasone intravitreal implant
 Laser photocoagulation
 Chorioretinal venous anastomosis
Follow -up


Regular follow –up
“babysit" for these eyes during that period when
they are at maximum risk of developing
neovascular glaucoma, i.e. first 7-8 months
Prognosis
For nonischemic CRVO,
complete recovery with good visual recovery occurs only in
about 10% of cases.
rd
 50% of patients will have 6/60 or worse vision. About 1/3
of patients convert to ischemic CRVO within 3 years; 15%
within the first 4 months.
For ischemic CRVO,
 more than 90% of patients will have 6/60 or worse vision.
 About 60% of patients develop ocular neovascularization
 About 10% of patients can develop CRVO or other type of
vein occlusions within either the same eye or the
contralateral eye within 2 years.

Conclusion




a 54-year-old school teacher presented with acute visual
loss in the left eye. He had history of uncontrolled
hypertension and open angle glaucoma. Laboratory tests
including complete hypercoagulability state and thrombotic
workup were completed.
Ophthalmologic exam showed best corrected visual acuity
(BCVA)of 6/9 OD, 6/60 OS . Pupil exam showed sluggish
left pupil with relative afferent papillary defect, and a
reactive pupil on the right side.
Intraocular pressures were 11 mmHg in the right, and 19
mmHg in the left.
Slit lamp exam showed normal anterior segments with open
angles bilaterally.



How many risk factors can you identify in this case?
What is the significance of relative afferent
papillary defect ?
What is the most likely diagnosis?
Case 02- History (06.03.2015)


A 65 year old man presented to the eye OPD with
the complaints of sudden painless loss of vision in
the left eye. He described the visual loss as seeing a
black spot in his vision which spread over the entire
visual field with in minutes. He didn’t have any pain
or discomfort prior to his symptoms. He gave history
of experiencing transient visual loss lasting for a
minute or two for the past 06 months.
He was a known hypertensive and had history of
Myocardial Infarction and CVA.
Physicals

VA : (BCVA) 6/12 OD, HM OS

Pupils: RAPD OS.

Fundus: normal OD, see photos OS

BP: 160/100 mm Hg

IOP 12 OD , 14 OS
Some questions

What is the most likely diagnosis?

Central Retinal Artery Occlusion

Is it a common disorder?

Fortunately, No

How severe could be the visual loss?


Loss of vision can be profound and permanent without
immediate treatment. Irreversible retinal damage
occurs after 90 minutes, but even 24 hours after
symptoms begin, vision can still be partially restored
Why is it considered an ophthalmic emergency?
Who can be affected?
Risk factors
 Age > 50 years
 Arteriosclerois
 Hypertension and other vascular disorders
 CAD and angioplasty
 Thromboembolic diseases
 Glaucoma
 Giant cell arteritis
 Retinal migraine
How can it be treated?

The goal of emergency treatment is to restore retinal
blood flow

Ocular massage

Paracentesis

Lowering of the IOP through medications


There are no proven medical or surgical
techniques for treating retinal artery occlusions
Oral vasodilators, intravenous fibrinolytic
agents tried with varying success.

Anti VEGF, if neovascularization happens

Risk modification
Degenerative Disorders