vasculaire geneeskunde meets oogheelkunde: arteriële en ... · occlusive disorders sudden loss of...
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Vasculaire geneeskunde meets
oogheelkunde:
arteriële en veneuze
problemen in het oog
Reinier Schlingemann
AMC
R.O.Schlingemann, Ocular Angiogenesis Group AMC
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Hoornvlies
RetinaVitreous
Choroid
Sclera
Rods and cones
Anatomy of the retina
Retinal vasculatuer
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Gezonde retina
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Visual acuity and daily activities
0,5
0,1
0,16
0,05
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Impact of retinal conditions on quality of life: time
trade-off values
Equivalent conditions
Mild AMD (0,5-1,0) 17% Symptomatic HIV
Moderate angina pectoris
Moderate AMD (0,1-
0,4)
30% Permanent kidney dialysis
Severe angina pectoris
Severe AMD(<0,05)
Total Blindness
35-65%
75%
Metastatic prostate cancer
with uncontrolled pain
Severe stroke with functional
loss
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Ocular neovascularization
Pterygium
Cornea
CornealNeovascularization
Retina
RetinalNeovascularization
VitreoretinalNeovascularization
SubretinalNeovascularization
Iris
R.O.P
•Main cause of visual loss in the Western world
•Affects the lives of millions of people
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B. Lafaut, 2000
Sub-retinal neovascularisation in AMD
Fluorescein angiogram
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Vascular leakage in Diabetic Macular Oedema
Normal
retina
Diabetic
macular
oedema
OCT
Loss of capillaries causes
leakage and oedema
Fluorescein angiogram
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Vaatgroei: Proliferatieve retinopathie
Littekenvorming
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Ocular vascular occlusive
disorders
Ischemic optic neuropathy
Central retinal vein occlusion (CRVO)
Branch retinal vein occlusion (BRVO)
Central retinal artery occlusion (CRAO)
Branch retinal artery occlusion (BRAO)
Cilioretinal artery occlusion
Ocular Angiogenesis Group AMC Amsterdam
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Vascular arcitecture in the optic
nerve head
R.O.Schlingemann, Ocular Angiogenesis Group AMC
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Central retinal artery occlusion (CRAO)– Non-arteritic CRAO-67%
CRAO secondary to CRVO-<1%
– Non-arteritic CRAO with cilioretinal sparing-14%
– Arteritic CRAO with Giant cell arteritis-4.5%
– Transient CRAO-16%
Branch retinal artery occlusion (BRAO)– Permanent BRAO-61%
– Transient BRAO-6%
– Cilioretinal artery occlusion
Non-arteric-6%
Non-arteritic secondary to CRVO-19%
Arteritic with GCA-6%
Cotton-wool spots
Amaurosis fugax
ACUTE RETINAL ARTERIAL OCCLUSIVE DISORDERS
Ocular Angiogenesis Group AMC Amsterdam
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Clinical presentation of acute arterial
occlusive disorders
sudden loss of vision in 1 eye
on initial ophthalmic evaluation retinal
opacity with cherry red spot
in eyes with transient CRAO, multiple
scattered patches of retinal opacity
“box-carring” (“cattle trucking”) of the
blood column in the retinal vessels
Ocular Angiogenesis Group AMC Amsterdam
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Non-arteritic CRAO with cilioretinal
sparing
Ocular Angiogenesis Group AMC Amsterdam
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Ocular Angiogenesis Group AMC Amsterdam
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Causes of CRAO and BRAO
Systemic associations (OR 2-5)
– diabetes mellitus
– Renal disease
– arterial hypertension
– ischemic heart disease
– cerebrovascular accidents
– smoking
Ipsilateral internal carotid artery– >50% stenosis-30%
– Plaques-70%
Abnormal echocardiogram with an
embolic source-52/42%
Ocular Angiogenesis Group AMC Amsterdam
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Causes of CRAO and BRAO
Direct cause in most cases
embolism
– Types of emboli
Cholesterol (Hollenhorst plaques)-74%
Calcific material-10.5%
Platelet-fibrin-15.5%
– Source
Carotid artery plaques
Heart
– Aortic and mitral valvular lesions
– Patent foramen ovale
– Left atrial myxoma
Ocular Angiogenesis Group AMC Amsterdam
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Clinical outcome in CRAO and
BRAO
CRAO
– Visual acuity usually < 0.1
– Improvement in first week 22% non-arteritic CRAO
66% in non-arteritic CRAO with cilioretinal sparing
0% in arteritic CRAO with Giant cell arteritis
82% in transient CRAO
BRAO
– Visual field defects
– Final visual acuity > 0.5
89% in permanent BRAO
100% in transient BRAO
100% in non-arteritic cilioretinal artery occlusion
Ocular Angiogenesis Group AMC Amsterdam
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Management of CRAO and BRAOHayreh: “a disease without any treatment has many treatments”.
No proven treatment for the eye
– Advocated treatments in CRAO ocular massage
a reduction of intraocular pressure
vasodilation of the CRA by sublingual isosorbide dinitrate,
rebreathing of expired CO2 in a bag, breathing Carbogen etc.
antiplatelet therapy or heparin therapy
Intra-arterial fibrinolysis
Prevention of CRAO/BRAO in the other eye
– Detect and treat source of emboli
– Anti-coagulants indicated
Ocular Angiogenesis Group AMC Amsterdam
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GIANT CELL ARTERITIS(Temporal or Cranial Arteritis)
Idiopathic vasculitis
– Same disease spectrum as
polymyalgia rheumatica
– Mainly women 65-80 years old
– Medium and large arteries in
head & neck involved
Presentation– Headache
– Scalp tenderness
– Thickened temporal arteries
– Jaw claudication
– Acute visual loss
– Weight loss, anorexia, fever, night sweats, malaise & depression
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GIANT CELL ARTERITIS
Ocular Complications
Transient monocular visual loss (amaurosis fugax)
Visual loss due to– Central retinal
artery occlusion (CRAO) or
– Anterior ischaemic optic neuropathy (AION)
Visual field defects
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Ischemic optic
neuropathy
Types
– Anterior (AION)– Arteritic
– Non-arteritic
– Posterior (PION)
Pathogenesis of NA-AION
– Acute ischemia of the optic nerve head
– Systemic and local risk factors
– Nocturnal hypotension
Treatment
– Aspirin not useful
– Early systemic steroids may be useful
Ocular Angiogenesis Group AMC Amsterdam
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Branch vein occlusion
Central Vein occlusion
Retinal vein occlusions
Ischemic Non-ischemic
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Central retinal vein occlusion Prevalence 0.1-0.4%
Most patients 60-70, any age possible,
10% <50 years
Ocular risk factors
– Glaucoma and ocular hypertension-30-70%
– Trauma-14%
Systemic risk factors
– Cardiovascular >50 years-OR 3-5
– Thrombophilia <50 years?
Hyperhomocysteinuria
Anti-phospholipid syndrome
– No clear association with hereditary
thrombophilic syndromes or other risk
factors for DVT
Cause of CRVO
– Steep venous pressure gradient
– Atherosclerosis
– Local hemodynamic factors
– Secundary EC proliferation and thrombosis
Ocular Angiogenesis Group AMC Amsterdam
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Pathogenesis of CRVO
R.O.Schlingemann, Ocular Angiogenesis Group AMC
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BRVO Prevalence 0.6-1.1%
Ocular risk factors
– Not glaucoma and ocular hypertension
Systemic risk factors– Systemic hypertension
Causes of BRVO
– Atherosclerosis
– Venous obstruction at arteriovenous crossing
– Secondary EC proliferation and thrombosis
Subtypes
– Major BRVO
– Macular BRVO
Ocular Angiogenesis Group AMC Amsterdam
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CRVO and BRVO Collaterals
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Blood-retinal barrier loss and macular edema in BRVO
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Anti-VEGF in macular edema secondary to
retinal vein occlusions
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Copernicus Study: Aflibercept in CRVOE
TD
RS
lett
ers
Week *P < 0.001
vs. Sham
LOCF; full analysis set; sham n=73; 2q4 n=114;
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VEGF-AProperties
– Glycoprotein dimer
– 4 isoforms: 121, 165, 189, 206 amino acids
– Secretion upregulated under hypoxic conditions
– Functions: survival, permeability and angiogenesis
In vitro effects:
– Mitogenic
– Tube formation
– Upregulation of
-urokinase and tpa
-urokinase PA-receptor
-integrins v3 and v5
-VEGFR1 and -2
Normal Embryo
Embryo w knockout of
VEGF gene - lethal
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VEGF-A induced iris neovascularization in the monkey eye
VEGF-A PBS
CD31
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Vascular occlusive disorders-
Take home messages Artery occlusions
– Retinal infarction caused by embolism
– Anticoagulants useful
– Beware of GCA
Ischemic optic neuropathy
– Optic nerve head infarction caused by vascular insufficiency
– Anticoagulants not useful
– Beware of GCA
Vein occlusions
– CRVO caused by atherosclerosis and local hemodynamic factors
Strong association with high intra-ocular pressure
Retinal thrombosis is misnomer
Anticoagulants not useful
Thrombophilia may contribute if <50 years
– BRVO caused by atherosclerosis
Strong association with systemic hypertension
– Anti-VEGF very effective in secondary macular edema
Ocular Angiogenesis Group AMC Amsterdam