VASCULAR DISORDERS
OF RETINA
Dr. Monika Mahat
Resident
Department of Ophthalmology
• Retinal artery occlusions
• Retinal vein occlusions
• Diabetic retinopathy
• Hypertensive retinopathy
• Sickle Cell retinopathy
• Retinopathy of Prematurity
• Retinal Telangiectasia.
RETINAL ARTERY OCCLUSION
RETINAL ARTERY OCCLUSION
• Occlusive disorders of retinal vessels are more
common in patients suffering from hypertension
and cardiovascular diseases
• BLOOD SUPPLY:
• The outer retina is supplied by the ciliary arteries via
the choriocapillaris and the inner retina by the
central retinal artery (CRA)
• The ophthalmic artery gives the major blood supply
ETIOLOGY:
• Atherosclerosis-related embolism and
thrombosis
RETINAL ARTERY OCCULSION
SYSTEMIC ASSESSMENT
• Smoking
• Symptoms of GCA (1–2% of CRAO), >55-60 yrs - headache, jaw claudication,
scalp tenderness, limb girdle pain, weight loss and existing polymyalgia
rheumatica (ESR, CRP)
• Pulse: Detect arrhythmia, particularly atrial fibrillation
• BP
• Cardiac auscultation: murmur
• Carotid auscultation: Bruit
• ECG: Arrhythmia and other cardiac disease
• Blood tests: CBC, glucose, lipids and urea and electrolytes
• Carotid Duplex Scanning: Non-invasive screening test, If significant stenosis
is present
• MRI or CT: Rule out intracranial or orbital pathology
• Echocardiography.: History of rheumatic fever, known cardiac valvular
disease
• Chest X-ray: Sarcoidosis, tuberculosis
• Other Blood Tests: Thrombophilia screen, Plasma protein
electrophoresis, Thyroid function tests, Autoantibodies., Syphilis
serology, Blood cultures.
RETINAL ARTERY OCCULSION
Clinically retinal artery occlusion may present
as:
1. Central Retinal Artery Occlusion (60%)
2. Branch Artery Occlusion (35%)
3. Cilioretinal artery occlusion (5%)
• It is more common in males than females
• Unilateral but rarely may be bilateral (1 to 2%
cases)
CENTRAL RETINAL ARTERY
OCCULSION
PATHOPHYSIOLOGY:
• EMBOLI--- ARTERIAL NARROWING–
ATHEROMA—TURBULENT BLOOD FLOW–
BREAK DOWN THE ATHEROMA–
LODGEMENT IN THE SMALL CALIBER
ARTERY– BLOCKAGE-- ISCHAEMIA
ETIOLOGY OF CRAO
CLINICAL FEATURES OF CRAO
• Symptoms: Sudden painless profound loss of
vision
• Signs:
• VA is severely reduced except if a cilioretinal artery
supplying a critical macular area preserves central
vision
• Direct pupillary reflex: Absent
• RAPD: Profound
• Fundus:
• Marked narrowing of retinal arteries
• Retina becomes milky white
• Cherry-red spot: In the center of macula
• Cattle tracking, i.e., segmentation of blood
column is seen in the retinal veins
• Emboli are visible in 20%
• Atrophic changes
• Rubeosis iridis
• Fundus fluorescein angiography (FFA)
shows delay in arterial filing (cilioretinal
artery when present will fill in early phase)
and masking of choroidal vasculature due to
retinal oedema.
BRANCH RETINAL ARTERY
OCCLUSION
• An abrupt diminution of blood flow through a
branch of central retinal artery severe enough to
cause ischaemia of inner retina in the territory of
affected vessels
• Usually occurs following lodgement of embolus
at a bifurcation
• Sudden and profound painless altitudinal or
sectoral visual field
• May go unnoticed if central vision spared
• VA is variable
• Initially remain clinically silent but later edematous opacification of
retina
• Permanent field defect
• RAPD: Present
• Fundus: Attenuation of arteries and veins, cattle trucking, Cloudy
white oedematous retina (ground glass), occluding emboli (at
bifurcation)
TREATMENT OF RETINAL ARTERY
OCCLUSION
1. Dislodging emboli:
• ocular massage
• Embolysis : surgical or Yag laser
2. Reducing IOP:
• Topical apraclonidine 1%, timolol 0.5% and intravenous
acetazolamide 500 mg to achieve a more sustained lowering
of intraocular pressure
• AC paracentesis
3. Vasodilatation: carbogen (95% O2 and 5% CO2), Nitrates
4. Maintaining the retinal oxygenation: hyperbaric oxygen
5. Thrombolytic : streptokinase, urokinase, tPA
Complications: Neovascular Glaucoma
RETINAL VENOUS OCCLUSIVE DISEASE
RETINAL VENOUS OCCLUSIVE DISEASE
• Occlusion of central retinal vein at the level of lamina cribrosa
• Retinal vein thrombosis is strongly associated with age-related local
and systemic factors
• Second most common retinal vascular disease after DR
RISK FACTORS
• Age : >65yrs
• Hypertension > 2/3rd of RVO patients over the age of 50 years and in
25% of younger patients
• Hyperlipidaemia
• Diabetes mellitus is present in up to 15% of patients over 50 years of
age
• Glaucoma and ocular hypertension
RISK FACTORS: (CONTN)
• Oral contraceptive pill
• Smoking
• Uncommon: Dehydration, myeloproliferative disorders (e.g. myeloma,
polycythaemia), thrombophilia (e.g. hyperhomocysteinaemia,
antiphospholipid antibody syndrome, factor V Leiden mutation),
inflammatory disease associated with occlusive periphlebitis (e.g.
Behçet syndrome, sarcoidosis, Wegener granulomatosis), orbital
disease and chronic renal failure.
ETIOLOGY
1. Pressure on the vein by an atherosclerotic retinal artery
2. HTN and DM
3. Hyperviscosity of blood as in polycythemia, hyperlipidemia,
macroglobulinemia, leukemia, multiple myeloma, cryoglobulinemia
4. Periphlebitis retinae which can be central or peripheral associated with
sarcoidosis, syphillis, and SLE
5. Raised intraocular pressure – common in primary open angle glaucoma
6. Local causes are orbital cellulitis, orbital tumors, facial erysipelas and
cavernous sinus thrombosis
SYSTEMIC ASSESSMENT
• BP
• ESR,CRP and CBC
• RBS and HDL
• Plasma protein electrophoresis
• RFT: Renal disease in HTN
• TFT: High prevalence of RVO
• ECG
• Chest X-ray. Sarcoidosis, tuberculosis, left ventricular hypertrophy in
hypertension
• Thrombophilia screen: PT, aPTT
• Autoantibodies. Rheumatoid factor, antinuclear antibody (ANA), anti-
DNA antibody, antineutrophil cytoplasmic antibody (ANCA)
• Treponemal serology
• Carotid duplex imaging
Classification
1. Central retinal vein occlusion (CRVO)
• Non-ischaemic CRVO (venous stasis retinopathy)
• Ischaemic CRVO (haemorrhagic retinopathy)
2. Branch retinal vein occlusion (BRVO)
3. Hemiretinal Vein Occlusion – Variant of
CRVO
CENTRAL RETINAL VEIN OCCLUSION
1. NON- ISCHEMIC CRVO:
• Most common clinical variety (75%)
• Venous stasis retinopathy
• RAPD: Absent
• EARLY:
• Mild venous congestion and tortuosity
• Few superficial flame-shaped haemorrhages – in periphery
• Mild papilloedema
• Mild or no macular oedema
• LATE:
• After 6–9 months
• Sheathing around the main veins
• Few cilioretinal collaterals around the disc
• Retinal haemorrhages are partly absorbed
• Chronic cystoid macular oedema
• COMPLICATIONS: About 15% cases of non-ischaemic CRVO are
converted to ischaemic CRVO in 4 months and about 30% in 3 years
2. ISCHEMIC CRVO
• Sudden complete occlusion of central retinal vein
• Haemorrhagic retinopathy
• Marked sudden visual loss
• RAPD present
• EARLY:
• Massive engorgement, congestion and tortuousity of retinal
veins
• Massive retinal haemorrhages (almost whole fundus is full
of haemorrhages giving a ‘splashedtomato’ appearance)
• Numerous cotton wool spots
• Disc oedema and hyperaemia
• Macular area is full of haemorrhages and is severely
oedematous
• Break through vitreous haemorrhage
• LATE:
• Marked sheathing around veins and collaterals is seen around the
disc
• Neovascularization may be seen at the disc (NVD) or in the
periphery (NVE)
• Macula shows marked pigmentary changes and chronic cystoid
oedema
• Complications:
1. Rubeosis iridis
2. Neovascular glaucoma
3. Vitreous haemorrhage
4. Proliferative retinopathy
Pathognomonic
features for Ischaemic
CRVO (Differentiating
from Non –Ischemic
• Presence of relative
afferent pupillary
defect (RAPD)
• Visual field defects
• Reduced amplitude of
b-wave of
electroretinogram.
BRANCH RETINAL VEIN OCCLUSION
(BRVO)
• More common than the central retinal vein
occlusion
• The commonest underlying cause: Systemic
hypertension
• Symptoms and VA:
• Depend on the anatomical location of the occlusion
• Macula involved: Sudden painless onset of blurred vision
and metamorphopsia
• Peripheral occlusion: Asymptomatic
• Iris neovascularization (NVI) and neovascular glaucoma (NVG) are
much less common in BRVO than in CRVO
Fundus
• Dilatation and tortuosity of the affected venous
segment, with flame-shaped and dot/blot
haemorrhages
• Cotton-wool spots and retinal oedema may be present
• Superotemporal quadrant is most commonly affected
• Site of occlusion may be identifiable as an
arteriovenous crossing point
• Retinal neovascularization -NVE are more common than NVD
• Chronic macular oedema
• Collateral vessels may form
• Recurrent vitreous and preretinal haemorrhage
MANAGEMENT OF RVO
• Treatment of systemic and ocular associations -Systemic arterial
hypertension and hyperlipidaemia
• Medical therapy:
• Intravitreal anti-VEGFs - Bevacizumab (Avastin), Ranibizumab (Lucentis)
• Intravitreal triamcinolone – Associated Cystoid Macular Edema
• Laser therapy
• Panretinal photocoagulation (PRP) – In neovascularization - in angle (NVA), iris
(NVE), retina (NVE & NVD)
• Scatter laser photocoagulation: Neovascularization else where (NVE)
• Surgical therapy
• Pars plana vitrectomy
• Pars plana placement of glaucoma drainage device – Neovascular glaucoma
• Radical optic neurotomy
THANK YOU
