RETINAL VASCULAR OCCLUSIONS

M O D E RAT O R : D R M A D H U R I M A N AYA KP R E S E N T E R : D R P O O JA

INTRODUCTIONANATOMYCLASSIFICATIONARTERIAL OCCLUSIONSVENOUS OCCLUSIONSREFERENCES

INTRODUCTION Retinal vascular occlusions are serious

diseases and significant causes of blindness that include arterial and venous obstructions

The clinical presentation aids in distinguishing the type of the occlusion, which may be classified according to the anatomical site of the occlusion

Blood supply of RETINA Outer 4 layers of RETINA: Choriocapillaries. Inner 6 layers of RETINA: Central retinal

artery The fovea is avascular and is mainly supplied

by Choriocapillaries. Cilio retinal artery is present in 20% of eyes The veins of the RETINA unite to form Central

retinal vein at the disc , which follows the corresponding artery

CLASSIFICATION

CENTRAL RETINAL ARTERIAL OCCLUSION

BRANCH RETINAL ARTERIAL OCCLUSION

CILIORETINAL ARTERIAL OCCLUSION

CENTRAL RETINAL VEIN OCCLUSION

BRANCH RETINAL VEIN OCCLUSION

HEMI RETINAL VEIN OCCLUSION

ARTERIAL OCCLUSION VENOUS OCCLUSION

COMBINED CENTRAL RETINAL ARTERY AND VENOUS OBSTRUCTION

RETINAL ARTERIAL OCCLUSIONS Visual loss from retinal arterial occlusion

(RAO) occurs from the loss of blood supply to the inner layers of the retina

CAUSES: ATHEROSCLEROSIS EMBOLISM

Hollenhorst plaques(Cholesterol) Fibrin platelet Calcific emboli

Systemic cardiovascular disease Coagulopathies Systemic vasculitis Oncologic Infective diseases Trauma Ocular conditions Oral contraceptives, Pregnancy, Drug

abuse, Migraine

CENTRAL RETINAL ARTERY OCCLUSION

Incidence and demographics: Frequency -1 per 10,000 outpatients visits CRAO accounts for (57%), BRAO(38%),

CRAO(5%) Mean age at the time of presentation is in the

early 60’s Men affected more then women 1-2 % of cases have B/L involvement, for which

the DD : should include cardiac valvular disease , GCA and other vascular inflammations.

CLINICAL FEATURES

Sudden and profound LOSS of vision, painless except in GCA.

VA is severely reduced RAPD present RUBEOSIS IRIDIS(1/5 eyes)

FUNDUS Superficial retinaYELLOW WHITE APPEARANCE CHERRY RED SPOT Cattle trucking/box caring Retinal/Disc NV(2%) LATE signs: Optic atrophy Narrowing of vessels Vessel sheathing RPE changes

CRAO with patent cilioretinal . A

Old CRAO

INVESTIGATIONS FA: Delay in retinal arterial filling (highest

SPECIFICITY). Delay in Retinal A-V transit time (Most common and highest SENSITIVITY)

OCT: shows highly reflective emboli plaque within superficial nerve headERG: Diminution of amplitude of “b” wave, with normal “a” wave

BRANCH RETINAL ARTERIAL OCCLUSION

BRAO occurs when the embolus lodges in a more distal branch of the retinal artery.

Typically involves the TEMPORAL retinal vessels

Clinical features Sudden and painless SECTORAL visual field loss VA is variable. RAPD is often present.

FUNDUS Cattletrucking/

boxcarring. Cloudy white

oedematous retina corresponding to the area of ischaemia.

Artery to artery collateral may develop in retina

INVESTIGATIONS FA shows delay in arterial filling and hypo

fluorescence of the involved segment due to blockage of background fluorescence by retinal swelling

CILIO RETINAL ARTERIAL OCCLUSION

Cilioretinal arteries-Temporal aspect of the optic disc , separate from the CRA

20% of eyes Provides second arterial supply to the

MACULA from posterior ciliary circulation.

On FFA fill concomitantly with choroidal circulation 1-2 seconds before retinal arteries

THREE VARIANTS

ISOLATED : • >40%• Young patients

with systemic vasculitis

• Good visual prognosis

• No ocular treatment required

WITH CRVO: >40% Reduced pressure in the CilioRA as compared to CRA Better visual prognosis No ocular treatment

required

WITH AION : 15% Both appear to

be manifestations of posterior ciliary insufficiency

Poor prognosis GCA as a cause

should be investigated.

TREATMENT OF ACUTE ARTERIAL OCCLUSION:

OCULAR Retinal artery occlusion is an emergency

because it causes irreversible visual loss unless the retinal circulation is re-established prior to the development of retinal infarction

The following treatments may be tried in patients with occlusions of less than 24 hours duration at presentation.

.

Adoption of a supine posture Ocular massage

Anterior chamber paracentesis Sublingual isosorbide dinitrate to induce vasodilation.

‘Rebreathing’ into a paper bag OR Breathing ‘CARBOGEN’.

Topical apraclonidine 1%, timolol 0.5% and intravenous acetazolamide 500 mg to achieve sustained lowering of intraocular pressure

Hyperosmotic agents. Mannitol or glycerol

Transluminal Nd: YAG laser embolysis.

SYSTEMIC General risk factors like smoking to be discontinued. Anti- Platelet therapy to be started , if not CI. Oral anticoagulants treatment (e.g.Warfarin) in

patients with AF Carotid endarterectomy in symptomatic stenosis

greater than 70% Asymptomatic retinal embolus if identified ,indicates

increased risk of stroke and IHD, evaluation and treatment of risk factors is required.

FOLLOW UP

CRAO: After 3-4 weeks and a minimum of twice subsequently at monthly intervals to detect neovascularization of Anterior segment

BRAO: After 3 months

RETINAL VENOUS OCCLUSIONS

RISK FACTORS: 1. AGE: 50% of cases occur in >65 years . 2. HYPERTENSION :73% in >50 years ,25% in younger patients 3. HYPERLIPIDAEMIA (total cholesterol >6.5 mmol /l) is present in 35% of patients 4. DIABETES MELLITUS 10% of cases over the age of 50 years 5.OCULAR: OAG, Ischemic optic neuropathy , Optic nerve head drusen

CENTRAL RETINAL VEIN OCCLUSION

Incidence and demographics : Prevalence of CVO - 0.1-0.4%. Age at the time of presentation is

above 60’s Men and women equally affected U/L ,with 1% risk of development in

the fellow eye by the end of 1 year, 7% risk by the end of 7 years.

NON-ISCHAEMIC CRVO Non-ischaemic CRVO is the most

common type, accounting for about 75%.

CLINICAL FEATURES: 1.Sudden painless unilateral loss of vision. 2.VA is impaired to a moderate-severe degree. 3.RAPD is absent or mild (in contrast to ischaemic CRVO)

FUNDUS Tortuosity and dilatation of all the branches Dot/blot and flame-shaped haemorrhages,

throughout ALL quadrants Cotton wool spots, Disc and macular oedema

are common. Most acute signs resolve over 6–12 months. OPTOCILIARY shunts/RETINOCHOROIDAL shunts

Conversion to ischaemic CRVO occurs in 15% of cases within 4 months and 34% within 3 years

Investigations o FA shows delayed A-V transit time, blockage by haemorrhages, good retinal capillary perfusion(<10 disc areas of non perfusion) and late leakage. o OCT is useful in the assessment of CMO(mild in NI-CRVO)

Follow up: Initial follow-up should take place after 3months. Subsequent review is usually at 18-24 months

Recent non-ischaemic CRVO

Old non-ischaemic CRVO

ISCHAEMIC CRVO Clinical features: 1. Sudden and severe painless unilateral loss of vision, occasionally can present with pain, redness or photophobia 2. VA is CF or worse 3. RAPD is present 4. Anterior segment findings : NVI , ANV, NVG(100 day glaucoma).CVOS STUDY

RUBEOSIS IRIDIS

FUNDUS

Tortuosity of all branches Extensive deep dot/blot

and flame-shaped haemorrhages,

Cotton wool spots are prominent, optic disc swelling usually present.

Most acute signs resolve over 9–12 months.

INVESTIGATIONS FA shows delayed arteriovenous transit

time, masking by haemorrhages, extensive areas of retinal capillary non- perfusion(10 or > disc areas in diameter)

OCT is useful in quantification of CMO

Electroretinogram (ERG).

Recent ischemic CRVO

MANAGEMENT

SYSTEMIC ASSESSMENT ALL PATIENTS BP ESR,CBC RBS HDL . Cholesterol OTHERS: Urea Creatinine Electrolytes

(renal disease @ with HTN) Thyroid function tests ECG(LVH is associated with

HTN)

SELECTED PATIENTS(<50 yrs, B/L, Common inv-negative, family h/o thrombophilia) Chest X ray: TB, Sarcoidosis CRP: sensitive indicator for

inflammation Plasma homocysteine level “Thrombophilia screen” Plasma Protein electrophoresis Autoantibodies: RF, ANA, ANCA,

anti-DNA antibody ACE: Sarcoidosis Treponemal serology Carotid duplex imaging

Medical therapy Treatment of MACULAR OEDEMA:

a) VA worse than 6/9 and significant central macular thickening on OCT b)Intravitreal anti-VEGF agents: Ranibizumab showed a significant visual benefit when used for CMO c) Intravitreal Dexamethasone implant d)Intravitreal Triamcinolone: The SCORE study showed an improvement in the vision of 3 or more lines at one year in over 25% of patients treated with an average of 2 injections of 1 mg triamcinolone versus 7% of controls.

e) Laser photocoagulationCVOS study: Grid pattern argon laser photocoagulation did reduce macular oedema by 1 year (31%), BUT it did not result in an improvement in visual acuity. OTHER treatments include Chorioretinal anastomosis Pars plana vitrectomy Radial optic neurotomy Recombinant tissue plasminogen activator(r-tPA)

Treatment of NEOVASCULARIZATION a) PRP in eyes with NVI or NVA:application of 1500–3000 burns (0.5–0.1 second, spaced one burn width apart). CVOS study: PRP should be given after the development of INV/ANV and not prophylactically, to be considered in patients with RF of developing INV/ANV or follow up not possible b) Intravitreal anti-VEGF agents

BRANCH RETINAL VEIN OCCLUSION

Macular BRVO involving only a macular branch Peripheral BRVO not involving the macular

circulation Clinical features: 1. Sudden painless onset of blurred vision Peripheral occlusion may be asymptomatic 2.VA is variable 3. NVI and NVG are much less common than CRVO (2-3% at 3 years )

FUNDUS

• Tortuosity with dot/blot & flame-shaped haemorrhages • Cotton wool spots and retinal oedema are present • SUPEROTEMPORAL quadrant • Resolution over 6–12 months. • Retinal neovascularization 8%

Superior branch vein occlusion

Residual findings- Venous sheathing and sclerosis, persistent /recurrent haemorrhages. Collaterals may form near areas of limited capillary perfusion. FA shows peripheral and macular ischaemia,

Venous filling delayed OCT is useful in quantification of CMO

Management Systemic assessment Observation without intervention if VA is

6/9 or better NVE/NVD: sector photocoagulation 400-500 µm

diameter for 0.05 sec duration and spaced one burn width apart are applied to ischaemic area.

NVI : Sector PRP Intravitreal anti-VEGF agents Intravitreal Dexamethasone implant

Macular laser: Eligibility criteria Method Intravitreal Triamcinolone Review : After 3months and then 3-6

monthly intervals for 2 years to detect neovascularization

HEMIRETINAL VEIN OCCLUSION

Hemiretinal vein occlusion is generally regarded as a variant of CRVO and may be ischaemic or non-ischaemic.

DIAGNOSIS Sudden onset altitudinal visual field defect. VA reduction is variable. NVI more common than BRVO , but less than

CRVO FUNDUS shows the features of BRVO,

involving the superior or inferior hemisphere , NVD more common

FA shows masking by haemorrhages , hyper fluorescence due to leakage and variable capillary non perfusion

Inferior hemiretinal vein occlusion

TREATMENT Depends on the severity of retinal

ischaemia Extensive retinal ischaemia carries the risk of neovascular glaucoma and should be managed in the same way as ischaemic CRVO.

Macular oedema usually responds poorly to grid laser due to extensive foveal capillary shutdown

Systemic treatment in retinal vein occlusion

Control of systemic risk factors Antiplatelet therapy with aspirin or an

alternative agent should be considered

COMBINED RETINAL ARTERY AND VEIN OCCLUION

References Ryan Retina American Academy of ophthalmology Kanski’s clinical ophthalmology Retinal vein occlusions by royal college

of ophthalmologists

THANK YOU