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Retina 2 Professor K N Jha, MS [email protected]

Retina 2 hypertensive changes crvo crao dr.k.n.jha -01.06.16

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Page 1: Retina 2 hypertensive changes crvo crao dr.k.n.jha -01.06.16

Retina 2

Professor K N Jha, [email protected]

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Learning Aims

• Hypertension and the Eye: Clinical features,

complications, relationship of retinal changes and

prognosis for life

• Retinal Vascular occlusions: Clinical features,

complications and treatment

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Hypertension and the Eye • Retinopathy: FIPTs, microaneurysms, intraretinal

microvascular abnormalities (IRMAs), blot haemorrhages,

hard exudates, venous beading. and new retinal vessels

• Chroidopathy: Elschnig spots, Siegrist streaks

• Optic neuropathy: flame-shaped haemorrhages,

blurring of the disc margins, florid disc edema with

secondary retinal venous stasis, and macular exudates

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• Hypertension is also associated with

-Intraretinal haemorrhages

- Branch retinal artery

occlusion(BRAO)

- Branch retinal vein occlusion(BRVO)

-Central retinal vein occlusion(CRVO)

-Retinal arterial macroaneurysms

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Focal Intraretinal Periarteriolar Transudate

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Elschnig spots

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Hypertensive Optic Neuropathy

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Hypertensive retinal change: Classification

Grade I : Arteriolar narrowing

Grade II: Arteriovenous crossing changes

Grade III: Hemorrhage and exudates along with the

changes in grade I and II plus

Grade IV: Hemorrhages, exudates, and papilloedema

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Retinal vascular occlusionArterial OcclusionVenous Occlusion

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Arterial Occlusive Disease

• Branch Retinal Artery Occlusion(BRAO)

• Central Retinal Artery Occlusion(CRAO)

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Arterial Occlusive Disease

Fundamentals:

• Retinal ischemia results from occlusion of

common carotid artery to intraretinal arteries

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Precapillary Retinal Arterial Obstruction

• Leads to NFL infarct(CWS/soft exudates)

• They are ¼ dd in size or smaller

• Fade in 5-7 weeks

• Effect on Va or field will depend on location

and size

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Etiology: BRAO/CRAO

Embolus/thrombosis :from carotids /heart-Cholesterol emboli -Platelet-fibrin thrombus-Calcific emboli-Infective endocarditis, fat emboli etc.

In addition in CRAO:-Hemorrhage under plaque-Spasm-Dissecting aneurysm

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Other rare causes

• Migraine• Trauma• Coagulation disorders• Sickle cell disease• MVP• Oral contraceptive• Toxoplasma/syphilitic retinochoroiditis

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Symptoms and signs

BRAO

• Initially may remain clinically silent

• Later: Edematous opacification of retina

• Permanent field defect

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Management:BRAO

• Determine systemic etiology

• No ocular therapy

• Massage of the globe may be tried

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Central Retinal Artery Occlusion

• Clinical presentation:Sudden, severe, painless loss of vision Ophthalmoscopic feature:-Retina :edematous and opaque-Foveola: Cherry-red spot-Cholesterol emboli at retinal arterial bifurcation -Arterioles and venules are markedly narrowed-Cattle-truck appearance- Pupil:-RAPD

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Central Retinal Artery Occlusion

• About 2/3rd of patients have Va of < 3/60 and

visual prognosis is poor.

• If cilioretinal artery is present central vision may

be preserved.

• Leading cause of death in these cases is

cardiovascular disease.

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Investigations

-Same as BRAO

-Look for evidences of giant cell arteritis

-Blood for ESR and C-reactive protein

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Management• To be started without delay• They include:

• Reduction of IOP by ocular massage

• Ant chamber paracentesis

• Retrobulbar anaesthesia

• Inhalation of 95% O2+ 5% CO2 mixture

• Oral acetazolamide and aspirin

• Corticosteroid therapy to save the other eye, if giant cell arteritis is

diagnosed

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Venous Occlusive Disease

• Branch Retinal Vein Occlusion(BRVO)

• Central Retinal Vein Occlusion(CRVO)

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Retinal venous occlusion

• Predisposing conditionsSystemic-Hypertension-Arteriosclerosis-Cardiovascular diseaseOcular-History of glaucoma

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Retinal venous occlusion

• In young people

-Infective periphlebitis

-Facial erysipelas

-Orbital cellulitis

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Pathology

• Common adventitia

• Thickening of the arterial wall

• Turbulence in blood flow, endothelial damage

• Thrombotic occlusion

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Pathophysiology of venous occlusion

Venous Occlusion

Stagnation

Increased extravascularpressure

Hypoxia

Oedema andhaemorrhage

Sec art narrowing

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Symptoms

BRVO

Depends on whether central vision (macula) is

involved or not

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Branch Retinal Venous Occlusion

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BRVO:Visual Prognosis

Depends on

• Capillary damage and macular ischemia

• Macular edema

• Retinal neovascularisation 40 %.

• 50-60 % will maintain 6/12 after 1yr.

• Secondary glaucoma, rarely.

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Management

• FFA• BRVO study• Photocoagulation

Focal for macular edemaPRP for retinal neovascularisation

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CRVO:Types

• Non-ischemic

• Ischemic (diagnosis by FFA)

• Papillophlebitis (combined inflammatory and

occlusive mechanism)

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CRVO

Clinical features: Symptoms: transient blurring of vision

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Ophthalmoscopic Features

• Dilatation and tortuosity of affected vein

• Superficial hemorrhages

• Retinal edema

• Cotton wool spots(soft exudates)

• Macular edema in case of macular involvement

• Fluorescein fundus angiography

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Vascular sheathing and collaterals Hard exudates

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Evaluation

Visual acuity and RAPD

IOP

Gonioscopy

Look for iris neovascularisation

FFA to determine whether the condition is ischemic or no-

ischemic

Exclude carotid occlusive disease

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Management

• CRVO study

• Associated medical condition

• Glaucoma

• Panretinal photocoagulation for iris

vascularization

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Hyperviscosity retinopathy

• Generally bilateral

• They are related to disproteinemias e.g.

Waldenstrom macroglobulinemia or,multiple

myeloma

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Macular edema

• Laser photocoagulation :No benefitmay benefit in young in improving VaCorticosteroid and aspirin:efficacy is

unprovenSystemic anticoagulation: not

recommendedIntravitreal triamcinolone acetonide

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Iris neovascularisation

• Predictive factor:Poor visual acuity• Risk factors:Retinal non-perfusion ,intraretinal

blood• Panretinal photocoagulation when iris

neovascularisation occurs• Prophylactic Panretinal photocoagulation if

close follow-up of patient is not possible

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BRVO:Visual Prognosis

Depends on • Extent of capillary damage and macular

ischemia• Integrity of parafoveal capillaries• Macular edema, retinal

hemorrhage,parafoveal retinal capillary occlusion

• Retinal neovascularisation

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Management

• Photocoagulation

• Pars plana vitrectomy

• Intravitreal trimcinolone

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Photocoagulation

• Indications:

-Chronic macular edema with intact perifoveal

retinal capillary perfusion

-Posterior segment neovascularisation

-Iris neovascularisation

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Photocoagulation

• Visual acuity 6/12 to 6/60

• Argon Laser grid pattern photocoagulation is

applied in areas of capillary leakage identified

by FFA

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Panretinal photocoagulation

• For areas of retinal capillary non-perfusion

• Disc neovascularisation

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Peripheral retinal cryoablation

• In those cases where hazy media due to

vitreous haemorrhage do not permit

photocoagulation

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Vitrectomy and/or RD Surgery

• For non-resolving vitreous hemorrhage

• Retinal detachment

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Points To Remember• Retinal Vascular Occlusions cause sudden painless

diminution of vision.

• Arterial occlusions result from atheromatous plaque,

emboli, or vasculitis.

• Venous occlusions in elderly result from arteriosclerosis

• Macular ischemia/edema, vitreous hemorrhage or

neovascularisation result in visual loss.

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Points To Remember

• Visual loss in arterial occlusion is irreversible.

• Macular edema is treated with laser,

intravitreal steroid/ anti-VEGF agents.

• Prognosis of Venous occlusions depend upon

the clinical features and the course.