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CRAO and BRAO

Jul 02, 2015

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Health & Medicine

Chacha Mashinka
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Epidemiology

Mean age – mid 60”s

Men > women

Bilateral in 1 – 2%

May have other retinal vascular disease

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Etiology Systemic hypertension seen in two thirds of patients

Diabetes mellitus

Cardiac valvular disease seen in one fourth of patients

Cardiac anomalies, such as patent foramen ovale

Embolism

Embolism is the most common cause. The carotid artery and the heart are the most common sources.

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There are 3 types of

emboli

1. Cholestrol

Hollenhorst plaques

Minute , bright , refractile,

Golden to yellow orange

crystals, often at

bifurcation

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2. Fibrin platelet

Dull grey , elongated

particles which are

usually multiple

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3. Calcific emboli

Single , white , non

scintillating particles

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PathophysiologyEmboli artery narrowing atheroma turbulent blood flow

break off atheroma lodge small caliber arteryt block

Ischemia Retinal artery occlusion

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Characteristics

Sudden severe visual loss in 1 eye

Painless

Retinal appearance

Opaque and edematous

Retina artery narrow,mild hemorrhage

Most prominent in posterior pole

Thickest ganglion cell layer

Cherry-red spot

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With time

Artery re-canalizes

Edema clears

Visual loss is

devastating and

permanent

Irreversible damage to

neural tissue after 90

minutes

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Diagnosis Ocular examintain

Cardiovascular examination

Labortory studies are helpful / blood sugar , cholesterol , triglycerid /

Carotid ultrasound

Fluorescein angiography

Electroretinogram

ECG and echocardiogram

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Dislodge the Embolus

“Burst the Dam”

Digital massage to dislodge embolus

A/C paracentesis

IV acetazolamide

Retrobulbar vasodilators

Inject fibrinolytic in supraorbital artery

Retrobulbar vasodilators

YAG laser embolysis

Surgical embolysis

Keep the Retina Alive

Carbogen inhalation

Oxygen inhalatioN

Hyperbaric oxygen therapy

Emergent TPPV with or without perfluorocarbonliquid infusion

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Ocular massage

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Sudden profound altitudinal or sectoral VF loss

VA – variable

Fundus – narrowing of arteries and veins with sludging and segmentation of the blood column / cattle trucking , box carrying/

One or more emboli may seen

Cloudy white retina that corresponds to the area of ischaemia.

Sign may sometimes be subtle.

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Management is directed toward determining systemic etiology factors. No specific ocular therapy has been found to be effective in improving the visual progmosis.pressureon the globe may dislodge an embolus from a large central vessel toward a more peripheral location , but the efficacy of this maneuver in improving visual outcomes is unknown

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Atherosclerosis is

the most common

etiology

but possible causes

include

Eisenmenger

syndrome , giant cell

arteritis , and other

inflammatory

conditions.

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A severe form of chronic ischemia of both anterior and posterior segments of the eye as well as other orbital structures supplied by the ophthalmic artery.

Usually unilateral

Age: 50-80 yrs

M&F 2:1

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Anterior Segment Dilated Episcleral

vessels Pain in orbit

Corneal edema AC Cells

Iris neovascularisation

NeovasuclarGlaucoma

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Proliferative diabetic

retinopathy

Ischemic CRVO

Carotid artery

ultrasoundCarotid occlusion, usually

90% or more

ERG

Diminished b- and a- waves

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Full scater PRP

Carotid artery stenting

Endarterectomy

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On fundusfluoresceinangiography, there was a delay in arterial filling and AV transit time was 70 sec

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fundus fluorescein

angiography showed

normal retinal

perfusion with AV

transit time of 12

seconds

One day after IAT, his

vision improved to

20/40

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Fundus photography 2

weeks after

thrombolysis . There is

no more retinal edema

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