42Fundus Angiography

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Introduction To Fundus Fluorescein Angiography (FFA)And Indocyanine Green(ICG)

- Dr HITESH SHARMA, JR1 , DEPT OF OPHTHALMOLOGY, IMS B.H.U.

FUNDUS ANGIOGRAPHY1. Fluorescein (FA) Characteristics of Fluorescein & General principles Excitation and emission Filters Photographic technique Phases of normal angiogram Causes of dark appearance of fovea Causes of hyperfluorescence Causes of hypofluorescence

2. Indocyanine green (ICG) General principles Phases of normal angiogram

Characteristics of Fluorescein Nontoxic, inexpensive, safe Alkaline solution Highly fluorescent Absorbs blue light (480-500 nm) Emits yellow-green (500-600 nm [525 nm]) Effective at pH 7.37-7.45 Removal from blood by kidneys and liver within 24 hrs.

General principles of FAFluorescein

85% bound to serum proteins 15% unbound free fluorescein

Inner blood-retinal barrier (retinal capillaries)

Impermeable to fluorescein

Outer blood-retinal barrier (zonula occludens)

Impermeable to fluorescein

Choriocapillaris

Permeable only to free fluorescein

Excitation and emission

Filters

Photographic technique

1. Take red-free photograph 2. Inject rapidly 5 ml of 10% solution 3. Take photographs at 1 sec intervals between 5-25 sec after injection 4. Take photographs after 10 min and 20 min, if appropriate

Normal FFA Arm-to-retina circulation time is 12-15 sec. Five angiographic phases: Pre arterial Arterial Arteriovenous Venous Recirculation

Phases of normal FA

Arterial

Arterial filling

Arteriovenous (capillary)

Early venous

Very early lamellar venous flow

Marked lamellar venous flow

Mid-venous

Late venous

Almost complete venous filling

Complete venous filling

Progressively weaker fluorescence Staining of disc

Late

Leak

Hyperfluorescence

Transmission increase

Abnormal vessels

Pooling (in a space) Leak Staining (in a tissue). Transmission increase Pigment epithelial window defect Retinal Abnormal Vessels Subretinal Tumors

Retinal Pooling (in a space) Subretinal Hyperfluorescence Leak Retinal Staining (in a tissue). Subretinal

Cystoid edema Sensory retina detachment Retinal pigment epithelium Noncystoid edema Perivascular staining Drusen Scars Sclera Lamina cribrosa

Pigment Hyperfluorescence Transmission Increase Epithelial Window Defect Atrophy Drusen

Retinal

Tortuosity and Dilation Neovascularization Microaneurysms Aneurysms Macroaneurysms Telangiectasias Shunts and collaterals Neovascularization Vessels in scar Angioma Retinal Retinoblastoma Hemangioma Melanoma Metastases

Hyperfluorescence

Abnormal Vessels Subretinal

Tumors Subretinal

Transmission Decrease (blocking effect) Hypofluorescence

Filling defect (delay and occlusion)

Pigment

Melanin Hemoglobin Xanthophyll Lipofuscin Hard Soft

Hypofluorescence

Transmission Decrease (blocked)

Exudates Edema and transudate

Other abnormal materials

Best`s disease Foreign body Fundus flavimaculatus

H y p o f l u o r e s c e n c e

Artery Retinal Vein Capillary bed

Filling defect (delay and occlusion)

Dystrophies Loss of tissue

Choroideremia Choroidal atrophy etc. Myopia Central areolar atrophy

Subretinal

Degeneration Nonperfusion

Causes of dark appearance of foveaAvascularity Blockage of background choroidal fluorescence by:

Increased density of xanthophyll Large RPE cells with more melanin

Causes of hyperfluorescence ( 1 )RPE window defect Pooling of dye

RPE atrophy(bulls eye maculopathy

Under RPE(pigment epithelial detachment)

(central serous retinopathy)

Under sensory retina

Causes of hyperfluorescence (2)Leakage of dye Prolonged dye retention ( staining )

(cystoid macular oedema)

Into sensory retina

(choroidal neovascularization

From new vessels

Associated with drusen

Causes of hypofluorescence (1)Blocked retinal or choroidal fluorescence

Blood under retinal pigment epithelium

Abnormal material Increased pigment

Preretinal or intraretinal blood

Causes of hypofluorescence (2)Vascular occlusion Loss of vascular tissue

Capillary non-perfusion (venous occlusion)

Choroideremia or high myopia

Side Effects Minimal relatively safe drug Use of dilating drops Red after images from the photoflash Temporary tan skin color Fl. Urine discoloration Interfere with serological tests 2-4% Transient nausea and occ. VOMITING Hives, asthmatic symptoms Laryngeal edema Rarely Syncope, anaphylactic rxn, MI, resp. or Cardiac arrest Rx oral or I.V. Benadryl or Cortisone A physician in the 1st few minutes

During Pregnancy and Lactation Controversial Fl. Crosses the placenta Has been done in pregnancy with no adverse effect Do it when necessary

General Principles of ICG Angiography1. Binding

98% bound to proteins Less leakage from choriocapillaris Much less than fluorescein Excitation peak 800 nm Emission at 835 nm Infrared barrier and excitation

2. Fluorescence

3. Filters

4. Safer than fluorescein

Phases of normal ICG angiogram (1)Early (20 sec) Early middle (3 min)

Disc hypofluorescence Poor perfusion of vertical (watershed) zone near disc Prominent filling of choroidal arteries Early filling of choroidal veins Filling of retinal arteries but not veins

Filling of watershed zone Fading of choroidal arterial filling Prominent filling of choroidal veins Filling of retinal arteries and veins

Phases of normal ICG angiogram (2)Late middle (6 min) Late (21 min)

Reduced filling of choroidal vessels Diffuse hyperfluorescence due to diffusion of dye from choriocapillaris Persistent filling of retinal vessels

Large choroidal and retinal vessels are empty Diffuse background hyperfluorescence

FFA

Things to remember Not all abnormal conditions of the ocular fundus will produce abnormal fluorescein angiograms.