FFA

Dr Aaron Ng

FFA Principles

• Fluorescence– Stimulated by light of shorter wavelength – Emission of light of longer wavelength

• Flurescein– Excitation peak 490nm– Emit light of about 530nm

FFA Principles: Filters

5 Phases of Angiogram

1.Choroidal (Pre-arterial): 9-15 sec

5 Phases of Angiogram

2.Arterial phase: 1 sec after choroidal phase

5 Phases of Angiogram

3.Arterio-venous (capillary) phase: early venous laminar flow

5 Phases of Angiogram

4a.Venous phase: Laminar venous flow

5 Phases of Angiogram4b.Venous phase – complete filling

•Max perifoveal capillary filling – 20-25 sec

•First pass of fluorescein circulation – 30 sec

5 Phases of Angiogram

5. Late (recirculation) phase

•Absent after 10 min

Timing of FFA phases• Arm to retina (ONH): 7-12s• Posterior ciliary artery 9s• Choroidal flush, cilio-retinal artery 10s• Retinal arterial phase 10-12s• Capillary transition phase 13s• Early venous/lamellar/a-v phase 14-15s• Venous phase 16-17s• Late venous phase 18-20s• Late phase 5-15 min

Foveal dark appearance

- Foveal avascular zone- High density of xanthophyll at the fovea- Foveal RPE larger and rich in melanin and

lipofuscin

Causes of hyperfluorescence

1. Autofluorescence2. Pseudofluorescence3. RPE window defect4. Dye pooling5. Dye leaking6. Tissue staining-disc, drusen, chorioretinal

scar

Autofluorescence

Optic disc drusen

Autofluorescence

Lipofuscin

Autofluorescence

Angioid streaks

RPE window defect

Atrophic ARMD

Dye pooling

Subretinal - CSCR

Dye pooling

Sub-RPE - PED

Dye leaking

Proliferative DR

Cystoid Macula Oedema

Late staining

Causes for hypofluorescence

• Masking of retinal fluorescence– Pre-retinal lesions block all fluorescence– Deeper retinal lesions e.g. intraretinal

haemorrhages and hard exudates block only capillary fluorescence

Pre-retinal lesions

Blockage to all fluorescence

Intraretinal lesions

Hard exudates Intraretinal haemorrhages

Causes for hypofluorescence

• Masking of background choroidal fluorescence– Conditions that block retinal fluorescence– Conditions that block only choroidal

• Sub-retinal or subRPE lesions• Increased RPE density• Choroidal lesions

• Filling defects– Vascular occlusions– Loss of vascular bed (myopic degen, choroidaeraemia)

Increased RPE density

CHRPE

Choroidal naevus

Filling defects

Capillary drop – out in DR (vascular occlusion)

Choroidaeraemia (loss of vascular bed)

CNVM subtypes

Classic

Atypical classic

Occult

Minimally classic

Indocyanine Green Angiography

• Advantages over FFA– Study of choroidal vasculature otherwise

prevented in FFA due to RPE blockage– Near-infrared light utilised penetrates melanin,

xanthophylls, exudates and subretinal blood– Infrared is scattered less cf visible light, thus

suitable in eyes with media opacities– 98% ICG molecules bound to protein, thus

remaining in the blood vessels

ICGA Principles

• Infrared excitation (805nm)• Infrared emission (835nm)

Phases of ICGA• Early phase (first 60 sec

post injection) – choroidal arteries

• Early mid phase (1-3 min) – choroidal veins and retinal vessels

• Late mid phase (3-15 min) – choroidal vessels facing but retinal vessels are still visible

• Late phase (14-45 min) – hypofluorescent choroidal vessels and gradual fading of diffuse hyperfluorescence

Causes for hyperfluorescence

• “Window defect”

• Retinal or choroidal vessel leakage

• Abnormal retinal or choroidal vessels

Causes for hypofluorescence

• Blockage– Pigment, blood, fibrosis, infiltrate, exudate, serous

fluid– PED are predominantly hypofluorescent on ICGA

as cf FFA

• Filling defect– Vascular occlusion– Loss of choroidal or retinal circulation

Clinical indications

• PCV• CSCR• Posterior uveitis (extent of disease

involvement)• Breaks in Bruch’s (lacquer cracks, angiod

streaks)• Contraindication for FFA

CSCR

FFA ICGA

CSCR

PCV