ffa dr aaron ng. ffa principles fluorescence – stimulated by light of shorter wavelength –...
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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