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 (Prearterial): 9-15
sec
5 Phases of Angiogram
2.
Arterial
phase: 1 sec
after
choroidal
phase
5 Phases of Angiogram
3.
Arteriovenous
(capillary)
phase: early
venous
laminar flow
5 Phases of Angiogram
4a.
Venous
phase:
Laminar
venous flow
5 Phases of Angiogram
4b.
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):
Posterior ciliary artery
Choroidal flush, cilio-retinal artery
Retinal arterial phase
Capillary transition phase
Early venous/lamellar/a-v phase
Venous phase
Late venous phase
Late phase
7-12s
9s
10s
10-12s
13s
14-15s
16-17s
18-20s
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.
2.
3.
4.
5.
6.
Autofluorescence
Pseudofluorescence
RPE window defect
Dye pooling
Dye leaking
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