FFA Dr Aaron Ng FFA Principles Fluorescence Stimulated

FFA Dr Aaron Ng

FFA Principles • Fluorescence – Stimulated by light of shorter wavelength – Emission of light of longer wavelength • Flurescein – Excitation peak 490 nm – Emit light of about 530 nm

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 4 a. Venous phase: Laminar venous flow

5 Phases of Angiogram 4 b. 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 -12 s 9 s 10 -12 s 13 s 14 -15 s 16 -17 s 18 -20 s 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 sub. RPE 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 (805 nm) • Infrared emission (835 nm)

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