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 Angiogram 4b. Venous phase – complete filling Max perifoveal capillary filling – 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 artery9s Choroidal flush, cilio-retinal artery 10s Retinal arterial phase10-12s Capillary transition phase 13s Early venous/lamellar/a-v phase14-15s Venous phase 16-17s Late venous phase 18-20s Late phase5-15 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.Autofluorescence 2.Pseudofluorescence 3.RPE window defect 4.Dye pooling 5.Dye leaking 6.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 exudatesIntraretinal 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 FFAICGA

CSCR

PCV