1. FFA Dr Aaron Ng

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

3. FFA Principles: Filters

4. 5 Phases of Angiogram 1. Choroidal (Pre- arterial): 9-15 sec

5. 5 Phases of Angiogram 2. Arterial phase: 1 sec after choroidal phase

6. 5 Phases of Angiogram 3. Arterio- venous (capillary) phase: early venous laminar flow

7. 5 Phases of Angiogram 4a. Venous phase: Laminar venous flow

8. 5 Phases of Angiogram 4b. Venous phase – complete filling Max perifoveal capillary filling – 20-25 sec First pass of fluorescein circulation – 30 sec

9. 5 Phases of Angiogram 5. Late (recirculation) phase Absent after 10 min

10. 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

11. Foveal dark appearance -Foveal avascular zone -High density of xanthophyll at the fovea -Foveal RPE larger and rich in melanin and lipofuscin

12. Causes of hyperfluorescence 1.Autofluorescence 2.Pseudofluorescence 3.RPE window defect 4.Dye pooling 5.Dye leaking 6.Tissue staining-disc, drusen, chorioretinal scar

13. Autofluorescence Optic disc drusen

14. Autofluorescence Lipofuscin

15. Autofluorescence Angioid streaks

16. RPE window defect Atrophic ARMD

17. Dye pooling Subretinal - CSCR

18. Dye pooling Sub-RPE - PED

19. Dye leaking Proliferative DR Cystoid Macula Oedema

20. Late staining

21. 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

22. Pre-retinal lesions Blockage to all fluorescence

23. Intraretinal lesions Hard exudatesIntraretinal haemorrhages

24. 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)

25. Increased RPE density CHRPE

26. Choroidal naevus

27. Filling defects Capillary drop – out in DR (vascular occlusion) Choroidaeraemia (loss of vascular bed)

28. CNVM subtypes

29. Classic

30. Atypical classic

31. Occult

32. Minimally classic

33. 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

34. ICGA Principles Infrared excitation (805nm) Infrared emission (835nm)

35. 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

36. Causes for hyperfluorescence “Window defect” Retinal or choroidal vessel leakage Abnormal retinal or choroidal vessels

37. 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

38. Clinical indications PCV CSCR Posterior uveitis (extent of disease involvement) Breaks in Bruch’s (lacquer cracks, angiod streaks) Contraindication for FFA

39. CSCR FFAICGA

40. CSCR

41. PCV