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FFA Dr Md Afzal Mahfuzullah

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FFA Dr Md Afzal Mahfuzullah

  1. 1. Fundus Fluorescein Angiography Dr Md Afzal Mahfuzullah MCPS,FCPS,Felow Vitreo-Retina Retina Specialist & Surgeon Bangabandhu Sheikh Mujib Medical University
  2. 2. WHY FFA  To confirms the elements already revealed by clinical examination.  Flow characteristics in the blood vessels as the dye reaches and circulates through the retina and choroid.  Gives a clear picture of the retinal vessels and assessment of their functional integrity.  To monitor the disease intensity and impact of therapy.  Provides guidance for application of focal laser in photocoagulation therapy.  To detect the leakages without clinical manifestation of edema
  3. 3. What are the informations we get from FFA FFA reveals:  Inflammatory status of retinal and choroidal blood vessels.  Localization of intra retinal lesions e.g. depth of pathological involvement in DR.  CNV  Neovascularisation in disc or retina
  4. 4. FFA reveals: Cont  Subretinal fluid status  Cystoid macular edema  Intraretinal/ preretinal haemorrhages  Optic nerve disorders  RPE integrity and disorders  Choroidal neovessels and chorioretinal atrophy
  5. 5. BASIC PRINCIPLES:
  6. 6. BASIC PRINCIPLES:  Based on luminescence and fluorescence.  Luminescence – is the emission of light from any source other than high temperature.  Fluorescence is luminescence that is maintained only by continuous excitation. Excitation occurs at one wave length and immediate emission occurs through a longer wave length.
  7. 7. FLUORESCENCE  Refers to fluorescein sodium (C20H10Na2O5)  A brown or orange red crystalline substance, alkaline in nature.  MW- 376 dalton  Readily diffuses through body fluids and choriocapillaries but does not diffuse through vascular endothelial cells and RPE (Blood retina barriers)
  8. 8. OPTICAL PRINCIPLE  Absorbs blue light (465- 490nm ) and Emits yellow-green light (520- 530nm)  Metabolized by liver and exerted by kidney
  9. 9. FILTERS 1.Blue excitation filter 2.Yellow-green filter
  10. 10. Blood supply to retina
  11. 11. Layers & blood supply
  12. 12. GENERAL PRINICIPLES OF FFA Fluorescein • 85% bound to serum proteins • 15% unbound ‘free’ fluorescein • Impermeable to fluorescein Outer blood-retinal barrier (zonula occludens) • Impermeable to fluorescein Choriocapillaris Permeable only to ‘free’ fluoresce Inner blood-retinal barrier (retinal capillaries)
  13. 13. Circulation of NaF Dye injected from peripheral vein Venous circulation Heart Arterial system INTERNAL CAROTID ARTERY Ophthalmic artery Short posterior ciliary artery) Central retinal artery (choroidal circulation.) ( retinal circulation) N.B. The choroidal filling is 1 second prior to the retinal filling.
  14. 14. ANGIOGRAPHIC PHASES  Five angiographic phases: • Pre arterial (Choroidal 9-15 seconds) • Arterial • Arteriovenous(capillary) • Venous • Recirculation
  15. 15. Basic anatomy :  The inner retina contains the retinal blood vessels.  The larger vessels in the Nerve fiber layer.  The retinal capillaries in the Inner nuclear layer.  Both are impermeable to dye.  The outer retina is primarily interstitial space of the retina, where hemorrhages, edematous fluid and hard exudates accumulate.  In normal conditions this layer does contain NaF as because of RPE tight junctions(Outer BRB)  Large choroidal vessels do not leake NaF but choriocapillaris does leak.
  16. 16. BASIC ANATOMY
  17. 17. PRE-ARTERIAL/ CHOROIDAL PHASE  Choroidal flush  Patchy Choroidal filling because of lobular arrangements of choriocapillaris  10-12 sec in young  12-15 sec in old  Cilioretinal artery fills at the same time with choroid circulation  Macula remains dark due to tall RPE and more pigments.
  18. 18. ARTERIAL PHASE
  19. 19. ARTERIAL PHASE Cont…
  20. 20. ARTERIOVENOUS PHASE
  21. 21. VENOUS PHASE
  22. 22. Recirculation phase
  23. 23. ABNORMAL ANGIOGRAPHIC FINDINGS  Hypofluorescence: Filling defect Blocking defect  Hyperfluorescence : Window defect Leakage Pooling Staining
  24. 24. Hypofluorescence  Blocked fluorescence (Transmission defects- blood, pigment, hard exudates etc)  Vascular filling defects (Circulation abnormality)  Blocked Retinal fluorescence 1. Arterial segment material 2. Vitreous material 3. Inner retinal material  Blocked choroidal fluorescence 1. Deep retinal material 2. Subretinal material 3. Sub RPE material 4. Choroidal material
  25. 25. Hypofluorescence.Cont
  26. 26. Hyperfluorescence Anomalous vessels Choroid Retina Optic nerve head Subretinal neovasculari- zation Tumor vessels Chorioretinal anastomosis Vascular tortuosities Dilation and shunts Anastomosis Neovascularization Aneurysms Teleangiectasia Tumor vessels Hamatoma Neovascularization Tortuosity Dilation Hamatoma Tumor vessels
  27. 27. Hyper- fluorescence In a preformed space (pooling) Into tissue (staining) Retinal Subretinal Retina Subretinal Cystoid edema Detachment of the pigment epithelium Detachment of the sensory retina noncystoid edema e.g.dursen
  28. 28. Leakage
  29. 29. Fluorescence without the administration of fluorescein Autofluorescence Pseudofluorescence Drusen of the optic nerve head Hamatoma Scleral exudate Myelinate nerve Fibers, optic nerve drusen Scar tissue Foreign body
  30. 30. Causes of dark appearance of fovea -Avascularity • Increased density of xanthophyll • Large RPE cells with more melanin -Blockage of background choroidal fluorescence by:
  31. 31. Causes of Hyperfluorescence RPE ‘ window’ defect RPE atrophy (bull’s eye maculopathy Pooling of dye Under RPE (pigment epithelial detachment) Under sensory retina (central serous retinopathy)
  32. 32. Causes of Hyperfluorescence Leakage of dye Prolonged dye retention ( staining ) Into sensory retina (cystoid macular oedema) From new vessels (choroidal neovascularization Associated with drusen
  33. 33. Vascular occlusion Capillary non-perfusion (venous occlusion) Loss of vascular tissue Choroideremia or high myopia Causes of Hypofluorescence
  34. 34. BRVO- HYPO F- BLOCKED F
  35. 35. BRVO
  36. 36. SUB HYLOID. Hge/ PRERETINAL Hge HYPO F- BLOCKED
  37. 37. STARGARDT'S DISEASE  Fundusflavimaculatus: (Stargardt disease (STGD) is the most common childhood recessively inherited macular dystrophy.  Blocked the choroidal fluorescence, so fundus background looks black.
  38. 38. AION – HYPO F OF DISC
  39. 39. Red-free Fundus photos Normal appearance Autofluorescence
  40. 40. Macular Hole
  41. 41. ARMD - HYPER- STAINING
  42. 42. CHOROIDAL NAEVUS
  43. 43. DIABETIC RETINOPATHY Diabetic retinopathy gives a combination of both hyper/ hypofluorescence. Several pathologies are seen in this frame:
  44. 44. DIABETIC RETINOPATHY  Hypofluorescence: Retinal haemorrhage (1) Ischaemia (2).  Hyperfluorescence: microaneurysms (3) and neovascularization (4) In addition, there are IRMA (5) between the retinal artery and vein and venous beading (6)
  45. 45. DIABETIC MACULOPATHY TREATED WITH LASER
  46. 46. PDR- HYPER F
  47. 47. BACKGROUND DIABETIC RETINOPATHY
  48. 48. CENTRAL SEROUS RETINOPATHY POOLING/ HYPER F Late phase of FFA shows a spot of pigment epithelium leakage has enlarged & fuzzy,in this case there is pooling of fluorescein under the detched retina
  49. 49. HYPER F- WINDOW/ POOLING EFFECT  Fundus photography shows PED & late phase of angiogram showing the corresponding well defined hyperfluorescent lesion
  50. 50. HYPERTENSIVE RETINOPATHY
  51. 51. Limitations of FFA
  52. 52. 1) Does not permit study of choroidal circulation details due to a) melanin in RPE b) low mol wt of fluorescein 2) More adverse reaction 3) Inability to obtain angiogram in patient with excess hemoglobin or serum protein.
  53. 53. Thank you

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