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Fundus Fluorescein Angiography Technique and Interpretation
- 1. Fundus fluorescein angiography PRESENTED BY: DR. VANDANA SHARMA
- 2. Brief history Dye synthesized by Adolf von Baeyer in 1871 Fundus camera introduced by Zeiss in mid-fifties Chaos and Flocks gave first description of fluorescein angiography First used in clinical practice by Novotiny and Alvis in 1961
- 3. Luminescence: Emission of light from any source other than high temperature Energy in the form of electromagnetic radiation is absorbed and then re-emitted at another frequency. Fluorescence: Luminescence that is maintained only by continuous excitation excitation at one wavelength occurs and is emitted immediately through a longer wavelength.
- 4. Properties of dye Physical: Water soluble crystalline powder Color: dark red to yellow green Chemical: Hydrocarbon: C20H10O5Na2 Molecular wt.: 376.27 kD
- 5. Fluorescence: Excitation occurs by light of wavelength between 465 to 490 nm Emits light of wavelength between 520 to 530 nm Pharmacokinetics: Excreted by kidney and liver Traces may be found for upto 1 week after injection After i.v. injection, 80% bound to blood proteins Permeates freely through blood vessels of all tissues except CNS and retina Also excreted in human milk
- 6. Side effects: Nausea, vomiting Skin rash, itching Yellow discoloration of urine for 1st 24 hours Yellow discoloration of skin, phototoxicity Gives positive test results for sugar in urine for several days Anaphylaxis and shock Painful local reaction in case of extravasation
- 7. Principle
- 8. Contraindications Absolute: Fluorescein allergy h/o severe allergic reaction to any allergen Relative: Pregnancy Renal failure Moderate to severe asthma Significant cardiac disease Iodine allergy is NOT a contraindication for FFA
- 9. procedure Explain procedure to the patient and obtain informed consent Full mydriasis Proper patient positioning Color photos, red free photos and photos with FA barriers in place taken before injecting the dye Injection of dye
- 11. Injection of dye Available solutions: Contain 500 mg of fluorescein Vials of 10 ml of 5% fluorescein or 5 ml of 10% fluorescein Also 3 ml of 25% fluorescein solution (750 mg) Greater the volume, the longer the injection time will be Smaller the volume, a significant percentage of fluorescein will remain in the venous dead space between the arm and the heart For pediatric patients, the dose is adjusted to 7 mg/kg of body weight
- 12. Scalp vein should be used (23 G) Ante-cubital vein is preferred Any vein on dorsum of hand or radial aspect of wrist may be used Timer started with injection of dye Rapid injection over 2-3 sec yields better photographs No extravasation of dye should be allowed
- 13. Taking fundus photographs Begin taking the initial transit fluorescein photographs 8 seconds after the beginning of the injection in young patient 12 seconds after injection for older patients Followed by approximately six photographs at intervals of 1.5 to 2 seconds Photographs taken as often as every second are not usually necessary
- 14. If no fluorescein entering and filling the retinal vessels is seen while the six initial-transit photographs are taken, continue to photograph the fundus until filling takes place Also check as to why no fluorescein is present Control pictures of opposite eye are also taken Photos during desired phases are taken Late photos at 10 min and 20 min may be taken Special emphasis to areas of interest
- 15. Ocular tissue response to fluorescein Bound dye Free dye Choroid: • Major choroidal vessels • Choriocappilaris Impermeable Impermeable Impermeable Permeable Bruch’s membrane Impermeable Permeable Retina: • Retinal pigment epithelium • Retinal vessels Impermeable Impermeable Impermeable Impermeable
- 16. Normal angiogram
- 17. Phases of normal angiogram Phase I: pre arterial phase/ choroidal phase( 9-15 sec) Phase II: arterial phase ( 1 sec after phase I) Phase III: arterio-venous phase/ capillary phase (16 – 20 sec) Phase IV: venous phase (20-25 sec) Phase V: late phase/ recirculation phase
- 18. Phase I Dye enters choroidal circulation 1 sec before retinal circulation Also called ‘choroidal flush’ Patchy choroidal filling Watershed zone between medial and lateral ciliary arteries Cilioretinal artery will fill in this phase Macula remains dark throughout the angiogram
- 19. Phase II • Starts 1 sec after phase I • Retinal arteriolar filing with continuation of choroidal filling
- 20. Phase III • Fluorescein from the venules enters the veins along their walls • Flow of fluorescein in the veins is laminar • The dark central lamina is nonfluorescent blood that comes from the periphery • The perifoveal capillary net can be seen best in young patients with clear ocular media about 20 to 25 seconds later • This is called the “peak” phase of the fluorescein angiogram.
- 21. Phase IV • As fluorescein filling increases, the laminae enlarge and meet • Complete fluorescence of the retinal veins.
- 22. Phase V • Approximately 30 seconds after injection, the first high concentration flush of fluorescein begins to empty from the choroidal and retinal circulations • The vessels of most normal patients almost completely empty of fluorescein in approximately 10 minutes • staining of Bruch’s membrane, the choroid, and especially the sclera may be visible if the pigment epithelium is lightly pigmented. • The disc and adjacent visible sclera remain hyperfluorescent because of staining • The lamina cribrosa within the disc also remains hyperfluorescent because of staining • the disc stains from the adjacent choriocapillaris, which normally leaks.
- 24. Hypofluorescencehypofluorescence blocked Retinal material Anterior segment Vitreous Inner retinal Choroidal material Deep retinal Sub retinal Vascular filling defects Retinal Artery Vein Capillary bed combination Disc Capillary non filling Choroidal Physiologic Posterior ciliary artery obstruction Absence of choroidal vascular tissue
- 25. blocked fluorescence: If material is visible ophthalmoscopically and corresponds to the area of hypofluorescenceIf vascular filling defect : no corresponding blocking material exists
- 26. Blocked fluorescence Further the opacification is in front of the fundus, the more it will affect the overall quality of the photographs Light scattered from the nonfluorescing opacities is not transmitted through the barrier filter and has no effect on the angiographic photograph When anterior segment and vitreous opacities are present, the angiogram may be of higher resolution and quality than the color photograph
- 27. Blocked retinal fluorescence • blocking material lies in front of the nerve fiber layer: block both planes of retinal vessels e.g. subhyaloid hemorrhage • Material lies beneath the nerve fiber layer but within or in front of the inner nuclear layer: will block only the retinal capillaries and choroidal vessels leaving the view of the large retinal vessels unobstructed e.g. flame shaped hemorrhage, severe retinal edema • Material lies deep to the inner nuclear layer: will not block the retinal vessels but will block the choroidal vascular fluorescence e.g. deep intra retinal hemorrhage
- 30. Blocked choroidal fluorescence • Fluid, exudate, hemorrhage, pigment, scar, and inflammatory material, accumulates in front of the choroidal vasculature and deep to the retinal vasculature
- 33. Vascular filling defects complete occlusion or complete atrophy of vascular tissue: hypofluorescence is complete and lasts throughout the angiogram Partial obstruction or incomplete vascular atrophy: the vascular fluorescein filling is delayed or reduced relative to corresponding areas that fill normally
- 34. Retinal vascular filling defects: Can be arterial, venous or capillary Easily distinguished by phase of angiogram Correspond to the normal vasculature of the retina
- 35. Retinal vascular filling defects
- 37. Filling defect of disc: Causes: Congenital absence of disc tissue e.g. optic pit, optic nerve head coloboma Atrophy of the disc tissue and its vasculature e.g. optic atrophy Vascular occlusion e.g. ischemic optic neuropathy Characterized by early hypofluorescence caused by nonfilling and late hyperfluorescence due to staining of the involved tissue
- 38. Choroidal vascular filling defect: Pigment epithelium depigmented or atrophied in chronic choroidal vascular filling defects Loss of ground-glass fluorescence from the choriocapillaris Filling defect does not correspond to retinal vasculature Patchy choroidal filling: early hypofluorescence followed by normal filling of whole choroid 2 – 5 sec later
- 39. Choroidal vascular filling defects
- 40. hyperfluorescence Preinjection fluorescence Autofluorescence pseudofluorescence Early (vascular) Abnormal retinal vessels Choroidal PE window defect Abnormal vessels Late (leak, extravascular) Vitreous Disc Retinal choroidal
- 41. Main causes are Preinjection fluorescence Transmitted fluorescence Abnormal vessels Leakage
- 42. Pre injection fluorescence: Autofluorescence: emission of fluorescent light from ocular structures in the absence of sodium fluorescein Seen in optic disc drusen and astrocytic hahartoma Pseudoflourescence: blue exciter and green barrier filters overlap i.e., the blue filter allows the passage green light or the green barrier filter allows the passage of blue light Seen from light colored or white fundus change e.g. sclera, exudate, scar tissue, myelinated nerve fibers, foreign body
- 45. Transmitted fluorescence: Also known as pigment epithelial window defect Occurs due to increased visibility of normal choroidal vasculature Appears early in angiography, coincidental with choroidal filling Increases in intensity as dye concentration increases in the choroid Does not increase in size or shape during the later phase of angiography Fades and sometimes disappear as the choroid empties of dye at the end of angiography
- 48. Abnormal vessels on retina and disc: tortuosity and dilation Aneurysms Neovascularization Anastomosis Telangiectasis tumor vessels
- 52. Abnormal vessels in choroid: Subretinal neovascularization: lacy, irregular, and nodular hyperfluorescence Tumor
- 55. Leak: Late extravascular hyperfluoresence which may be normal fluorescence of the disc margins from the surrounding choriocapillaris Fluorescence of the lamina cribrosa fluorescence of the sclera at the disc margin if the retinal pigment epithelium terminates away from the disc, as in an optic crescent Fluorescence of the sclera when the pigment epithelium is lightly pigmented
- 56. Disc leak: Normal to some extent Disc edema shows initial hyperfluorescence due to dilated capillaries followed by leakage of dye Vitreous leak: Retinal neovascularization: localized snowball like appearance Intraocular inflammation: diffuse white haze Tumor: localized to area of tumor
- 57. Retinal leak Cystoid edema: dye lies in small loculated pockets Leakage of large retinal vessels leads to perivascular staining Seen in traction, occlusion and inflammation Choroidal leak Pooling: accumulation of dye in anatomic spaces such as under areas of detachment as in CSR, and PED Staining: accumulation of dye in tissue and material such as sclera, RPE and drusen
- 60. Stargardts Disease exhibits a ‘silent choroid’ and a central bulls-eye fluorescence pattern in the macula APMPPE demonstrates a characteristic ‘block early, stain late’ pattern
- 64. CSR
- 67. Recurrent CSR
- 75. Bibliography Fundus fluorescein angiography in Retina. Ryan Acquired macular disorders in Clinical Ophthalmology. Kanski and Bowling Albert and jacobiec’s principles and practices of ophthalmology