basic info on fudus florescence angiography
TRANSCRIPT
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NALIN NAYAN OPTOMETRIST
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It is a medical imaging technique used to visualize the inside of blood vessels and organs of the body, with particular interest in the arteries, veins and the heart chambers.
traditionally done by injecting a radio-opaque contrast agent into the blood vessel and imaging using X-ray based techniques
The word itself comes from the Greek words angeion, "vessel", and graphein, "to write or record".
The film or image of the blood vessels is called an angiograph, or more commonly, an angiogram.
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- Fundus Fluorescein angiography refers to photographing fluroscein dye in the retinal vasculature following intravenous injection of fluroscein sodium.
- Described in 1959 by MacLean and Maumenee
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Fluorescein (C20H12O5) refers to Fluorescein sodium (C20H10Na2).
Is a brown or orange-red crystalline substance first synthesized in 1871 in Germany by Von Baeyer
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1882 – Ehrlich introduced Fluorescein into investigative ophthalmology
1940 – Gifford studied aqueous dynamics after injecting intravenous Fluorescein
1960 – 2 medical students Novotny & Alwis experimented on each other and developed FFA
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Non toxic, inexpensive, safe Alkaline solution Highly fluorescent Absorbs blue light (480-500 nm) Emits yellow-green (500-600 nm [525
nm]) Effective at pH 7.37-7.45 Removal from blood by kidneys and
liver within 5 hrs.
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Inner and Outer blood retinal barriers control movement of fluid, ions & electrolytes from intravascular space to extracellular space in retina
FFA – method of examining competence of blood retinal barriers and making permanent record
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GENERAL PRINCIPLES:- -Fluorescein binding. -Inner blood retinal barrier. -Major choroidal vessels. -Outer blood retinal barrier. -Excitation peak. -Types of filters.
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70-85% fluorescein molecules bind to serum proteins (mainly albumin) on entering the circulation.
The rest unbound molecules are referred to as free fluorescein.
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At level of retinal capillary endothelium (tight junctions, non-fenestrated) and basement membrane
Prevents all leaks of free fluorescein and albumin-bound fluorescein.
in vascular permeability caused by changes in intravascular pressure or tissue hydrostatic pressure, or by change in capillary walls themselves, will permit leakage of both bound & free fluorescein molecules in extra vascular space.
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-impermeable to both bound & free fluorescein molecules.
- walls of choricapillaries are extremely thin & contain multiple fenestrations through which free fluorescein molecules are able to escape into the extra vascular space & across Bruch’s membrane.
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Composed of intact RPE (tight junctions b/w RPE cells).
Impermeable to free fluorescein. RPE presents an optical barrier to
fluorescein and masks choroidal circulation
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490 nm (blue part of spectrum). represents maximal absorption of
light energy by fluorescein. Molecules stimulated by this
wavelength will be excited to higher energy level & will emit light of longer wavelength ( green portion of spectrum i.e. at 530 nm ).
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2 types of filters:- - cobalt-blue excitation. - yellow-green barrier.Ensures blue light enters the eye &
only yellow green light enters the camera.
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Light emitted from retinal camera passes through blue excitation filter, emerging blue light enters the eye & excites Fluorescein molecules in retinal & choroid circulation of longer wavelength (yellow green).
Yellow green barrier filter thus blocks any blue light that may leave eye, allowing only yellow-green light to pass through unimpaired to be recorded on film.
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- Pupil should be dilated.TECHNIQUE:-- Patient seated in front of camera with one arm
out stretched.- Fluorescein 5 ml of 10% solution is drawn up
into syringe. In opaque media, 3 ml of 25% solution may be
preferred, because it gives better result.
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- Red free photograph is taken.- Fluorescein injected rapidly into antecubital
vein.- Photographs are taken at approx 1 sec
interval between 5 & 25 sec after injection.- After transit phase has been photographed
in eye, control pictures are taken of opposite eye.
If necessary, late photograph can also be taken after 10 min & occasionally after 20 min if leakage is anticipated.
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Red after image. Transient nausea. Flushing of skin. Itching. Hives. Excessive sneezing. Discolouration of urine & skin.
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Baseline photos and red free 5 Phases of FFA Choroidal phase Arterial phase Capillary phase Venous phase Late phase
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1) CHOROIDAL OR PRE-ARTERIAL PHASE:- -Choroidal circulation is filling, but no dye
has reached the retinal arteries.2) ARTERIAL PHASE:- -follows 1 sec after pre-arterial phase. -extends from first appearance of dye in the
arteries until whole arterial circulation is filled.
3)CAPILLARY OR ARTERIOVENOUS PHASE:- -characterized by complete filling of the
arteries & capillaries with early lamellar flow in the veins.
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4) VENOUS PHASE:- - subdivided into early, mid & late stages according
to extent of venous filling & arterial emptying. early venous phase:- shows complete arterial &
capillary filling, & lamellar venous flow. mid venous phase:- shows almost complete venous
filling. late venous phase:- shows complete venous filling. -arteries are beginning to show decreasing fluorescence. -Recirculation of dye occurs within 3-5 min. -The intensity of fluorescence begins to diminish
so that arteries & veins appear equally fluorescent.
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5) LATE PHASES:- - shows effects of continuous
recirculation, dilution & elimination of dye.
- with each succeeding wave, the intensity of fluorescence becomes weaker.
- late staining of optic nerve is a normal finding.
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Arm to retina (ONH) 7-12s Posterior- ciliary artery fill 9s Choroidal flush, cilio-retinal artery 10s Retinal arterial phase 10-12s Capillary transition phase 13s Early venous/lamellar/a-v phase 14-15s Venous phase 16-17s Late venous phase 18-20s Late phase 5 – 15 mins
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12s arterial phase 15s early venous
20s venous phase 52s late phase
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Arterial phase may range from 2-30s; may be affected by:
- cardiac disease - blood viscosity- vessel calibre- CCF- GCA - ↑BP- carotid artery stenosis.
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Superior arterioles fill before inferior and temporal before nasal
Choroidal & scleral fluorescence depends on pigment density of RPE & its integrity
Macular hypo fluorescence – due to ↑’d density of RPE & xanthophyll blocking choroidal fluorescence
No retinal capillaries – FAZ 500μm; foveola 350μm
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Only 2 fundamental principles in FFA
- HYPER fluorescence or HYPO fluorescence !
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MAY BE CAUSED BY:- 1) AN RPE WINDOW DEFECT: -RESULTING FROM ATROPHY OF
OVERLYING RPE CELLS WITH UNMASKING OF NORMAL BACKGROUND CHOROIDAL FLUORESCENCE.
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2) POOLING OF DYE:- -UNDER A DETACHMENT OF RPE OR
IN IN THE SUB RETINAL SPACE. - CAUSED BY A BREAKDOWN OF
OUTER BLOOD RETINAL BARRIER.
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3) LEAKAGE OF DYE:- - into the sensory retina as a result
of breakdown of inner blood retinal barrier.
- may be:- ~from choroidal new vessels. ~from retinal new vessels. ~from the optic nerve head (in papilloedema).
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4) STAINING OF TISSUES:- - as a result of prolonged retention
of fluorescence.
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Permeability defects cause pooling & staining
Pooling – serous RPE detachment, SRF (↑ in size, shape & intensity in later phases)
Staining – sclera, ON, drusen, vasculitis. (Leak into tissue rather than anatomical space)
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May be caused by :- 1) BLOCKAGE OF FLUORESCENCE:- - by increased density of pigment (xanthophyll -sensory retina,
melanin- RPE) - deposition of abnormal materials ( hard exudates in sensory retina,
lipofuscin in Best’s disease) - Blood.
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2)obstruction of retinal and choroidal circulation:-
- preventing access of fluorescein to the tissues.
3) loss of vascular tissues:- - in severe myopic degeneration or
choroideremia.
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Due to the 2 barrier filters not having mutually exclusive transmission spectra
Light from bright fundal structures can pass through both filters & expose film. e.g. ONH drusen, astrocytic hamartomas
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Autofluorescence can be diagnostic
FFA can exclude papilloedema
Saves pt from invasive neuro diagnostic procedures!
Optic nerve head drusen
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CB readily leaks fluorescein during aqueous production, into ocular fluids.
Green light emitted when excited by blue light. Illuminates light coloured structures eg: MNF’s, white lesions
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To aid diagnosis
Decisions on whether to Rx or not
Always study FFA’s with other relevant investigations before making final diagnosis
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Start by describing obvious abnormality
Describe hypo/hyperfluorescent components
Intensity of fluorescence with time Area of fluorescence & changes with
time
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Run through anatomical list describing any other abnormalities affecting structures below:
Macula Disc Major arcades Capillaries
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Early venous phase
HyperF – NVD, ma’s
HypoF – blocked due to blood
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HypoF retinal haem 1 ischaemia 2
HyperF ma’s 3, nv’s 4
IRMA 5 Venous beading 6
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HyperF – ma’s (leak) & laser spots (stain)
HypoF – pigmented scars, blood, capillary drop out
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HypoF – massive retinal capillary dropout, pigmented laser scars
HyperF – laser scar staining
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HypoF – retinal capillary closure, SRF, blood
HyperF – retinal vein damage – staining collagen, leaking through damaged endothelial walls
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HyperF – damaged veins staining and leaking, ma’s
HypoF – subretinal and preretinal haems
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Collaterals don’t leak!
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Non-perfusion of retinal vasculature. Vessels appear dark against light background
No capillary perfusion, so empty veins (cattle-trucking)
Choroidal perfusion intact (hence “cherry red spot”); C-R artery sparing in 15%
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RPE atrophy allows choroidal fluorescence through with choroidal “flush”
Does not change size or shape with time
Fades with choroidal fluorescence
Red Free
Late
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Large area of GA
Clear view of choroidal vessels
FFA shows unmasking of choroidal vessels
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RPE “show-through”
Loss of masking
Early lighting up with choroid
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Small defect in outer BR barrier
F enters RPE defect & fills serous retinal elevation “blister” (7% cases)
HyperF - ↑’s in size & intensity
Early
Late
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Breakdown of internal BR barrier
Early leak from parafoveal retinal vessels – hyperF, ↓ in FAZ
Late pooling in classic “petalloid” appearance (NFL)
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Ischaemia & vasculitis incompetent endothelial TJ’s
F leaks into CT of bv’s & stains it. This persists
Late disc staining is normal
ARN
Pars planitis
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Early lacey hyperF “classic”
HypoF “halo” – blood &/or macula pigment
Late leak, blurred margins & apparent ↑ in size
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Type I – PED – well-defined area of early hyperF, margins unchanged
Type II – late leak of undeyermined source – not obvious from early phase
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Choroidal naevus blocking choroidal fluorescence in arterial phase
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Stargardt’s – “dark choroid” (early)
Lipofuscin deposition at RPE
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Fluorescein Angiography, technique interpretation & application, Max Nanjiani (OMP)
www.mrcophth.com/ffainterpretation