OCT, FFA, ICG and FAF Flashcards
OCT mechanism
A broadband low coherence light source (in the infrared range) is directed at the
target
A beam splitter simultaneously directs the light source at a reference mirror
The reflected light from the target and the reference mirror are recombined and
directed to a detector
OCT interfernece pattern
is analysed using low coherence interferometry
The structures of the target reflect varying amounts of light depending on their
distance from the source, producing different interference patterns
Fourier-domain scanner
show more detail and have shorter acquisition time
compared to time-domain scanners (which also leads to less motion artefact)
Limitations of OCT
Requires a transparent media
Patient co-operation
Susceptible to motion artefact
Requires moderate dilation
OCT and GCL
50% of retinal ganglion cells in the macul
RNFL _ GCL + ipl - ganglion cell complex
causes of poor OCT image
small pupil
corneal or vitreous opaicty
non-co-operative patient
most common OCT protocls
3D scan, raster scan, radial scan
3D oct scan
o Horizontal line scans
o Composing of a rectangular box
o Examples: 6mm by 6mm, 7mm by 7mm, 12mm by 9mm
o Generates 3D view of retina which allows for topographic maps, volumetric analysis
raster scan
o Series of parallel lines
o Can be oriented at different angles, usually higher resolution
OCT radial scane
o 6-12 line scans arranged in equal angles with common axis
o Good for picking up pathology like macular holes
OCT retinal thickness
Value in microns between the RPE and internal limiting membrane
OCT retinal thickening
thickness minus population means of the particular variable in consideration , eg: centre point ( CP) , CP thickness
OCT centre point
Intersection of 6 radial scans of the fast macular thickness protocol of OCT
OCT central subfield
o Circular area of 1mm diameters centered around CP
o Correlates with visual acuity
o 128 thickness measurements are made in this circular area in fast macula protocol
OCT subfiled mean thickness
Mean value of 128 thickness values obtained in CS
OCT and diabetes - focal changes
Leakage from microaneurysms and surrounding exudates
OCT and diabetes - diffuse retinal thickening
No structural changes, however muller cells swelling occur in the outer nuclear layer
OCT and diabetes - CMO
(caused by muller cell necrosis, and cystic fluid spaces), this occurs in the outer nuclear layer/outer plexiform
o Acute: Small cystic spaces
o Chronic: Coalesce to form large cystic spaces, with retinal tissue loss
o cystic swelling in diabetic macula disease usually extends to ganglion cell layer (GCL)
OCT and diabetes - tractional macular oedema
epiretinal membrane (ERM), taut posterior vitreous) and lamellar hole formation
OCT and diabetes - cotton wool spots
o Lasts between 4-12 weeks
o Sign of ischaemia
o Arise from the retinal nerve fibres layer (RNFL)
OCT and diabetes - retinal laser
o In the acute stage, there can be hyper-reflectivity of the outer nuclear layer (ONL)
o There can be loss of the retinal pigment epithelium (RPE) layer following laser treatment
OCT and diabetes - flame haemorrhages
these are found in the retinal nerve fibre layer (RNFL)
OCT and diabetes - hard exudate
found in the outer plexiform/ outer nuclear layer ( OPL/ ONL)
OCT and diabetes - mirco-aneurysms
occur in the inner plexiform/ inner nuclear layer (IPL/INL)
OCTangiography (OCTA_
- Non-invasive technique to visualize the vasculature of the retina and choroid
- Multiple OCT B-scans are taken at the same point in the retina.
- OCTA is good at detecting abnormal choroidal vessels
Limitiations of OCTa
o presence of artifacts related to eye movement
o superimposition of images from different planes
o artifacts from eye disease/ eye properties, eg: intravitreal opacities, subretinal fluid
fluorescein angiography (FFA)
White light from the camera passes through a blue excitation filter
Blue light (wavelength of 490nm) is therefore transmitted to the fundus and is
absorbed by the fluorescein molecules in the retinal and choroidal vasculature
They are stimulated to emit yellow-green light (530nm)
Fluorescence
he property of emitting a longer wavelength light when stimulated
by a shorter wavelength
why does fluorescein work for
Can easily pass between endothelial cells in the choriocapillaris and other
capillary beds in the body (therefore, in other tissues it does not stay
intravascular)
The RPE tight junctions normally prevent this leak into the neural retina (outer
barrier)
The tight junctions between retinal vascular endothelial cells also prevent leak
normally (inner barrier)
Fluorescein is 80-85% bound to serum protein (it is primarily hydrophilic)
Leaks readily from fenestrated choriocapillaris
Side effects of FFA
Discolouration of skin and urine
Nausea and vomiting
Urticarial rash
Flushing
Photosensitivity
Itch
Discomfort at injection sit
why is the diameter of retinal vessels larger on FFA compared to fundus photography
A photo only visualises the axial blood column whereas fluorescein reaches the
peripheral blood in the vessel
why is the macular darker on FFA
xantophyllic pigment
greater pigmentation of cell in the RPE
absence of cappillaries in avascular zone
normal phases
Arm to retina - 10-12 seconds
Chorodial from 12 seconds
Arterial 1-3 seconds after chorodial
Ateriovenous / capillary lasts for 1-2 seconds
Venous
Late phase
Tissue phase - 5-10minutes
chorodial phase
10-12 seconds after injection in young patients but depends on vascular
health
NB: a cilioretinal artery, if present, is a branch of the short posterior ciliary
artery so fills during the choroidal phase
highlights chorocapillaries, ciliary retinal ateries
arterial phase
1-3 seconds after the choroidal phase
Neovascularisation of the disc (part of the retinal circulation) is visible during
the early arterial phase
arteriovenous phase
Demonstrates laminar flow: the veins are fluorescent near their walls and darker
centrally
Lasts for 1-2 seconds
venous phase
laminar flow with penetration of fluro into vein walls
later phase
Useful to highlight cystoid macular oedema, CSR, or occult subretinal
neovascular membranes
tissue phase
always pathological as there should be no fluro at this phase
leakage on FFA
increases in size and intensity of hyperfluorescence over time
Incompetence of the inner or outer blood-retinal barriers
Neovascularisation: defective inner barrier
Defective choroidal circulation eg. AMD
Window defect on FFA
unmasking of the normal choroidal fluorescence
RPE atrophy
Window defects are seen early
Hyperflueorescen on FFA
e due to staining of dye: appears late
Drusen
Disciform scars
Pseudo-autofluorescence on FFA
: overlap in the spectral transmission of the excitation and
barrier filters
Indocyanin green angiography
Useful to provide more information about the choroidal circulation
ICG absorption
ICG peak absorption (790-805nm) and fluorescence (770-880nm) are within the
infrared range of wavelengths (>800nm) and thus can penetrate the overlying RPE,
pigments and any overlying haemorrhages
properties of ICG
circulates 98% bound to plasma protein (it is amphiphilic, ie. both hydro- and
lipophilic therefore binds lipproteins and phospholipids) so less leakage
Excreted by the hepatobiliary system: discoloured stool for several days
ICG used for
Occult/poorly defined CNVM: can be more easily measured
Polypoidal CNV
Fibrovascular PEDs
Medial opacities/vitreous haemorrhages
Photophobic patients (they cannot see the infrared lights)
Inflammatory disease: to identify possibly occult choroidal disease (crucial
investigation for inflammatory disease)
white dot syndromes
Wogt Koyangi Harda disease
Sympatheitc ophthalmeia
concentration of ICG
40mg in 2ml
side effects of ICG
nausea/ vomiting
back pain
discolouration of the stool
vasovagal syncope
severe anaphylaxis 1 in 2000
contraindicated in pregnancy
Phases
Early phase 2s-60s
choroidal arteries fill and appear tortuous
1-3 minutes
choroidal vein becomes prominent , appear straight, drain towards vortex vein
3-15 minutes
diffuse hyperfluorescence, diffusion of dye from choriocapillaries
Late phase 15-30mins
dye can remain in neovascular tissue after it is has left choroidal and retinal circulation
Hyperflurorescent causes
Window defect- retinal pigment epithelium defect
Leakage of dye
- choroidal neovascularization
- idiopathic polypoidal choroidal - vasculopathy
Abnormal blood vessel -
choroidal haemangioma
Hypofluorescent causes:
Transmission defect:
RPE detachment
blood
pigments
exudate
Filing defects
choroidal infarcts
choroidal atrophy
FAF
- FAF is based on the detection of fluorophores
- Fluorophores are primarily from RPE lipofuscin. Other sources are subretinal fluid
lipofuscin granules
are residual outer photoreceptor segments found in the RPE
o Referred to as a wear and tear pigment
o Lipofuscin accumulation increases with age
o Lipofuscin cause autofluorescence
how to detect autofluosrecence
488nm laser. This is the same as the laser used in fundus fluorescein angiography
o The barrier filter separates the excitatory light and the fluorescent light
Red free images in FAF
are used for pathologies with low contrast compared to red colours
o Red-free filter essentially blocks out ‘noise’ from images
o Confusingly sometimes known as ‘Green Filter’ because you are blocking red and seeing ‘Green’ wavelength of between 540-570nm
When to use FAF
o Detection of microhyphaema in anterior chamber
o Assessing retinal nerve fibre layer for glaucoma damage
o Better visualisation of retinal pathologies such as dot/blot haemorrhages
two main ways of measuring FAF
fundus camera
scanning laser ophthalmoscopy
fundus camera
- Uses green light.
- Uses a single flash of light
- Reduces lens interference
- Matches the wavelengths of fluorophores in the retina.
- Better for detecting fluorophores in the subretinal space eg: central serous retinopathy . This is more pronounced as detachment becomes chronic.
- Retinal fluorophores are thought to be outer retinal segments that could not be phagocytosed
scanning laser ophthalmoloscopy
- Typically uses 488nm excitation filters. Usually can perform fundus fluorescein angiography on the same machine etc.
- Reduces lens interference and scattered light
- Considered the gold standard for FAF.
- Infrared SLO uses a 787nm excitation filter
- This detects a product that arises from the interaction of melanin and lipofuscin called melanolipofuscin.
FAF increased autofluorescence
RPE dysfunction (increased metabolism), loss of retinal luteal/photopigment and subretinal autofluroscent material
FAF decreased autofluorescence
RPE atrophy and blockage of RPE cells
FAF uveitis
posterior uveitis, active disease is generally associated with increased autofluorescence. Inactive disease is associated with reduced autofluorescence.
FAF and lyonization
autofluorescence diseases with lyonization produce a mottled appearance.
lyonization
o X-linked recessive traits typically don’t manifest in women
o However, lyonization causes random X chromosome inactivation
o This can produce mild or very rarely, severe disease
examples of lyonization
Choroideremia
X-linked ocular albinism
X-linked RP
Lowe syndrome
Fabry diseases
FAF on melanoma
o The orange pigment on melanomas is autofluorescent.
o Recent leakage is associated with increased autofluorescence, while old leakage is associated with reduced autofluorescence due to RPE death.
FAF optic disc
o Optic nerve drusens are associated with increased autofluorescence
o Ultrasound scan is more sensitive than FAF in detecting drusen.
FAF birdshort
Associated with reduced placoid autofluorescence.
FAF best disease
Vitelliform material causes increased autofluorescence
FAF APMPEE
- Acute posterior multifocal placoid pigment epitheliopathy ( APMPPE): Inactive disease: patchy reduced autofluorescence.
