OCT, FFA, ICG and FAF Flashcards

(71 cards)

1
Q

OCT mechanism

A

 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

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2
Q

OCT interfernece pattern

A

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

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3
Q

Fourier-domain scanner

A

show more detail and have shorter acquisition time
compared to time-domain scanners (which also leads to less motion artefact)

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4
Q

Limitations of OCT

A

 Requires a transparent media
 Patient co-operation
 Susceptible to motion artefact
 Requires moderate dilation

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5
Q

OCT and GCL

A

50% of retinal ganglion cells in the macul
RNFL _ GCL + ipl - ganglion cell complex

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6
Q

causes of poor OCT image

A

small pupil
corneal or vitreous opaicty
non-co-operative patient

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7
Q

most common OCT protocls

A

3D scan, raster scan, radial scan

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8
Q

3D oct scan

A

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

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9
Q

raster scan

A

o Series of parallel lines
o Can be oriented at different angles, usually higher resolution

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10
Q

OCT radial scane

A

o 6-12 line scans arranged in equal angles with common axis
o Good for picking up pathology like macular holes

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11
Q

OCT retinal thickness

A

Value in microns between the RPE and internal limiting membrane

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12
Q

OCT retinal thickening

A

thickness minus population means of the particular variable in consideration , eg: centre point ( CP) , CP thickness

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13
Q

OCT centre point

A

Intersection of 6 radial scans of the fast macular thickness protocol of OCT

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14
Q

OCT central subfield

A

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

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15
Q

OCT subfiled mean thickness

A

Mean value of 128 thickness values obtained in CS

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16
Q

OCT and diabetes - focal changes

A

Leakage from microaneurysms and surrounding exudates

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17
Q

OCT and diabetes - diffuse retinal thickening

A

No structural changes, however muller cells swelling occur in the outer nuclear layer

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18
Q

OCT and diabetes - CMO

A

(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)

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19
Q

OCT and diabetes - tractional macular oedema

A

epiretinal membrane (ERM), taut posterior vitreous) and lamellar hole formation

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20
Q

OCT and diabetes - cotton wool spots

A

o Lasts between 4-12 weeks
o Sign of ischaemia
o Arise from the retinal nerve fibres layer (RNFL)

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21
Q

OCT and diabetes - retinal laser

A

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

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22
Q

OCT and diabetes - flame haemorrhages

A

these are found in the retinal nerve fibre layer (RNFL)

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23
Q

OCT and diabetes - hard exudate

A

found in the outer plexiform/ outer nuclear layer ( OPL/ ONL)

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24
Q

OCT and diabetes - mirco-aneurysms

A

occur in the inner plexiform/ inner nuclear layer (IPL/INL)

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25
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
26
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
27
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)
28
Fluorescence
he property of emitting a longer wavelength light when stimulated by a shorter wavelength
29
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
30
Side effects of FFA
 Discolouration of skin and urine  Nausea and vomiting  Urticarial rash  Flushing  Photosensitivity  Itch  Discomfort at injection sit
31
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
32
why is the macular darker on FFA
xantophyllic pigment greater pigmentation of cell in the RPE absence of cappillaries in avascular zone
33
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
34
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
35
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
36
arteriovenous phase
Demonstrates laminar flow: the veins are fluorescent near their walls and darker centrally  Lasts for 1-2 seconds
37
venous phase
laminar flow with penetration of fluro into vein walls
38
later phase
Useful to highlight cystoid macular oedema, CSR, or occult subretinal neovascular membranes
39
tissue phase
always pathological as there should be no fluro at this phase
40
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
41
Window defect on FFA
unmasking of the normal choroidal fluorescence  RPE atrophy  Window defects are seen early
42
Hyperflueorescen on FFA
e due to staining of dye: appears late  Drusen  Disciform scars
43
Pseudo-autofluorescence on FFA
: overlap in the spectral transmission of the excitation and barrier filters
44
Indocyanin green angiography
Useful to provide more information about the choroidal circulation
45
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
46
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
47
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
48
concentration of ICG
40mg in 2ml
49
side effects of ICG
nausea/ vomiting back pain discolouration of the stool vasovagal syncope severe anaphylaxis 1 in 2000 contraindicated in pregnancy
50
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
51
Hyperflurorescent causes
Window defect- retinal pigment epithelium defect Leakage of dye - choroidal neovascularization - idiopathic polypoidal choroidal - vasculopathy Abnormal blood vessel - choroidal haemangioma
52
Hypofluorescent causes:
Transmission defect: RPE detachment blood pigments exudate Filing defects choroidal infarcts choroidal atrophy
53
FAF
* FAF is based on the detection of fluorophores * Fluorophores are primarily from RPE lipofuscin. Other sources are subretinal fluid
54
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
55
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
56
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
57
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
58
two main ways of measuring FAF
fundus camera scanning laser ophthalmoscopy
59
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
60
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.
61
FAF increased autofluorescence
RPE dysfunction (increased metabolism), loss of retinal luteal/photopigment and subretinal autofluroscent material
62
FAF decreased autofluorescence
RPE atrophy and blockage of RPE cells
63
FAF uveitis
posterior uveitis, active disease is generally associated with increased autofluorescence. Inactive disease is associated with reduced autofluorescence.
64
FAF and lyonization
autofluorescence diseases with lyonization produce a mottled appearance.
65
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
66
examples of lyonization
 Choroideremia  X-linked ocular albinism  X-linked RP  Lowe syndrome  Fabry diseases
67
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.
68
FAF optic disc
o Optic nerve drusens are associated with increased autofluorescence o Ultrasound scan is more sensitive than FAF in detecting drusen.
69
FAF birdshort
Associated with reduced placoid autofluorescence.
70
FAF best disease
Vitelliform material causes increased autofluorescence
71
FAF APMPEE
* Acute posterior multifocal placoid pigment epitheliopathy ( APMPPE): Inactive disease: patchy reduced autofluorescence.