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Investigations > OCT, FFA, ICG and FAF > Flashcards

OCT, FFA, ICG and FAF Flashcards

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
Q

OCTangiography (OCTA_

A
  • 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
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26
Q

Limitiations of OCTa

A

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

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27
Q

fluorescein angiography (FFA)

A

 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)

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28
Q

Fluorescence

A

he property of emitting a longer wavelength light when stimulated
by a shorter wavelength

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29
Q

why does fluorescein work for

A

 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
Q

Side effects of FFA

A

 Discolouration of skin and urine
 Nausea and vomiting
 Urticarial rash
 Flushing
 Photosensitivity
 Itch
 Discomfort at injection sit

31
Q

why is the diameter of retinal vessels larger on FFA compared to fundus photography

A

A photo only visualises the axial blood column whereas fluorescein reaches the
peripheral blood in the vessel

32
Q

why is the macular darker on FFA

A

xantophyllic pigment
greater pigmentation of cell in the RPE
absence of cappillaries in avascular zone

33
Q

normal phases

A

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
Q

chorodial phase

A

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
Q

arterial phase

A

1-3 seconds after the choroidal phase
 Neovascularisation of the disc (part of the retinal circulation) is visible during
the early arterial phase

36
Q

arteriovenous phase

A

Demonstrates laminar flow: the veins are fluorescent near their walls and darker
centrally
 Lasts for 1-2 seconds

37
Q

venous phase

A

laminar flow with penetration of fluro into vein walls

38
Q

later phase

A

Useful to highlight cystoid macular oedema, CSR, or occult subretinal
neovascular membranes

39
Q

tissue phase

A

always pathological as there should be no fluro at this phase

40
Q

leakage on FFA

A

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
Q

Window defect on FFA

A

unmasking of the normal choroidal fluorescence
 RPE atrophy
 Window defects are seen early

42
Q

Hyperflueorescen on FFA

A

e due to staining of dye: appears late
 Drusen
 Disciform scars

43
Q

Pseudo-autofluorescence on FFA

A

: overlap in the spectral transmission of the excitation and
barrier filters

44
Q

Indocyanin green angiography

A

Useful to provide more information about the choroidal circulation

45
Q

ICG absorption

A

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
Q

properties of ICG

A

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
Q

ICG used for

A

 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
Q

concentration of ICG

A

40mg in 2ml

49
Q

side effects of ICG

A

nausea/ vomiting
back pain
discolouration of the stool
vasovagal syncope
severe anaphylaxis 1 in 2000
contraindicated in pregnancy

50
Q

Phases

A

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
Q

Hyperflurorescent causes

A

Window defect- retinal pigment epithelium defect
Leakage of dye
- choroidal neovascularization
- idiopathic polypoidal choroidal - vasculopathy
Abnormal blood vessel -
choroidal haemangioma

52
Q

Hypofluorescent causes:

A

Transmission defect:
RPE detachment
blood
pigments
exudate
Filing defects
choroidal infarcts
choroidal atrophy

53
Q

FAF

A
  • FAF is based on the detection of fluorophores
  • Fluorophores are primarily from RPE lipofuscin. Other sources are subretinal fluid
54
Q

lipofuscin granules

A

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
Q

how to detect autofluosrecence

A

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
Q

Red free images in FAF

A

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
Q

When to use FAF

A

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
Q

two main ways of measuring FAF

A

fundus camera
scanning laser ophthalmoscopy

59
Q

fundus camera

A
  • 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
Q

scanning laser ophthalmoloscopy

A
  • 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
Q

FAF increased autofluorescence

A

RPE dysfunction (increased metabolism), loss of retinal luteal/photopigment and subretinal autofluroscent material

62
Q

FAF decreased autofluorescence

A

RPE atrophy and blockage of RPE cells

63
Q

FAF uveitis

A

posterior uveitis, active disease is generally associated with increased autofluorescence. Inactive disease is associated with reduced autofluorescence.

64
Q

FAF and lyonization

A

autofluorescence diseases with lyonization produce a mottled appearance.

65
Q

lyonization

A

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
Q

examples of lyonization

A

 Choroideremia
 X-linked ocular albinism
 X-linked RP
 Lowe syndrome
 Fabry diseases

67
Q

FAF on melanoma

A

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
Q

FAF optic disc

A

o Optic nerve drusens are associated with increased autofluorescence
o Ultrasound scan is more sensitive than FAF in detecting drusen.

69
Q

FAF birdshort

A

Associated with reduced placoid autofluorescence.

70
Q

FAF best disease

A

Vitelliform material causes increased autofluorescence

71
Q

FAF APMPEE

A
  • Acute posterior multifocal placoid pigment epitheliopathy ( APMPPE): Inactive disease: patchy reduced autofluorescence.

Investigations (8 decks)

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