2. INTRODUCTION
• Makita et al. in 2006
• noninvasive
• 3D and cross sectional data
• real-time volumetric data on chorioretinal vasculature and its flow pattern.
• generates images that resemble an angiogram.
3. Principle
• In OCT scan - patient's retina consists of multiple individual A-scans, which when
compiled into a B-scan provides cross-sectional structural information.
• In OCT A- To generate the image of the retinal microvascularization, each B-
scan of the examination pattern is consecutively repeated several times.
• The contrast comparisons on consecutive B-scans at the same location
reveal some areas with a contrast change over time and some areas with
a constant contrast.
• The temporal change in contrast in a specific location is attributed to the
movement of erythrocytes, which therefore indicates the location of the
vessels.
4. • OCT-A employs two methods for motion detection:
amplitude decorrelation
phase variance.
• Amplitude decorrelaration detects differences in amplitude between two different OCT
B-scans.
• Phase variance is related to the emitted light wave properties, and the variation of phase
when it intercepts moving objects.
• To improve visualization and reduce background noise from normal small eye movements,
two averaging methods were developed.
split spectrum amplitude decorrelation technique
volume averaging
5. Terminologies
Amplitude/Magnitude/Intensity - refer to the amount of light detected by the OCT
system.
• Intensity is related to the power reflected from the sample
• optical field amplitude or magnitude is related to the square root of the intensity
Intensity Variance –
o the variance of signal amplitude (aka magnitude), intensity, or their log transforms.
o These refer to methods which detect motion or flow by looking for change in the OCT
signal over time
6. • PhaseVariance - Phasevariance useschanges in the phase of the OCTsignal as the
means of detecting flow.
• Split-spectrum Amplitude decorrelation Angiography(SSADA)is an efficient
algorithm which improves the signal-to-noise ratio of flow detection by
maximizing the extraction of flow information from speckle variation. This is
achieved by splitting the OCTspectrum, which increasesthe number of usable
image frames and reduces noise from axial bulk motion.
7. Amplitude Decorrelation or Flow Signal:
• Decorrelation is a way to quantify variations in the OCTsignal amplitude without being
affected by the average signal strength.
• The decorrelation value ranges from 0 (no variation) to 1 (maximum variation).
• A higher decorrelation value implies higher flow velocity, up to a limit.
• The slowest flow that can be detected by SSADAis the sensitivity limit, while the
saturation limit is the fastest flow beyond which the decorrelation value cannot
increase further.
• The linear range lies between the sensitivity and saturation limits.
• The decorrelation value is also referred to as the flow signal in OCT angiography.
8. Various algorithms used in OCTA devices are as follows:
1. OCT-based optical microangiography (OMAG)
2. Split-spectrum amplitude decorrelation angiography (SSADA)
3. OCT angiography ratio analysis (OCTARA)
4. Speckle variance
5. Phase variance
6. Correlation mapping
9. • OCTA can be full spectrum (e.g., OMAG, OCTARA) or split spectrum (e.g., SSADA).
• OMAG uses both amplitude and phase in the OCT signals to show the blood flow
within the tissue.
• The OCTARA (OCTA ratio analysis) is the intensity ratio calculation (not amplitude
decorrelation).
• SSADA is based on the decorrelation of OCT signal amplitude due to flow.
10. Scan architecture
• As every OCTA obtained is essentially a cube scan, it is a three-
dimensional (3D) assessment of the retinal vasculature ( traditional
fluorescein or ICG angiography, which is two dimensional.)
• Evaluate the scans from the inner retinal surface right down to the choroid in a
continuous manner.
11. OCT samples a discrete tissue volume and generates a numerical value based on the
reflectivity.
This numerical value corresponds to a Voxel
Each voxel is an estimation of the reflective properties of a small volume of tissue
OCTA repeatedly scans the same discrete tissue volume and detects changes in the
reflectivity signal.
If the changes are above a selected threshold, flow is considered to be present. Thus,
OCTA allows a volumetric rendering of blood vessels.
12. • After processing of the volume scans, the Decorrelation of the images is
calculated.
• The imaging characteristics of the scan for stationary tissues a low decorrelation
high blood flow tissue - High Decorrelation.
• This gives rise to an image that resembles an angiogram
13.
14. En Face Segmentation of Tissue Slab
The 3 macular capillary plexuses are –
1. Superficial retinal vascular plexus is in the nerve fiber layer, ganglion cell layer,
and the superficial portion of the inner plexiform layer.
2. Intermediate capillary plexus is located at the junction between the inner
plexiform layer and the inner nuclear layer.
3. Deep capillary plexus is located at the junction between the inner nuclear layer
and the outer plexiform layer.
• Spaide and colleagues suggested that the intermediate capillary plexus could be
mixed with the deep plexus.
15. 4 en face zones with currently commercially available OCTA devices -
a) Superficial plexus: the capillary network in ganglion cell layer.
b) Deep plexus: the network of capillaries between the outer boundary of the inner
plexiform layer and the midpoint of the outer plexiform layer with total thickness
about 55 microns.
c) Outer retina (photoreceptors): although they do not have vessels, the perfusion
indices are still obtained.
d) Choriocapillaris (choroid): with offshoot of 30 microns below retinal pigment
epithelium
16. Showing the location of 4 en face zones on OCTA in relation to SD-OCT and histology of retina.
Superficial plexus (A) the capillary network in ganglion cell layer and nerve fiber layer;
Deep plexus (B) network of capillaries in inner plexiform layer with offshoot of 55 microns;
Outer retina (C ) in zone of photoreceptors and
Choriocapillaris (D) in zone of inner choroid with offshoot of 30 microns.
17. Superficial Capillary Plexus, (SCP) 25-μm-thickness OCT-A C-scan, shaped on the Inner limiting membra
(ILM) profile. Arteries are clearly distinguishable from veins by the presence of the surrounding hypo-inten
halo due to
the absence of efferent vessels directly coming out from the walls. It is shown as a fine capillary network,
which corresponds to the superficial capillary plexus (SCP). The peri-foveal arcade is clearly visible on 36
18. Deep Capillary Plexus, DCP). 25-μm-thickness OCT-A C-scan, shaped on the ILM profile.
Scan is taken at the level of the inner nuclear layer (INL), 130 μm below the ILM [as shown with the
red line ]. Clearly distinguishable dense capillary network, present all around the perifoveal area,
corresponding to the DCP. very dense, regularly anastomosed, with sinuous arborization, and without
visibility of arterioles and venules.
19. At the level of the Choriocapillaris (CC) 10-μm-thickness OCT-A C-scan, shaped on the Bruch’s
membrane (BM) profile. The scan is taken at 10 μm below the BM . Diffuse hyperintense signal without a
fine capillary network appreciable. Relatively homogenous grayish image that seems composed by a large
number of tiny dots either hyper or hypo-intense. This pattern could correspond to the very richly
anastomosed vascular layer of the choriocapillaris.
20. At the level of the Sattler’s Layer (medium choroidal vessels), 10-μm-thickness OCT-A
C-scan shaped on the Bruch’s membrane (BM) profile. The C-scan is taken at 70 μm below the BM .
The diffuse hyperintense signal due to the choriocapillaris does not allow a clear visualization of the
medium
choroidal vessels. Several hypointense linear structures are appreciable in this C-scan section, probably
representing the choroidal vessels present at this level and partially masked by the signal
absorbed/diffused by
21. At the level of the Haller’s Layer (large choroidal vessels), 10-μm-thickness .
The C-scan is taken at 140 μm below the BM .Numerous hypo-intense linear structures are evident.
These could be related to large choroidal vessels present at this level. As it was for the Sattler’s
layer, the decorrelation signal in this vessels is masked by the absorption of the structures above.
22. Quantification of flow information
• For disease diagnosis and management, objective quantification of flow
information of retinal vasculature is of great interest.
> Two metric perfusion indices -
• Vessel density (VD) - defined as percentage area occupied by vessels in the
segmented area.
• Flow index (FI) - defined as the average flow signal (which is correlated with flow
velocity) in a selected region.
24. HEIDELBERG SPECTRALIS OPTICAL COHERENCE
TOMOGRAPHY ANGIOGRAPHY
• Spectralis OCTA prototype (Spectralis OCT2; Heidelberg Engineering)
• An amplitude decorrelation algorithm developed by Heidelberg Engineering was
applied to a volume Scan ,which was composed of 131 B-scans (35 frames per
scan) at a distance of 11 microns each.
• The automated real-time mode combined with the eye-tracking system of the
Spectralis OCT 2 prototype (TruTrack) improves the signal-to-noise ratio; this,
associated with the reduced distance between 2 consecutive Bscans (11 microns),
facilitates high resolution.
25. • The OCTA software (Heyex Software version 1.9.201.0; Heidelberg Engineering)
provides an automated segmentation algorithm for retinal and choroidal layers.
• 2 automatically segmented lines separated by 30 microns and shaped on the
basement membrane profile can be manually fine-tuned to be located
immediately above the RPE and then moved progressively deeper in 30-micron
steps upto the choroidal-scleral interface.
26. INTERPRETATION OF OCTA
• As OCTA provides information at different layers of retina, it needs careful axial
segmentation to preserve important data on perfused structures and to avoid the
risk of generating superimposed images, which are typical of dye angiographies.
• An automated segmentation algorithm for both retinal and choroidal layers is
provided by most different OCTA devices, which may not correctly correlate to
relevant anatomic layers or the results.
• In the case of accentuated macular retinal/choroidal disruptions (various
pathologies) causing potential segmentation errors, specific manual correction
allows modification of the shape and the localization of each layer.
29. • Fluorescein angiography image of the central macula in a healthy subject .
• OCT angiography image (3 × 3 mm) of the superficial vascular plexus showing the vascular
centripetal distribution “web-like shape” towards the fovea.
• OCT angiography image (3 × 3 mm) of the deep vascular plexus showing a close-knit pattern of
vessels around the foveal avascular zone.
OCT angiography identifies more about details of the capillary beds (superficial and deep) than
standard Fluorescein Angiography.
a b c
30. ARTIFACTS IN OCTA
Motion artifacts in a subject with
• eye movements
• repeated optical coherence tomography angiography with no eye
movements.
31. Motion correction technology incorporated to the Optovue XR Avanti with AngioVue software.
(a) Fast-X and (b) Fast-Y raster scan- the white lines (yellow arrows) due to motion artifacts, before the
incorporation of motion correction technology.
(c) The two orthogonal volumes are then merged to form a single optical coherence tomography
angiography volume. MCT
32. Poor-quality optical coherence tomography angiograms (a, superficial plexus; b, deep plexus; c, outer
retina; d, choriocapillaris) due to gross eye movements. Neither quantitative nor qualitative
assessment would be possible in this situation
33. Projection artifacts in a subject with choroidal neovascular membrane (CNV).
OCTA image of the A: superficial plexus projects its vessels (blue arrows) in
B: deep plexus.
In-built software removes projection artifacts in C: outer retinal
(photoreceptor zone) allowing better visualization of CNV.
35. OCTA IN WET AMD
CRITERIA FOR DIAGNOSING CNVM
C Scan between RPE and Bruch’s membrane
1. Shape: A well-defined (tortuous vessels, lacy-wheel or sea-fan shaped) CNV
lesion in contrast to one with long filamentous linear vessels.
36. 2. Branching pattern: Numerous tiny capillaries in contrast to rare
large mature vessels.
38. 4. Morphology of the vessel termini : Presence of a peripheral arcade in contrast to
a “dead tree” appearance.
39. 5.C SCAN - Below the Bruch’s membrane, at the level of the choriocapillaris layer.
Perilesional Halo : Presence of a perilesional hypo-intense halo, considered as regions of
choriocapillaris alteration, either corresponding to flow impairment and/or localized
atrophy.
41. • Color fundus photo shows multiple
drusen with some pigmentary change.
No subretinal fluid, exudate or
hemorrhage is apparent.
• Arterial phase FA.
• Early venous phase FA demonstrates
fluorescein uptake by the drusen and
an area of hyperfluorescence with low
grade oozing.
• Late venous phase FA shows slight
increased hyperfluorescence in the
same area without a well-defined net.
42. • SD-OCT shows irregularity of RPE and ellipsoid zone with drusen. Mild subretinal fluid is present (yellow arrow)
• OCTA with manual shows no abnormal vessels in the outer retina.
• OCTA “default outer retina slab setting” up to the RPE to avoid picking up flow signal from beneath the RPE.
No CNV is detected above the RPE.
• OCT angiography of the choroid slab clearly demonstrates blood flow in a neovascular net.
43. Type 1 CNV poorly identified by FA
• Color fundus photo shows multiple small to medium size drusen with pigment stippling. Radiating
petalloid RPE atrophy is also noted.
• SD-OCT reveals multiple drusen with irregularity of the RPE and the ellipsoid zone.A small amount of
subfoveal fluid is present.
• Early venous phase FA demonstrates a pigment window defect and some fluorescein staining of drusen.
No definite leakage is present.
• Late venous phase FA: slight increased fluorescence of the area with radiating petalloid pigment atrophy.
There is no definite leakage to confirm a CNV.
44. • OCT angiography of the superficial retina slab. No abnormal vessels are present in this
section.
• OCT angiography with manual segmentation by moving the lower border of “default outer
retina slab setting” up to the RPE to avoid picking up flow signal below the RPE. No definite
CNV is detected.
• OCT angiography of the choroid slab demonstrates the small, multi-looped CNV (in yellow
45. Type 1 CNV with vascularized PED.
• Color fundus photo shows an old chorioretinal scar
with RPE atrophy temporal to the macula. No
significant drusen or geographic atrophy are
present. The foveal reflex is absent. No classic PED
with well demarcated border can be demonstrated.
• Arterial phase FA shows pigment window defect
corresponding to the chorioretinal scar. There is
irregular increased transmission of choroidal
fluorescence surrounding the fovea.
• AV phase FA shows no definite dye pooling or
leakage. An extensive irregular pigment window
defect is present in the macular area.
• Late venous phase FA shows faint fluorescein
dye pooling temporal to the fovea in addition to the
pigment window defect with hyperfluorescence.
A
46. • SD-OCT demonstrates moderately elevated PED with irregular surface, and some mild hyper-reflective
spots adherent to the inner surface of the dome-shaped PED (yellow arrow). A significant amount of
subretinal fluid is present (red arrow).
• OCT angiography with manual full thickness retinal segmentation shows no abnormal blood flow from the
inner retina to the inner RPE surface.
• Manual segmentation of OCT angiography with a curved reference line at the outer retina above the RPE
• Manual segmentation of OCT angiography with a curved reference line under the dome of the PED reveals
a tree-branch like CNV underneath the RPE (in yellow circle).
47. Type 1 Neo. AMD
Fundus –macular drusen
Early phase –hyperfluorescence
of drusen
Late phase –hyperfluorescent
stain with no obvious leak
OCT–drusenoid PEDwith
mild SRF
OCTA–CNVM complex
deep to RPE
48. Active type 1
neovascularization (left)
and color-coded
highlighting of thevessel
complex for density analysis
(right).
Mature vascular complex
with prominent feeder
and dilated core vessels
and finer interlacing and
anastomosing vessels
toward the periphery of
the lesion.
49. ACTIVE CNV TYPE-I SUB-EPITHELIAL OR OCCULT CNV
FFA-In mid AV phase, an irregular
hyper-fluorescence is evident with
pinpoints in the macular area, with poorly
defined irregular borders.
FFA-late phase: Well-defined hyper fluorescent
area due to staining phenomena, mainly in the
centre of the CNV lesion and some fluorescein
leakage at the border of the lesion
50. OCT-A: C-scan (30 μm above the RPE): No evidence of clear
decorrelation signal that could be attributed to CNV. The highly
hypo-intense areas are caused by subretinal fluid accumulation.
Some slightly hyper-intense signals are due to “pseudo-images”
of the retinal vessels (yellow
arrows) caused by the reflectivity of the RPE or by the proximity
of some intensely perfused structures (choriocapillaris).
51. C-scan (above the Bruch’s Membrane)shows almost the
whole extension of the neo-vascular network. (yellow dashed
line). This part of the lesion is mainly made by large mature
vessels with a “dead-tree” aspect. Some tiny ones forming
loops, anastomoses and a peripheral anastomotic arcades
(green arrows). This could be an index of very localized
activity or recurrence of this part of the lesion
• C scan below bruchs membrane diffuse hyper-intense
signal, probably due to remnants of the choriocapillaris
and the Sattler’s layer. Some large choroidal vessels
(green arrows) are also visible as hypo-intense tubular
structure. This could be due to the presence of highly
hyper-intense signal from the structures above (i.e.
choriocapillaris or CNV), able to hide the decorrelation
signal coming from the large choroidal vessels layer
52. • The OCT-A allows a clear visualization of almost the entire neo-vascular network.
• In the centre, large «mature» vessels, long, linear with few branches.
• But at the periphery of the lesion, development of a typical sea fan shaped CNV
branch with fine tiny vessels, with anastomoses and loops and a peripheral
arcade, mainly in the inferior and nasal part
• This is a mixed lesion with a centre already stabilized and a peripheral part again
active, suggesting a recurrence and indication for (re) treatment.
53. ACTIVE TYPE I CNV (SUB-EPITHELIAL/OCCULT CNV)
FFA AV PHASE-Irregular hyper-fluorescence with pinpoints in the macular area, the borders are poorly
defined and irregular, with a hypo-fluorescent halo.
FFA (late phase): Hyper fluorescent areas due to the staining phenomena mainly in the centre of the CNV
and slight fluorescein leakage at the border of the lesion
54. Large, fibrovascular PED, almost involving the entire
macular area, with a heterogeneous pattern (some
hyperreflective structures and several hypo-reflective
spaces), has resulted in an upward dislocation of the
neuro sensory retina and a downward one of the
Bruch’s membrane,the latter is seen to be detached
from the RPE layer
OCT-A: C-scan (30 μm above the RPE): No evidence of
clear decorrelation signal that could be attributed to CNV.
Some slightly hyper-intense signals are due to “pseudo-
images” of the retinal vessels (yellow arrows) caused by
the reflectivity of the RPE or by the proximity of some
intensely perfused structures (choriocapillaris)
55. OCT-A: C-scan (back surface of the RPE): The 30-μm C-
scan section is positioned at the back surface of the RPE
and therefore inside the PED. Neo-vascular network,
mainly composed of numerous finely anastomosed
sinuous vessels (green arrows), with a peripheral arcade
(yellow arrows) is clearly seen
OCT-A: C-scan (below the Bruch’s Membrane):
The 30-μm C-scan section is positioned below the
Bruch’s membrane, directly inside the choroid.
Some areas of hyper-intense signals, while several
confluent large choroidal vessels are also visible as
hypo-intense structures (yellow arrow)
56. • OCT-A shows a broad neovascular network, mainly composed of
numerous, finely anastomosed, sinuous vessels and a peripheral
arcade.
• This is a lesion, with a centre with a partially stabilized centre and a
periphery that is still moderately active, suggesting persistence of
activity and thus indicating prolongation of treatment.
57. TYPE I CNV (SUB-EPITHELIAL/OCCULT CNV) QUIESCENT/RECURRENT
FFA (AVphase): Large hyper fluorescent macular lesion, with well-defined borders. The lesion appears to be
composed of two major hyper fluorescent components, separated by a sickle-shaped hypo fluorescent
area. Numerous hyperhypo fluorescent pinpoints are also seen, involving the entire macular area.
FFA(late phase): Marked hyperfluorescence of the two components of the lesion due to a staining effect
there are no clear signs of fluorescein leakage.
58. A large, “dome-shaped” fibro vascular PED, almost involving the entire macular area, has resulted in
an upward dislocation of the neurosensory retina. The PED has a heterogeneous hyper reflective
appearance, probably due to the concomitant presence of new vessels and scar tissue.
The choroid is significantly thinned and in some areas, only the large choroidal vessels (Haller’s layer)
are seen.
59. OCT-A: C-scan (30 μm above the RPE): No evidence
of a clear decorrelation signal that could be
attributed to CNV. The hyper-intense signal is due to
“pseudo-images” of retinal vessels (yellow arrows)
caused by the reflectivity of the RPE or by the
proximity of some intensely perfused structures
(choriocapillaris).
OCT-A: C-scan (back surface of the RPE): The
30-μmC-scan section is positioned at the back
surface of the RPE and therefore inside the
PED. Some tiny vessels are seen, forming a
poorly defined neo-vascular network (yellow
dashed line).
60. OCT-A: C-scan (below the Bruch’s Membrane. A diffuse
hyper-intense signal is appreciable probably
caused by remnants of the choriocapillaris and the
Sattler’s layer. There are high hypo-intense tubular
structures (yellow arrows) due to large choroidal draining
vessels immediately below the lesion
OCT-A shows a well-circumscribed CNV
The centre of the lesion is mainly filled
with large mature vessels.
There is concomitant presence of large
mature vessels in the centre and tiny
ones at the borders of the lesion, but
without a well defined arcade and
having a "dead-tree" pattern.
This appearance suggests a quiescent
CNV but is till doubtful due to the
numerous tiny vessels;
suggesting close follow up is
recommended.
61. CNV TYPE I QUIESCENT
FFA (arterio-venous phase): Poorly circumscribed hyper fluorescent macular lesion, with irregular borders
and pinpoints. Numerous hyper-fluorescent tiny spots are seen almost involving the entire macular area
,these are due to the presence of hard drusen.
FFA (late phase): The hyper fluorescent area (staining effect) does not increase or show appreciable signs of
fluorescein leakage.
62. Focal interruptions in the Ellipsoid Zone. A “dome-shaped” fibro
vascular PED almost involving the entire macular area has resulted in
an upward dislocation of the neurosensory retina
63. OCT-A: C-scan (30 μm above the RPE): No evidence of
a clear decorrelation signal that could be attributed to
CNV. The hyper-intense signal is due to “pseudo-
images” of the retinal vessels caused by the
reflectivity of the RPE or the proximity of some
intensely perfused structures (choriocapillaris).
OCT-A: C-scan (back surface of the RPE): The 30
μm C-scan section is positioned at the back
surface of the RPE, therefore inside the PED.
Several mid-diameter vessels that seem to have
a radial distribution are seen.
64. OCT-A: C-scan (above the Bruch’s Membrane): It
shows a “spiked-wheel” shaped CNV. The centre of
the lesion is mainly composed of large mature vessels
that branch into some smaller ones toward the
periphery. The number of anastomoses is limited and
the vessel’s termini have a relative “dead-tree”
appearance
OCT-A: C-scan (below the Bruch’s Membrane):.
A diffuse hyper-intense signals evident probably
due to the remnants of the choriocapillaris and
the Sattler’s layer. There are also several high
hypo-intense tubular structures due to the large
choroidal vessels draining just below the lesion
65. • OCT-A shows a “spiked wheel” shaped CNV. The centre of the lesion is
mainly composed of large mature vessels that branch into some
smaller ones toward the periphery. The number of anastomoses is
limited and the vessel’s termini have a relative “dead-tree”
appearance.
• The “dead tree” appearance suggests a quiescent neo-vascular
lesion. It does not appear to be necessary to prolong the treatment.
67. TYPE II CNVM
• Color fundus photo shows a dirty
grayish type 2 CNV with adjacent
subretinal hemorrhage and
surrounding retinal edema.
• SD-OCT demonstrates a small
subretinal CNV (white arrow) and
subretinal fluid.
• Early venous phase FA at shows a
lacy pattern fluorescein filling of
the small CNV temporal to the
macula with surrounding blocked
fluorescence.
• Late phase FA - intense leakage
from the CNV.
68. • Superficial retina slab of the OCT angiography shows no abnormal vascular flow.
• Manual OCT angiography segmentation with the lower border of tissue slab set just above the RPE ,
shows a small subretinal CNV.
• OCT angiography of the outer retina and RPE slab shows a significant flow signal from the CNV.
• OCT angiography of the choroid slab shows the CNV as well. A 360 degree dark zone surrounds the CNV
net, corresponding well to the area of blocked fluorescence in FA.
E
69. • Color fundus photo shows a thick fibrovascular CNV
and significant subretinal fluid surrounding the CNV
complex. Subretinal hemorrhage at the upper border
of the CNV complex is also present.
• Venous phase FFA reveals a cnv with fluorescein
leakage. There is fluorescein blockage surrounding the
CNV.
• Late phase FA shows fluorescein leakage from cnv
with complete staining of the whole complex. The
subretinal blood at the upper border of the CNV is
causing significant fluorescein blockage.
• SDOCT demonstrates a thick fibrovascular membrane
under the sensory retina and RPE (yellow arrow).
Significant subretinal fluid is present nasal to the
fibrovascular membrane (red arrow). Retinal
architecture, especially the outer retina in the
macular area, is distorted.
A
70. • OCT A with manual full-thickness retinal segmentation demonstrates a see-through large CNV net with
significant blood flow.
• OCT A using the default outer retina shows a large CNV with multiple branches.
• OCT A of the choroid slab shows significant blood flow in the thick CNV. A feeder vessel is visible centrally.
A 360 degree dark zone surrounds the CNV net, corresponding well to the area of blocked fluorescence in
FA.
71. Type 2 Neo AMD
Medusa- shaped type 2
neovascular complex
located above the
retinal pigment
epithelium (RPE).
The high- flow core
feeder vessel (arrow) is
the likely entry point
into the subretinal
space.
72. Images of a patient with choroidal neovascular membrane (CNV) showing typical Medusa Head
appearance. Optical coherence tomography angiography (OCTA) images (A-C ) depicts the en face
images (top panel ) with corresponding SD-OCT images (bottom panel ).
The superficial plexus (A) shows disruption of vascularity due to fluid accumulation in the retina; the
photoreceptor zone (B) shows CNV lesion (white arrows) which is better visualized in the
choriocapillaris zone (red arrows) (C ).
An analogous medusa head (D) image where face of medusa represents central dark area of panels B
and C and the vessels represent the serpents
73. Effect of Anti-VEGF treatment in Exudative AMD
En face OCTA images of patient with CNVM before and after treatment with anti-VEGF
with corresponding SD-OCT (bottompanel).
The pretreatment baseline image (A) shows prominent CNV lesion which regresses 1
week after treatment (B) and reoccurs after a month (C ).
75. ATROPHIC AMD
FFA (AV phase): Well-circumscribed hyper fluorescent macular lesion, with pinpoints. There are also some
hypo fluorescent areas inside the lesion (RPE hyperplasia).
FFA (late phase): The hyper fluorescent area does not increase (staining effect) or show appreciable signs of
fluorescein leakage.
76. The foveal depression is substantially impaired without sub/intra-retinal fluid
accumulation. There is a diffuse outer retinal atrophy in the macular area, involving almost all the layers, from
the Inner Nuclear Layer to the photoreceptors.
The RPE is not visible in the sub-foveal area. There appears to be areas of focal thickening at the border of
the atrophy, probably due to RPE hyperplasia.
The choroid is significantly thinned in the macular area and only some large choroidal vessels are appreciable.
77. OCT-A: C-scan (30 μm above the RPE in foveal area):
at the level of the Ganglion Cells Layer where the
superficial capillary plexus (SCP) is normally located.
In this case, a significantly enlarged perifoveal arcade is
seen due to the extensive retinal impairment caused
by severe geographic atrophy. The SCP appears to be
almost fully preserved and normally perfused.
OCT-A: C-scan (back surface of the RPE): There is clear
visualization of some mid-diameter vessels (Sattler’s
Layer) and large choroidal vessels (Haller’s Layer) due to
diffuse atrophy of choriocapillaris. There is no evidence
of any decorrelation signal that could be attributed to a
neo-vascular network
78. • On OCT-A, some mid-diameter vessels (Sattler’s and large choroidal
vessels are seen.
• This is due to the diffuse atrophy of the choriocapillaris.
• There is no evidence of a neo-vascular network at the centre or at the
borders of the lesion.
• Therefore, this is a typical case of atrophic AMD without any neo-
vascular complications.
• There is no indication for treatment with intra vitreous injections.
79. DIABETIC MACULAR EDEMA
BEFORE ANTI VEGF
• Superficial inner retina- few pockets of edema
as dark spaces between vessels .
• Deep inner retina- multiple cysts
AFTER ANTI VEGF
• Superficial inner retina - decreased cystic
changes. Corresponding OCT B-scan does not
show edema
• Deep inner retina demonstrates that the
edema is mostly improved. The corresponding
OCT B-scan does not show evidence of DME
EN FACE OCT OF DEEPER LAYERS IS BEST
FOR VISUALISATION OF CYSTIC PLACES
80. • Patient with diabetic macular edema. OCT-A depicts vascular loops and cysts in superficial and deep plexus .
• En face OCT is best technique to outline cystic changes in DME
• OCT scan.
81. MICROANEURYSMS
• FFA-Microaneurysms are circled in yellow.
• OCT A-. Microaneurysms that are seen on FA that are also seen on OCTA are circled in
yellow. Microaneurysms on FA that are seen as areas of capillary nonperfusion on OCTA are
circled in blue.
• Areas where microaneurysms are seen on FA, but not on OCTA are circled in red.
82. • Since some microaneurysms may have slower flow than the sensitivity threshold,
these microaneurysms are not detected by the OCTA. If the interscan time is
increased, sensitivity to visualizing microaneurysms (slow flow lesions) will
increase, but there is a tradeoff of increased noise from eye motion.
• FA in the eye of a patient with diabetic macular edema, showing one leaking
microaneurysms and some nonleaking microaneurysms.
• The OCT A demonstrates these microaneurysms.
• When the OCT thickness map is superimposed over the OCTA, the pattern of
edema is consistent with leakage from one, but not from theother
microaneurysms.
83. FAZ area estimated by OCT Angiography (A) and fluorescein angiography (B) in healthy subject.
Note the same area in square millimeters measured in both noninvasive and invasive imaging
techniques
84. Nondiabetic eye.
The foveal avascular zone (FAZ) is demarcated in
yellow and measures 0.16 mm2
the perifoveal intercapillary area is delineated in
white and measures 0.35 mm2.
Diabetic eye
(FAZ) and perifoveal intercapillary area appear
enlarged. FAZ is demarcated in yellow and
measures 0.394 mm2 while the perifoveal
intercapillary area is delineated in white and
measures 0.881 mm2.
85. OCT A
• healthy young subject
• child with albinism
Shows absence of FAZ. Note retinal capillaries crossing the central foveal area where capillaries are
usually absent.A
86. OCT angiography showing interindividual variation in shape and size of FAZ area
in young healthy subjects
87. An eye with NPDR showing a greatly enlarged FAZ , surrounding
microaneurysms (examples circled in yellow), and telangiectatic vessels
(examples marked by yellow *).
88. OCT angiogram of different sizes (8 x 8 mm, 6 x 6 mm and 3 x 3 mm) at superior temporal
arcade of the left of a patient with non-proliferative diabetic retinopathy (A-C). Note better
vascular details and non-perfusion areas with 3 x 3 mm scan .
89. Capillary Perfusion Density
Mapping (ANGIOANALYTICS)
OCTA color-coded capillary
perfusion density mapping.
Bright red represents a
density of greater
than 50% perfused vessels,
dark blue represents no
perfused vessels,
90. Arterial Occlusions
Color fundus photograph
demonstrates retinal
whitening with a
“cherry-red spot” at the
(a) foveola .
Macular edema and
increased thickness on
optical coherence
tomography (OCT)
91. CRAO
Decreased arterial perfusion
is evident in the macula on
FFAby comparing areas of
hypofluorescence to the
fellow eye.
OCTangiography of similar
regions demonstrates flow
void with more capillary
detail. This further enables
enhanced visualization of the
foveal avascular zone.
92. BRAO
A- fundus photo
B-FFA showing non perfusion
I,j-superficial and deep retina
capillary network
D,e- capillary perfusion
analysis
93. CHRONICBRAO
3333
Chronic BRAO
OCT reveals inner
retinal atrophy
inferotemporal to the
macula.
OCTA shows decreased
capillary perfusion in
both retinal capillary
networks .
Arteries and arterioles
remain perfused over
areas of ischemia.
C-superficial plexus
D-deep plexus
The extent of capillary nonperfusion appears less in the (c, d) superficial capillary
network slabs compared to the (e, f) deep.
94. Vein occlusion
Morphological differences of the superficial
plexus between a normal eye and in the
case of a retinal vein occlusion
Morphological differences of the deep
plexus between a normal eye and in the
case of a retinal vein occlusion
95. OCT-angiography of ischemic area in a vein
occlusion. The ischemic area is clearly perceived
as absence of flows in the occluded area. Note
the initial formation of anastomoses and
collateral circulation at the edges of the ischemic
area.
Truncated vessels, with abrupt interruptions in the
areas of non-perfusion in a vein occlusion seen with
OCT-angiography. Note the absence of collateral
branches in the occluded area.
96. CRVOwith CME
a. (OCT) showing hyporeflective areas
that represent intraretinal cysts.
b. OCT en face
c. OCT angiography at the level of
the deep vascular network
showing lack of OCT signal in
well-defined rounded or oblong
areas with smooth borders
corresponding to the intraretinal
cysts
98. Ischemic BRVO
a. Magnified FFA of alocalized area, superior to
the macula.
b. OCT A - Vascular tortuosity, formation of
collaterals, and areasof capillary non perfusion
c. Manual selection followed by automatic
calculation of the capillary dropout/nonflow
areasat the level of the superficial vascular
network.
d. The vascular density is automatically
calculated in the whole scan and in each grid
pattern area.
99. • Multiple areas of leakage corresponding
to preretinal neovascularization are
observed in the fluorescein angiogram.
• A 3 × 3 mm OCTA of the corresponding
yellow dashed square in showing details
of a preretinal neovascularization
complex (green arrowhead) that was
completely obscured by dye leakage in
the fluorescein angiographic image
100. MACULAR TELANGIECTASIA
• Neurodegenerative disease involving Müller cells
• Ectasis of the perifoveal vessels and loss of both inner and outer retinal tissue
• Mac Tel 1- aneurysmal dilatation
• Mac tel 2 –perifoveal telangiectasia
• Mac Tel 1 is the original Gass type 1, which is Coat’s disease in reality. Gass type
2a and 2b were renamed to Mac Tel 2, the Gass 2b was dropped due to the rarity
of the disease.
101. MACULAR TELANGIECTASIA
• Mac Tel 2, Stage1
• Color fundus photo shows no obvious vascular change except for some loss of tissue transparency with
grayish color change at the macular area.
• Early venous phase FA shows very minimal fluorescein oozing at the temporal perifoveal area.
• Late venous phase FA shows a mild increased fluorescein staining at the temporal perifoveal area.
• SD-OCT with horizontal sectioning through the central fovea shows a hyporeflective cystic cavity with a
disruption of the ellipsoid zone. The foveal contour has remained normal
102. • OCT angiography of the superficial
retinal capillary plexus slab shows no
definite vascular abnormal changes.
• OCT angiography of the deep retinal
capillary plexus slab shows early
telangiectatic capillaries at the
temporal perifoveal area.
• OCT angiography does not show any
abnormalities in the outer retina, RPE
or choroid slab
103. Mac Tel 2, Stage 2
• Color fundus photo shows some
telangiectatic vascular change at the
temporal perifoveal area with significant
amount of crystalline deposits at the
superficial retina in a circular fashion.
• Mid venous phase - FA shows fluorescein
dye filling in the dilated temporal
perifoveal capillaries with low grade
leakage.
• Late venous phase FA shows a moderate
amount of dye leakage from 7 to 12
o’clock of the temporal perifoveal area.
• SDOCT- shows cystic cavity with tissue
loss mainly involving IPL, INL,OPL and part
of ONL. Bending and slight irregularity of
the ellipsoid zone is noted.
104. • OCT A of the deep capillary plexus slab
shows capillary ectasia predominantly
involving temporal area with club-head like
dilatation at 11 o’clock of the perifoveal
capillaries, and some disruption of the
inner circle of the perifoveal capillary
network.
• There is also widening of the intervascular
spaces. Segmentation of the outer retina,
RPE and choroidal reveal no abnormal
blood flow.
105. Mac Tel 2, Early stage 3
• Numerous crystalline deposits with mild pigment clumping.
• Early venous phase FA shows a right-angled venule at 3 o’clock in the perifoveal area, and low-grade
fluorescein leakage from the temporal telangiectatic capillaries.
• Late venous phase fa shows moderate fluorescein leakage from the temporal perifoveal dilated
vessels, and mild leakage from the nasal perifoveal area. There are also small hypofluorescent spots
noted due to fluorescein blockage by the pigment clumps.
106. • SD-OCT-multiple hyperreflective spots on the surface of the retina (yellow arrows) corresponding to the
crystalline deposits surrounding the central fovea. A cystic cavity at the fovea, disruption of the ellipsoid zone.
• OCT A of the superficial retina slab shows right-angled draining venule at 3 o’clock, and some vascular drop out with
disruption of the circular perifoveal capillary net.
• OCT A with deep retina slab shows telangiectatic vascular changes predominantly on the temporal side, but there is also
nasal involvement. Significant widening of the intervascular space is noted.
• Manual segmentation with OCT A down to the RPE to avoid picking up any flow signal above the RPE, shows the invasion
of the telangiectatic vessels reaching to the RPE.
• There is no choroidal involvement in the choroid slab.
107. Mac Tel 2, Stage 4 (with SRNV invading the RPE and choroid)
• Color fundus photo shows pigment clumping surrounded by a mild creamy color change temporal to the
fovea.
• Early venous phase and late venous phase FA show fluorescein leakage from the temporal and nasal
perifoveal dilated vessels. There is a pigment clump with fluorescein blockage.
• SD-OCT shows prominent deep retinal hyperreflective spots with optical shadowing effect temporal to the
foveola. Small hyporeflective cavities are also noted along with a disrupted ellipsoid zone.
108. • OCT A of the superficial retina slab and
deep retina slab show irregular dilated
capillaries involving 360º of the perifoveal
area. There is an irregular and widened FAZ,
along with moderate degree of capillary
drop out.
• OCT angiography with manual segmentation
by moving the upper border of the “default
outer retina slab setting” down to the RPE,
to avoid picking up any flow signal above
the RPE, further confirms SRNV invasion
(yellow circle) to the RPE.
• The choroid slab shows SRNV (yellow circle)
in the choroid.
109. Mac Tel 2, Stage 5
patient with disciform fibrovascular membrane.
• Color fundus photo shows a large disciform fibrovascular proliferative membrane with surrounding
retinal edema.
• late venous phase FAs show the fluorescein staining of the whole disciform fibrovascular membrane with
a more intense hyperfluorescent spot in the middle of the complex. Low grade fluorescein leakage is
noted.
• The SD-OCT shows a disciform fibrovascular membrane with increased reflectivity in the outer retina and
RPE . The normal retinal architecture has been disrupted with poor delineation of retinal layers. There is a
cystic cavity temporal to the central fovea
110. • OCT A of the superficial retina slab shows loss of
vessels with capillary drop out temporal to the fovea.
There is disruption of the perifoveal capillary
network.
• The deep retina slab shows vascular ingrowth to the
central fovea with patchy loss of the vascular tree in
the perifoveal area. There is significant dilatation of
the temporal vessels with disturbance of the normal
vascular pattern.
• A neovascular membrane is connected to dilated,
coarse outer layer retinal vessels.
• The SRNV membrane has invaded through the RPE to
reach the choroid
111. CSCR
OCTAscan at the level of the
outer retina shows trace flow
asaresult of projection
artifacts from the superficial
and deep capillary flow.
OCTAat the level of the
choriocapillaris demonstrating
an area of increased choroidal
flow among adark area
(yellow trace) that
corresponds to theoverlying
SRD.
112. CSCR related CNVM
Late frame fluorescein angiogram showing the
CNVasan area of subretinal dye leakage (arrow).
(OCT)scan through the fovea showing serous
retinal detachment with an irregular retinal
pigment epithelium detachment.
OCTA scan at the level of the outer retina
showing the presence of a distinct vascular
network representing a CNV.
The CNV could also be seen on the OCTA scan taken
at the choriocapillaris level.
113. POLYPOIDAL VASCULOPATHY
• OCT notched PED with serous retinal detachment.
• En-face OCT shows a rounded image that may correspond to the polyp (yellow arrow).
• OCT-A: The scans performed at the pigment epithelium detachment in the choriocapillaris (B) and in
the choroid (C) show vascular anomalies within the lesion forming an abnormal vascular network
called a branching vascular network (red arrows).
114. Characterizing Branching Vascular Network Morphology in Polypoidal Choroidal
Vasculopathy by Optical Coherence Tomography Angiography
• Three distinct morphologic patterns of BVN were identified.
(1) The “Trunk” pattern (47%) exhibited major vessel trunk with features including presence of drusen, thin
choroid, and larger BVN area.
(2) The “Glomeruli” pattern (33%) showed anastomotic vascular network without major trunk.
(3) The “Stick” pattern (20%) had localized BVN and the thickest choroid.
• Subtypes 2 and 3 held higher recurrence rate.
• In conclusions, the precise visualization of BVN on OCTA supported that OCTA might be a noninvasive tool to
study the morphology of BVN in PCV, which exhibits three different morphological types.
• Identifying the morphology of BVN has the potential to prognosticate outcomes in PCV patients.
115. Type 1: “The Trunk pattern”: presence of one or more main trunk of neovascular vessel
and may have radiated branches pointing toward periphery of the vascular network.
Type 2: “The Glomeruli pattern”: a vascular network with intensely interconnecting
anastomosis, but without visible major trunk.
Type 3: “The Stick pattern”: localized fine neovascular network without definite pattern.
116. LIMITATIONS
• Inability to show leakage, pooling, staining .
• A tendency for image artifacts.
. Poor repeatability of segmentation algorithms that reliably identify specific retinal vascular layers in the
diseased poorly-fixating eye.
• In the presence of extensive exudation, hemorrhage, edema, and large PED, it was difficult to visualize
neovascular networks on the en face plane using OCTA. This is because OCTA uses automated segmentation
techniques with predetermined anatomical constraints, to resolve flow-based information.
• When there is distortion of retinal layers because of disease in advanced stage, the reconstructed image
observed are inherently imprecise.
117. CONCLUSION
• OCTA is an evolving, but exciting, technology that is non invasive and dyeless.
• OCTA will potentially improve patient care by decreasing the disease morbidity
through earlier detection and intervention.
• Further studies are required in larger cohorts to establish the possible association
between the retinal flow compromise and retinal pathologies.
118. OCTA IN GLAUCOMA
• Glaucoma is associated with reduced blood flow in the optic nerve head (ONH) and retina.
• For glaucoma, the optic nerve head and the peripapillary retinal perfusion in the retinal
nerve fiber layer, and the superficial perifoveal macular vasculature are the areas of interest
• For both research purposes and glaucoma practice, the most informative parameters are
peripapillary vessel density (angioflow vessel density) in the peripapillary retinal nerve fiber
layer (RNFL) and superficial perifoveal vessel density in the macula
119. Peripapillary OCTA report of a healthy eye with
• A) Scanning laser ophthalmoscopy image of
the measurement area
• B) Vitreous-retinal perfusion map
• . C) Perfusion map in the radial peripapillary
capillaries layer which corresponds to the
retinal nerve fiber layer.
• D) Perfusion map in the choroid level.
• E) Optic nerve head and retinal nerve fiber
layer thickness measurement results.
• F) Color-coded retinal nerve fiber layer
thickness image.
• G) Color-coded vessel density map and its
sectors in the radial peripapillary capillaries
layer.
• H) Capillary and all-vessels density values for
various sectors of the peripapillary area in the
radial peripapillary capillaries layer
121. QUANTIFICATION OF PERIPAPILLARY RETINAL
FLOW INDEX AND VESSEL DENSITY
• glaucomatous eye shows reduced density of the peripapillary microvascular network
with patches of nonperfusion that correlated well with the locations of NFL and visual
field (VF) defects on en face OCTA
122. • radial peripapillary capillary(RPC) network- is a unique plexus of capillary beds lying in
the inner part of the RNFL and oriented parallel to the RNFL axons. It has fewer
anastomoses compared to other retina layers, which makes it particularly vulnerable to
glaucoma damage .
• superficial vascular plexus(SVP), which is supplied by the central retinal artery and
composed of larger vessels primarily in the ganglion cell layer (GCL)
• intermediate capillary plexus (ICP)
• deep capillary plexus (DCP)
123. • loss of both flow and reflectance signal in the normal ONH are located in the large retinal vessels
and is most likely due to the high velocity flow –OCTA is unable to capture
• Therefore, low index and vessel density measurements inside the optic nerve heard (ONH) were
unreliable.
• But to determine it in peripapillary area, it is still possible
• The peripapillary region was defined to be a 0.7 mm wide elliptical annulus extending outward
from the optic disc boundary
(a) Whole en face image centered on the optic nerve head (ONH); (b) papillary region; (c) peripapillary or
circumpapillary; and (d) within disc
124. • The peripapillary retinal flow index was defined as the average decorrelation value on
the en face retinal angiogram in the peripapillary region.
• The vessel density was defined as the percentage area occupied by blood vessels in the
peripapillary region in the en face retinal OCT angiogram.
NORMAL EYE GLAUCOMA EYE
PERIPAPILLARY RETINAL
FLOW INDEX
0.086 0.070
PERIPAPILLARY VESSEL
DENSITY
88.5% 78.9%
125. A localized retinal nerve fiber bundle defect and the spatially corresponding localized
peripapillary vessel density reduction (arrows) in glaucoma
126. • open-angle glaucoma- in which vascular dysregulation frequently plays a role in
the development of the disease, vessel density measurements may offer
advantages in early diagnosis
• angle closure glaucoma- in which intraocular pressure elevation has a major or
exclusive pathophysiological role, the structural parameters like RNFL thickness,
sector RNFL thickness, inner macular retina thickness and its hemifields perform
better
127. CORRELATION BETWEEN PERIPAPILLARY RETINAL
OCT ANGIOGRAM, NERVE FIBER MAP, AND
VISUAL FIELD
• Peripapillary retinal nonperfusions are associated with areas of NFL thinning, ganglion
complex thinning, and VF defects
128. • ONH and peripapillary vascular changes correlated well with the severity of
glaucoma and can be an important marker for disease progression.
• Study of the peripapillary vessel density and RNFL thickness in glaucoma,
glaucoma suspect, and normal eyes showed
inferotemporal and superotemporal sectors, and the temporal and inferonasal
sectors showed significant correlation between vessel density and visual field loss –
specially in POAG
129. • strong relationship was found between mean paracentral visual field defect
values in perimetry and temporal peripapillary vessel density values
• This indicates that some mild vascular dysfunction or damage may start in the
papillomacular area much earlier than previously thought
• Similarly , correspondence was found between the presence of central visual field
defects(perimetry 10-0) and increased size of the foveal avascular zone in
glaucoma.
130. High Myopia
• Peripapillary assessment is difficult in highly myopic eyes because of structural variability
(e.g., peripapillary atrophy, tilted disc or steep retinal slope), making it difficult to distinguish
between glaucoma-induced and myopia-induced RNFL thinning.
• In myopic glaucoma , the relationship of visual field and peripapillary vessel density is
significantly greater than that with the corresponding RNFL thickness
• In myopia without glaucoma, peripapillary vessel density is lower than in normal eyes, and in
myopic glaucoma it is even more reduced.
• Thus, in myopic glaucoma we cannot expect considerably better diagnostic accuracy from
OCTA than from structural OCT parameters ,but ,it can be used for monitoring
131. MACULA
• The macula has the highest density of retinal ganglion cells (RGCs)
and macula damage has been demonstrated in early glaucoma
(a) Whole en face macula image; (b) parafoveal; and (c) perifoveal-SCP,DCP
132. Superficial perifoveal macular vessel density and
the corresponding macular inner retina thickness
and retinal nerve fiber layer thickness in
healthy eye - (A to D)
an advanced glaucoma eye -(E to H).
A and E: Color coded perfusion maps
B and F: Vessel density measurement values,
C and G: Macular inner retina thickness maps,
D and H: Retinal nerve fiber layer thickness
maps
133. Various studies showed
• Progressive reduction of the inner macula vessel density over a mean period of 1 year ,
whereas the inner macula thickness remained unchanged
• Another study-the inner macular thickness was better than the inner macula vessel
density for detection of glaucoma
• the differences were due to difference in the region of interest selected for
measurements of inner vessel density and inner retinal thickness.
• the exact role of macula vessel density measurements in glaucoma diagnosis and
progression remains unclear
134. CHOROID
• Deeper peripapillary vessels and the deep optic nerve head share the same blood supply,
from the short posterior ciliary arteries.
• Choroidal vascular impairment within b-zone parapapillary atrophy (bPPA) adjacent to
the optic disc, seen using OCTA in glaucomatous eyes .
• These choroidal vascular impairment area are most often found at inferotemporal
locations within bPPA regions surrounding the optic disc in eyes with glaucoma
• In glaucoma -impairment in blood supply occurs not only in superficial layers, but also at
the deep layers of the retina and choroid.
• Additionally, deep-layer microvasculature dropout seems to be associated with more
advanced disease status.
135. Artifacts in OCT A
• most commonly vitreous
floaters.
• Collagen opacities, which are
common in glaucoma, may
cause shadow effect by blocking
the return of the illumination
light from the retina
136. HOW TO DIFFERENTIATE FROM OTHER OPTIC
NERVE DISEASE
A) Compression due to optic
nerve head drusen
B)Old Retinal vein occlusion
C) Chronic non-arteritic
anterior ischemic optic
neuropathy
D) Advanced glaucoma
NEEDS CLINICAL CORELATION
137. Influence of Intraocular Pressure on Measured Vessel Density Values
• The structural parameters (RNFL
thickness and inner macular
retina thickness) do not react in
an active way to pressure-
lowering treatment.
• OCT A significant improvement
in peripappillary vessel density
on owering the IOP
• Therefore ,OCTA can be used for
assessment of intervention by
anti glaucoma drugs
A) Untreated eye with high intraocular pressure.
B) B) The same eye one month later under combined intraocular
pressure lowering medication and with more than 50%
intraocular pressure reduction. The peripapillary vessel density
map shows a clear increase in capillary perfusion
138. Can We Use Vessel Density for the Measurement of
Glaucomatous Progression?
• vessel density reflects intraocular pressure changes, status of systemic perfusion,
glaucomatous vascular dysregulation, retinal oxygenation, and hypercapnia.
• Thus, vessel density is less stable than RNFL thickness.
• Therefore, we cannot expect to see an easy-to-understand vessel density progression
pattern when the gradual glaucoma-related perfusion changes are small, or smaller than the
fluctuations induced by factors which are not related to glaucomatous progression
139. CONCLUSION
• OCTA provides the quantification of microcirculation in the superficial optic
nerve, peripapillary retina, and the macula of glaucoma in a noninvasive fashion.
• OCTA has emerged as a new objective approach to the diagnosis and disease
progression monitoring in glaucoma, however it remains controversial
