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Optical Coherence Tomography Angiography (OCT-A) Principles and Applications

2 CPD in Australia | TBA in New Zealand | 30 January 2017


By Dr. Anmar Abdul-Rahman.   

Optical Coherence Tomography Angiography (OCT-A) is a nascent non-invasive imaging OCT modality with a potential wide applicability to retinal and optic nerve vascular disease. The basic function is generating a structural map representative of the microvascular network.1

OCT-A relies on interferometric detection of low temporal coherence light back-scattered by moving red blood cells. The resultant B-scan images are analysed for relative change in tissue reflectivity induced by the cells between two sequential scans.2, 3, 4, 5

Makita et al reported the first in vivo macular OCT angiography in 2006.6 Since then a rapid array of algorithms have been implemented to analyse the resulting motion-contrast signal. These can be roughly categorised but not limited into three groups. Each method has its own merits due to its unique physics and mathematics behind the flow contrast mechanism.7

1. Angiography based on the magnitude of the OCT signal: a key advantage is less sensitivity to phase noise, making it particularly helpful in situations where the phase stability of light source is an issue, as it is independent of the Doppler angle, e.g. OCT Angiography Ratio Analysis (OCTARA), Speckle Variance (SV-OCT), Split-spectrum Amplitude Decorrelation Angiography (SSADA), correlation mapping, scattering OCT.8, 9

2. Angiography based on the phase of the OCT signal (phase Doppler approach) associated with time domain OCT in which the flow monitoring is based on the Doppler shift in back-scattered light induced by moving objects. This is additive to the carrier frequency associated with the reference arm of the OCT signal e.g. Doppler Variance OCT, Phase Variance OCT (PV-OCT).10

3. Angiography based on both the magnitude and phase of the OCT signal (complex signal): Instead of operating on phase or intensity alone, subtraction to calculate motion contrast between sequential scans is performed directly upon the raw spectrum, followed by Fourier transform to generate the flow image, e.g. Optical Microangiography (OMAG), Phase Contrast OCT (PC-OCT), Ultrahigh- Sensitive Optical Microangiography11 and Eigen Decomposition OCT-A.12

Although algorithms provide qualitatively interpretable resolution images, the quantitative results in analysing flow velocity remain limited.9



In spite of the use of newly available OCT-A, there is limited information on normative databases.13 The macula scan of the DRI Triton Swept Source OCT (SS-OCT) printout generates the following seven images (Figure 1).


Figure 1. Normal OCT-A of the macula 4.5 x 4.5 mm area scans. The standard DRI Triton macular printout images consist of: (a) the superficial vascular plexus; (b) the deep vascular plexus; (c) the outer retina; (d) the choriocapillaris; (e) composite image of all retinal layers; (f) colour fundus photograph; (g) OCT B-scan.

1. The superficial vascular plexus, located in the ganglion cell and the nerve fibre layer: Course retinal vessels appear in this layer that demonstrate dichotomous branching pattern converging on the foveal avascular zone (FAZ). The finer branches of this network form a continuous circumferential vascular plexus around the FAZ.

2. The deep vascular plexus, located in the inner nuclear and the external plexiform layer: These vessels originate from vertical anastomoses with the superficial vascular plexus the terminal ends forming a network of a fine interconnected network of vessels with a concentric pattern around the FAZ.9,14 The FAZ area is variable, reported normal population mean values are 0.266 ± 0.097 mm2 in the superficial plexus and 0.495 ± 0.227 mm2 in the deep plexus. Therefore FAZ area is larger in the deep plexus (P< 0.0001) as compared to the superficial plexus15

3. The outer retina (photoreceptor layer): A fine granular layer, normally devoid of vascularity

4. The choriocapillaris: A homogenous granular layer. The texture and pattern are indicative of the high blood flow in this layer

5. OCT B-scan provides a central vertical cross-section through the examined retino-choroidal interface, which provides an overview of the distribution of the pathologic process in the vertical plane

6. Composite angiogram of all retinal layers

7. Colour fundus photograph centered on the area of interest.

The optic nerve is supplied by two main vascular sources: the superficial layers (nerve fiber layer) by the central retinal artery, and the deeper layers (the prelaminar, lamina cribrosa, and retrolaminar regions) by the posterior ciliary artery.16

Structural differences of these fine capillary networks are not discernable by OCT-A. The optic nerve scan of the DRI Triton Swept Source OCT (SS-OCT) in addition to images 5 and 7 above, displays the images for the following reference levels (Figure 2):

1. The superficial optic nerve head scan

2. The deep scan at the level of the vitreoretinal interface

3. The radial capillary network, which resides in the retinal nerve fiber layer (RNFL)

4. The optic nerve at the level of the choroid

5. OCT projection, which is a composite of surface points generated from all scans of the optic nerve and peri-papillary retina.

Figure 2. Normal OCT-A of the optic nerve. 4.5 x 4.5 mm area scans. The standard Triton optic disc printout images consist of scans at the following levels: (a) the superficial scan; (b) vitreo-retinal interface; (c) the radial capillary network; (d) the choroidal level; (e) OCT projection; (f) colour optic disc photograph; (g) OCT B-scan.


Comparison of OCT-A with Fluorescein and Indocyanine Green Angiography (ICG)

Due to the similarity of OCT-A and the more familiar conventional angiography images, it is prudent to note when interpreting OCT-A images there is a poor concordance in regards to hyperfluorescence (FFA/ICG) and hyperreflectivity (OCT-A). The two methods are complementary and not comparative.9

Conventional angiography depends on dye leakage or staining to generate a high contrast signal, whereas OCT-A operates on the principle of detection of motion contrast of cells in a blood vessel between successive B-scans; therefore a lesion detectable by conventional angiography may not be amenable to the same imaging properties by OCT-A due to intralesional flow characteristics; by the same token, lesion margins, particularly at the boundaries of capillary closure in ischemic areas are not blurred by dye leakage. Table 1 highlights the characteristics of these imaging modalities.



Choroidal Neovascularization

The ability to combine lesion morphology, depth of retino-choroidal involvement with qualitative changes in response to therapy have been the most significant contributions of OCT-A in the management of Choroidal Neovascularization (CNV).17,18

The role of quantitative functional data regarding CNV flow and area indices on the horizon remains a promising development.18

Currently the role of OCT-A resides in non-invasive qualitative monitoring of the retinal and choroidal microvasculature, supplementing Fluorescein (FFA) in diagnosis and treatment decisions.19,20

The features summarised below, are characteristic of neovascular AMDdescribed by Coscas et al in a prospective case series of 80 eyes.17

CNV in age related macular degeneration (AMD) is classified by location in the deep retinal layers; below (Type I ‘occult’) or above (Type II ‘classic’) the retinal pigment epithelium, or within the neurosensory retina (Type III ‘retinal angiomatous proliferation (RAP)’).21 OCT-A can enhance lesion features obscured by angiographic dye leakage, especially in Type I lesions, or identify the occult component in mixed lesions.22, 23

Treatment naïve Type I and II membranes have a characteristic pathophysiologic stage dependent appearance in the form of a fan like arborescent mesh. The irregular flow gives the membrane a faint signature. Associated anastomoses and feeder vessels are common (Figure 3).

Figure 3. OCT-A 6.0 x 6.0mm scan. An 86-year-old female with treatment naive type II CNV due to AMD, the intensity of the signal from the membrane is directly proportional to the speed of blood flow in the lesion. In this example arborescent fan shaped vessels extend to the level of: (a) the outer retina; surrounded by a patchy loss of choriocapillaris; (b) particularly along the upper border of the membrane; (c) a composite image of all retinal layers degraded in the upper portion by blink artifact; (d) B-scan OCT showing the presence of subretinal fluid, retinal pigment epithelial irregularity and choroidal thinning.

Treatment causes fragmentation of the lesion in addition to reducing the number of secondary branches (Figure 4). This appearance precedes regression of the associated exudative changes. Intralesional fine vessels are seen in the presence of longstanding fibrosis.9


Figure 4. A 78-year-old female with a type II CNV due to AMD, partially treated with intravitreal Bevacizumab. A 4.5 x 4.5 mm area OCT-A demonstrating a mesh of fragmented abnormal vessels seen at the level of: (a) the deep capillary plexus; (b) the outer retina, which is normally devoid of vascularity; (c) the choriocapillaris where it is surrounded by a patchy loss of homogeneity; (d) composite image from all retinal layers; (e) the abnormal vessels exist both below and above Bruch’s membrane and extend to the deep capillary plexus. Vascular architecture of the deep capillary plexus is disrupted by intra-neurosensory edema as demonstrated on the OCT B-scan.

A post anti-VEGF time dependent change in Type II lesion appearance has been described by Lumbroso et al. Twenty-four hours after injection, there is a decrease in the dimensions of CNV with loss of smaller vessels and narrowing of larger vessels. Between days seven and 12, there is continued decrease in the size of CNV, whereas the central trunk remains unchanged. The maximum decrease in vessels is noted between days 13 and 18. Re-proliferation is noted after day 28.24

Quantitative alterations of intra and peri-lesional blood flow patterns have diagnostic and therapeutic advantages. In an observational, cross-sectional study of five cases of Type I, II and mixed CNV in AMD, Jia et al identified reduced choroidal flow adjacent to the CNV in all cases. Higher flow indexes were associated with larger and Type II CNV.18

Sensitivity and specificity comparable to FFA have been reported in other disorders associated with CNV as chronic CSCR,25 pathologic myopia,26, 27 polypoidal choroidal vasculopathy,20 and adult vitelliform macular dystrophy.19 However, fluorescein angiography remains the gold standard for determining the presence of a neovascular network.19

Although a high specificity (91 per cent) has been reported in the diagnosis of CNV, Talisa et al in the same study of 48 eyes, reported a sensitivity of 50 per cent.28 Caution should be exercised when attempting to establish a diagnosis of CNV on the basis of OCT-A only as exudative and fibrotic changes can mask the characteristic appearances.


Diabetic Retinopathy

Non-proliferative retinopathy: OCT-A features, due to microangiopathy related structural changes in the superficial and deep capillary layers, include capillary loops, anastomoses, microaneurysms, widening of the FAZ, and remodeling of the fine perifoveal capillaries (Figure 5).29,30


Figure 5. Diabetic maculopathy in a 68-year-old patient. OCT-A 4.5 x 4.5 mm area scan of the right eye demonstrating microangiopathic non-proliferative changes: (a) microaneurysms (yellow circles) in the superficial and; (b) deep plexuses; (d) foveal avascular zone expansion, loss of the normal radial deep capillary plexus architecture and intraretinal fluid (yellow arrow) also detected on the OCT B-scan nasal to the foveola. Areas of capillary closure in both plexus layers (white arrow) appear as dark patches. (c) a punctate loss of choriocapillaris homogeneity can be noted secondary to patchy blood flow in this layer. Vessels of the superficial retinal layers are artifactually projected in the choriocapillary layer in this example.

Preclinical microangiopathic changes could be detected by OCT-A. In a prospective observational study on 61 eyes, with diabetes without detectable clinical retinopathy; foveal microvascular changes not detected by clinical examination (Foveal avascular zone remodeling 36 per cent, capillary non-perfusion 21 per cent, microaneurysms and venous beading < 10 per cent) were imaged by OCT-A.30

There is a poor concordance in both the shape and size of microaneurysms between FFA and OCT-A; where they are less abundant than FFA as the detection depends on scan resolution and intralesional flow. Microaneurysms appear smaller, multivariate, typically solid, and round in shape with dark centers, or fusiform. They are mainly (80 per cent) located in the deep capillary plexus.

Cotton wool spots show intralesionalimpaired perfusion. Vascular Looping and Intraretinal Microvascular Abnormalities (IRMA) demonstrate larger caliber capillary loops than that of surrounding areas of involvement, which extend across more than one retinal layer.29,31,32,33,34

Capillary non-perfusion is of particular prognostic importance. Agemy et al have reported a significant decrease in retinal capillary perfusion density with increased severity of DR.35

There is good concordance between FFA and OCT-A in the area of capillary closure. In OCT-A the extent of the impaired perfusion is more evident at any point of fluorescein transit.

Patches of impaired perfusion are rarely identical between capillary layers. This finding is predominantly in the superficial than the deep capillary plexus, where disruption of the normal vortex pattern is in turn a more common feature.34

Capillary closure contributes to expansion of the FAZ,33,36,37,38,39,40,41 Diabetic eyes show a statistically significant FAZ enlargement in both superficial and deep capillary layers compared with healthy eyes, regardless of the presence of retinopathy.33

In the superficial capillary plexus the FAZ area measures 0.25 ± 0.06 mm² in healthy eyes. It is 0.37 ± 0.07 mm² in diabetic eyes without retinopathy and 0.38 ± 0.11 mm² in eyes with diabetic retinopathy.33

Vascular tortuosity is found to be a poor indicator for the presence of diabetic microangiopathy.30

Proliferative Diabetic Retinopathy: Early detection of neovascularization (NV) at the posterior pole is a useful application of OCT-A. Figure 6 highlights the significance of this technology in the assessment of suspicious vascular lesions, where clinical examination alone may under-represent the extent of the pathological change. Assessment of therapeutic interventions could be documented and quantified even when the lesion, seen clinically, cannot be imaged by conventional means (Figure 7). The diagnostic efficacy of this technology compared to other imaging modalities in this setting is yet to be studied.


Figure 6. OCT-A in proliferative diabetic retinopathy demonstrating the ability of OCT-A to detect neovascularization at the disc (NVD). Composite photograph of the optic discs and corresponding OCT-A images at the level of the vitreo-retinal interface in a 41-year-old patient prior to instituting treatment. Advanced NVD of the right optic disc and early neovascularization of the superior temporal quadrant of the left optic disc (yellow arrow) are seen. Note the discrepancy of the appearance of the neovascular complex particularly on the right optic nerve compared to the corresponding color image.


Figure 7. OCT-A in proliferative diabetic retinopathy. Composite photograph of the left optic disc and corresponding OCT-A images at the level of the vitreoretinal interface in a 33-year-old patient; demonstrating neovascularization of the lower pole of the left optic disc: (a) although detected on slit-lamp biomicroscopy, the lesion could not be demonstrated on a colour fundus image; (b) the treatment naive lesion can be seen as a network of vessels at the lower pole of the optic nerve; (c) eight weeks after PRP to the retinal mid and far periphery; the lesion is demonstrating regression.

Differentiating NV of the disc from optic disc collateral vessels can pose a clinical challenge; as a diagnosis of the latter lesion precludes laser treatment and in addition to diabetes,42 it may indicate other etiologic possibilities (previous retinal vein occlusion,43, glaucoma,44 optic disc drusen,45 meningioma of the optic nerve sheath and compressive optic neuropathies46,47,48); therefore distinction between these two lesions is a significant clinical decision. OCT-A can enhance diagnostic accuracy by outlining the depth of the lesion. Maximum lesion depth for a neovascular complex is at the level of the optic nerve head and vitreoretinal interface, whereas collaterals will demonstrate a maximal depth at the choroidal layer (Figure 8).


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Figure 8. OCT-A in the differential diagnosis of optic disc vascular lesions. Composite photograph of the left optic disc of two patients: (a) a 29-year-old female with proliferative diabetic retinopathy; (b) a 67-year-old male diabetic without retinopathy and optic disc collaterals. Note the neovascular complex in image demonstrated in all layers above the level of the choroid (yellow arrows), whereas in image b the collateral vessels represented maximally at the choroidal layer and disappeared in the opposite direction to that of the neovascularization.

The main disadvantage of OCT-A, in the assessment of lesions characteristic of proliferative retinopathy, is the constrained field of view requiring a directed examination for lesions limited to the posterior pole.22



The significant contributions of OCT-A in the management of Retinal Vein Occlusion (RVO) are in the ability to simultaneously evaluate both macular perfusion and edema. Additionally, this is the only modality capable of imaging the deep capillary plexus.

There is a greater involvement of the deep compared to the superficial capillary plexus in RVO. Transmitted hydrostatic pressure is thought to have a greater effect on the deep capillary plexus due to a direct connection with the major retinal venules in this layer.49 The superficial capillary plexus is directly connected to the retinal arterioles with a higher perfusion pressure and oxygen supply. These factors explain the discrepancy of the pathological changes.50

In a retrospective observational case series of 54 cases of RVO, Coscas et al reported on the significance of perifoveal capillary arcade disruption on OCT-A as this sign correlated with peripheral ischemia on FFA. Their results suggested that foveal arcade involvement mirrored peripheral ischemia as determined by FFA, further directing the identification of cases requiring FFA in the course of management of the disease (Figure 9).

Salles et al reported that the size of the FAZ correlates strongly with Best- Corrected Visual Acuity (BCVA) in central retinal vein occlusion without macular edema. Enlargement of the FAZ was associated with a poorer BCVA.51


Figure 9. OCT-A in central retinal vein occlusion with ischemic maculopathy. There is a strong correlation between perifoveal capillary arcade disruption on OCT-A with peripheral ischemia on FFA. An 82-year-old female with vision loss for six months: Images a,b,c show superficial, deep capillary plexuses and the choroidal layers with disruption of all layers, loss of the choroidal layer homogeneity secondary to disrupted flow and extensive intraretinal cystic changes. Images d and e show B-scan OCT demonstrating the intraneurosensory cystic change; (f) Arterio-venous and (g) late phase fluorescein angiogram showing vascular tortuosity, ischemic maculopathy parallel to the horizontal raphe and perimacular late angiographic leakage along the superior and inferior margins of the ischemic area particularly temporally.



The role of OCT-A in the management of glaucoma and other optic neuropathies is yet to be determined. The current role may lie in the differential diagnosis of optic neuropathies, more specifically, in distinguishing vascular from non-vascular pathogeneses.

Abnormal Optic Nerve Head (ONH) blood flow in glaucoma patients is a recognised phenomenon.52,53,54,55 Arterio-venous transit time delay, diffuse disc and focal sector hypoperfusion has been demonstrated in patients with primary open-angle glaucoma and normal tension glaucoma.53,54,55 Fluorescein filling defects in the disc have been found in ocular hypertensive eyes.56,57

Alterations in the peripapillary perfusion detected by OCT-A have been reported to precede the development of clinically significant retinal nerve fiber layer damage and visual field defects.58 In addition to the physiologic changes, glaucomatous optic discs demonstrate a lower peripapillary and optic nerve head vessel density compared with aged-matched normal eyes (Figure 10).59,60,61 These changes correlate with both structural and functional impairment. In a study of 261 eyes, differentiating healthy from glaucomatous optic discs, Yarmohammadi et al reported a similar diagnostic accuracy for OCT-A vessel density at the peripapillary retina and ONH compared to retinal nerve fiber layer (RNFL) thickness measurements.62


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Figure 10. OCT-A in primary open angle glaucoma. An 82-year-old female with advanced glaucomatous optic nerve cupping: (a) minimal residual paracentral visual field just inferior-temporal to fixation is seen on the Humphrey visual field 24–2 printout. (b) generalised thinning of the retinal nerve fiber layer, particularly inferiorly. (c) absence of the neuroretinal rim and a paucity of peripapillary vessels is seen on OCT-A.

Functional parameters represented by visual field indices are better correlated with perfusion indexes (total retinal blood flow, ONH peripapillary flow index and peripapillary vessel density) than structural measures.60,59,52,63

Liu et al reported a reduced peripapillary flow index using a swept source system and found a spectral source system less reliable in this parameter.59

In patients with normal tension glaucoma, a strong correlation exists between disc flow index and cup-to-disc ratio, suggesting poorer perfusion in discs with larger cups and more severe damage in this group of patients. No correlation is seen with other measured factors including mean deviation, pattern standard deviation, and RFNL thickness.64

High myopia and congenital optic nerve disorders can mimic glaucomatous changes, especially megalopapilla, coloboma, tilted disc, optic nerve pit and optic nerve hypoplasia.65,66 Delineation of optic nerve vascular architecture may aid in the diagnosis of these neuropathies by distinguishing areas of peripapillary atrophy, from the neuroretinal rim and highlighting pathological features of the optic disc (Figure 11).


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Figure 11. OCT-A in normal tension glaucoma. A 39-yearold female with an incidental left superior nasal step on automated visual field assessment. Family history was negative for glaucoma. Visual acuity =6/6 OU intraocular pressure on phasing averaged 19 mmHg. Gonioscopy showed open angles. The left optic nerve showed a C/D ratio of 0.6 with an inferior notch, a nerve fiber layer hemorrhage and a visible retinal nerve fiber layer defect. (a) Humphrey visual field 24-2 of the left eye showing a superior nasal step; (b) OCT retinal nerve fiber layer analysis demonstrating an inferior nerve fiber bundle defect; (c) a retinal nerve fiber layer bundle defect can be seen from the superficial through to the radial capillary layer, in addition to the colour fundus photograph (arrow). A notch is seen in the lower pole of the optic nerve in the OCT projection image (yellow circle).

Adding to the armamentarium of diagnostic tests to distinguish optic disc drusen from papilledema, are tests including B-scan ultrasound, Spectral Domain Optical Coherence Tomography (SD-OCT), short wave-length fundus autofluorescence, Computed Tomography (CT), Confocal Scanning Laser Ophthalmoscopy and facial X-rays.67,68,69 70,71,72 OCT-A provides a non-invasive means of establishing the integrity of the ONH circulation, a reduced density of ONH vessels in optic disc drusen compared to papilledema in a comparison of these cases (Figures 13, 14). The efficacy of this test as a discriminator between these diagnoses warrants further evaluation.



1. Decorrelation artifact: appear as white lines in the image, these result from eye motion during scan acquisition

2. Blink artifact: appear as black lines in the image

3. Projection artifact: the image from superficial retinal vessels appears as a faint hyper-reflective image superimposed on the deeper layers

4. Vascular shadowing: the image from larger caliber superficial retinal vessels appears as a hypo-reflective image superimposed on the deeper layers

5. Image defocus artifact results in the loss of detail of fine vascular structures in the superficial and deep vascular layers, in addition to the loss of accuracy of layer segmentation.



Because OCT-A is new technology there is limited clinical experience compared with other imaging modalities in the assessment of various disorders. This means the implications of the imaging results may be difficult to translate into clinical practice.

Additionally, distinguishing the normal vasculature from pathologic changes can be difficult in certain cases. OCT-A is prone to imaging artifacts during image acquisition that require steady fixation and clear optical media.

Finally, a limit of resolution for lesion detection is at a blood flow below the scanning speed threshold, which is the interval between two consecutive B-scans. This may limit detection of lesions with slow or irregular vascular flow.



Ultra high speed swept source OCT-A with scan speeds of 400-kHz A-scan rate, 5-10x faster than current commercially available devices, allows a wider field of view (12x12mm), faster acquisition of images and higher image resolution.73, 74 This technology, using variable interscan time analysis (VISTA) – which allows visualisation of relative flow speed – is especially valuable when assessing diseases in which progression is linked to flow impairment, rather than vasculature loss, thereby offering possible quantitative data.73

Jones matrix optical coherence tomography in this technique, tissue pigment contrast is used to enhance the interpretation of vascular images. 75


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Figure 12. OCT-A in superior segmental optic disc hypoplasia (topless disc syndrome). A 41-year-old female presented with an inferior right arcuate visual field defect on automated visual field assessment: (a) Humphrey visual field 24–2 of the right eye showing an inferior arcuate defect; (b) pallor of the superior pole of the right optic nerve, the temporal margin of the optic disc is ill defined by conventional imaging. OCT retinal nerve fiber layer analysis demonstrated a superior nerve fiber bundle defect; (c) there was a decrease in density of the optic nerve head capillary network in all layers, represented by the radial peripapillary network in this image (left). A clear distinction of the area of peripapillary atrophy from the neuroretinal circulation could be seen at the level of the choroidal circulation (yellow arrows C central image), the temporal neuroretinal rim is also highlighted in the OCT projection image (right).


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Figure 13. OCT-A in optic disc drusen. A 50-year-old female with bilateral inferior arcuate visual field defects on automated visual field assessment. Visual acuity =6/6 OU. (a) Humphrey visual field 24–2 of the left eye showing an inferior arcuate defect; (b) OCT retinal nerve fiber layer analysis demonstrating bilateral generalised thinning, drusen are visible in the images; (c) paucity of the optic nerve head vasculature, particularly at the level of the vitreo-retinal interface and the radial peripapillary capillary layer.



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Figure 14. OCT-A in papilledema secondary to idiopathic intracranial hypertension. A 54-year-old asymptomatic diabetic female referred with bilateral optic disc swelling detected at the time of diabetic photo-monitoring. Weight =125kg, visual acuity=6/6 OU. (a) optic disc images four years apart demonstrated some regression of the edema; (b) generalised thickening of the retinal nerve fiber layer on OCT; (c) OCT-A of the right optic nerve demonstrating intact optic nerve head vasculature in contrast to Figure 13.


Figure 15. Imaging artifacts: (a) decorrelation artifact; (b) blink artifact; (c) projection artifact; (d) vascular shadowing; images e and f show defocus artifact of the (e) superficial; and (f) deep capillary plexuses in an aphakic patient.



      Dr. Anmar Abdul-Rahman is a Medical Retina and Glaucoma subspecialist at Counties Manukau DHB, Auckland. The first to be awarded a degree of Masters of Ophthalmology from the University of Otago with distinction for his study “Fourier analysis of digital retinal images in estimation of cataract severity”, he has a special interest in medical image analysis.


All images in this article were obtained using the DRI Triton Swept Source OCT (SS-OCT), which uses central wavelength 1,050 nm, allowing some level of imaging through optical opacities. Scan speed 100,000 axial-scans/sec. There are three selections of area scan 3x3, 4.5x4.5 and 6x6 mm, from high to low resolution respectively (image resolutions 256x225, 320x320).



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' Caution should be exercised when attempting to establish a diagnosis of CNV on the basis of OCT-A only '