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Next-level imaging

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Dr Graham Lakkis
BScOptom GradCertOcTher FACO

Product
Nidek RS-3000 Advance OCT with AngioScan

Supplier
Designs For Vision

 

With each new generation of OCTs, scanning speed, resolution and eye tracking ability have improved. The latest advance in technology is OCT Angiography (OCT-A), which offers the practitioner the ability to image both large and small retinal vessels and capillaries without the injection of fluorescein dye.

OCT-A technology relies on the ability to sequentially image exactly the same location. The retinal structures are fixed and unchanged in the sequential image; however, the blood inside the vessels is in motion and will change position. The OCT-A software is able to subtract all the stationary information, revealing only the blood flow.

Because OCT-A does not use an injection of intravenous dye, it is unable to provide information on blood flow rates and arteriovenous transit times, or show areas of vascular leakage. However, it has an advantage over traditional fluorescein angiography in being able to image different layers of the retina and choroid, and provide much greater resolution of the capillary beds.

Figure 1 shows an en face OCT image of a normal eye. The upper row provides OCT structural details at the internal limiting membrane (ILM), inner retina, outer retina and the choroid, respectively.

 

161 Figure 1A OCT Normal - online.jpg

Figure 1A. OCT of normal eye. OCT scan shows the structural details, (L-R) internal limiting membrane (ILM), inner retina, outer retina and choroid

 

 161 Figure 1B OCTA Normal - online.jpg

Figure 1B. OCT of normal eye. OCT-A scans shows the vasculature at the equivalent retinal layer

 

The lower row of images shows the OCT-A scans of the vasculature at the equivalent retinal layer. Note how the first upper OCT image at the ILM gives great detail on the nerve fibre layer axons, while the equivalent OCT-A layer reveals the previously unseen retinal blood flow in the arterioles and capillaries. The 500 micron foveolar avascular zone is very obvious as a round area of minimal signal due the absence of capillaries at the fovea.

CASE REPORT 1

An 83-year-old male with a 27-year history of type 2 diabetes attended for a diabetic eye examination.

He was found to have R mild to moderate non-proliferative diabetic retinopathy with clinically significant macular oedema (Figure 2).

 

161 Figure 2 DME - online.jpg

Figure 2. Mild to moderate non-proliferative diabetic retinopathy with clinically significant macular oedema

 

Nidek OCT Macular Map scans confirmed the location and severity of the centre-involving macular oedema (Figure 3).

 

161 Figure 3 OCT DME - online.jpg

Figure 3. Macular Map scans confirm macular oedema

 

A 4.5 mm OCT-A scan centred on the fovea was taken (Figure 4). The first pair of scans at the ILM/vitreous interface did not show any obvious ocular pathology on OCT or OCT-A but the second set of scans at the inner retina revealed significant capillary drop-out, particularly superior to the foveola (enlarged view Figure 5).

 

161-Figure 4 OCT and OCTA - online.jpg

Figure 4. The first pair of scans at the ILM/vitreous interface did not show any obvious ocular pathology on OCT (top row) or OCT-A (bottom row)

 

161 Figure 5 OCTA DME capillary drop out - online.jpg

Figure 5. OCT-A image of the inner retina reveals significant capillary drop-out

 

Glycaemic damage to the vascular wall of the capillaries leads to loss of pericytes, fluid leak and eventual destruction of the capillary itself, resulting in areas of capillary non-perfusion. These areas of non-perfusion and diminished blood supply are hypoxic and therefore upregulate the production of vascular endothelial growth factor (VEGF) in an attempt to produce new vessels and improve tissue oxygenation. The excessive VEGF leads to worsening of the macular oedema and eventual neovascularisation.

Diabetic macular oedema can be treated in different ways including focal laser, infrared micropulse laser, intravitreal steroid injections and/or anti-VEGF injections. In this case, the perifoveal capillary non-perfusion may best be treated with a series of anti-VEGF injections to reduce VEGF drive and minimise the potential for further leakage and neovascularisation.

A referral to a medical retina specialist was made.

In this instance, OCT-A was able to reveal the presence of capillary non-perfusion of the inner retina without the need for fluorescein injection.

CASE REPORT 2

A 77-year-old female with a past ocular history of R exudative and L atrophic macular degeneration was treated with a series of R anti-VEGF injections from 2012 to 2014. She returned for her annual review.

Dilated fundus examination revealed areas of drusen, atrophy and scarring in the R macula. An OCT line scan was taken through the fovea but due to central damage, the patient used eccentric fixation of the upper macula to fixate the target.

The vertical line scan revealed a sub-retinal choroidal neovascular membrane (CNVM) (see asterisks, far right, Figure 6) without the presence of sub-retinal or intra-retinal fluid or cystoid spaces. The inner retinal structures above the CNVM appeared to be anatomically normal.

 

161 Figure 6 OCT CNVM - online.jpg

Figure 6.  Choroidal neovascular membrane (asterisks, far right) without sub-retinal or intra-retinal fluid

 

A 3.0 mm OCT-A scan was taken over the area of CNVM (Figure 7). Assessment of the upper row of OCT images revealed a general loss of detail in all layers compared to en face scans of a normal eye. Assessment of the lower row of OCT-A scans showed significant absence of signal only in the outer retina and choroid. This was due to the lack of functioning active blood vessels in the neovascular membrane, indicating an inactive CNVM.

 

161 Figure 7 OCT and OCTA - online.jpg

Figure 7. OCT scan (upper row) reveals a general loss of detail in all layers. OCT-A scan (bottom row) shows significant absence of signal only in the outer retina and choroid.

 

OCT and OCT-A scans were able to confirm that no active disease process was occurring in the area of the CNVM, so there was no need to recommence anti-VEGF therapy at this time. Routine review was scheduled and no referral was necessary.



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