This hour long webinar will begin with an overview and introduction to OCT Macula. Then, a disease or specific OCT macula finding from A-Z will be reviewed with cases. Each slide from “A-Z” will have an image followed by a detailed discussion of the finding.
Lecturer: Dr. Sowmya Srinivas, OD, MS, ABO, FAAO, Dartmouth-Hitchcock Medical Center, New Hampshire, USA
DR SRINIVAS: Hello, everyone. Thank you so much for joining me today. My name is Sowmya Srinivas. I’m in practice at Dartmouth Hitchcock Medical Center, and I’ll be discussing interpreting OCT retina today. There were a lot of excellent questions, which I hope will be answered throughout the presentation, and there were some questions about fluorescein angiography, OCT glaucoma, and fundus autofluorescence, which is out of the scope of today’s talk, but let’s begin with some of the objectives for today’s presentation. So first you’ll be testing your knowledge, and second, we’ll be overviewing the introduction to OCT technology. And the goal for today is to help novices and expert clinicians better understand OCT capabilities in clinical practice. And finally, we’ll go over a disease or specific OCT finding macula or feature from A to Z, and this will be reviewed. And to take full advantage of the remarkable images revealed by SD OCT, we have to first learn to meaningfully interpret the various lines, layers, contours, and shapes in normal eyes. And once the findings in normal eyes are appreciated, we can then transition to detecting variations in different retinal, choroidal, and vitreal abnormalities. And today we will review some features specific to common and rare ocular pathologies. So please choose which eye you think this is an OCT retina of. Is it the right eye, A, or B, left eye? So the second question here is: What do you think this is a diagnosis of? A, is it choroidal neovascular membrane? B, pigment epithelial detachment? C, diabetic macular edema? D, clinically significant macular edema? Or E, central serous chorioretinopathy? Great. And we’ll go over the answers to these polling questions at the end. So first I’d like to complete the talk. Thank you for your answers. What do you think the diagnosis is for this image? So is it A, a retinal detachment, B, vitreous hemorrhage and retinal traction, C, vitreomacular traction, or D, none of the above? Thank you for your answers. We’ll go over this question at the end of the presentation. The next question here is: What is your diagnosis? Is it a normal OCT retina? Does it indicate B, Plaquenil toxicity? Or C, acute middle maculopathy? Or D, none of the above? Thank you for your answers. Here’s the next diagnosis slide. So is it A, choroidal nevus? B, wet macular degeneration? C, pigment epithelial detachment? D, sclerochoroidal calcification? Or E, drusen? So next we’ll go into the introduction and history of optical coherence tomography. So optical coherence tomography was first introduced in 1991, and due to the transparency of the eye — so the retina can be viewed through the pupil — OCT has become an invaluable ophthalmic diagnostic tool. Initially, there was time domain OCT, and then nowadays, we use spectral or Fourier domain OCT. So here you can see the quality of time versus spectral domain OCT. So OCT images were initially acquired in a time domain fashion. So what that meant was: Time domain systems acquire approximately 400 A-scans per second, using 6 radial slices, oriented at about 30 degrees apart. And so this meant that we had the potential of missing pathology between the slices. Spectral domain technology, on the other hand, scans approximately 20,000 to 40,000 scans per second. So the increased scan rate and the number diminishes the likelihood of motion artifact, enhances resolution, and decreases the chance of missing any lesions. So time domain OCTs are accurate to about 10 to 15 microns, and newer spectral domain machines may approach even 3 microns resolution. So whereas most time domain OCTs image 6 radial slices, spectral domain continuously image a 6-millimeter area. So again, this reduces chance of missing any ocular pathology. So here you can see a comparison between time and spectral domain OCTs. On the left hand side, you see a time domain OCT, with the scan generated sequentially. One pixel at a time, at 1.6 seconds. And then time domain OCTs have a moving reference mirror. It scans 400 scans per second. Resolution is 10 microns. And this is slower than your eye movement. On the other hand, Fourier domain OCT or spectral domain — entire A-scan is generated at once, based on Fourier transformations of spectrometer analysis. And you can see a stationary reference mirror, and this scans about 26,000 scans per second, with a resolution of 3 to 5 microns. And this is faster than your eye movement. So down below, you can see two images. The one on the left is your time domain OCT, and the one on the right is the Fourier domain, and you can see a much higher resolution with the spectral domain or Fourier domain with the OCT on your right. Here we see a pathology of our epiretinal membrane with a pseudohole on time domain OCT on your left, and spectral domain OCT on the bottom, and a couple of other epiretinal membrane scans on the right. So you should think of OCT technology as identifying changes in optical density, which are either depicted in either color or gray scale. So color on your left, gray scale on your right. When two adjacent structures demonstrate large differences in the refractive indices, more light is reflected upon their interface. By convention, large reflections are depicted by vivid colors, such as red, whereas less reflective structures are depicted in the blue part of the spectrum. And zones without reflection are black or nearly so. So hence, when you see a normal patient, in the vitreous, it’ll appear dark or even black. So on your right hand side, you can see an epiretinal membrane here, with an intact sort of outer retinal layer, and you can see this tiny reflective area up top, which is your epiretinal membrane. Here you see a loss of foveal contour, and on the slide down below, there is an intact, almost intact, foveal pit. So this epiretinal membrane is more parafoveal, so away from the fovea here. And this epiretinal membrane on your left shows a pseudohole, because not all of the layers here are affected. And we’ll go over more of this in detail coming up in the presentation. And so time domain OCT — the advantage is intensity information is acquired in time domain with a 10 micron resolution. The disadvantage is limited acquisition rate due to moving reference mirror. Spectral OCT has several advantages. So it’s higher sensitivity than your time domain OCT, and there’s no moving reference mirror which is required. There’s the high scanning speed, and sends axial resolution throughout the tissue by evaluating frequency spectrum of the interface between the reflected light and the stationary reference mirror. And this can scan up to 5 microns of resolution. And the increase in resolution can decrease motion artifacts. And furthermore, you get repeatability for tracking progression of different ocular pathologies. One disadvantage is a noticeable signal dropout with depth. And I had an excellent question about different commercially available spectral domain OCT models. So I’ve included four of them here. Heidelberg, Topcon, Optovue, and Carl Zeiss. And this slide is a busy slide here, but it goes over what different commercial OCT scans show. So on your left is a printout of the Avanti RTVue XR. And as you can see, there’s horizontal cross line scans, which show intact foveal pit and good scan alignment, with the right eye up top and left eye down below. On your right hand side, you see a Heidelberg OCT image, with a macular thickness B-scan of the right eye, and on your left hand is an overlying infrared fundus image. And on the bottom, you see the left eye with horizontal line scans, and you can see RPE disruption in both eyes, and some drusen as well. So the next here is a picture of 3D OCT 2000, and you can see the report that it shows you on your left. And on your right hand side here is an HD OCT 5000 with a macular cube of the left eye here, with intact RPE, and sector macular thickness thinning, compared to the normative data. So what are some of the advantages of OCT? Firstly, it’s non-invasive, it’s non-contact, it’s painless, fast, reliable, sensitive, and finally radiation-free. So when would we get an OCT of the retina? So if we want to examine the retinal layers. If we want to monitor progression of ocular pathology. If we want to plan treatment. Or if we want to monitor response to therapy. And what are some limitations of getting an OCT? So the first point here is: A good lacrimal layer is needed. And number two, transparent media is needed. Number three, dilation may be necessary. And four, it is limited to the posterior pole. So in the presentation, coming forward, we’ll go over keratoconus and how that may affect the OCT scans. So this here is a spectral domain OCT of a normal right eye. And you can see the retinal layers, along with the choroid here on the bottom of the slide. And posterior hyaloid, which I have a picture of coming up next. And notice the marked change in reflectivity between the vitreous here and the internal limiting membrane complex, which depicts the vitreoretinal interface. And please notice how the outer and inner nuclear layers appear relatively dark due to the change in optical density, because light traverses the tightly and uniformly packed nuclei. In contrast, the inner and outer plexiform layers show increased reflectivity here. So here’s a picture of the posterior hyaloid that you can see on the scan to your right. And here this dark space is your retrohyaloid space. On your left side, you can see a nice posterior vitreous detachment, where the vitreous has separated here. And the first question you had to answer was: Which eye was this OCT scan of? And this is an important point, because if you were just shown an OCT macula slide, notice how the nerve fiber layer in the right eye is very thick and hyperreflective here. So this is a scan on your left of your right eye. And on the right hand of your slide, you can see an image of the left eye up here, and notice how the nerve fiber layer here is thick and hyperreflective here. So therefore the image on your right is a scan of your left eye. And this OCT shows a retinal pigment epithelial defect here, in both of your eyes. So again, the image on your left hand side is a scan, OCT scan, of the right eye, and the image on your right is an OCT scan of a left eye. So I like this image here, because you can appreciate how thick each layer is. So it is color coded, with the internal limiting membrane here, up top, on your view, and choroidal stroma here down below. And ST or spectral domain OCTs are presented as a cross section of the retina, which appears as a typical histological slice in textbooks. And so by convention, the inner retina is close to the center of the eye, the vitreous, and the outer retina is close to the choroid and sclera. Remember that the outer retina contains the RPE and photoreceptors, and the inner retina contains the retinal nerve fiber layer and ganglion cells. So the next important piece of information to go over is with regards to the photoreceptor integrity line. So the foveal pit here is an important landmark on any OCT scan. And you can notice here there’s a very thin hyperreflective band here, and this is called the photoreceptor integrity line. So if you notice, the photoreceptor integrity line is not present under the fovea. The visual acuity will be quite reduced. And with some clinical experience, you can actually estimate the visual acuity, based on the appearance of the photoreceptor integrity line, based on the appearance of this line under the fovea. And I’ll go over a couple of examples of this on the next slide. The photoreceptor integrity line is important, because it’s a biomarker of photoreceptor integrity, both rods and cones. And the term PIL for the receptor integrity line does not limit the usefulness of the concept of a biomarker, regardless of the precise anatomical location, which is subject to debate and change. So the right photoreceptor integrity line here, the PIL, has dark inner segments of photoreceptors above it, and dark outer segment below it. So the two layers here are not imaged on this slide, though. And you’ll notice this subtle blip here of the PIL in this figure. Directly under the foveal pit. And this is not a cyst, but indeed a normal finding. It likely occurs because outer segments of the cones under the foveal pit are longer and more narrow than cones and rods in any other zone of the retina. And note that here the PIL is a very bright band, with a dark band above and below it. So the dark band on the inner side here, above it, is the inner segment, IS, of the photoreceptors. While the outer band below it is the outer segment, OS. So you may have heard the term IS-OS junction. And this essentially is referring to the PIL line. But recent anatomical evidence has demonstrated that this is imprecise, and the more recent term for this you may have heard of is IS, so inner segment ellipsoid. But clinicians dislike this term, because it fails to convey the importance of this line, and hence photoreceptor integrity line is preferred. So if you look at these two slides here, I want to highlight the fact that up here on your top left hand side the photoreceptor integrity line here is intact and present, even though you see vitreomacular traction here. So because the photoreceptor integrity line is normal, the visual acuity in this top left hand eye will be good. And here down on your bottom right hand side, you can see the separation of the entire neurosensory retina from the RPE, temporal to the fovea, in this patient’s right eye. However, notice that the PIL line here is intact, and so the vision here is actually 20/20, because the macula is still attached and the PIL is present here. So therefore this is a macula on retinal detachment that requires immediate treatment to prevent vision loss. And one of the questions I had was whether we can see a retinal detachment here on the OCT, and here is a nice image of this here. And another question I had was with regards to macular thickness. I’ll go over briefly what this is. So according to the ETDRS map, the macula is divided into nine sections, with three concentric rings measuring 1 millimeter, which is the innermost ring, 3 millimeters, inner ring, and 6 millimeter diameter outer ring. And this is all centered on the fovea. The innermost 1 millimeter ring is in the fovea, while the 3 millimeter inner ring and 6 millimeter outer ring are further divided into four equal regions. So this identifies the layers of the retina and determines macular thickness by measuring the distance between the inner limiting membrane, ILM, and the inner boundary of the retinal pigment epithelium, RPE, in each of these nine regions. So the macular thickness measurements generated by the OCT systems in all the nine regions of the ETDRS map were documented from each subject and were averaged for the purpose of analysis. So the foveal thickness was defined as macular thickness within the innermost 1 millimeter ring. And the mean macular thickness was defined as average macular thickness from 9 regions of the ETDRS map. And it was found to be about 229 microns thick, and the mean macular thickness was 262.8 micrometers. And so the macular thickness of the 9 regions of the ETDRS map was presented, and it was the thinnest in the fovea, so the innermost 1 millimeter ring, and the thickest within the inner 3 millimeter ring, and it diminished peripherally. So the normative values for macular thickness in otherwise healthy eyes were measured to be about 227 microns, foveally, and 270 microns using commercially available Spectralis OCT. And this was similar to the Topcon OCT as well. And so now we’ll get into the A to Z of the cases, findings, and features of the OCT. And first with A. We’ll start with age-related macular degeneration, which you can see a slide of up here. And this is dry macular degeneration, because you can see drusen, which appear as undulations and elevations in the hyperreflective band of the RPE, with less reflective material beneath them. Notice how the inner retinal layers remain generally intact here. And the drusen are located under or occasionally immediately above the retinal pigment epithelium. And please compare this slide here with age-related macular degeneration, the dry form, to the wet form here. And on your left hand side, you can see a subretinal hemorrhage here, due to wet macular degeneration. And here on this yellow arrow, you can see that the blood here is collected between the RPE detachment and the neurosensory retina. And you noticed how in the previous slide, the drusen here were seen as undulations here, compared to the wet macular degeneration, where you can see the blood, again, collected between the RPE detachment here and the neurosensory retina. So this here is a branch retinal vein occlusion on your left, and down below is our central retinal vein occlusion. So with the branch retinal vein occlusion here, you can see cystoid macular edema with intraretinal fluid here, which is this open arrow here, and you can also see the subretinal fluid here. And which appears hyperreflective, with a little shadow down beneath here. So some characteristic findings of a branch retinal vein occlusion on OCT are cystoid macular edema, intraretinal hyperreflectivity from hemorrhages, shadowing, as you can see here, from edema, and occasionally subretinal fluid. And you can see here: Observe that we talked about the photoreceptor integrity line here. And this is not intact here. So as you can imagine, the vision here will be reduced. On your top right hand side, you can see that once the edema has resolved, there is a disruption or absence of the PIL line here. Which is an indication of photoreceptor cell death or disarrangement, which results in poor visual outcome here. Down below here, in the central retinal vein occlusion, you can see intraretinal edema here, and you can also see a loss of that PIL line here. So the vision will here, again, be greatly reduced. And so this is another example here of intraretinal edema from a branch retinal vein occlusion. And here on your right you can see that there is a disruption here, and thinning of the inner retinal layers here. However, notice that the PIL line here is intact, so the visual acuity for this patient will not be affected, as compared to the visual acuity after the resolution of edema for the previous patient you saw here. So again, the important point is: The PIL line is a good marker of how the visual acuity will be. So here is another example of a choroidal neovascular membrane or wet macular degeneration. And you can see how this blood is collected between the RPE detachment here and the neurosensory retina. And you can also see subretinal fluid here on either side of this scan here. And so you’ve seen so far that intraretinal thickening can be associated with many different diseases. So we saw branch retinal vein occlusion just now. And choroidal neovascular pathology can be different from retinal neovascular pathology. So how do we differentiate? So what we do is look at accompanying features and the way they grew as ways to differentiate pathology. So here on this top slide you can see intraretinal fluid with a large pigment epithelial detachment and hyperreflective material. So this here would be a slide of CNVM. But down below, you can see again intraretinal fluid with speckling here. You can see reduced reflectivity, and notice that there’s no pigment epithelial detachment here. And therefore with age, a good history, medications, medical conditions, the scan down below is a scan of diabetic macular edema, and the scan up above here is a scan of choroidal neovascular membrane. So this slide here shows hard exudates here. So these are showing scattered hyperreflectivity, and they’re located in the outer plexiform layer. So these are consistent with hard exudates. And you can also notice some subretinal fluid here on this scan as well. And recall that exudates are located in the middle of the retina, specifically in or adjacent to the outer plexiform layer, and drusen, on the other hand, are located either under or occasionally immediately above the retinal pigment epithelium. And so here is another scan of fluid that you may see on OCT macula. So notice that there’s subretinal fluid here, intraretinal fluid to the right of your screen, and then you can also see that pigment epithelium detachment here. So we talked about dry and wet AMD. And here’s a slide of geographic atrophy. So you can see an OCT scan showing a thinning band of hyperreflective external band, corresponding to attenuation of the RPE and Bruch’s complex. And you can see deeper hyperreflectivity, because of the loss of outer layers, including photoreceptors. And this shows hyperreflective clumps again, at different levels, segmented plaques of the outer band, and elevations with variable hyperreflectivity. In the perilesional area, there are elevations of the outer retinal layers, as well as thickening of the outer hyperreflective band. And at the junction here, you can see different degrees of loss. And again, notice here that the PIL line is lost, so therefore this patient would again have reduced visual acuity from geographic atrophy. And one interesting point to note is: Recently there were changes in OCT that actually preceded the development of geographic atrophy, and these have been identified. So these changes include the presence of hyperreflective foci in the retina, overlying drusen, a subsidence of the inner nuclear layer and outer plexiform layer, with the development of hyperreflective web-shaped bands, and increased signal transmission below the level of the RPE. So these anatomic changes might be used to identify patients early in the course of geographic atrophy development, who may still be at a reversible stage, and therefore amenable to intervention. So the OCT imaging can contribute to a better understanding of the underlying pathologic mechanisms in macular degeneration and geographic atrophy, and it may suggest new biomarkers related to disease progression, and might potentially indicate new therapeutic targets in macular degeneration. So this hyporeflectivity is a feature that you can see here on OCT. And this is a scan of central serous chorioretinopathy. And this is characterized by a buildup of subretinal fluid that you can appreciate here on this scan. In the macula. Caused by abnormalities of the choroidal circulation. And the fluid here leaks from the choroidal circulation, and passes through the hyperpermeable areas of the retinal pigment epithelium, accumulating in the subretinal space. So on examination, you can see the characteristic finding is a posterior neurosensory retinal detachment caused by a leakage of fluid from the level of the retinal pigment epithelium. And as you can see here again, the OCT shows a smooth, diffuse elevation of the neurosensory retina, which is wider than it is tall. And the RPE will be noted underneath the pocket of the optically blank fluid. And you can notice here that the pigment epithelium detachment is almost always smaller, with similar height and width. And sometimes the blister that you can see in central serous chorioretinopathy occurs by itself, but sometimes in the middle of the blister, there’s a tinier blister of the pigment epithelium layer. So you can see this down below here. And this is a PET or pigment epithelial detachment, which can sometimes occur in central serous chorioretinopathy. And we talked about how intraretinal thickening can show up in many different ocular pathologies, so you can see another slide here of intraretinal fluid, and also down below here, you can see subretinal fluid. So the next diagnosis we’ll talk about is juxtafoveal macular telangiectasia. And as you can see here, there’s significant areas of hyperreflectivity in the central retina, due to intraretinal fluid here. Which are, as you can see here, cystic in nature. And there are also areas of scattered hyperreflectivity, located in the outer plexiform layer. And so these here are consistent with exudate. So you can see — marked by A here — which are exudates. And you can also notice that there is some thinning of the ellipsoid zone and the external limiting membrane. And there is also hyperreflectivity, which is this B here, that you notice here. And this is located temporal to the fovea, which is located just deep to the inner nuclear layer. And this is an area of hyperreflectivity that is consistent with MacTel. So this patient was also known to have a small choroidal neovascular membrane on OCT angiography. And so this is a paper I came across, which I’ll give you in references, if you want to read this paper. But this patient was a 38-year-old female who had reduced vision in her left eye. And she had… Because of the reduced vision, and OCT was done, and she was also diagnosed with keratoconus. And as you can see here, the high quality OCT images were captured here, but are of poor quality, due to her keratoconus. And then they used a lens here, optically — so the question was here: Optical imperfections of keratoconic corneas impaired the OCT signal to levels of diagnostic utility. But what was done was neutralization of anterior irregularity of the keratoconic cornea with the fundal contact lens, and this was sufficient to overcome the keratoconic introduced degradation of the OCT signal. So the second question that this study has asked was: Does keratoconus alter macular anatomy? So they used a fundal contact lens to neutralize the effect of the anterior corneal curvature for the first part of the study, and they noticed some studies show that keratoconic patients have some changes in macular thickness. And so more studies are needed to see if keratoconus patients have any altered macular anatomy. So this here is a slide of lamellar hole. And although the macular pseudohole is funduscopically similar to a full thickness lamellar macular hole, a macular pseudohole has no retinal tissue loss. Often, though, there’s mild to moderate retinal thickening, corresponding to an epiretinal membrane. So remember that a macular pseudohole will always be associated with a perifoveal epiretinal membrane. So you’ll need a macular scan to differentiate these lesions and any vitreomacular interactions. So how do you distinguish between a full thickness macular hole, versus a lamellar hole, with irregular foveal contour and defect in the inner fovea? And remember, a pseudohole has an irregular foveal contour with steep edges, without true absence of retinal tissue, which is often associated with an epiretinal membrane. So you can see that there’s an inner retinal defect here on the top left hand slide, and you can also see the foveal contour irregularity here in the layers, inner retinal layers, here. And the next slide here is a full thickness macular hole. And remember, this is in contrast to a lamellar hole with irregular foveal contour and defect in the inner fovea, like we saw before, or pseudohole, which is an irregular foveal contour, with steep edges — but remember that the pseudohole does not have any absence of retinal tissue, and is often associated with an epiretinal membrane. So you may have heard of this anvil-shaped deformity of the full thickness macular hole here. So I looked up — and I have a picture here of an anvil. So if you flip this upside down, you can kind of see that this cystic space here is sort of lifted off, and imagine kind of rotating this 360 degrees, and you can see sort of this upside down anvil kind of being lifted off, as you see on the picture on your left. So the high resolution image here can allow evaluation of the macula in cross section, three-dimensionally. And so the OCT can be extremely helpful in detecting subtle macular holes, as well as staging obvious macular holes. And OCT can also assist in determining whether there’s an associated epiretinal membrane, or if the posterior hyaloid is still attached or not, and this can be critical in deciding their treatment approach. And you can also use OCT to aid in gauging the prognosis of the affected eye. And notice here there’s a full thickness defect here. But you notice that the RPE or retinal pigment epithelial layer here is intact. And you can see again on the top left hand side the RPE is intact, and you can see it as being hyperreflective in both of these scans. So the next slide here is a picture of retinal neovascularization that is showing up here on this slide. So you can see the early retinal neovascularization with fibrovascular growth kind of breaking the ILM and extending here into the vitreous. And remember that retinal neovascularization first develops in the intraretinal layers, but will then extend into the vitreous cavity and disrupt the inner limiting membrane, forming fibrovascular proliferations. And you can see here the OCT, when scanned over the retinal neovascularization will reveal hyperreflective lesions that disrupt the ILM, and it protrudes into the vitreous cavity, connecting to the posterior hyaloid membrane, if this is present. And on the bottom right hand side here, you see a neovascularization of the disc. With this fibrovascular membrane growing over the optic disc here. And this fibrovascular membrane is attaching to the posterior hyaloid membrane and blocking the view of the optic disc cup. So this patient here has high risk proliferative diabetic retinopathy. So this here is a slide of outer retinal tubulations in a patient with non-exudative age-related macular degeneration. So the outer retinal tubulation is believed to be a rearrangement of the photoreceptors, secondary to retinal damage. And it was first discovered by OCT scans and confirmed on histopathologic sections. So in this condition the ORT can be seen in exudative age-related macular degeneration, non-exudative macular degeneration, and other chorioretinal conditions. The ORT can be mistaken as choroidal neovascular membrane on SD OCT. And you can see here different shapes of the ORTs here, on the bottom right hand corner, so it’s highlighted by these yellow arrows here. So this here is a slide of Plaquenil toxicity. And remember that the OCT can detect early retinopathy via RPE and photoreceptor loss in the parafoveal regions that you see here. And you can see this sort of spaceship sign that you see classically with Plaquenil toxicity. And newer technologies such as SD OCTs and autofluorescence even can detect earlier retinopathy, before visual loss. And you can see here these boxes represent the damage of these outer retinal layers here. Again with this sort of spaceship sign that you can classically see in Plaquenil toxicity. And you can see outer retinal atrophy here on both of these slides. So we talked about central serous chorioretinopathy. So as you can see here, this is an image of central serous chorioretinopathy as it resolves. And you can see a progressive elongation of the photoreceptor outer segments in acute central serous chorioretinopathy. So you can see here that when it is acute, there’s a neurosensory retinal detachment here, and as it resolves over time, you can see the progressive elongation of the photoreceptor outer segments over the course of CSCR resolution. And this causes an outer segment disruption here, and this is within the dotted lines here on the bottom slide, and this creates this window defect that you can see on the slide here, down below. And the next slide here for R is the radiation retinopathy that we see on this slide. And as you can see on this slide, there’s significant retinal swelling. And this is due to the series of cysts located predominantly at the junction of the outer plexiform layer and the outer nuclear layer. And there are significant areas of hyperreflectivity located at this junction here. And this here is consistent with exudates. And this patient was also noted to have a microaneurysm. So as you can see, this A here represents a microaneurysm. Despite the fact that they were not known to have diabetes. So this patient was known to have been previously treated with brachytherapy for ocular melanoma. And so for that reason, she was diagnosed with radiation retinopathy. And you can see some hyperreflectivity here as well. The higher part, which is intraretinal fluid, and this large cystic edema here. So this next slide is a picture of a serous retinal detachment. And you can see it can be visualized on an OCT as a smooth, diffuse elevation of the neurosensory retina, which is wider than it is tall. And the RPE will be noted underneath the pocket of the optically blank fluid. So you can see the pigment epithelial detachment, right adjacent to this serous retinal detachment on your left. And remember that the blister CSCR can occur by itself, but sometimes, like we talked about, in the middle of a blister, there’s also a tiny blister of pigment epithelial detachment underneath. And you can see in the slide on your left and the image on your right that there is indeed a pigment epithelial detachment, as in this photo. During the further part of the talk, we talked about — we saw a slide of a retinal detachment. And that was most likely a rhegmatogenous retinal detachment. And here you see a tractional retinal detachment, as a physical separation of the neuroretina from the retinal pigment epithelium. So this is an important physiological ramification of the creation of a detachment, as it increases the physical distance between the photoreceptor cells and their blood supply and the choriocapillaris. And this detachment here recreates a space that disappears during early embryonic development. And you can recall that tractional retinal detachment involves proliferative membranes on the surface of the retina or the vitreous. And remember that these membranes can pull on the neurosensory retina, causing a physical separation between the neurosensory retina here and the retinal pigment epithelium. And this is called tractional retinal detachment. It can be seen in proliferative retinopathy, due to diabetic disease, sickle cell, and other disease processes, leading to neovascularization of the retina. And tractional retinal detachments can also happen due to proliferative vitreoretinopathy after trauma or surgery. And here you can see a focal sort of vitreomacular traction here. And down below, you can see that focal vitreomacular traction, and you can also see this schisis-like intraretinal change here on this slide. And please also appreciate the subretinal fluid on the bottom right hand portion of the slide here. So this here is a slide of a patient with Usher’s syndrome, and a normal patient on your left. So unfortunately, I could not make the quality of this slide come through here. But you’ll have to believe me on this one. So in the patient on your left, there’s a normal OCT retina here. But in the patient on the right with this Usher syndrome retinopathy, you can see they only retain a central island of their diminished outer nuclear layer in Usher syndrome. And the abnormal outer nuclear layer and the RP layers are accompanied by severely reduced vision. And another great question I had was: Using the OCT retina to look at uveitis. And as you can see, uveitis shows different forms of macular edema that you can see here. And the top one here is cystoid macular edema in serpiginous choroidopathy. And on slide B here, you can see diffuse macular thickening with cystic changes in chronic uveitis, and on the bottom slide here, in C, you can see subretinal fluid in Vogt-Koyanagi-Harada disease. Detection and monitoring of uveitic macular edema using OCT has been extensively studied. And so you see three different patterns of fluid distribution in the macula here. So again, cystoid macular edema, diffuse macular edema, which is in B, and the serous retinal detachment that you see in C. And you can see that the CME here, or cystoid macular edema, appears as low reflective intraretinal spaces that are separated by thin retinal tissue with high reflectivity. And you can see here with the diffuse macular edema in B here, you can see small areas of hyperreflectivity, and this sort of spongy appearance to some of these retinal layers here. And this results in an increased macular thickness. And lastly, on the bottom here, you can see the serous retinal detachments are characterized by separation between the neurosensory retina and the RPE. And isolated anterior uveitis can also cause non-cystic retinal thickening that correlates well with disease activity. Epiretinal membrane can also be seen in uveitis, and appears on OCT, as you saw, in the beginning of the presentation, as this jagged hyperreflective line, adhering to the innermost layer of the retina. And the ERM formation is often found in conjunction with vitreoretinal traction, and the tractional mechanism can also contribute to the onset of macular edema that you see here in uveitis. So these slides here show vitreomacular traction. So these are examples of vitreomacular traction and a full thickness macular hole that you see here on C here, down below. So what is the difference between the vitreomacular adhesion and vitreomacular traction? So VMA, or vitreomacular adhesion, was defined as macular attachment of the vitreous cortex within a 3 millimeter radius of the fovea without a change in retinal morphology. And VMT, vitreomacular traction, was differentiated from VMA by the presence of retinal morphological changes. As you can see here, A and B. And then in C you can see this full thickness macular hole defect. And this full thickness macular hole defect was defined as a foveal lesion, involving all of the retinal layers, as you can see here, compared to A and B. So the next slide here — it’s important to distinguish between a full thickness macular hole versus a lamellar hole, versus a pseudohole, which we talked about. And this is Watzke Allen’s sign. It’s commonly used in clinical practice, to have a patient look at a line on your slit beam and say whether it’s broken or not. And you can see there’s a macular hole here. The patient’s point of view will be this, where they a break in this line here. So the next slide here for X is X-linked retinoschisis, and this is an inherited retinal disorder which causes early vision loss in males. And you can see on a funduscopic exam, a patient will have a foveoschisis. And you can see this as a spoke-like pattern here, radiating from the fovea, with a dome-like elevation of the thin layer of the retina here. And schisis is most often in the macula, but it can also extend to the periphery, and it occurs in more than half of the patients. And these bullous retinoschises may improve over time. So again, this is an OCT macula of a patient with an X-linked retinoschisis, and you can see this large inner retinal layer pretty well. I also have seen some questions about macular dystrophies here. I have here… A Best’s disease patient on the right, and Stargardt’s dystrophy here on — excuse me. Best’s disease on your left and a Stargardt patient on your right. So in early stages of Best disease, our typical lesion has an egg yolk appearance, so hence the name vitelliform. And this is later replaced here, as you can see, with atrophy and scarring. This is B, here. So notice that this patient’s right eye here had more advanced disease than her left, and you can see this on her OCT. So notice in her right eye there’s a loss of the outer retinal layers that you can see with this yellow arrow here and pigment epithelium, which corresponds — when you do an FAF, you can see this hypofluorescent area here. And in her left eye, you can see the splitting of the retinal layers, and you can also see this area of subretinal fluid with this blue arrow here on this slide here. Her initial visual acuity here was 20/20 in the right eye and 20/30 in her left eye, and notice that her visual acuity is not severely affected, because the lesions were eccentric to the fovea. So on your right hand side is a picture of Stargardt’s disease. And you can see that the inner segment/outer segment junction, the photoreceptors, the outer nuclear layer, and the retinal pigment epithelium are lost in the center macula of both of her eyes. And remember, Stargardt’s disease is the most commonly inherited single gene retinal disease, and it usually has a autosomal recessive inheritance. So next we’ll review the answers to the quiz questions. So this, I believe, most of you had done. So this is a slide of central serous chorioretinopathy. And you can see it is characterized by a buildup of subretinal fluid in the macula, and it’s caused by abnormalities in the choroidal circulation. So this fluid here leaks from the choroidal circulation and passes through the hyperpermeable areas of the RPE layer, and it accumulates here in the subretinal space. So again, on examination, you can see a characteristic finding is a posterior neurosensory retinal detachment caused by leakage of fluid from the level of the RPE. And you can see a serous retinal detachment is visualized with an OCT as a smooth, diffuse elevation of the neurosensory retina, which is wider here, as you notice in both of these slides, than it is tall. And please also recall that in some cases of CSCR, you can also see a pigment epithelial detachment that is noted underneath the pocket of this optically blank fluid. And recall that the PED here is almost always smaller with a similar height and width as the larger piece here. So the diagnosis for this slide was vitreal hemorrhage and retinal traction. So here you can see that the posterior vitreous is detached from the underlying retina here. On the posterior side of the vitreous are significant fibrotic membranes. And these membranes are associated with significant retinal traction, and there’s an elevation of the retina here, due to the traction. And this here is causing intraretinal cysts. And there is also evidence of a previous laser photocoagulation, as there is some outer retinal thinning and a reverse shadow that there’s geographic atrophy. So this is evidenced by this A here. So points to the A on this slide. And so therefore this patient was diagnosed with a recurrent vitreous hemorrhage and traction here that you can see. So the answer to that question here was B. Vitreal hemorrhage and retinal traction. So the answer to this slide was C, acute middle maculopathy. And here you notice there was a segmental swelling of the middle retina here, and this actually is a newly identified condition on OCT. So it is related to the schema of the superficial capillary plexus. So on OCT here, the nerve fiber layer and the ganglion cell layer are within normal limits, as you can see. And there’s middle retinal hyperreflectivity that you can see here. Specifically, the inner plexiform layer, IPL, and the outer plexiform layer, are hyperreflective, due to this swelling. So the inner nuclear layer is somewhat obscured, due to the swelling of the two plexiform layers that you can see here. And this is showing up as almost this train track appearance on this scan. So the swelling of these layers is causing that shadowing of the outer nuclear layer that you see. So therefore this patient was diagnosed with acute middle maculopathy, and this is a type of acute macular neuroretinopathy. And these rare lesions are believed to be related to a segmental ischemia of the superficial capillary plexus. And this patient was also diagnosed with a stroke, which caused temporary paralysis. So remember, there are up to four retinovascular networks in the macula. So the superficial vascular plexus, SVP, is supplied by the central retinal artery, and composed of larger arteries, arterioles, capillaries, venules, and veins. And there are two deeper capillary networks above and below the INL, or inner nuclear layer, and these are referred to as the intermediate and deep capillary plexi, or ICP and DCP. And these are supplied by the vertical anastomoses of the SVP. And the fourth network here is a regional layer called a radial peripapillary capillary plexus. So again, this patient had a segmental ischemia here, due to the superficial capillary plexus. So the diagnosis for this slide was scleral choroidal calcification. So you can see here there’s a white lesion, just outside of the vascular arcade. And so what is this? So all the retinal tissue is still normal to your left and to your right. This lesion here is noted to be elevated, as opposed to a depression or absence of tissue, which can also present as a depigmented lesion. So the retinal tissue overlying the lesion is normal. With the exception of some compression of the outer nuclear layer. So the ELM, or external limiting membrane, and underlying ellipsoid, are visible in the area here to your right. There is an elevation of the RPE from the underlying Bruch’s membrane, and this is shown by A, showing the Bruch’s membrane. And the hyperreflective area of the retina is normal, and is related to the retinal blood vessel that has been sectioned here. So this lesion itself is located at the level of the sclera, and it is hyperreflective here. So therefore this patient was diagnosed with sclerochoroidal calcification. And you saw this slide in the beginning of the presentation. So we’ll go over briefly what the diagnoses are. So again, on 1A, you can see intraretinal edema here. So this is a slide of diabetic macular edema. And here in 1B, you can see a macula-off retinal detachment, which exhibits extensive subretinal fluid here. On 1C, you can see an AMD patient with some small subretinal fluid here, with this photoreceptor loss. And on 1D, you can see this pigment epithelial detachment here, with adjacent intraretinal exudates, which, remember, causes some hyperreflectivity on OCT retina. Here on figure 1E, you can see a CSCR, with this focal PED right beneath it. And in figure 1F, you can see these multifocal large PVDs, and this is a patient with polypoidal choroidal vasculopathy, which is a disease of choroidal vasculature. And this is characterized by serosanguineous detachments of the pigment epithelium, and you can also see exudative changes that can commonly lead to subretinal fibrosis. So clinical pearls from today were to understand OCT’s capabilities in clinical practice. You can learn to meaningfully interpret various lines, layers, and contours in normal eyes, so you can then learn how to interpret OCT in retinal pathology. And then you can transition to variations in different retinal, choroidal, and vitreal abnormalities. And remember that the PIL line, the photoreceptor integrity line, gives you an estimate of the visual acuity based on its appearance right beneath the fovea. And I’m happy to send you a list of references, if you need to review the papers I alluded to in this presentation. And thank you so much for your time. And I’m happy to answer any questions you may have. So with regards to glaucoma diagnosis, so here I was covering the OCT retina, so I’m happy to address glaucoma diagnosis using the retinal nerve fiber layer, in a different presentation. So Stargardt’s disease, we had a slide on Stargardt’s. So here you can see on the right hand side of your slide Stargardt’s disease. And in Stargardt’s, notice that there are atrophic macular lesions. So notice how the inner segment/outer segment junction has been disrupted here. On these slides on your right. And the retinal pigment epithelium is also lost in the center of the macula in both eyes here. So right eye on top, left eye on the bottom here. And I see a lot of questions about OCT and glaucoma, which are, again, out of the scope for this presentation. But I’m happy to address in the future. And in terms of getting good OCT images of highly myopic patients, remember we talked about how they used the fundus contact lenses for a keratoconic patient, so perhaps more studies are needed to see if we can get good images in highly myopic patients, as well, with OCT. And with regards to reading OCT step by step, I’m going to go back to the slide of the normal OCT here. And remember that it’s really important to know a normal OCT retina here. And so with this normal OCT retina, you can know all the layers. Sort of these layers here on the retina. And then you can then compare the pathological OCT retina slides to these layers, to see which layers are disrupted. So we went over a lot of features you can see on OCT, as well as some diagnoses, where you saw edema, exudates, and so it’s important to see which layer of the retina the pathology is happening in, to make the diagnosis. You can use the age of the patient, medical history, medications, to kind of read an OCT, and come up with a diagnosis. And chronic CSCR on OCT is also an excellent question. So remember that this is a picture of an acute CSCR. And when you have chronic CSCR, what happens is… You can see sort of, as the acute CSCR resolves, you can see the outer segment disruption here that is within these dotted lines. And so this creates a window defect, once the edema from the acute CSCR resolves over time. Thank you all for joining me today, and I’m happy to address any other questions when it’s been posted on Orbis. Thank you so much for having me.
July 11, 2019