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- CTX? Never Heard of It: Part 2
- Early-age Vision Screening is Crucial
- Clinical Experience with Lifitegrast
- OSD in 2017: A Device Summary
- Level 3 Dry Eye Treatments: Scleral Lenses
- The Pyramids of Dry Eye Disease: A Simplified Model to Guide DED Management
- Tips for Novice Scleral Lens Fitters
- The Role of OCT in the Comprehensive Optometry Office
- AMD Monitoring at Home
- Choices Matter in Postoperative Inflammation
- Ocular Manifestations of Graft vs. Host Disease
- From Naysayer to Believer: Using PERG to Diagnose Early Glaucoma
- A New Low Vision Tool
- Introduction: AOC’s Last Waltz
- From 2010: Hordeolum and Chalazion
- From 2011: Capitalizing on Growth Categories
- From 2012: Taking Ownership of Ocular Allergies
- From 2016: Take Care of the Ocular Surface in Glaucoma
- From 2017: Scleral Lenses: From the Renaissance to the 21st Century
- Alternative Treatment Leads to Personal, Professional Growth
- Optometry and Diabetes: Beyond the Exam Room
- Clinical Experience Shapes the Educational Experience
- Get to Know Leslie O’Dell, OD, FAAO
The ophthalmoscope may be the primary tool for viewing the fundus, but it is not by any stretch the best one. Can you imagine all the disease that would be missed if we still relied solely on Hermann von Helmholtz’s 150-year-old invention?
Optical coherence tomography (OCT) provides retinal information and histopathologic information that is often invisible on ophthalmoscopy. Retinal diseases such as age-related macular degeneration (AMD), diabetic retinopathy, epiretinal membrane, vitreomacular traction, central serous chorioretinopathy, and optic nerve elevation are examples of conditions commonly seen in our offices for which OCT can provide valuable information.
The use of this technology in everyday primary eye care helps us to care for our patients more completely. It is crucial that we employ OCT, not only to make appropriate referrals to specialists for retinal consultations and emergent conditions, but also to monitor and manage disease in the office and clinic.
OCT uses light from a super luminescent diode to create in vivo cross-sectional views of the retina. In early iterations, OCT images were acquired using a time-domain function (approximately 400 A-scans per second using six radial slices 30° apart). Spectral-domain (SD) technology subsequently increased scan speeds to 20,000 to 70,000 per second. This greater speed enhances the resolution, decreases artifact, and diminishes the chance of missing pathology.
SD-OCT images reveal the retina, retinal nerve fiber layer (RNFL), and optic nerve in real time. We can directly visualize pathology and obtain quantitative measurements of the retinal architecture and density changes at high resolution.
The SD-OCT unit I use is the 3D OCT-1 Maestro (Topcon). With this technology, I can see all of the layers of the retina (Figure 1). The outer plexiform layer is the dividing line between the inner retina and outer retina (Figure 2). Examples of inner retinal disease include hypertensive retinopathy (flame-shaped hemorrhage), glaucoma (affecting the ganglion cell complex), and early diabetic disease. Outer retinal diseases include macular degeneration (involving the choroid, Bruch membrane, retinal pigment epithelium [RPE], and photoreceptors), photoreceptor disease, and central serous chorioretinopathy (CSCR).
The landmarks visible on OCT include the vitreoretinal interface, the RNFL, the photoreceptor integrity line (PIL)–ellipsoid portion of the inner segments, and the RPE. When interpreting an OCT scan, we read horizontally, starting away from the lesion. We can then identify arrangement and symmetry located anterior and then posterior to RPE line 4 and look for the alteration of features (Figure 3).
The 3-D Wide Report on the Maestro includes several useful components: an optic nerve head photo, B-scan images, retinal analysis, ganglion cell complex (GCC) data, and RNFL analysis (Figure 4).
A SAMPLING OF CLINICAL APPLICATIONS
OCT is invaluable in a diabetic retinal evaluation. For example, for a patient with dot and blot hemorrhages and hard exudates, should the optometrist monitor or get a consultation? We must keep in mind that cotton wool spots and flame-shaped hemorrhages last about 6 weeks, dot and blot hemorrhages usually last less than 6 months, and microaneuyrsms last longer than 6 months. Therefore, to differentiate these entities, we should evaluate the patient again in 6 months. Flame-shaped hemorrhages occur in postarteriole retinal capillaries, located in the RNFL. Dot and blot hemorrhages occur in prevenule capillaries, located in the inner nuclear layer.
GCC assessment is indicated in diabetic patients. Diabetes can have a neurodegenerative effect on the retina, even absent a vascular component. Diabetic macular edema is difficult to visualize at the slit lamp, so SD-OCT is key in evaluating these patients. Other pathologies in which GCC assessment is helpful include neovascularization elsewhere and proliferative diabetic retinopathy.
When do macular changes (Figure 5) necessitate referral? In an RPE detachment (Figure 6) the basal cells lift up and detach. (This can reveal the Bruch membrane under the RPE.) Drusen are remnants of cholesterol, macrophages, photoreceptor components, and other cellular waste products seen on funduscopy as small hard deposits or as larger soft confluent deposits. On OCT, drusen are seen as elevations of various sizes between RPE and Bruch membrane with a turbid mass of material inside.
OCT is essential for monitoring neovascular AMD (Figure 7). The proliferation of abnormal blood vessels in AMD is a result of excess of vascular endothelial growth factor (VEGF). When proliferation occurs under the RPE, it is called occult neovascular AMD. When the membrane penetrates and courses above the RPE, it is known as classic neovascular AMD. On OCT, we can spot subtle changes in the RPE from drusen and identify breakdowns in the RPE. We can visualize subretinal fluid and even a choroidal neovascular net coursing through the RPE. OCT makes it possible to see when dry AMD turns wet.
In a serous RPE detachment, there will be a break in the continuity of the PIL and the RPE. The space under the RPE will either be black, indicating a cyst, or turbid, indicating a mass.
CSCR (Figure 8) is caused by choroidal congestion and vessel hyperpermeability. This is thought to be a result of elevated plasma catecholamine levels and may also be related to cortisol. Dysfunction of the RPE pump function or vascular permeability is thought to cause CSCR.1,2
Patients with CSCR should be monitored, as they may return months later with signs of metamorphopsia that can indicate the presence of disruption due to subchoroidal neovascularization.
Cystoid macular edema (CME) occurs in the outer plexiform layer and is a result of the hyperpermeability of abnormal perifoveal capillaries. Pseudophakic CME, also known as Irvine-Gass syndrome, occurs most often at 6 to 10 weeks after cataract surgery. About 20% of patients develop some CME after cataract surgery, but only 1% have significant visual impairment as a result.3
See what you might be missing with that ophthalmoscope?
Many situations that present to us in primary ocular care can visualized using OCT, including vitreomacular traction, macular holes and pseudoholes, epiretinal membranes, retinoschisis, and retinal detachment, to name a few. The importance of incorporating new technologies such as SD-OCT into your practice cannot be overstated.
1. Leveque TK, Yu L, Musch DC, et al. Central serous chorioretinopathy and risk for obstructive sleep apnea. Sleep Breath. 2007;11(4):253-257.
2. Tewari HK, Gadia R, Kumar D, et al. Sympathetic-parasympathetic activity and reactivity in central serous chorioretinopathy: a case-control study. Invest Ophthalmol Vis Sci. 2006;47(8):3474-3478.
3. Rotsos TG, Moschos MM. Cystoid macular edema. Clin Ophthalmol. 2008;2(4):919-930.
Travis Johnson OD, FAAO
• owner, Music City Eyecare, LLC, Murfreesboro, Tenn.
• firstname.lastname@example.org; 651-230-3554
• financial disclosure: none