QUALITATIVE ANALYSIS OCT/FA BOOT CAMP. OCT Layers 4/17/2017. Holly Cheshier, CRA, OCT-C, COT

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1 OCT/FA BOOT CAMP Holly Cheshier, CRA, OCT-C, COT OCT Layers QUALITATIVE ANALYSIS Reflectivity- hotter colors (yellow, orange, red) highly reflective structures (Hyper-reflective). Cooler colors (green, blue) lower reflectivity (Hypo-reflective). White represents the highest reflective structures and black represents the least reflective structures. Highest reflective anatomical layers are the NFL and RPE. Highly reflective anomalous structures include areas of dense pigmentation, scar tissue, neovascularization and hard exudates. Low reflectivity are the vitreous space and bottom of the scan (light does not penetrate past the choroidal tissues). Low reflective anomalous structures are areas of edema (fluid). Shadowing-dense structure prevents light from penetrating below the structure. Shadow cones can appear below normal retinal blood vessels, a dense hemorrhage, exudates, densely pigmented formation (choroidal nevus) and a thick CNVM. 1

2 PHASES OF A FLUORESCEIN ANGIOGRAM Choroidal Filling The fluorescence that first appears in the eye is from the choroidal circulation. Choroidal filling is diffuse or patchy and is seen before the appearance of dye in the retina. A retinal artery supplied from the choroid (cilioretinal artery) provides blood to a portion of the macula. Ciloretinal arteries are found in 15% of individuals. When present, cilioretinal vessels will fill with the choroidal circulation. CHOROIDAL PHASE EARLIEST RECORDING OF DYE RETINA RELATIVELY QUIET EXCEPT THE CILIORETINAL ARTERY. DYE IN ARTERIES ONLY VERY SHORT- LESS THAN 1-2 SECONDS VEINS STILL DARK ARTERIAL PHASE ARTERIOVENOUS PHASE/EARLY VENOUS ARTERIES FILL WITH FLUORESCEIN LAMINAR FLOW IN VEINS 2

3 VENOUS PHASE RECIRCULATION PHASE VEINS GENERALLY BRIGHTER THAN ARTERIES VEINS ARE FILLED WITH FLUORESCEIN USUALLY OCCURS BETWEEN 1-3 MINUTES ARTERIES AND VEINS OF EQUAL BRIGHTNESS FLUORESCENCE BEGINNING TO DECREASE LATE PHASE OCCURES FROM 5-10 MINUTES SLOW DECREASE IN TOTAL FLUORESCENCE LATE PHASE Abnormal Fluorescein Angiogram Patterns HYPERFLUORESCENCE INCREASED FLUORESCENCE. Staining-Hyperfluorescence late. No change in shape or size over time. Window Defect/Transmission Defect- Hyperfluorescence early, then slow decrease in intensity. No change in shape or size over time. Leakage-Early hyperfluorescence with late increased intensity, diffusion, and enlargement of dye. Pooling-Slowly developing hyperfluorescence with sharply demarcated borders. STAINING-DRUSEN STAINING-Hyperfluorescence late. No change in shape or size over time. 3

4 WINDOW DEFECT-GEOGRAPHIC ATROPHY WINDOW DEFECT-Hyperfluoresce early, then slow decrease in intensity over time. No change in shape or size. LEAKAGE-CLASSIC AMD LEAKAGE-Early Hyperfluorescence with late increased intensity, diffusion and enlargement of dye. POOLING-PED Abnormal Fluorescein Angiogram Patterns HYPOFLUORESCENCE-DECREASED FLUORESCENCE Filling Defects-Results from decreased vessel perfusion. Blockage-Usually blood which is often visible with shape or size corresponding to the area of decreased fluorescence. 4

5 FILLING DEFECTS-Results from decreased vessel perfusion. BLOCKAGE-Usually blood which is often visible with shape or size corresponding to the area of decreased fluorescence. A gel-like structure. It occupies approximately four fifths of the volume of the globe. The vitreous is composed of 99% water, it has a viscosity two times that of water due to the presence of hyaluronic acid. The vitreous is also made up of hyalocytes and type II collagen. The vitreous has attachments at the optic disc, along the retinal vessels and in the fovea/parafovea area. Vitreous Floaters Floaters are deposits of various size and shape, consistency within the eye s vitreous humour, which is normally transparent but as one ages, imperfections gradually develop. Floaters are visible because of the shadows they cast on the retina or refraction of the light that passes through them. They can appear alone or together with several others in one s visual field. They may appear as spots, threads, or fragments of cobwebs, which float slowly before the patient s eyes. Floaters are able to catch and refract light in ways that somewhat blur vision temporarily until the floater moves to a different area. Often they trick people who are troubled by floaters into thinking they see something out of the corner of their eye that really is not there. Most people come to terms with the problem, after a time, and learn to ignore their floaters. For people with severe floaters it is nearly impossible to completely ignore the large masses that constantly stay within their central vision. Scanning the Vitreous Line Scan Showing Floaters #3 Step 1: Start with Line Scan (Default setting of 30 degree A scan with ART set at 100) Step 2: Make sure HR is selected. Step 3: Center scan over fovea and bring retina scan below the blue guide to show vitreous. Focus on vitreous if needed. #1 #2 5

6 Diopter Setting Vitreous Layer Asteroid Hyalosis Asteroid hyalosis is a degenerative condition of the eye involving small white opacities in the retina. Asteroid hyalosis does not usually severely affect vision, the floating opacities can be quite annoying, and may interfere significantly with visualization and testing of the Vitreous. Asteroid Hyalosis Red Free Asteroids Remain Asteroids Not Seen On FA 6

7 Vitreous Syneresis Hyaloid Degeneration of the vitreous humor with loss of gel consistency to become partially or completely fluid. May precede a vitreous detachment. Layer of collagen separating the vitreous humour from the rest of the eye. At least two parts have been identified anatomically. The posterior hyaloid membrane separates the rear of the vitreous from the retina. The anterior hyaloid membrane separates the front of the vitreous from the lens. VMA (Vitreomacular Adhesion) When the vitreous begins to shrink and liquefy, it can become stuck to the retina and begin to pull leading to VMA. VMT (Vitreomacular Traction) The macula is the small area at the center of the retina, which is the thin tissue that lines the inside of the back of the eye. The macula is the most sensitive part of the retina. It is the macula that gives us the vision we use to read and to do detailed visual tasks. As we grow older the thick vitreous gel that fills the eye shrinks and pulls away from the macula. Sometimes as the vitreous pulls away from the macula, it remains partially stuck and pulls on the surface. This pulling and distortion of the normal macular structure is called Vitreomacular Traction (VMT). VMT (Vitreomacular Traction) VITREOMACULAR TRACTION (VMT) The vitreous gel shrinks and pulls away from the macula at different rates in each person, but it occurs in everyone with time. VMT only occurs when there is an abnormally tight adhesion between the shrinking gel and the macula. VMT may cause no symptoms at all in its mildest forms. Sometimes, VMT worsens and the increased traction results in blurred or distorted central vision. Traction on the retina frequently causes retinal distortion and cystoid macular edema (CME). VMT can also lead to the development of epiretinal membranes and macular holes. OCT is extremely useful in monitoring the progression of VMT. 7

8 VITREOMACULAR TRACTION (VMT) How Do I Do A Dense Scan For VMT? Step #1: Choose FAST scan Step #2: Shorten your A-scans by hitting your - buttons horizontal & vertical to reflect 15x5. Step #3: Increase your sections by hitting your + to reflect um. # 1 Align dense scan over macula #2 #3 IT S IMPORTANT TO USE A DENSE SCAN TO LOOK FOR MACULAR HOLES THAT THE VMT MAY CAUSE DENSE SCAN 15X5 25 LINES Internal Limiting Membrane (ILM) Internal Limiting Membrane The inner limiting membrane is the boundary between the retina and the vitreous body, formed by astrocytes and the end feet of Muller cells. It is separated from the vitreous humor by a basal lamina. 8

9 Inner Retina (Subhyaloid Hemorrhage & Flame Hemorrhage) ILM/Subhyaloid Hemorrhage (Vertical Orientation-90 degrees) ILM/Subhyaloid Heme (Horizontal Orientation-180 degrees) Epiretinal Membrane ERM termed macular pucker and cellophane maculopathy. Symptoms-variable reduction in visual acuity. Alterations in the normal anatomy of the macula may lead to significant distortion, binocular diplopia, or even macropsia (objects appear larger in size). Features-Examination demonstrates the presence of a glistening, crinkled sheen to the retinal surface corresponding to the location of the ERM. Contracture of the ERM may lead to distortion of the retinal vasculature and retinal folds. Severe cases may be associated with retinal whitening, retinal edema, or occasional retinal or preretinal hemorrhage. Testing for Epiretinal Membrane Testing-OCT may allow better visualization of the relationship of the ERM to the retinal surface. Fluorescein angiography helps look for damaged vessels that can cause edema from the traction. The most common form of ERM usually forms after posterior vitreous detachment (PVD). ERM may arise in association with retinal vascular disease including vein occlusions and diabetic retinopathy, uveitis, trauma or following retinal detachment. Treatment of ERM Patients with significant visual symptoms may elect to undergo pars plana vitrectomy with removal of the ERM tissue. Approximately 70% to 80% of patients will gain at least two lines of visual acuity with successful removal of the ERM. Vitrectomy for ERM is associated with a significant risk of cataract progression. ERM are generally not associated with systemic diseases. 9

10 ERM #1 ERM #2 Red Free Enhances ERM FLUORESCEIN ANGIOGRAM LOOKS FOR HYPERFLUORESCENCE (TYPE IS: LEAKAGE) FROM DISTORTED VESSELS. What Do You See? DX? 10

11 Color Photo-What Do You See? Early FA-What Do You See? Late FA-What is the DX? Nerve Fiber Layer Represents the innermost layer of the fundus. The nerve fiber layer collects the visual impulses that begin with the rods and cones. Carries neural impulses to the optic disc. Lack of function causes loss of visual acuity or scotoma. The thickness of the RNFL increases toward the optic disc. RNFL thickness decreases in glaucoma. Nerve Fiber/Myelin Nerve fiber is a thread like extension of a neuron, which is formed by the axon and its covering. Larger axons are covered by a myelin sheath and are termed myelinated or medullated fibers. Myelin is a fatty substance that covers neurons. Myelin sheath (a layer of myelin) helps increase the speed at which information can travel on the neurons. The fatty nature of myelin is responsible for the glistening whiteness of the peripheral nerve trunks and white matter of the CNS. Damage to the myelin sheath causes neurological disease, as in multiple sclerosis. MNFL/MRNFL(Myelinated Retinal Nerve Fiber Layer) Myelinated retinal nerve fiber layers (MRNFLs) are relatively common and generally benign. They appear as white, sharply demarcated patches on the surface of the retina that block the underlying retinal vessels. They have frayed or feathered borders that correspond in shape and distribution to ganglion cell axons. Myelination of the RNFL is often congenital but can be acquired or even progress in childhood or adolescence. Myelination does not normally extend onto the retina. They do not interfere with vision. Myelinated nerve fibers are often mistaken for cotton wool spots or retinal infiltrates. 11

12 MNFL/MRNFL MNFL/MRNFL MNFL/MRNFL FA Shows: Hypofluorescence Type Is: Blockage Cotton Wool Spots (CWS) CWS are caused by retinal nerve fiber layer micro-infarcts. Cotton wool spots are found around the optic disc and along the temporal vascular arcades. Cotton wool spots have several causes. Any process that occludes small retinal arterioles will do this: hypertension, diabetes, HIV, vein occlusion, severe anemia, connective tissue disorders, viruses, Purtscher Retinopathy, Behçet's and many others. Usually a sign of ischemia. Cotton Wool Spot Cotton Wool Spots (CWS) sign of ischemia 12

13 FA Shows HypoFluoescence Type is: Filling Defect FA Shows HypoFluoescence Type is: Filling Defect Intra Retina (GCL, IPL, INL, OPL, ONL & ELM ) Cystoid Macular Edema CME is most commonly encountered after cataract surgery but may arise in association with a number of conditions including retinal vascular disease, retinitis pigmentosa, uveitis, and secondary to the use of several drugs such as epinephrine, latanoprost, and nicotinic acid. Postcataract CME is most commonly observed 1 to 3 months postoperatively. Symptoms-Patients present with decreased vision. Some patients may note metamorphopsia or micropsia. Features-Refraction may demonstrate a hyperopic shift. CME is characterized by a honeycomb pattern of retinal thickening in the fovea and parafoveal region. You may have a yellow spot in the fovea due to retinal thickening with loss of the normal foveal reflex. Angiogram Features-Accumulation of edema fluid in the outer plexiform layer leads to the characteristic petaloid pattern of cystoid spaces observed around the fovea. Characteristic features are late accumulation of dye within the cystoid spaces and late staining of the optic disc may occur. CME arises from accumulation of edema fluid within the retina due to disruption of the normal blood-retinal barrier. Inflammatory mediators are hypothesized to trigger the breakdown of the blood-retinal barrier. Treatment of CME OCT-CME Preoperative topical nonsteroidal anti-inflammatory drugs (NSAIDs) reduce the incidence of CME. Topical NSAIDs and steroids have been demonstrated to be effective in the resolution of postoperative CME. Patients whose conditions fail topical therapy are considered for periocular steroid therapy. In cases of chronic CME pars plana vitrectomy has been shown to improve the visual outcome. The therapy of CME associated with chronic uveitis is primarily directed at treatment of the underlying inflammation. Postoperative CME is not associated with systemic disease. Patients with uveitis and associated CME may have underlying systemic inflammatory diseases that require evaluation. 13

14 Central Retinal Artery Occlusion (CRAO) CRAO occurs in older patients as a complication of atherosclerosis. Rarely, CRAO in the elderly may be related to giant cell arteritis. When CRAO occurs in younger patients, other etiologies such as coagulopathy (sickle cell, oral contraceptive use, pregnancy, protein S or antithrombin III deficiency), cardiac emboli, or collagen vascular disease with vasculitis must be considered. Symptoms-sudden, severe, painless loss of vision characterizes the onset of CRAO. Episodes of transient visual loss lasting minutes (amaurosis fugax) may precede permanent visual loss. If eye pain is associated with CRAO, unusual causes such as carotid dissection or orbital cellulitis must be considered. Symptoms of giant cell arteritis including jaw claudication, scalp tenderness, headache, fatigue and myalgia (muscle pain) may occur in some patients. Central Retinal Artery Occlusion (CRAO) Findings-An afferent pupillary defect (APD) is present. A cherry red spot is characterized with CRAO. The cherry red spot refers to the macular appearance of a central red spot surrounded by superficial retinal whitening. Occlusion of the central retinal artery results in ischemia and infarction of the inner retina. The occlusion is manifest by whitening and edema of the inner retina in the macular area. The fovea retains its reddish color because the inner retinal layers are displaced laterally and the underlying choroidal circulation remains intact. Blood flow within retinal arteries may appear slow and segmented, referred to as box-car formation. Iris neovascularization may be seen in up to 20% of patients with CRAO. Central Retinal Artery Occlusion (CRAO) Testing-fluorescein angiography may show delay or absence of filling in the retinal arteries. Boxcar segmentation can be seen in both veins and arteries. Retinal blood flow may be restored by the time the patient seeks attention, in which the FA will appear normal. Irreversible damage to the neurosensory retina occurs after 90 minutes of complete CRAO. Treatment-for embolic CRAO of less than 24 hours, the physician may attempt to improve perfusion pressure and dislodge the embolus (by lowering the IOP-anterior chamber paracentesis). Treatment rarely alters the visual outcome. Panretinal photocoagulation is used for eyes that develop iris or anterior chamber angle neovascularization. CRAO typically results in severe visual loss in the range of 20/200 to light perception. Major risk factors for CRAO include hypertension, diabetes mellitus, carotid artery disease and coronary artery disease. 14

15 Common Findings in OCT of Central Retinal Artery Occlusion (CRAO) Increased Intraretinal thickening & Hyper- Reflectivity due to retinal edema & Optic Nerve swelling in the early stages of CRAO Increasing Your Length and Width of Your A-scans Will Give You a Broader View Step #1: Start with Fast scan. Step #2: Increase your A-scans by hitting your + both horizontal & vertical. Step #3: At maximum length this will default your sections to 31. No need to dense your sections. Step #4: Optional...You can choose HR if you notice too much Noise/Snow. This will decrease the amount you have. #1 start with Fast scan #2 Increase A- scans #3 #4 Important Facts to Remember When Doing Fluorescein Angiography for CRAO Accurate timing of the sequence of the dye filling/transit is important in helping with the evaluation of some of the many therapies recommended. Montaging your Fluorescein Angiogram (FA) photos are important. Begin montaging between 2-4 minutes, depending on filling/transit phase. This provides helpful information for the physician to better evaluate and provide best treatment options to the patient. Fluorescein Angiography (FA) of Central Retinal Artery Occlusion (CRAO) Montage of Fluorescein Angiography (FA) of Central Retinal Artery Occlusion (CRAO) 15

16 Central Retinal Vein Occlusion (CRVO) CRVO is a common retinal vascular disease that is usually seen in adults over 50 years. Men are more commonly affected than women, especially in younger age groups. Risk factors-systemic vascular disease (hypertension, cardiovascular disease, diabetes mellitus), primary openangle glaucoma and in younger patients hypercoagulable states (abnormal increase of blood clotting). Symptoms-may be asymptomatic or present with profound visual loss. Loss of vision may be sudden or gradual. Other symptoms include central scotoma, photopsias (appearance of sparks, flashes or colors due to retinal irritation), transient visual obscurations, pain and eye redness. CRVOs are classified as perfused or nonperfused. Central Retinal Vein Occlusion (CRVO) Features-visual acuity of less than 20/200 and the presence of an APD (afferent pupillary defect) suggest ischemia. It is also important to measure IOP and perform an undilated slit lamp exam and gonioscopy to examine for iris or anterior chamber angle neovascularization. Acute findings include dilated and tortuous veins, scattered intraretinal hemorrhages in all four quadrants of the retina, cotton wool spots, macular edema and optic disc edema. Major complications of CRVO are macular edema and neovascular glaucoma. Approximately 1/3 of eyes with CRVO are classified as nonperfused or ischemic. Of those, 1/3 to ½ will develop neovascular glaucoma as a result of iris and anterior chamber angle neovascularization. Central Retinal Vein Occlusion (CRVO) Testing-fluorescein angiography demonstrates a delay in the filling of the retinal veins with prolongation of the arteriovenous transit time. Leakage is routinely observed from the optic disc and retinal vessels. Varying degrees of macular ischemia and leakage occur and also vary in the extent of peripheral retinal nonperfusion. Eyes with areas of at least 10 disc diameters of retinal nonperfusion are classified as nonperfused. Treatment-Anti-VEGF injections (Avastin & Lucentis), macular focal laser for macular edema and PRP in eyes with significant nonperfusion. Approximately 1/3 of eyes initially judged as perfused progressed to the nonperfused by 3 years. Patients should by closely followed by careful examination for neovascularization of the iris or anterior chamber angle at each visit. Central Retinal Vein Occlusion (CRVO)-Nonperfused FA-Central Retinal Vein Occlusion (CRVO)-Nonperfused Important Facts to Remember When Doing Fluorescein Angiography for CRVO Accurate timing of the sequence of the dye filling/transit is important in helping with the evaluation of some of the therapies recommended. Montaging your Fluorescein Angiogram (FA) photos are important. Begin montaging between 2-4 minutes, depending on filling/transit phase. This provides helpful information for the physician to better evaluate and provide best treatment options to the patient. 16

17 Central Retinal Vein Occlusion (CRVO)-Perfused Fluorescein Angiogram of Central Retinal Vein Occlusion (CRVO)- Perfused OCT of Central Retinal Vein Occlusion (CRVO)-Perfused Intraretina Cysts Common OCT findings are Cysts. Cysts are Hypo-Reflective on an OCT. Cysts are found in the Intra-Retina of an OCT. Longer A-scans are helpful in looking at CRVO s. 17

18 Branch Retinal Artery Occlusion (BRAO) BRAO most often occurs in older patients as an embolic complication of atherosclerosis. In younger patients, inflammatory (infectious and autoimmune) diseases, thrombotic states, cardiac valvular disorders or embolic sources must be considered in the differential diagnosis. BRAO are usually unilateral and unifocal but may be bilateral or multifocal in unusual cases. Branch Retinal Artery Occlusion (BRAO) Symptoms-characterized by sudden, painless loss of visual field or visual acuity. Occasionally, episodes of transient visual loss lasting minutes (amaurosis fugax) precede permanent retinal arteriolar occlusion. Findings-opacification of the inner retina (ischemic retinal whitening) in the distribution of the occluded branch retinal artery. In some patients, an embolus may be visible at an arterial bifurcation. The most common forms of emboli are fibrin platelet, cholesterol, and calcific emboli. The ischemic retinal whitening usually clears within 3 weeks. Late fundus changes include segmental disc pallor and narrowing of the involved arteriole. Multiple BRAOs may be observed in one or both eyes with or without associated systemic disease. Testing-Fluorescein angiography may demonstrate delay or absence of filling in the affected retinal arteriole. However, particularly with fibrinplatelet or cholesterol emboli, retinal blood flow may be restored by the time the patient seeks attention. Branch Retinal Artery Occlusion (BRAO) Retinal arteriolar emboli originate from various sites including the carotid artery (platelet, cholesterol, or calcific emboli), cardiac valves and exogenous sources (such as talc or steroidal suspensions injected intravascularly). Treatment-has two components: first-to minimize the effects or the retinal arteriolar occlusion, and second to address the underlying systemic cause, if known. The physician may attempt to move or dislodge the embolus by anterior chamber paracentesis. If the occlusion is thought to be secondary to a systemic inflammatory disorder, treatment with systemic corticosteroids or immunosuppressive drugs, managed in cooperation with an internist may be indicated. The visual prognosis for BRAO is generally favorable, with most eyes retaining vision of 20/40 or better, provided that the fovea is not involved. Visual field defects correspond to the distribution of the BRAO are permanent. 18

19 Emboli are usually found in front of the retinal whitening and usually located in the arterial bifurcation (splitting of the vessel in 2 different directions fork in the road ). Embolus. Important Facts to Remember When Doing Fluorescein Angiography for BRAO Accurate timing of the sequence of the dye filling/transit is important in helping with the evaluation of some of the therapies recommended. Montaging your Fluorescein Angiogram (FA) photos are important. Begin montaging between 2-4 minutes, depending on filling/transit phase. This provides helpful information for the physician to better evaluate and provide best treatment options to the patient. OCT of Branch Retinal Artery Occlusion (BRAO) Retinal Whitening Emboli/Plaque Beautiful montage! The physician may want you to montage the color photos to look for additional plaque/emboli elsewhere. Normal macula. Macula has been spared in this BRAO. 19

20 OCT Superior of Branch Retinal Artery Occlusion (BRAO) #1 #2 The red arrows are directing you to the Hyperreflective increased thickening in the intra retina vs. the blue arrow (temporally #1). Notice the decreased reflectivity of the outer retinal layers (including the pigment epithelial layer) compared to the blue arrow (temporally #2). By increasing your A-scans and placing them over the pathology you can scan effectively for the physician in one scan. Branch Retinal Vein Occlusion (BRVO) BRVO appears most frequently between the ages of and affects men and women equally. BRVO is unilateral, with a 5% to 10% risk to the fellow eye. Risk factors for BRVO include hypertension, cardiovascular disease, increasing age, elevated body mass, glaucoma, and possibly diabetes mellitus. Symptoms-blurred vision, metamorphopsia, visual field loss, and floaters. Features-venous dilation and tortuosity, superficial and deep retinal hemorrhages, cotton wool spots, and retinal edema. Major complications of BRVO are macular edema and retinal neovascularization with vitreous hemorrhage. Branch Retinal Vein Occlusion (BRVO) OCT-BRVO Testing-fluorescein angiography shows delayed venous filling and prolonged venous circulation time of the involved vein. Microvascular abnormalities such as microaneurysms, telangiectasis and macroaneurysms formation. Leakage of fluorescein from microvascular abnormalities is common. Capillary nonperfusion and disruption of the foveal ring may be seen due to macular ischemia. Areas of neovascularization are characterized by intense hyperfluorescence and usually located at the junction of perfused and nonperfused retina. Treatment-In general, BRVO are followed up for 3-4 months for spontaneous improvement. Macular laser to areas of macular edema increases the likelihood of visual recovery and reduces the risk of visual loss. Laser is also used if neovascularization develops. Branch Retinal Vein Occlusion (BRVO) Branch Retinal Vein Occlusion (BRVO) It is important to get a color mini montage of the area of pathology for documentation. 20

21 Montage of FA is Important Branch Retinal Vein Occlusion (BRVO) Branch Retinal Vein Occlusion (BRVO) Branch Retinal Vein Occlusion (BRVO) Branch Retinal Vein Occlusion (BRVO) Increasing Your Length and Width of Your A-scans Will Give You a Broader View Step #1: Start with Fast scan. Step #2: Increase your A-scans by hitting your + both horizontal & vertical. Step #3: At maximum length this will default your sections to 31. No need to dense your sections. Step #4: Optional...You can choose HR if you notice too much Noise/Snow. This will decrease the amount you have. #1 start with Fast scan #2 Increase A- scans #3 #4 21

22 Diabetic Retinopathy:Nonproliferative NPDR DR is the most common retinal vascular disease. It is the leading cause of new blindness in adults years of age. Risk-duration of diabetes and the level of diabetes control, uncontrolled hypertension, hyperlipidemia, intravascular fluid, renal disease, anemia, pregnancy and intraocular surgery may aggravate the risk and severity of NPDR. NPDR is the most common form of diabetic retinopathy. Symptoms-no or minimal symptoms. Patients usually do not complain of vision loss until moderate NPDR develops with macular edema or ischemia. Features-presence of microaneurysms, intraretinal hemorrhages, lipid exudate, and cotton wool spots. As the condition progresses, most patients have increased vasodilation and tortuosity and macular edema. Macular edema is associated with most cases of visual loss in NPDR. CSME (clinically significant macular edema) is used to describe those eyes at risk for visual loss related to macular edema. Eyes with severe NPDR have any one of the following features: 4 quadrants of dot/blot hemorrhage, 2 quadrants of venous beading or 1 quadrant of intraretinal microvascular abnormality (IRMA). Testing-fluorescein angiography is performed to determine the degree of macular perfusion and identify the location and extent of treatable lesions in patients with CSME. Treatment-control of blood glucose levels, cardiovascular risk factors (hypertension, fluid overload, hyperlipidemia, anemia) must be treated. Focal laser in eyes with CSME and microaneurysms. Patients with diabetes should undergo regular examination and treatment by their primary care provider or endocrinologist to optimize control of their diabetes. Photograph ALL Diabetics at 50 degree/widest Field Photograph ALL Diabetics at 50 Degrees Diabetic Retinopathy:Proliferative PDR is an advanced form of DR characterized by neovascularization on the optic disc (NVD), retina (NVE) or iris as a result of widespread retinal ischemia. Complications include vitreous hemorrhage, fibrovascular proliferation, traction retinal detachment (TRD) and neovascular glaucoma. Symptoms-may be asymptomatic or complain of visual loss and floaters related to vitreous hemorrhage. In neovascular glaucoma, patients may present with eye pain and redness in addition to loss of vision. Features-PDR exhibits the same findings as patients with NPDR: microaneurysms, retinal hemorrhages, cotton wool spots, lipid exudates and macular edema. In addition, neovascularization arises. NVE is observed most commonly along or just anterior to the temporal retinal vascular arcades. The vitreous plays a critical role in the development of PDR. The vitreous provides a scaffold for the growth of new vessels. The interaction between the vitreous and the neovascular tissue contributes to the development of vitreous hemorrhage and TRD. PDR Testing-fluorescein angiography reveals nonperfusion, NVD or NVE hyperfluoresces early and leaks throughout the study. NVE usually is observed at the junction of the perfused and nonperfused retina. VEGF (vascular endothelial growth factor) is a leading cause linking retinal ischemia and intraocular neovascularization. Treatment-PRP laser is successful in reducing VEGF levels and decline in neovascularization. Patients with non clearing vitreous hemorrhage or TRD a pars plana vitrectomy may be performed. Iris and neovascular glaucoma are treated with PRP. 22

23 Neovascularization Neovascularization 23

24 24

25 OCT of NVE/TRD OCT of NVE/TRD OCT of NVE/TRD 25

26 Neovascularization-Hyperfluorscense in an FA-Type is Leakage NVD Your Turn Color FA-What is This DX? 26

27 Inner Segment/Outer Segment (IS/OS) or Ellipsoid Layer Inner Segment/Outer Segment (IS/OS) or Ellipsoid Layer IS/OS Layer contains two types of photoreceptor cells, rods and cones. Rod cells mediate dim light vision, while cones function in bright light and are responsible for color vision. The names of these cells are derived from the shapes of their outer segments, which contain the visual pigments. Plaquenil (Hydroxychloroquine)Toxicity Plaquenil tablets contain 200mg hydroxychloroquine sulfate and are used in the treatment of malaria, systemic lupus erythematosus, and rheumatoid arthritis. Plaquenil is classified as a disease-modifying antirheumatic drug (DMAD). Retinal toxicity from hydroxychloroquine is quite rare, considering the number of people who use Plaquenil. For those patients who develop retinal toxicity, permanent vision loss may result, even after stopping the medication. PLAQUENIL (Hydroxychloroquine) TOXICITY This OCT defect is know as Flying Saucer Plaquenil FA-Plaquenil 27

28 Dystrophies OCT-Best s/vitelliform Lesion Retinal dystrophy is a term for a group of rare hereditary disorders that cause deterioration to the layers of the retina, including the following: Macular dystrophy Stargardt s Vitelliform macular dystrophy (Best s) Retinal dystrophy is caused by genetic disorders. Symptoms vary widely, but often impact the macula within the retina. When the macula is affected, there is significant noticeable vision loss. Some types of retinal dystrophy appear as early in life as childhood. A dilated retinal examination, fluorescein angiogram, autofluorescence and an optical coherance tomography scan will assist in the diagnosis. Genetic testing will confirm the diagnosis. Best s/vitelliform Lesion FA-Best s/vitelliform Lesion Dystrophy #1 Dystrophy #2 28

29 Dystrophy #2 Retinal Pigment Epithelium Layer of pigment-containing specialized cells that maintain the health of the retina. This pigment prevents visualization of the choroid to varying degrees, depending on the pigment density. In the center of the normal macula there is an increased pigmentation of the RPE cells. Fluorophores called Lipofuscin accumulate in the RPE. Since the choriocapillaries are leaky the RPE acts as a barrier to prevent this leakage from entering the retina. Bruch s Membrane Layer between the RPE and the choroid. It is composed of elements from the base of the RPE and the choriocapillaries. Barrier that keeps Choroidal Vessels at bay. Provides a route for water, solutes, macromolecules that transfer between the RPE and Choroid while supporting the structural integrity of both. Oxidation of lipid deposits in Bruch s membrane initiates an inflammatory process that leads to lesion formation and CNVM in AMD. Age-Related Macular Degeneration: Nonexudative (Dry) Approximately 90% of individuals with AMD have the nonexudative or dry form of the disease. Types of dry AMD include drusen, retinal pigment epithelial alterations, and geographic atrophy. Risk factors for AMD include age (45 and older), family history of AMD, and cardiovascular factors including hypertension and a history of smoking. Symptoms-majority of people with dry AMD are asymptomatic. Individuals with drusen may complain of mild distortion or visual loss. Individuals with more extensive RPE changes or geographic atrophy complain of difficulty reading or recognizing details, and have paracentral or central scotomas. Visual loss associated with geographic atrophy is slow. AMD-Nonexudative (Dry) Clinical features-findings are drusen. Drusen are small, discrete yellowish white deposits. They are most common in the macula but may be found in every area of the fundus. Drusen tend to be bilateral and symmetric. Types of Drusen Hard Drusen-small, yellowish white, discrete deposits. Hard drusen are not associated with the development of wet AMD and considered to be a normal aging phenomenon. Soft Drusen-larger yellowish deposits with less distinct borders. They are found in the fovea region. Soft drusen are associated with an increased risk for the development of CNVM. Calcified Drusen-small refractile deposits associated with AMD and geographic atrophy. Basal Laminar or Cuticular Drusen-innumerable small, round, discrete nodular deposits that are more apparent on fluorescein angiography. The fluorescein reveals a Milky way appearance. Drusen are localized deposits found between the basement membrane of the RPE and the remainder of Bruch s membrane. Treatment-There is no known treatment for dry AMD. The Age-Related Eye Disease Study (AREDS) demonstrated a reduction in progression of AMD in patients taking zinc, beta-carotene, vit C and E. The majority of individuals with dry AMD do very well with excellent visual function. Visual loss is the result of progressive geographic atrophy or CNVM. 29

30 Hard Drusen Soft Drusen Soft Drusen Mix Up Mix Up Calcified Drusen 30

31 Cuticular Drusen Cuticular Drusen OCT-Drusen Drusenoid PED Pigment Epithelium Detachment (PED) Pigment Epithelium Detachment (PED) 31

32 POOLING-Slowly developing hyperfluorescence with sharply demarcated borders Geographic Atrophy (GA) Geographic Atrophy (GA) OCT-Geographic Atrophy (GA) Age-Related Macular Degeneration:Exudative (Wet) Approximately 10% of individuals with AMD have the wet form of the disease. Exudative AMD accounts for the majority of cases of significant visual loss in AMD. Manifestations of wet AMD may include CNVM, pigment epithelial detachment (PED), retinal pigment epithelial tear, subretinal hemorrhage (SRH), fibrovascular scar, vitreous hemorrhage. Symptoms-complain of visual loss, metamorphopsia (distortion), scotoma, micropsia, photopsia, and formed hallucinations. Features-CNVM appears as a grayish green lesion associated with subretinal fluid, subretinal hemorrhage and lipid exudation. Serous PEDs are round or oval, sharply demarcated dome-shaped elevations of the RPE. Complications of CNVM include RPE tear, subretinal hemorrhage. Ultimately, most individuals develop a fibrovascular scar (disciform scar) in the macula. RPE RIP 32

33 PED RPE RIP RPE RIP AMD-Exudative (Wet) Fluorescein angiography is used to determine the type and location of the CNVM. The type of CNVM is divided into two categories: CLASSIC-lacy vascular network with well-demarcated borders during the early phase of the angiogram followed by late leakage. OCCULT-Includes fibrovascular PEDs that appear as poorly defined areas of hyperfluorescence early followed by late leakage, late leakage of undetermined source. OCT Classic CNVM Classic Choroidal Neovascular Membrane (CNVM) 33

34 Classic Choroidal Neovascular Membrane (CNVM) Classic Choroidal Neovascular Membrane (CNVM) Occult Choroidal Neovascular Membrane Occult Choroidal Neovascular Membrane Occult Choroidal Neovascular Membrane Occult Choroidal Neovascular Membrane 34

35 The choroid is located between the retina and the sclera. The choroid is the vascular part of the eye that includes the connective tissue. The main purpose of the choroid is to send oxygen and other nutrients to the retina. The choroid consists of four layers. The layer of the choroid that contains the capillaries is called Choriocapillaries. These are leaky vessels. Since the eye relies on blood supply to function, the choroid must remain healthy at all times. The choroid regulates retinal heat and assists in the control of intraocular pressure. Choroid CHRPE (Congenital Hypertrophy of the Retinal Pigment Epithelium) Benign condition that has been mistaken for a melanoma and nevus. No treatment is required and the visual prognosis is excellent. Grouped CHRPE can be seen in familial adenomatous polyposis, which is associated with a high risk of colon cancer. CHRPE (Congenital Hypertrophy of the Retinal Pigment Epithelium) CHRPE (Congenital Hypertrophy of the Retinal Pigment Epithelium) CHRPE (Congenital Hypertrophy of the Retinal Pigment Epithelium) Nevus/Nevi 35

36 OCT of Nevus #1 EDI of Nevus #1 Nevus #2 OCT of Nevus #2 Line of Nevus #2 EDI of Nevus #2 36

37 EDI of Nevus #2 White Dot Syndrome White dot syndromes are inflammatory diseases characterized by the presence of white dots on the fundus, the interior surface of the eye. The majority of individuals affected with white dot syndromes are younger than fifty years of age. Symptoms include blurred vision and visual field loss. There are many theories for the etiology of white dot syndromes including infectious, viral, genetics and autoimmune. Classically recognized white dot syndromes include: Acute Posterior Multifocal Placoid Pigment Epitheliopathy (APMPPE) Birdshot Chorioretinopathy Multiple Evanescent White Dot Syndrome (MEWDS) Acute Zonal Occult Outer Retinopathy (AZOOR) Multifocal Choroiditis and Panuveitis (MCP) Punctate Inner Choroiditis (PIC) Serpiginous Choroiditis MEWDS Affects young adults between the ages of 20 and 45 years. Mostly seen in females. Usually unilateral, but bilateral cases have been documented. Spontaneous recovery usually occurs within several weeks or months. Cause of MEWDS is unknown but viral etiology has been suggested. Symptoms-Sudden visual problems in one eye such as blurred vision, temporal or paracentral scotomas and photopsia. OCT Line Scan EDI MEWDS 37

38 MEWDS Line Scan EDI 38