1. health and fitness
2. disease

9/16/2013
Financial Disclosure
Mastering OCT: Pattern Recognition in Context
Robert A. Sisk, MD
• I have no financial interest in the content of this presentation
JCAHPO CE Program
September 21, 2013
Discussion Outline
• Background: What is OCT?
What is OCT?
• Optical coherence tomography (OCT)
– Noninvasive, noncontact, laser‐based technology that evaluates the reflectivity of • OCT Findings of Common Vitreoretinal light in semi‐transparent materials (ocular tissues)
Pathologies
– Similar to how radar or ultrasound uses sound waves to provide information about density and • Applying Relevant History
spatial orientation
– Light waves are faster and shorter wavelength than sound – greater resolution and speed of capture
Why is OCT Suitable for Retinal Imaging?
• The internal structures of the eye and the retina are optically clear, except in states of disease • The retina is organized in predictable, fixed layers circumferential and parallel to the eye wall
• The macula, the “focusing point” for vision, is also the fixation point of gaze and the area of interest for microanatomic study
A‐scan vs B‐scan
• A‐scan = “A” single scan
– Provides information about a singlel
pathway of light and the objects that i t f ith th t th li ht i interfere with that path as light is reflected back towards the sensor
• B‐scan = “Bunches” of scans
– Provides a 2‐dimensional picture representation from several A‐scans
– Conventional representation for OCT
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The Macula
Scanning the Macula
Retinal Anatomy
Time Domain vs Spectral Domain
• The retina is arranged in 9 layers
• Light must traverse the entire retina before activating photoreceptors
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• Inner retinal layers are displaced at the fovea to allow light to pass unimpeded
• OCT accurately represents retinal histology and can provide a safe, non‐invasive “optical biopsy” to yield anatomic information
• Time domain imaging depends on the time for a moving mirror to reach its excursion and return to its originating point
• Spectral domain uses a fixed mirror and a diffusion grating that breaks light information into a spectral profile analyzed for greater resolution and with far greater speed than time‐domain
Ways OCT Information is Displayed
• Raster Lines – Variable length, orientation, number, spacing
• Retinal Thickness Maps
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– Volume, Segmentation Scans (ILM, RPE)
• 3D (C‐scan)
• Positive vs Negative
• Grayscale vs Color
OCT Terminology
• Hyper‐/Hyporeflective – standard is medium gray or yellow
• Blockage/Shadowing Hypo
H
Hyper
• Transmission Defect – reference is RPE band
• Cyst/Schisis – Cavity within solid tissue; appearance may distinguish between exudative and tractional etiologies
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OCT Terminology
• Hyper‐/Hyporeflective – standard is medium gray or yellow
OCT Terminology
• Hyper‐/Hyporeflective – optical density
– standard is medium gray or yellow
• Blockage/Shadowing • Blockage/Shadowing • Transmission Defect • Transmission Defect – reference is RPE band
• Cyst/Schisis – Cavity within solid tissue; appearance may distinguish between exudative and tractional etiologies
Image Processing
• Image Averaging
– Multiple raster scans through the same area can enhance image resolution/clarity by eliminating artifacts
– Oversampling can prevent detection of subtle findings
• Eye Tracking/Image Registration/Reproducibility
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g/
g
g
/ p
y
– The eyes are never still in awake patients; otherwise the image would “bleach out”
– Anomalous hyperreflectivity posterior to RPE band
• Cyst/Schisis – Cavity within solid tissue; appearance may distinguish between exudative and tractional etiologies
Most Useful Clinical Applications for OCT Imaging
• Diagnosis – VR interface diseases, Exudative diseases, rare diseases (white dot, hereditary)
• Guiding Treatment – Retinal vascular diseases, choroidal neovascularization
– Microsaccades maintain fixation but move the OCT reference
– A second laser can follow the retina during eye movements
• Correlating Vision to Anatomy –
– Retinal vessels can be used as stable landmarks in most patients
Organization/Lamination, IS/OS integrity, Outer – Reproducibility allows accurate quantitative analysis of therapy or disease states
retinal and NFL thicknesses
Approaches for Interpreting OCT
Common Types of Vitreoretinal Pathology by Anatomic Location
• Normal vs Abnormal – Compare measured retinal thickness to areas corresponding to an ETDRS grid with reference values provided by manufacturer
• Warning: values vary by as much as 15% from one maker to another • Retinal Surface ‐ Vitreous and ILM • Inner Retina • Raster scans can not be ignored! (devil’s in the details)
• Qualitative vs Quantitative
• Outer Retina/RPE/Choroid
• Stepwise Evaluation by Layers
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Posterior Vitreous Detachment
Vitreous
• Collagen and hyaluronic acid gel matrix congenitally adherent to the retina and optic nerve • Degrades over decades as gel matrix dehydrates and coalesced p
,
y
g
p
fluid pockets forms, ultimately resulting in separation of the vitreous from the posterior retina and optic nerve (posterior vitreous separation)
– Accelerated by trauma, inflammation, hemorrhage, myopia, ocular surgery, degenerative retinal diseases
• Vitreous separation is a discrete window when retinal tears or retinal detachment typically occur (1% risk in general population)
PVD with Retinal Flap Tear
Tear = Vitreous Traction on Retina
Bridging Vessel
Vitreoschisis
• The vitreous gel is arranged in layers, like skins of an onion
• The layers closest to the innermost layer of the retina (ILM) are tightly adherent and may strip away from the vitreous body in pathologic states
Vitreous Attachment/Detachment
•
Vitreous consistency is like epoxy glue (sticky and stringy more than gooey)
•
Pathologic states involve abnormal excessive adhesion between gel and g
retina
•
Symptomatic retinal breaks usually accompany PVD
•
Completion of PVD significantly reduces risk for future retinal breaks
•
Surgical approach for RD repair depends on PVD status
Vitreomacular Traction Syndrome
• Aka “Vitreomacular adhesion”
• Partial macular vitreous separation with anomalous foveal adherence, creating schisis ( p
(splitting)
g)
• Analogous to ripping wires of an electrical system apart, which reduces function
• Chief complaints: – metamorphopsia – scotoma
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Vitreomacular Traction Syndrome
VMT
VMT
Diabetic Tractional Retinal Detachment
• Proliferative (neovascular) diabetic retinopathy thickens/toughens the ILM‐
vitreous interface (adhesion) while prematurely aging the vitreous body (contraction)
• Degree of tractional forces depends on quantity (more) and quality (fibrotic) of new vessels
Full Thickness Macular Hole
• More severe form of VMT resulting in full thickness foveal defect
• Stages:
1 = outer retinal defect
2 = full thickness defect with vitreous traction on one edge
3 = operculum
4 = PVD
• Chief complaint: scotoma
FTMH
Operculum
Schisis
Window Defect
• Treatment: Surgery, Intravitreal Ocriplasmin
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FTMH
Stage 2
Surgical Outcomes
Focal Adherence with Severe Traction
IS/OS Defect
Vitreous Opacities
Vitreous Hemorrhage
• Opaque objects in the vitreous block the OCT’s laser, producing
of deeper layers • Examples: Asteroid hyalosis
(calcium), hemorrhage, inflammation, intraocular foreign bodies, vitreous opacities
• Treatment: Surgery
Vitreous Hemorrhage
Epiretinal Membrane
• Thickened mass of cells at the VR interface (hyaloid, reactive, RPE) • Very common (25% after PVD) b PVD), but most not visually i ll significant
• Chief Complaints: metamorphopsia, blurred vision
• Treament: Surgical Removal
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ERM
Macular Pseudohole
ERM
ERM
Schisis
Disorganization of Retinal Layers
Intact Outer Retinal Layers
Lamellar Macular Hole
ERM with Vitreous Strand to PVD
Correspondence of Thickness Map to ERM Morphology
ILM Cleaved
ERMs
Progression of ERMs
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Effects of Membrane Peeling
Effects of Membrane Peeling
Myopic Macular Schisis
Myopic Macular Schisis
• Pathologic myopia disproportionately elongates posterior aspect of eye (egg shaped)
of eye (egg‐shaped)
• Posterior hyaloid face acts like ERM and contracts against excessive posterior curvature of myopic macula
• Results in splitting (schisis)
Staphyloma
Retinal Detachment
•
Contraction of vitreous body, often with PVD, can result in retinal tears if VR traction exceeds retinal integrity
•
Retinal breaks become an avenue for subretinal fluid and overwhelm the RPE pump, creating RD
RD
ERM
• Macular status determines urgency of repair and prognosis about visual outcome
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Inner Retina
• Responsible for processing light information from multiple photoreceptors and transmitting it through the optic nerve towards the brain
• Contains nerve fiber layer, ganglion cells; bipolar, amacrine, and Contains nerve fiber layer ganglion cells; bipolar amacrine and horizontal cells; Müller cells
• The retina receives oxygen from two sources
Retinal Artery Occlusion
• Acute obstruction of a retinal artery results in ischemia (dysfunction) and ultimately infarction (death)
• Acutely, inner retinal edema seen clinically as • Obstruction of the retinal circulation produces visible changes on OCT
Central Retinal Artery Occlusion
Hyperreflectivity
Swelling
Disorganization
Macular
Nonperfusion
paracentesis, globe compression, YAG laser embolysis aspirin
embolysis, aspirin
• Workup: R/O GCA, Carotids, Echo, Hypercoagulability – Inner 2/3 supplied directly by retinal blood vessels
– Outer 1/3 supplied by diffusion from the choroid
• Treatment controversial: workup, Vasculitis/Uveitis • Chief complaint: workup
– scotoma, blindness
CRAO
Diffuse inner layer thickening
Shadowing
CRAO
Bilateral CRAO
Cilioretinal artery sparing
Atrophy of Inner Retinal Elements
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Branch Retinal Artery Occlusion
Retinal Vein Occlusion
•
Venous obstruction releases contents of the bloodstream (water, blood cells, and cholesterol) into the retina
Bartonella Granuloma
•
Plumbing problem
•
Chief Complaints: blurred vision, •
Treatment: manage underlying scotoma, metamorphopsia
vascular disease (HTN, DM, OSA) and/or glaucomas, retinal lasers, intravitreal anti‐VEGF and/or corticosteroids
Central Retinal Vein Occlusion
CRVO
• Venous Dilation and Tortuosity
• Retinal Edema
• Optic Disc Edema
• Intraretinal Hemorrhages
• Ischemia: CWS, Severe Retinal Edema and Minimal Subretinal Fluid
BRAO
Unusual Manifestations
Treatment of CRVO
Chronic E d ti
Exudation
Reversible Ischemia
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Branch Retinal Vein Occlusion
Veinous
Obstruction
Collateral Vessels
Diabetic Retinopathy
Diabetic Macular Edema
•
Diabetes preferentially damages capillary beds, creating microaneurysms and avascular zones •
Clinically edema, exudates, and hemorrhage are seen in varying degrees associated with vascular anomalies
•
Similar to RVO, intraretinal hyperreflective areas and inner and outer retinal cystic hyporeflective cavities are seen on OCT
Severe CME with SRF
BRVO
Diabetic Macular Edema
Macular Edema
Exudate Rings
Exudates with Shadowing
Extensive MAs
Telangiectasia
Increased Foveal Avascular Zone
Diffuse DME
Macular Telangiectasia Type 2
• Idiopathic macular VMT Component
disease associated with
– Retinal telangiectasia
– Cystic macular degeneration
– RPE hyperplasia
– Intraretinal crystals
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IMT Type 2
Outer Retina/RPE/Choroid
•
Outer Retina ‐ retinal photoreceptors are highly specialized neurons that Disorganization of Cystic Retinal Retinal Layers
Degeneration
generate electrical responses to light. •
RPE – multipurpose layer needed to maintain outer retinal function and health
•
Choroid – high flow blood vessel layer that sustains outer retina by diffusion Age‐Related Macular Degeneration
•
Most common cause of blindness in the US in adults over 50
• “Dry” = progressive loss of /
/
RPE/outer retinal function/cells (atrophy) with accumulation of drusen (hallmark lesion)
Drusen
•
• Chief Complaints: • Blurred Vision
• Metamorphopsia
• Scotoma
• Treatment
recycled visual cycle pigments that could not be returned to the photoreceptors in conjunction with complement cascade components/inflammatory debris
•
that leak water, blood, or cholesterol into the subRPE or subretinal space
Accumulate progressively, but distribution can fluctuate in some • “Wet” = development of new choroidal vessels outside the choroid Accumulation of incompletely patients
•
Loss of drusen frequently accompanied by RPE atrophy (geographic atrophy)
Basal Laminar Drusen
Drusen
RPE clumping with shadowing
Thin Choroid
Transmission Defects
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Vitelliform Lesion
Pigment Epithelial Detachment
(Geographic) RPE Atrophy
FAF and OCT reveal
occult RPE atrophy
Transmission Defect
Choroidal Neovascularization
Manifestations of CNV
Subretinal Fluid
• A break in Bruch’s membrane and/or RPE associated with leaky vessels
• Type 1: SubRPE
– Wet AMD
• Type 2: Subretinal
T S b i l
– Inflammatory
– Pathologic Myopia
• Type 3: Retinal Angiomatous
Proliferation
Pigment Epithelial Detachment
– Wet AMD
– Macular Telangiectasia
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Manifestations of CNV
Subretinal Hemorrhage
Resolution with Treatment
Loss of IS/OS Integrity indicates damage from prior SRH
RPE Tear
Manifestations of CNV
Subretinal Scarring
Overlying Retinal Degeneration
MASSIVE Subretinal Hemorrhage
Pathologic Myopia
• Axial myopia, commonly called “near‐sightedness,” in its extreme form
•
Represents a connective tissue weakness – Elongates the eye, thinning the layers of the eye wall (cornea, sclera, l
h
h
h l
f h
ll
l
choroid, RPE, retina)
– Degenerating the vitreous early (collagen and hyaluronic acid) – Creating traction between the stretched retina and vitreous
– Predisposes to vitreoretinal interface disorders, retinal tears, and retinal detachment
Myopic Macular Degeneration
• Thinning of the posterior eye wall layers
• Increased posterior curvature (staphyloma)
– Diffuse or focal
• RPE thinning/atrophy (lacquer cracks, geographic atrophy)
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Central Serous Chorioretinopathy
Myopic Macular Degeneration
Increased Visibility of Large Choroidal Vessels
Tilted Disc and α‐zone Parapapillary Atrophy
• Idiopathic condition in young adults that may mimic CNV, producing SRF, PED, and CME
• Precipitated or aggravated by P i it t d t d b steroids, stress, and caffeine/analogs
• Treatment: Remove offending agent, Observation (self‐limited), Posterior Staphyloma Choroidal Thinning
Chronic Steroid‐Induced Central Serous Chorioretinopathy
rfPDT guided by FA or ICG
Photoreceptor Dystrophies
•
The outer retina is dominated by photoreceptors, highly‐specialized Chronic SRF, CME, and IS/OS defects
neurons that convert light information into electrical signals for the brain to process as vision
•
•
Rods – dim light, peripheral vision
Cones – bright light, color perception, visual acuity
• Chief complaints – Night blindness (nyctalopia)
– Day blindness (hemeralopia)
Retinitis Pigmentosa
(Rod‐Cone Dystrophy)
Retinitis Pigmentosa
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Cone Dystrophy
Stargardt Disease
Role of Clinical History in Segregating Diagnoses
Example #1
• Although some OCT findings are pathognomonic (i.e. macular • Floaters – Vitreous
• Distortion – Retinal surface, hole), most need a chief complaint and limited history to • Distortion with scotoma – severe intraretinal or subretinal
• Scotoma – any layer except • Specific visual complaints can help localize pathology
– Age < 50 – CSR, especially if bilateral
,
intraretinal, or subretinal
add context and get the right treatment
• SRF without evidence of inflammation – Age > 50, Caucasian – Wet AMD
– Age > 50, darkly pigmented skin, +/‐ SRH ‐ IPCV
vitreous
• Amaurosis – inner retinal circulation
Example #2
• Numerous yellow spots OU
– Age > 50 – Dry AMD
– Age < 50, centered in the Applications
• Most clinical decisions for injection‐based therapies in exudative diseases are guided more by OCT findings than biomicroscopy
• My technicians can briefly screen the OCT before seating the temporal macula – dominant temporal macula patient and facilitate the clinical encounter with appropriate ti t d f ilit t th li i l t ith i t drusen
paperwork (consents, H+P form, lab form, etc)
– Age < 50, centered on fovea – genetic causes: Stargardt disease, pattern dystrophy, North Carolina macular – New Visits: RD (mac‐on vs mac‐off), Wet AMD (injection consent), Diabetic (focal laser and/or injection consent)
– Return Visits: For patients receiving chronic anti‐VEGF injections, detection of new fluid prompts preparation for injection procedure
dystrophy
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Conclusions
Thank You
• OCT is a powerful diagnostic tool for macular diseases
• OCT augments clinical examination by providing g
yp
g
high‐resolution structural information about the posterior segment
• As with any test, it does not replace a thorough history and physical examination
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