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Papadopoulou Caterina
Thessaloniki – GREECE
catepapgr@hotmail.it www.tvrs.gr
OCT was first reported by Huang et al. in 1991.
In vivo retinal imaging was first demonstrated in 1993, and early
studies in 1995 provided the first demonstration of OCT imaging
of the normal retina and of macular pathology.
OCT is a noninvasive (non contact) medical imaging technology
similar to ultrasound and MRI that provides high resolution, cross
sectional images of the retina and the retina nerve fiber layer and
the optic nerve head.
In medicine, the technique has been compared to an in-vivo optical
biopsy.
TIME DOMAIN OCT (TD-OCT) : is the early version of this technology.
Low-coherence infrared light (800-1310nm) is transmitted into the eye through
use of an interferometer (Michelson type interferometer)
The infrared light is transmitted through the pupil and then penetrates through
the transparent nine layers of the retina. Subsequently, the light backscatters and
returns through the pupil, where detectors can analyze the interference of light
returning from the layers of the retina compared with light traveling a reference
path (mirror). An algorithm mathematically uses this information to construct a
gray-scale or false-color image representing the anatomy of the retina
Uses a moving reference mirror for measuring the time it takes for
the light to be reflected. This relatively slow mechanical process
limits both the amount of data that can be captured as well as
image quality.
TD-OCT data is acquired at approximately 400 axial scans (or A-
scans) per second with an axial resolution of 8-10μm.
Because of the eye motion, it is not feasible to use TD-OCT to
precisely map retinal tissue in three dimensions
In 2006, the first commercially available SD-OCT system was introduced.
SD-OCT uses a significantly faster non mechanical technology.
SD-OCT employs detection of the light echoes simultaneously by
measuring the interference spectrum, using an interferometer with a high
speed spectrometer.
This technique achieves scan rates of 20.000-52.000 A scans per second
and a resolution of 5-7μm in tissue.
The increase speed and number of scans translates into higher resolution
and better chance of observing disease
 Improved resolution
 Improved acquisition speed
 Reduces motion artifacts
 Digital processing not required to align adjacent axial
scans = More accurate retinal scans
 3D views
 More accurate segmentation
 Precise registration/orientation
Time Domain OCT
400 axial scans per second (Zeiss Stratus-2002)
8-10μm axial resolution
Spectral/Fourier Domain OCT-spectrometer
25.000-50.000 axial scans per second (2006)
5-7μm
Next Generation Spectral/Fourier OCT
70.000-100.000 axial scans per second
3-5μm axial resolution
Swept Source/Fourier OCT-swept laser
200.000+axial scans per second
5-7μm axial resolution at 1050nm wavelengths
In time-domain OCT, output of a low-
coherence source is split between two arms,
one of which scans the sample, while the
other provides an adjustable time delay. The
two arms are phase-matched so the returned
light inerferes constructively only for light
backscattered from a particular depth.
Spectral-domain OCT splits light from a
broadband source between the sample and the
reference arms, then recombines the beams
through a spectrometer onto a detector array
Swept-spectrum OCT splits light from a high
speed wavelength-swept laser source between the
sample and reference arms, then recombines the
light a a detector array
• OCT performs “optical biopsy” imaging tissue pathology in
situ and in real time
• Retinal pathology can be examined at the level of
indivudual retinal layers
• 3D OCT provides comprehensive information about
structure
• Reproducible registration, longitudinal follow up,
quantitative assessment
Derived form a latin word “vitrum” which means glass.
The vitreous is the trasparent, colourless, gelatinosous mass
that fills the space between the lens and the retina. It
comprises about 80% of the total volume of the globe
(~4ml).
98-99% water
Collagen fibers with glycosaminoglycan hyaluronic acid
Very few cells (phagocytes, hyalocytes of Balazs)
NO BLOOD VESSELS
Refractive index 1,336
The collagen fibers of the vitreous are held apart by electrical charges.
In children, the vitreous has a consistency similar to an egg white. With age
it gradually thins and becomes more liquid because of the reductions of
these charges
Vitreous base
Optic disc
Perifoveal/macular region
Vessels
Posterior lens - Weigert’s ligament
Uchino et al, ARVO 2000, Arch Ophthalmol 2001
PVD begins around the macula
before 50 y , 60 % of normal eyes have some degree of partial PVD
Mark W Johnson , Arch Ophth Feb 2001
Ultrasonography
Caused by partial posterior vitreous detachment: the posterior
hyaloid is incompletely detached from the posterior pole and
remains attached to the optic disc and the foveal center exerting
traction on the foveal tissue.
Traction on macular tissue produces gradual anatomic and
functional deterioration in proportion to traction forces
(anterior-posterior or tangenzial) and their duration of action.
 Macular hole formation
 Macular pucker formation
 Macular detachment
 Cystic changes
ETIOLOGY
 Idiopatic disease
 Diabetic retinopathy
 Myopia
 Inflammation of the eye
Asymptomatic: normal or near-normal vision (initial
stages).
Most common
Metamorphopsia e central scotoma
Blurred vision
Less common
Monocular diplopia: caused by foveal ectopia if
occurs.
Central photopsia
Macropsia
FUNDUS EXAMFUNDUS EXAM
FAGFAG
OCTOCT
GASS (1988, 1995)
Stage 1 : Impending MH
A : foveal yellow spot
B : foveal yellow ring (occult hole)
Stage 2 : Full thickness early MH
 Stage 3 : Full thickness MH with
foveal vitreomacular separation
 Stage 4 : Full thickness MH with
complete PVD
The cysts develop in the inner part of the foveal center
due to vitreofoveal traction. Often some degree of
changes at the level of photoreceptors.
Expanding of the cyst in the outer retina
Posterior hyaloid is still attached to the edge of the hole via the operculum
Ø < 400μm
Stage 3
 Thickened and elevated edge
 No PVD
 Operculum in front of the hole
 A non contractile ERM may be present around the hole
 White spots may be present in the center of the hole
 The diameter is variable
Stage 4
 same characteristics, but complete PVD
If the vitreo-foveal separation have already occurred
No risk for MH
If there is no vitreo-foveal separation at all, or an incomplete vitreo-
foveal separation
50% risk of MH
If presence of an ERM
little risk of MH
If Lamellar hole
little risk of evolution to FTMH
SURGICAL TREATMENT (25GPPV)
Release any vitreomacular traction
Remove the vitreous cortex (kenalog assisted)
Remove as much vitreous gel as possible
Peel off any ERM
ILM peeling
Gas tampponade and face down positioning
MEDICAL TREATMENT
Microplasmin: phase IIIMicroplasmin: phase III
The use of intravitreal vital dyes has facilitated the peeling of
the ILM.
Several drugs may be used:
ICG
Trypan blue
Brilliant blue
Triamcinolone
The first popular dye in retinal surgery: ICG staining of ILM started in
1998
Tornanbee. Vitreous Society 1999
Kadodonoso. Arch Ophthalmol 2000
Is the use of ICG safe ?
ICG is potentially toxic for RPE cells
Engelbrecht et al, Am J Ophthalmol Jan 2002
Specific affinity of ICG for RPE cells
RPE atrophy after prolonged contact
depends on its concentration and the duration of contact
ICG stains the ganglion cell axons (toxicity unknown)
central microscotomas have been attributed to the use of ICG
several studies show that final VA is worse when ICG have been used
than without ICG.
Staining of ILM with Trypan blue has started in 2001
Feron, 2002 Arch Ophthalmol : PVR dissection
Li, 2003 Br J Ophthalmol : ILM peeling for MH
TB 0.15%
CE mark , FDA approval, for VR surgery,
TB can be diluted in 10% glucose 50/50%, for better contact with retina
2 min contact
Exposure of cultured RPE cells to TB shows evidence for cytotoxicity specially in the
presence of light and with concentration > 2 mg/ml
Cox CA, ARVO 2003; Veckeneer M, Gaefe’s 2001
ICG is taken up by RPE at concentrations < clinically used, and TB is not.
Hirasawa H, Retina 2007
Substantial retinal damage with Subretinal 0.05% ICG > 0.15% trypan blue
Penha FM, Ophthalmology 2007
Clinical comparison with ICG
Author Year Nb eyes Dye MH Closure VA Gain
Beutel 2000 20 ICG 90% 59% ≥ 2l
99 TB 87% 71% ≥ 2l
Lee 2005 19 ICG 98.5% 1.79 l
19 TB 97% 2.94 l
Unlike ICG, BBG does not cause apoptosis of retinal
glial cells: safer adjuvant during VR surgery
Kawahara S, IOVS 2007
With BBG, No significant reduction in RGC numbers or
morphological alterations in rat eyes, AND No toxic effects
attributable to the dye in patients
Remy M, BJO 2008
Triamcinolone for ILM peeling: “to free from the possible toxicity of
dyes”
Frazer , 2005 Retina
Shah , 2003 Retina
Triamcinolone does not stain the ILM , but its deposit on the macular
surface
Cheapest…
4 mg IVTA complications are known:
Glaucoma, cataract … and possible retinal toxicity
Preservatives
Adverse effect suspicions:
Toxicity for bared retina and RPE
Reduces success rate of MH surgery
The gas bubble helps to the healing process
Insulate the macula from the liquid of the vitreous cavity
which results in
dehydration of the hole edge
flattening of the cystic cavities
reattachement of the hole edge to the RPE
narrowing of the hole aperture
Decreased visual acuity and metamorphopsia
VISUAL ACUITY
RE 2/10
LE 10/10
Decreased visual acuity in the LE 5/10
25PPV after 5 days
VISUAL ACUITY
RE 4/10
LE 10/10
Vitreomacular traction sydromes often can be
bilateral
Sometimes should be treated as an emergency!!!
Our clinical experience shows that the sooner
we operate the better is going to be the visual
outcome.
THANK YOU FOR YOUR
ATTENTION

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Understanding OCT Imaging of the Retina

  • 1. Papadopoulou Caterina Thessaloniki – GREECE catepapgr@hotmail.it www.tvrs.gr
  • 2. OCT was first reported by Huang et al. in 1991. In vivo retinal imaging was first demonstrated in 1993, and early studies in 1995 provided the first demonstration of OCT imaging of the normal retina and of macular pathology. OCT is a noninvasive (non contact) medical imaging technology similar to ultrasound and MRI that provides high resolution, cross sectional images of the retina and the retina nerve fiber layer and the optic nerve head. In medicine, the technique has been compared to an in-vivo optical biopsy.
  • 3. TIME DOMAIN OCT (TD-OCT) : is the early version of this technology. Low-coherence infrared light (800-1310nm) is transmitted into the eye through use of an interferometer (Michelson type interferometer) The infrared light is transmitted through the pupil and then penetrates through the transparent nine layers of the retina. Subsequently, the light backscatters and returns through the pupil, where detectors can analyze the interference of light returning from the layers of the retina compared with light traveling a reference path (mirror). An algorithm mathematically uses this information to construct a gray-scale or false-color image representing the anatomy of the retina
  • 4. Uses a moving reference mirror for measuring the time it takes for the light to be reflected. This relatively slow mechanical process limits both the amount of data that can be captured as well as image quality. TD-OCT data is acquired at approximately 400 axial scans (or A- scans) per second with an axial resolution of 8-10μm. Because of the eye motion, it is not feasible to use TD-OCT to precisely map retinal tissue in three dimensions
  • 5. In 2006, the first commercially available SD-OCT system was introduced. SD-OCT uses a significantly faster non mechanical technology. SD-OCT employs detection of the light echoes simultaneously by measuring the interference spectrum, using an interferometer with a high speed spectrometer. This technique achieves scan rates of 20.000-52.000 A scans per second and a resolution of 5-7μm in tissue. The increase speed and number of scans translates into higher resolution and better chance of observing disease
  • 6.  Improved resolution  Improved acquisition speed  Reduces motion artifacts  Digital processing not required to align adjacent axial scans = More accurate retinal scans  3D views  More accurate segmentation  Precise registration/orientation
  • 7. Time Domain OCT 400 axial scans per second (Zeiss Stratus-2002) 8-10μm axial resolution Spectral/Fourier Domain OCT-spectrometer 25.000-50.000 axial scans per second (2006) 5-7μm Next Generation Spectral/Fourier OCT 70.000-100.000 axial scans per second 3-5μm axial resolution Swept Source/Fourier OCT-swept laser 200.000+axial scans per second 5-7μm axial resolution at 1050nm wavelengths
  • 8. In time-domain OCT, output of a low- coherence source is split between two arms, one of which scans the sample, while the other provides an adjustable time delay. The two arms are phase-matched so the returned light inerferes constructively only for light backscattered from a particular depth. Spectral-domain OCT splits light from a broadband source between the sample and the reference arms, then recombines the beams through a spectrometer onto a detector array Swept-spectrum OCT splits light from a high speed wavelength-swept laser source between the sample and reference arms, then recombines the light a a detector array
  • 9. • OCT performs “optical biopsy” imaging tissue pathology in situ and in real time • Retinal pathology can be examined at the level of indivudual retinal layers • 3D OCT provides comprehensive information about structure • Reproducible registration, longitudinal follow up, quantitative assessment
  • 10.
  • 11. Derived form a latin word “vitrum” which means glass. The vitreous is the trasparent, colourless, gelatinosous mass that fills the space between the lens and the retina. It comprises about 80% of the total volume of the globe (~4ml).
  • 12. 98-99% water Collagen fibers with glycosaminoglycan hyaluronic acid Very few cells (phagocytes, hyalocytes of Balazs) NO BLOOD VESSELS Refractive index 1,336 The collagen fibers of the vitreous are held apart by electrical charges. In children, the vitreous has a consistency similar to an egg white. With age it gradually thins and becomes more liquid because of the reductions of these charges
  • 13. Vitreous base Optic disc Perifoveal/macular region Vessels Posterior lens - Weigert’s ligament
  • 14. Uchino et al, ARVO 2000, Arch Ophthalmol 2001 PVD begins around the macula before 50 y , 60 % of normal eyes have some degree of partial PVD Mark W Johnson , Arch Ophth Feb 2001 Ultrasonography
  • 15.
  • 16.
  • 17. Caused by partial posterior vitreous detachment: the posterior hyaloid is incompletely detached from the posterior pole and remains attached to the optic disc and the foveal center exerting traction on the foveal tissue. Traction on macular tissue produces gradual anatomic and functional deterioration in proportion to traction forces (anterior-posterior or tangenzial) and their duration of action.
  • 18.
  • 19.  Macular hole formation  Macular pucker formation  Macular detachment  Cystic changes ETIOLOGY  Idiopatic disease  Diabetic retinopathy  Myopia  Inflammation of the eye
  • 20. Asymptomatic: normal or near-normal vision (initial stages). Most common Metamorphopsia e central scotoma Blurred vision Less common Monocular diplopia: caused by foveal ectopia if occurs. Central photopsia Macropsia
  • 22. GASS (1988, 1995) Stage 1 : Impending MH A : foveal yellow spot B : foveal yellow ring (occult hole) Stage 2 : Full thickness early MH  Stage 3 : Full thickness MH with foveal vitreomacular separation  Stage 4 : Full thickness MH with complete PVD
  • 23. The cysts develop in the inner part of the foveal center due to vitreofoveal traction. Often some degree of changes at the level of photoreceptors.
  • 24. Expanding of the cyst in the outer retina
  • 25. Posterior hyaloid is still attached to the edge of the hole via the operculum Ø < 400μm
  • 26. Stage 3  Thickened and elevated edge  No PVD  Operculum in front of the hole  A non contractile ERM may be present around the hole  White spots may be present in the center of the hole  The diameter is variable Stage 4  same characteristics, but complete PVD
  • 27. If the vitreo-foveal separation have already occurred No risk for MH If there is no vitreo-foveal separation at all, or an incomplete vitreo- foveal separation 50% risk of MH If presence of an ERM little risk of MH If Lamellar hole little risk of evolution to FTMH
  • 28.
  • 29. SURGICAL TREATMENT (25GPPV) Release any vitreomacular traction Remove the vitreous cortex (kenalog assisted) Remove as much vitreous gel as possible Peel off any ERM ILM peeling Gas tampponade and face down positioning MEDICAL TREATMENT Microplasmin: phase IIIMicroplasmin: phase III
  • 30. The use of intravitreal vital dyes has facilitated the peeling of the ILM. Several drugs may be used: ICG Trypan blue Brilliant blue Triamcinolone
  • 31. The first popular dye in retinal surgery: ICG staining of ILM started in 1998 Tornanbee. Vitreous Society 1999 Kadodonoso. Arch Ophthalmol 2000 Is the use of ICG safe ? ICG is potentially toxic for RPE cells Engelbrecht et al, Am J Ophthalmol Jan 2002 Specific affinity of ICG for RPE cells RPE atrophy after prolonged contact depends on its concentration and the duration of contact ICG stains the ganglion cell axons (toxicity unknown) central microscotomas have been attributed to the use of ICG several studies show that final VA is worse when ICG have been used than without ICG.
  • 32. Staining of ILM with Trypan blue has started in 2001 Feron, 2002 Arch Ophthalmol : PVR dissection Li, 2003 Br J Ophthalmol : ILM peeling for MH TB 0.15% CE mark , FDA approval, for VR surgery, TB can be diluted in 10% glucose 50/50%, for better contact with retina 2 min contact Exposure of cultured RPE cells to TB shows evidence for cytotoxicity specially in the presence of light and with concentration > 2 mg/ml Cox CA, ARVO 2003; Veckeneer M, Gaefe’s 2001 ICG is taken up by RPE at concentrations < clinically used, and TB is not. Hirasawa H, Retina 2007 Substantial retinal damage with Subretinal 0.05% ICG > 0.15% trypan blue Penha FM, Ophthalmology 2007 Clinical comparison with ICG Author Year Nb eyes Dye MH Closure VA Gain Beutel 2000 20 ICG 90% 59% ≥ 2l 99 TB 87% 71% ≥ 2l Lee 2005 19 ICG 98.5% 1.79 l 19 TB 97% 2.94 l
  • 33. Unlike ICG, BBG does not cause apoptosis of retinal glial cells: safer adjuvant during VR surgery Kawahara S, IOVS 2007 With BBG, No significant reduction in RGC numbers or morphological alterations in rat eyes, AND No toxic effects attributable to the dye in patients Remy M, BJO 2008
  • 34. Triamcinolone for ILM peeling: “to free from the possible toxicity of dyes” Frazer , 2005 Retina Shah , 2003 Retina Triamcinolone does not stain the ILM , but its deposit on the macular surface Cheapest… 4 mg IVTA complications are known: Glaucoma, cataract … and possible retinal toxicity Preservatives Adverse effect suspicions: Toxicity for bared retina and RPE Reduces success rate of MH surgery
  • 35. The gas bubble helps to the healing process Insulate the macula from the liquid of the vitreous cavity which results in dehydration of the hole edge flattening of the cystic cavities reattachement of the hole edge to the RPE narrowing of the hole aperture
  • 36. Decreased visual acuity and metamorphopsia VISUAL ACUITY RE 2/10 LE 10/10
  • 37.
  • 38. Decreased visual acuity in the LE 5/10
  • 39. 25PPV after 5 days VISUAL ACUITY RE 4/10 LE 10/10
  • 40. Vitreomacular traction sydromes often can be bilateral Sometimes should be treated as an emergency!!! Our clinical experience shows that the sooner we operate the better is going to be the visual outcome.
  • 41. THANK YOU FOR YOUR ATTENTION