*reviewed and approved by the conflict of interest ... · vitreomacular traction syndrome (vmts)...
TRANSCRIPT
1
1
PETER K. KAISER, MD
C h a n e y F a m i l y E n d o w e d C h a i r i n O p h t h a l m o l o g y R e s e a r c h , P r o f e s s o r O f O p h t h a l m o l o g y
C l e v e l a n d C l i n i c L e r n e r C o l l e g e o f M e d i c i n e , C l e v e l a n d , O H
OCT of Vitreomacular Interface Disorders
22
Financial Disclosure*Reviewed and approved by the Conflict of Interest Committee of the Cleveland Clinic
Alcon (C)
Alimera (C, R)
Allegro (C, S)
Bayer (C)
Genentech (C, R)
InSitu Therapeutics (C, S)
Kanghong Biotech (C)
National Eye Institute (R)
National Institute of Health (R)
Novartis (C)
Ophthotech (C, S)
Oraya (C, S)
Regeneron (C, R)
Research to Prevent Blindness (R)
SKS Ocular (S)
Thrombogenics (C)
33
Loss of interfibrillar hyaluronan
Degenerative breakdown of the collagen network
Liquefied lacunae increase with age in number, size, and coalescence
Age-related changes of vitreous gel
Sebag, J. The Vitreous. Springer-Verlag New York, NY,1989
76 year old vitreous
44
Vitreoretinal Adhesion
There is progressive age-related weakening of the adhesion between the posterior vitreous cortex (posterior hyaloid) and the internal limiting membrane (ILM)
2
55
Posterior Vitreous Detachment
Natural with aging (common over 50 years of age)1
Characterized by2
– Synchisis: vitreous gel liquefaction
– Syneresis: separation of the vitreous at the vitreoretinal interface Natural Aging
1. Hikichi T, et al. Ophthalmic Surg. 1995;26(1):39‐43.
2. Sebag J, Wang MY. In: Holz FG, Spaide RF, eds. Medical Retina: Focus on Retinal Imaging. Berlin, Germany: Springer‐Verlag; 2009:157‐168.3. Faulborn J, et al. Ophthalmologica. 1998;212(6):369‐376. 4. Gandorfer A, et al. Eye (Lond). 2002;16(1):95‐97. 6
Normal Vitreous Aging
Stage 1 – Vitreomacular adhesion (VMA)
7
Normal Vitreous Aging
Stage 2 – Separation from macula
8
Normal Vitreous Aging
Stage 3 – Separation for entire posterior retina except optic nerve
3
9
Complete PVD is rare
Faulborn Oph 1998. Gandorfer Eye 2002 1010
Liquefaction without vitreoretinal dehiscence
Macular
Pucker
Macular
Pucker
VMT
Syndrome
VMT
Syndrome
Vitreopapillary
Traction
Vitreopapillary
Traction
Retinal
Tear
Retinal
Tear
Anomalous
PVD
Anomalous
PVD
Peripheral Separation
Posterior Traction
Centripetal (inward)
Contraction
Premacular
Membrane
Premacular
Membrane
J. Sebag, Retina 2009;29(7):871-874.
Centrifugal (outward)
Contraction
Full Thickness,
but partial PVD
Peripheral Separation
Peripheral Traction
Macular
Hole
Macular
Hole
11
International VMI Consensus Working Group
Jay Duker, MDNew England Eye CenterBoston, MassachusettsUSA
Peter K Kaiser, MDCole Eye InstituteCleveland, OhioUSA
Susanne Binder, MDRudolf Foundation ClinicVienna, Austria
Marc de Smet, MD, PhDMontchoisi ClinicLe Mont‐sur‐Lausanne, Switzerland
Alain Gaudric, MDLariboisière HospitalParis Diderot UniversityParis, France
Elias Reichel, MDNew England Eye CenterBoston, MassachusettsUSA
SriniVas Sadda, MDDoheny Eye InstituteLos Angeles, CaliforniaUSA
Jerry Sebag, MDVMR InstituteHuntington Beach, CAUSA
Richard Spaide, MDVitreous‐Retina‐Macula ConsultantsNew York, New YorkUSA
Peter Stalmans, MDUZ LeuvenLeuven, Belgium
1212
Goals of the Classification Scheme
Simple, easy to use, easy to remember
Objective – no symptoms, no clinical findings
Based on OCT alone
Applicable to clinical practice
Helpful in predicting surgical outcomes
Useful for clinical trials
Allow retina community to speak a “common language”
4
1313
Vitreomacular adhesion (VMA)
1515
Vitreomacular Adhesion (VMA) –International Classification
Exclusively an OCT “finding”– No symptoms
– No clinical findings
Due to age-related changes of the vitreous
Rarely pathologic
Common
1616
Swept Source
17
Focal versus Broad
Why 1500 microns?– Known site of strong VM adhesion by histology– Pre-existing cut-off employed by reading centers
< 1500 = focal
= 1500 microns
5
1818
Isolated versus Concurrent
Isolated = isolated finding on OCT in absence of posterior segment disease
Concurrent = associated with a posterior segment diseaseoVMA may or may not be directly attributable to concurrent disease
oVisual affects, if present, may be due to VMA or the secondary disease or both
19
Isolated Focal VMA
19
Otherwise normal macula = Isolated focal VMA
2020
Concurrent Focal VMA
20
Concurrent focal VMA (associated with CSC)
2121
Clinical Course of VMA
Asymptomatic
VMA
SpontaneousResolution
VMT
6
2222
Vitreomacular Traction (VMT) –International Classification
Definition = VMA with ANY abnormal macular retinal architecture
OCT diagnosis
“symptomatic VMA” = VMT
2323
VMT
2424
Isolated Focal VMT
VMT = VMA with retinal architectural changes
2525
Isolated Focal VMT
VMT = VMA with retinal architectural changes
7
2626
Isolated Focal VMT
VMT = VMA with retinal architectural changes
27
Isolated Broad VMT
28
Isolated Broad VMT
2929
Pathology at the vitreoretinal interface
Growth factors at the vitreoretinal interface– Laminin, fibronectin, and others
May contribute to fibrocellular proliferation at the retinal surface in the presence of vitreous remnants
“Vitreoschisis”: collagen and cells left firmly attached to the ILM
8
3030
VMT Becomes ERM
52 year old high myope
VA = 20/25
Mild metamorphopsia
3131
VMT Becomes ERM
2 years later
Worsening symptoms
VA = 20/50
3232
Epiretinal Membrane
Cellular proliferations ona layer of native vitreous collagen
The ILM and/or vitreous collagen serves as a scaffold for cellular proliferation
Adhesion of vitreous collagen transmits tangential tractionalforces to the retina
3333
Epiretinal membrane
9
3434
C-Scan ERM
3535
Vitreomacular traction syndrome (VMTS)
Characteristic clinical appearance at macular surface (wrinkling, tightening, thickening)
Typically has double membrane due to hyaloidal splitting or surface profileration
3636
Vitreomacular traction syndrome (VMTS)
3737
Vitreomacular traction syndrome (VMTS)
An ERM is present in the VMT syndrome (VMTS)
10
3838
Full Thickness Macular Hole
A full-thickness defect of retinal tissue involving the anatomic fovea
– First described in 1869 following ocular trauma by Knapp
3939
Pseudohole
Differentiate macular holes, lamellar holes, and pseudoholes
Macular hole Lamellar hole
OCT in vitreoretinal interface disorders
4040
Pseudohole
Steepened foveal contour, small foveal aperture
Thickening of macular edges (without thinning of foveal center)
Reduced macular diameter
4141
OCT of Pseudohole
Steep profile consistent with Allen and Gass' hypothesis of centripetal ERM constriction
11
4242
ERM with Pseudohole
4343UHR-OCT Courtesy of Jay Duker, MD
ERM with PseudoholeERM with Pseudohole
4444
Lamellar Hole
Gass definition: aborted macular hole
Complete PVD - pulls off inner retinal tissue leaving outer retina (photoreceptors) intact
Vision usually good - 20/20 to 20/30
Usually stable
4545
Lamellar Hole
Visual Acuity 20/30Followed 18 months
12
46
Lamellar Hole
48
Gass Classification
Stage 1
Stage 2
Stage 3/4
4949
“Stage 1a Macular Hole” = VMT
5050UHR-OCT Courtesy of Jay Duker, MD
“Stage 2 Macular Hole” = FTMH
13
5151
“Stage 2 Macular Hole” = FTMH
5252
Full Thickness Macular Hole
5353UHR-OCT Courtesy of Jay Duker, MD
“Stage 3 Macular Hole” = FTMH
5454
“Stage 3 Macular Hole” = FTMH
14
5555
Swept Source
56
Stage 3 Macular Hole
5757
“Stage 4 Macular Hole” = FTMH
5858
Full Thickness Macular Hole
15
5959
OD = 20/50 OS = 20/20
Stage “0” hole = VMA
• Stage 0 macular hole has a 42% risk of going to full thickness macular hole
• If contralateral eye does not have a stage 0 only 3% risk
6060
OCT for Macular Hole
Diameter of macular hole associated with initial closure rates
– Prognosis better for eyes with small diameter macular holes
– Late re-opening of macular holes with larger diameter more common
Ip MS, et al. Arch Ophthalmol 2002;120:29-35
6161
Size for FTMH
Size (not stage) most important variable to predict anatomic success (eg Stage 4 holes can be small)
SMALL: < 250 microns near 100% closure
MEDIUM: > 250 < 400 about 95% closure
LARGE: ≥ 400 microns about 75% closure
6262
FTMH International Classification System
Based on size of full thickness defect
VMT = present or absent
Primary versus secondary
Note:– No stages
– No “idiopathic” . Now referred to as Primary. Due to VMA VMT
16
6363
FTMH Subclassification – Small (< 250 microns)
80 microns
6464
FTMH Medium (251 – 400 microns)
390 microns
6565
FTMH Large (> 401 microns)
516 microns
6666
FTMH – VMT Present or Absent
Small FTMH –VMT released
Small FTMH –VMT present
17
6767
FTMH Primary vs Secondary
Primary = due to VMA leading to VMT (formerly “idiopathic” macular hole)
Secondary– Not initiated by VMA or VMT
– Secondary to preexisting or concurrent condition or disease
6868
Secondary FTMH
Pre-existing or concurrent condition or disease without evidence of VMT
– TraumaoBlunt trauma
oLightning strike
oSurgical procedure
– Myopia
– Macular schisis
– MacTel Type 2
– Choroidal neovascularization (CNV) treated with anti-VEGF
6969
OCT of the Vitreomacular Interface
OCT is invaluable for evaluation of the vitreomacularinterface
Diagnosis and management will be altered based on OCT findings
OCT can visualize subtle findings that may be impossible to see clinically
7070
Thank you...