nice palatable presentation for residents & retina specialists

1. Disorders of vitreomacular interface

2. Anatomy
Vitreous is a gel like transparent
extracellular matrix that fills the cavity
behind the lens .
It occupies an avarage volume of about 4.4
ml in adulthood.
Outer vitreous cortex is made up of dense
collagen(Type 2) whichis firmly attached to
internal limiting membrane.

3. Vitreous Attachment
Physiological:
1.Vitreous base,very strong
ring shaped area encircling ora
serrata(2mm anterior and 4 mm
posterior to it)
2.Optic disc mergin,fairly strong
3.Perifoveal,fairly weak
4.peripheral blood vessels,usually
weak

4. vitreoretinal interface
• It is an adhesive sheet that connects
the of posterior vitreous cortex to ILM
of the retina.
• The viteroreinal interface consists of
matrix protein Lamnin,Fibronectin and
collagen type4 and these act as an
extra cellular matrix glue.

5. Posterior vitreous detachment(PVD)
• Separation between the posterir vitreous cortex and the
neurosensory retina,with the vitreous collapsing anteriorly
towards the vitrous base.
• PVD affects mostly by eighth decade,but initiation occurs in sixth
to seventh decade,and men and women are equally affected.
• PVD occurs earlier in Myopic eyes,inflammatory disease and in
Blunt trauma or Cataract surgery(especially when there is surgical
vitreous loss).

6. Incomplete posterior vitreous detachment.posterior hyaloid is
detached from fovea and remains partially attached to optic disc

7. Vitreomacular interface disorders
• Vitreomacular Adhesion(VMA):Focal adhesion of vitreous face
within maculae region.
• Vitreomacular Traction(VMT):VMA causing focal tractional
distortion of macula
• Macular hole
• Epiretinal membrane

8. Viteromacular Adhesion(VMA)
OCT based Classification
I. Focal:Width of attachment ≤1500 micron.
II. Broad:Width of attachment > 1500 micron
I. Concurrent:Associated with other macular abnormalities(e.g
age related macular degenaretion,Retinal vein
occlusion,Diabetic macular oedema)
II. Isolated:Not associated with other maculr abnormalities.

9. Vitreomacular Traction(VMT)
The main differenc of VMT from VMA is-
Presence of change in foveal contour or retinal
morphology(distortion of foveal surface,intra retinal structural
changes such as pseudocyst formation,elevation of fovea from
the RPE,or a combination of any of these features)

11. VMT-OCT based Classification
I. Focal:Width of attachment ≤1500micron
II. Broad:width of attachment >1500micron
i. 'V' shaped:
• Vitreous cortex detached from both temporal and nasal to fovea.
• Attached only to the fovea.
i. 'J' shaped or arch shaped:
• Vitreous cortex detached from the rtina temporal to the fovea
• Remain attached to retina nasal to the fovea and to fovea itself.

12. HD OCT images of VMT syndrome based on the pattern of
vitreomacular adhesion a) V shaped VMT b)J shaped
VMT.OCT images of the VMT syndrome based on the
diameter of the vitreomacular adhesion c)Focal and d)broad
VMT

13. VMT &VMA
Symptoms
• VMA:Asymptomatic
• VMT:symptomatic-
• Blurred or reduced vision,
• Metamorphopsia,
• Micropsia
• Scotoma and
• Difficulties with daily vision related task such as reading.Onset and
progression of symptoms are gradual except in few cases of sudden onset of
loss/scotoma due to severe traction causing foveal detachment.

14. Complications
1. Full thickness macular hole
2. Tractional macular schisis
3. Tractional macular/foveal detachment

15. MANAGEMENT
1. Observation
2. Surgery
PPV and release of tangenital traction with ILM
peeling
3.Medical Therapy:
pharmacological vitrolysis with Ocriplasmin

17. Macular Hole
• Incidence:0.3%
• 12%Bilateral.
• Common in Women 3:1 aged 70 years.
• In other eye if PVD present less than
1% chance to have a macular hole.
• If PVD not present risk increase by
20%.

18. ETIOLOGY
•Common causes:
Idiopathic-90%
•Other Causes:
Trauma
High Myopia
ERM
Cystoid Macular Oedma
Solar Retinopathy

19. Classification
• Primary macular hole:Is commonly an idiopathic macular
hole.
caused by vitreous traction on the fovea.
• Secondary macular hole:
Caused by other pathologies not associated with vitreomacular
traction-
Blunt trauma,High myopia,Macular talengiactasia,ERM.

20. Stage 1a
• Impending Macular Hole
a) Signs:Yellow spot
b) Pathology:Muller cell
cone detach from the
underlying
photoreceptor layer,with
formation of a schysis
cavity(pseudocyst).
impending macular hole with a
foveal cyst

21. (A)showing a cyst in the inner part of the fovea due to the traction exerted by
incompletely detached posterior hyaloida(arrows)
(B)Magnification of (A)showing that central cyst is devided into several
cystic spaces by septa.The inner segment/Outer sgment(IS/OS)line is intact
but the cone outer segment tips(COST)line is elevated at a foveal center.
cont.

22. Stage 1b
•Occult maculr hole
a) Signs:a yellow
ring(donut
shaped)200-
300micron in
diameter.
b) Pathology:Photorecep
tor layer undergo
centrifugal
displacement
The posterior hyaloid(PH) still
attached to the roof of the cyst.
The cystic space extend poste-
riorly.

23. Stage2
• Small full thickness hole
a) Signs:<400micron,centra
l,slightly eccentric or
crescent shaped.
b) Pathology:dehiscence
centrally or eccentrically
seen in the roof of the
schitic cavity,pseudo
operculam
vitreous is attached to the lid of
the hole and cystic change

24. stage 3
• Full size macular Hole
a) Signs:>400micron
Red base with yellow-
white dots
surrounding grey cuff
of subretinal fluid
b) Ptahology:avulsion of
roof of the cyst with an
operculum and persistent
peripapillary attachment of
the vireous cortex.
medium sized FTMH with intra
retinal cystic space

25. Stage 4
• Full size macular hole with
compete PVD
a) Signs:As in stage3
a) Pathology:PVD is
complete(Weiss ring) FTMH with intra retinal cystic space
and an overlying operculum

26. Clinical Features:
• Visual acuity the first indicator
but sometimes misleading.
• Mild loss of central vision(Stage
1a & 1b)
• Metamorphopsia
• Amsler Grid:
Non specific distorsion rather than
scotomas.

27. Watzke RC,Allen L. subjective slit beam sign for
macular disease.
• FTMH is diagnosed on lit
lamp biomicroscopy.
• By slowly sweeping a
vertical or Horizontal narrow
slit beam accross the eye we
can study the contour of
hole and vitreous interface
Positive and negative Watzke
Allen sign.it differentiates
FTMH from other lesions.

28. Macular pseudohole
• This lesion mimics the clinical appearence of a FTMH
• But it is caused by distorsion of the perifoveal retina into
heaped edges by ERM,without any loss of retinal tissue,and
near normal foveal thickness.
• There is a central defect in the membrane.
• VMT may be present.

30. Investigations
• OCT:
Gold standard
Confirm the diagnosis of macular hole
Stage of the hole can be detected
Helpful in prognosticating
For fol
• FFA:
Usuall not indicated in diagnosis of macular hole
But generally demonstrates early hyperflurosence(Window
defect)low up

31. Differntial diagnosis
• Epiretinal membrane with pseudomacular hole
• Lamellar macular hole
• Chronic cystoid macular oedema

32. Epiretinal membrane
• This is an avascular fibrocellular membrane that proliferates on the inner
surface of the retina to produce verious degrees of macular dysfunction.
Key features
Transparent,Translucent,Opeque membrane on
inner retinal surface.
Tangenital traction on macula.
Partial or complete posterior vitreous separation.

33. Classification
• Idiopathic
• Secondary
• Iatrogenic
Pathology
ERM consists of avascular fibrous sheet of-
• Native vitreous
• Newly synthesized collagen
• Fragments of ILM
• Glial cells
• Myofibroblastic cells:RPE cells,Fibrous
astrocytes,Macrophages

34. Symptoms
• Mild cases often asymptomatic
• Blurring
• Metamorphopsia
• Visual acuity depends on severity

35. Cellophane Maculopathy
• Early ERM
• Irregular translucent sheen
• Best detected using green(red
free)light
Macular pucker
• Membrane thickens&contracts
• Becomes more obvious
• Mild distrsion of blood vesels

36. Advanced ERM
• Severe distorsion of blood
vessels
• Marked retinal wrinkling and
striae
• May obscure underlying
structures

37. Investigations
• Amsler grid:
Shows distorsion
• OCT :
Highly reflective surface
layer
Retinal thickening
Disruption of IS/OS
junction(poor prognosis)

38. Treatment
• Observation-
Mild &non-progressive
Spntaneous resolution of visual symptoms sometimes occurs
Due to separetion of ERM from retina as previously incomplete
PVD completes.
• Treat in case of-
Significant visual loss
Metamorphopsia
Intolerable binocular diplopia

39. Surgical Removal
• Peeling of ERM from surface of macula
• Goal of treatment is to reduce or eliminate
most common mechanisms of visual loss-
 Macular distorsion
 TRD
 Foveal ectopia
 Retinal vascular leakage with macular
 oedema

41. Lamellar Macular Hole
• Sharply circumscribed.
• Partial thickness defects of the macula.
• Reprasents either as an aborted full
thickness lesions or a complication of
chronic cysoid macular oedema.
• Charecterized by a flat,reddish hue type
with intact outer retinal tissue.
• Careful evaluation will reveal retinal
tissue in the base of the lesion.
• No evidence of sub retinal fluid.
• Do not progress to full thickness lesions.

42. Management
• Surgical and Medical
• Depending on the stage-
stage1>50%resolve sponteniously-observation.
stage2,3,4-surgery is benificial for both functional and anatomical
closure.
-
ParsPlanaVitreactomy+ILM peeling and Temponade.

44. Pharmacological Vitreolysis
• New nonsurgical option that can
aid closure of macular holes
associated with
VMT.(Ocriplasmin)
• Degrades the macromolecular
vitreous attachment complex.
• Relieves the traction forces that
cause the foveal lesion.

45. Advantages of ILM peeling
• Removes the scaffold for proliferation of celluler components like
myofibroblasts,fibrocytes,RPE cells,fibrous astrocytes.
• Eleminate tangenital traction around fovea.
• The benifit of ILM peeling is that it ensures complete removal of the
posterior hyaloid or any overlying epiretinal membranes.
• ILM peeling may reduce the duration of face-down positioning required
for macular hole closure.

46. Take Home Message
• Disorders of vitreomacular interface always associated with
visual impairment.
• Treatment option is usually vitreoretinal surgery
• In time skillful itervension is madatory to regain anatomical
integrity and functional outcome(visual outcome)