Vitreoretinal interface disorders involve abnormal adherence between the vitreous gel and the retina. Posterior vitreous detachment normally occurs in older individuals as the vitreous liquefies and separates from the retina. Vitreomacular adhesion and traction occur when the vitreous remains abnormally attached to the macula, which can cause macular edema or hole formation. Optical coherence tomography is useful for diagnosing and monitoring these disorders. Treatment may involve observation, pharmacologic vitreolysis to release attachments, or vitrectomy surgery to remove tractional forces on the macula.

1. Vitreoretinal Interface Disorders
Eranda Wannigama

2. Overview
• Anatomy.
• Posterior Vitreous Detachment (PVD).
• Types Vitreoretinal Interface Disorders.
• Management of Vitreoretinal Interface Disorders.
• Summary.

3. Anatomy
• The vitreous gel is a transparent
extracellular matrix that fills the
cavity behind the lens of the eye.
• It occupies an average volume of
4.4 ml in adulthood
• The outer cortex of vitreous which
is made up of dense collagen (Type
II) is firmly attached to internal
limiting membrane (Type IV
collagen).

4. Vitreous Attachments
• Vitreous Base-
a ring shaped area
encircling the ora serrata
(2mm anterior and 4mm
posterior to it).
• Peripheral margin of the
Optic nerve head
• Margin of the fovea
• Main retinal vessels
Abnormal areas
– Lattice degeneration
– Cystic retinal tufts
– Chorioretinal scars

5. • Posterior Vitreous Detachment (PVD)
• Is a separation between the posterior vitreous cortex and the neurosensory retina, with
the vitreous collapsing anteriorly towards the vitreous base.
• PVD affects most eyes by the eighth decade of life. Age at onset is generally in sixth to
seventh decade and men and women appear to be equally affected.
• PVD occurs earlier in myopic eyes, in eyes with inflammatory disease and following blunt
trauma or cataract surgery (especially when there is surgical vitreous loss).
Incomplete posterior vitreous detachment. Posterior hyaloid is detached from fovea and remains
partially attached to optic disc.

6. Pathophysiology of PVD
• The initial event is liquefaction (Synchisis)
• Then the collapse (Syneresis) of the central vitreous.
Synchysis Syneresis
A rupture develops in the posterior hyaloid (or vitreous cortex) through
which liquefied vitreous flows into the retrovitreous space, separating
the posterior hyaloid from the retina.

7. • It typically starts as a partial PVD in the perifoveal region and is usually asymptomatic
until it progresses to the optic disc, when separation of the peripapillary glial tissue
from the optic nerve head occurs, usually with formation of a Weiss ring and
accompanying symptoms
PVD ctd

8. Vitreoretinal Interface
• Is an adhesive sheet that facilitates the
connection of the posterior vitreous cortex of
the vitreous body to ILM the of the retina.
• The vitreoretinal interface consists of matrix
proteins including laminin, fibronectin and
collagen IV, and it is thought that these may act
as an extracellular matrix 'glue'
Disorders of the vitreo-retinal interface characterized by incomplete PVD, and an abnormally
strong adherence of the posterior hyaloid face to the macula ,and anteroposterior traction
exerted by the synchytic vitreous pulling at adherent sites on the macula causing morphologic and
often functional effects.

9. Vitreoretinal Interface Disorders
• Vitreomacular Adhesion: focal adhesion of the vitreous face within macular
region.
• Vitreomacular Traction: VMA causing focal tractional distortion of macula.
• Macular Hole
• Macular oedema with Posterior hyaloid traction(PHT)
Vitreoretinal Interface imaging with Optical coherence tomography (OCT)
has contributed significantly to the diagnosis and management of
Vitreoretinal Interface diseases

10. Case 1
66year old Female retired teacher from Kolonnawa
OD-BCVA 6/6
OS-BCVA 6/9
3D OCT -OD 3D OCT -OS

11. VMT• VMA

12. Vitreomacular Adhesion
In VMAThe following must be present on at least one OCT image
(i) Partial vitreous detachment as indicated by elevation of cortical vitreous above the retinal surface in the
perifoveal area
(ii) Persistent vitreous attachment to the macula within a 3-mm radius from the center of the fovea
(iii) Acute angle between posterior hyaloid and inner retinal surface
(iv) Absence of changes in foveal contour or retinal morphology.
Focal vitreomacular adhesion with normal foveal contour and retina morphology.

13. VMA-OCT-based classification
(i) Focal: Width of attachment ≤1500 μm
(ii) Broad: Width of attachment >1500 μm
(i) Concurrent: Associated with other macular abnormalities (e.g.
age-related macular degeneration, retinal vein occlusion, diabetic
macular edema)
(ii) Isolated: Not associated with other macular abnormalities

14. Vitreomacular traction (VMT)
The following must be present on at least one OCT image:
(i) Partial PVD as indicated by elevation of cortical vitreous above the retinal surface in the perifoveal area
(ii) Persistent vitreous attachment to the macula within a 3-mm radius from the center of the fovea
(iii) Acute angle between posterior hyaloid and inner retinal surface
(iv) Presence of changes in foveal contour or retinal morphology (distortion of foveal surface, intraretinal
structural changes such as pseudocyst formation, elevation of fovea from the RPE, or a combination of any of
these three features)
(v) Absence of full thickness interruption of all retinal layers

15. VMT-OCT-based classification
(i) Focal: Width of attachment ≤1500 μm
(ii) Broad: Width of attachment >1500μm
(i) V shaped - the vitreous cortex is detached from the retina both temporal and nasal to the
fovea, and attached only to the fovea,
(ii) J shaped or arc shaped - the vitreous cortex is detached from the retina temporal to the
fovea, but remains attached to the retina nasal to the fovea and to the fovea itself.
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1752um

17. VMT & VMA
Symptoms
• VMA: Asymptomatic
VMT: Symptomatic with blurred or reduced vision, metamorphopsia, micropsia, scotoma,
and difficulties with daily vision-related tasks such as reading. Onset and progression of
symptoms are usually gradual, except in a few cases of sudden onset of vision
loss/scotoma due to severe traction causing foveal detachment.
Complications can include:
1. Full thickness macular hole
2. Tractional macular schisis
3. Tractional foveal/macular detachment

18. Management
1. Observation
2. Surgery
Release anteroposterior traction by means of pars plana vitrectomy (PPV) and
tangential traction with ILM peeling is a common treatment for VMT The
reconstitution of retinal architecture is expected to occur with time, after
removal of the tractional forces.
Symptomatic and visual improvements are expected to follow. Outcomes are variable depending
on morphology and duration
3. Medical therapyThe medical therapy of VMT consists of
pharmacologic vitreolysis.-Ocriplasmin (formerly, microplasmin) is a recombinant
truncated form of human plasmin that has proteolytic activity against these proteins
anchoring the vitreoretinal interface.
4 pneumatic Vitreolysis ;risk of Glaucoma and Inducing tears

20. Macular hole
• Incidence 0.3% in 3in 1000
• 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%.

21. Etiology
• Common causes:
• Idiopathic -90%
• Other causes:
• Trauma
• high myopia
• ERM
• cystoid macular edema
• proliferative diabetic retinopathy
• severe hypertensive retinopathy
• Choroidal neovasculatrisation
• Solar retinopathy

22. Classification
• Primary macular hole: is commonly an idiopathic
macular hole
• Caused by vitreous traction on the fovea from an
abnormal vitreous separation
• Secondary Macular hole: caused by other pathologies
not associated with vitereomacular traction
• blunt trauma, high myopia, macular
telangiectasia,ERM

23. Stages of Macular hole
• Gass first described a series of
stages of formation of idiopathic
macular hole 1988.

24. Stage 1 a
• Anteroposterior traction by prefoveolar cortical
vitreous split the foveolar retina
Stage 1a: ‘Impending’ macular hole
a Signs: yellow spot
b Pathology: Müller cell cone detach from the
underlying photoreceptor layer, with the formation
of a schisis cavity (pseudocyst)
pseudocyst

25. Stage 1 a
(A)showing a cyst in the inner part of the fovea (asterisk) due to the traction exerted by the incompletely
detached posterior hyaloid (arrows).
(B)(B) Magnification of (A) showing that the central cyst is divided into several cystic spaces (asterisks) by
septa. The inner segment/outer segment (IS/OS) line is intact, but the cone outer segment tips (COST)
line is elevated at the foveal center.

26. Stage 1 b
Stage 1b: Occult macular
hole
a Signs: a yellow ring
(donut-shaped) 200-300μm in
diameter
b Pathology: photoreceptor
layer undergo centrifugal
displacement
The posterior hyaloid (PH) is still attached to the roof
of the cyst. The cystic space extends posteriorly and
there is a break in the photoreceptor layer. Note also
the cystic cavities around the central defect. Stage 1B
is an occult macular hole.

27. Stage II
Stage 2: Small full-thickness hole
a Signs: < 400 µm , central, slightly
eccentric or crescent-shaped.
b Pathology: dehiscence centrally or
eccentrically seen in the roof of the
schitic cavity, pseudo-operculum
The posterior hyaloid (PH) is still attached to the operculum
(aarrow). The operculum is only partially detached from the hole
edge.

28. Stage III
Stage 3: Full-size macular hole
a Signs:
- > 400 µm
- red base with yellow-white dots
- surrounding grey cuff of
subretinal fluid
b Pathology: avulsion of the roof
of the cyst with an operculum and
persistent peripapillary
attachment of the vitreous
cortex.
The posterior hyaloid (PH) is detached from the
macular surface and contains the operculum (blue
arrow). The edge of the hole has been thickened by
cystic spaces and the photoreceptors are elevated
(black arrows mark the end of the outer segments of
the elevated photoreceptors).

29. Stage IV
Stage 4: Full-size macular hole with
complete PVD
a Signs: as in stage iii
b Pathology:PVD is complete (Weiss
ring)
Stage iv Hole

31. Case 2

32. OD -1A OS -1B

33. Clinical features
• Visual acuity the first indicator but sometimes
misleading
• Mild loss of central vision (Stage 1a & 1b)
• Metamorphopsia
Amsler Grid
• Non specific distortion rather than scotomas.But Small absolute
scotomas can be detected in 30 -40 % of patients

34. Watzke RC, Allen L. Subjective slit-
beam sign for macular disease.
• FTMH is diagnosed on slit lamp biomicroscopy
• By slowly sweeping a vertical or horizontal narrow slit beam across the
eye we can study the contour of hole and vitreous interface
differentiates FTMH from other lesions
Positive & Negative Watzke - Allen Sign

35. Investigations
• OCT-gold standard
-Confirm the diagnosis of macular hole.
-Stage the hole
-Helpful in prognosticating
anatomical-hole form factor(ratio between base
diameter and height)
functional- Continuous IS/OS junction and external limiting membrane as well as
increased photoreceptor outer segment thickness predicts a better
functional outcome
-For follow up
• FFA
Usually not indicated in diagnosis of macular hole
But generally demonstrates early hyperfluoresence (window defect)

36. Differential Diagnosis
• Epiretinal membrane with pseudomacular hole
• Lamellar macular hole
• Chronic cystoid macular edema

37. Lamellar macular hole
• Sharply circumscribed
• Partial-thickness defects of the macula
• Represents either as an aborted full-
thickness lesions or a complication of chronic
cystoid macular edema.
• Characterized by a flat, reddish hue-type
lesion with intact outer retinal tissue
• Careful evaluation will reveal retinal tissue in
the base of the lesion
• No evidence of subretinal fluid
• Do not progress to full-thickness lesions

38. Management
• Depending on the Stage
Stage i > 50% resolve spontaneously -Observation
Stage ii,iii,iv- Surgery is benefitial for both Functional and Anatomical
closure.
Surgery
TPPV +ILM peeling and Tamponade
Release anteroposterior traction by means of pars plana vitrectomy (PPV) and
tangential traction with ILM peeling is a common treatment for MH The
reconstitution of retinal architecture is expected to occur with time, after
removal of the tractional forces
• Surgical and Medical

39. Pharmacologic vitreolysis
• New nonsurgical option that can aid closure of macular holes
associated with VMT.
• degrades the macromolecular vitreous attachment complex
• relieves the tractional forces that cause the foveal lesion

40. • On the basis of post operative OCT findings closed macular
holes are:
• Type 1 & type 2 closure
Types of closure

41. • Indicates that macular hole is closed without foveal defect of the
neurosensory retina
• U shape-perfect closure
• V shape-closure with central thinning
• .
Type 1 closure

42. Type 2 closure
• Indicates a foveal defect of neurosensory retina persists
postoperatively(w shape closure)
• Although the whole rim of macular hole is attached to the
underlying RPE with flattening of the cuff

43. Post operative parameters
• OCT parameters: Type 1 closure of MH without
neurosensory defect) has a better visual outcome
compared to Type 2 closure (with neurosensory defect)
• Continuous IS/OS junction and external limiting
membrane as well as increased photoreceptor outer
segment thickness predicts a better functional
outcome

44. Pre operative parameters
Hole form factor > 0.9 and Macular Hole
index > 0.5 also have a better prognosis
a = base diameter, b = minimum diameter
c = left arm length, d = right arm length

45. Case 3
73 year old female house wife came
with reduced visual acuity in right
eye
OD-BCVA 2/60
OS-BCVA 6/9

46. Advantages of ILM peeling
• Removes the scaffold for proliferation of cellular components Like
myofibroblasts, fibrocytes,RPE cells, fibrous astrocyts.
• Eleminate tangential traction around fovea.
• The benefit 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.

47. Case 4

49. Macular oedema with Posterior
hyaloid traction(PHT)
• Vitrectomy including removal of the ILM leads to expedited
resolution of diffuse diabetic macular edema and
improvement of visual acuity without subsequent epiretinal
membrane formation.
• Complete release of tractional forces and inhibition of
reproliferation of fibrous astrocytes seem to be prudent in
the eyes of patients with diabetes and advanced
vitreoretinal interface disease of the macula.