This document provides an overview of epiretinal membrane (ERM). Key points include: - ERMs are cellular sheets that form on the macular surface due to various etiologies. They were first described in 1865. - Presentation can vary but ERMs often cause mechanical distortion of the macula due to their contractile properties. - Prevalence increases with age, peaking between 70-79 years old. Studies show a prevalence of 7-11.8% and bilateral involvement in 19.5-31% of cases. - Classification includes idiopathic ERMs and secondary ERMs associated with other ocular conditions. Formation involves glial cells, extracellular matrix

1. EPIRETINAL MEMBANE
Dr Amit Srivastava

2. Definition
• Acquired formation of semi-transparent
cellular sheets on the macular surface, which
are formed due to varied etiologies.
• 1865, first described by Iwanoff

3. Introduction
• Premacular fibroplasia, Macular pucker,
Cellophane maculopathy, and Premacular
gliosis
• Contractile properties, often leading to
mechanical distortion of macula.
• Wide spectrum of presentation and clinical
findings

4. Epidemiology
• Beaver Dam Eye Study and the Blue Mountains
Eye Study
• Prevalence of ERM was 7–11.8%, with a 5-year
incidence of 5.3%.
• Idiopathic ERMs were bilateral in 19.5–31%, with
13.5% 5-year incidence of second eye
involvement.
• Age distribution shows a peak between the ages
of 70 and 79 (11.6%), with ERMs being
uncommon before the age of 60(1.9%)

5. Indian Scenario
7.6%

6. Classification
• Idiopathic ERMs (no associated ocular
abnormality)
• Secondary ERMs with a pre-existing or
coexisting condition has had a significant
impact on development
• Iatrogenic if they occur following medical or
surgical intervention

8. Pathogenesis
• Reactive gliosis in response to retinal injury or
disease involving inflammatory and glial cells.
• Involves
– Cellular & Extracellular component
– Growth Factors
• Two main components of ERM
– Extracellular matrix (consisting of collagen, laminin,
tenascin, fibronectin, vitronectin, etc.)
– Cells of retinal and extra retinal origin (such as glial
cells, neurites, retinal pigment epithelium, immune cells
and fibrocytes).

9. Growth factors
(formation, progression and transformation of membranes)

10. Pathogenesis
(PVD +)
• Müller cells have proliferated and migrated onto the
inner surface of the retina.
• PVD exerts traction on the retina and induces
– Müller cell gliosis (cellular hypertrophy)
– Upregulation of cellular proteins such as vimentin and
– Transient cellular proliferation.
• Migrate to epiretinal surface via small defects in ILM,
either natural (near retinal vessels) or as a result of
larger paravascular breaks observed following PVD

11. Pathogenesis
(PVD -)
• Vitreomacular traction cause chronic irritation
of Müller cells inducing gliosis and vascular
leakage.
• Glial cells appear to grow through the
posterior hyaloid which then in turn becomes
incorporated into the membrane

12. Clinical Features
(Symptoms)
• Grade 0 Incidental finding
• Grade I ERM involving fovea causes
–
–
–
–
–
distorted or blurred vision
loss of binocularity,
Central photopsia,
Macropsia.
Monocular diplopia
• Grade 2 ERM
– blurred vision or
– metamorphopsia

13. Clinical Classification
Grade 0 Translucent membrane
with no underlying retinal
distortion
Grade 1 ERM with irregular
wrinkling of Inner retina
Grade 2 ERM with opaque membrane and vascular tortuosity

14. Clinical Features
• Grade 2 ERM associated with cotton-wool spots,
exudates, blot hemorrhages and
microaneurysms
• Cystoid macular edema (20–40%)
• Vascularization of the ERM and underlying RPE
rare and indicate more severe disease
A posterior vitreous detachment (PVD) is present in approximately
60–90% of patients at the time of diagnosis

15. Clinical Features
• Macular pseudoholes (steepened foveal
contour) 20%
• Lamellar holes (retinal cysts ERM rupture)
• Full-thickness macular holes (Tangential
traction).

16. Clinical Assesment
• Distinguish between idiopathic/Secondary/
iatrogenic ERM.
• Good ophthalmic and general medical history.
• Visual acuity that is lower than expected for
the degree of ERM indicate underlying retinal
disease
• Intraretinal hemorrhages, exudates or
cottonwool spots,

17. • Best corrected Visual Acuity for distance and
Near.
• Thick ERM cause decreased VA
• Amsler grid distortion
– Does not allow for the quantification of the
severity of metamorphopsia;
– Difficult to monitor the visual function over time

18. M-chart
– Developed by Matsumoto
– Quantifying metamorphopsia
Metamorphopsia score
MV 0.4
MH 0.5

19. OCT
• Detects ERM in up to 90% cases
• Assess the anatomical relationship between
vitreous face and the retinal surface
• Diagnosis, monitor the clinical course prior to
and following surgery.
• IS-OS junction
• More recently, intraoperative OCT has also
been used

20. OCT
•
•
•
•
•
Hyper-reflective layer retinal surface.
Underlying corrugation of the retinal surface,
Blunting of the foveal contour,
Increased retinal thickness and
Intraretinal cysts

21. Globally adherent ERM
Focally Adherent ERM
• Idiopathic ERMs tend to be adherent globally to the
underlying retina,
• Secondary ERMs are more likely to be characterized by
focal retinal adhesion

22. OCT Patterns

24. • Inner retinal layer thickness (IRT) distance
from the vitreoretinal interface to the inner
border of the outer nuclear layer at the foveal
center.
• The outer retinal layer denoted layers of
photoreceptor, encompassing the outer
nuclear layer and inner segment/outer
segment (IS/OS) junction line in OCT scan
images

25. Fovea attached type ERM
• Group 1A included ERM with outer retinal thickening;
the inner retina, however, showed a minimal increase
in thickness and maintained a nearly normal
configuration.
• Group 1B included ERM with more exaggerated tenting
of the outer retinal layer in the foveal area; the inner
retinal layer was slightly thickened and its configuration
was distorted by centripetal and anteroposterior
tractional forces due to ERM.
• Group 1C included ERM with prominent inner retinal
thickening, with inward tenting of the outer retinal
reflectivity in the foveal area.

26. • Group 2A included ERM with the formation of a
macular pseudohole,
• Group 2B included ERM with macular
pseudohole accompanied by marked intraretinal
splitting

27. Cone outer Segment tips
Attributed to scattering from the tips of the cone OS, in the region of interdigitation
between the photoreceptor OS and the RPE cell processes that extend into the OS layer

28. Fibrillary Changes
• Alternating linear hyperreflective and hyporeflective signal between ERM and Retinal
Surface
• Extent of ERM retinal adherence and presence of fibrillary changes gives reliable method
of intraoperative difficulty of membrane peeling

29. Fluorescein Angiography
• Recently decreased diagnostic utility
• Underlying vascular event or CNVM is
suspected
• Highlight the extent of retinal wrinkling,
degree of retinal vascular tortuosity and
presence of macular
edema

30. • Extensive leakage from retinal capillaries or
veins was associated with more rapidly
progressing lesions*
• Displacement or distortion of the foveal
capillary network may indicate foveal ectopia
* Wise G. Clinical features of idiopathic preretinal macular fibrosis. Am J Ophthalmol
1975;79:349–57.

32. Course
• Appiah et al 324 idiopathic ERMs with a mean
follow-up of 33.6 months,
– 49.5% maintained a visual acuity within 1 line of the
initial acuity;
– 37.4% showed a reduction in vision, and
– 13.1% stayed the same.
• Blue Mountains Study, the area of retina occupied
by the ERM remained over 5 year
– Stable 39%,
– Regressed 25.7% and
– Progressed 28.6%
(where change was defined as a change in area of >25%).
Course is one of stability or slow progression over years

33. Surgery Indication
• Patient-reported symptoms of reduced visual
acuity with or without metamorphopsia.
• Reduction in acuity to ≤20/60,
• Better than 20/60 if
– Annoying metamorphopsia
– Diplopia
– Occupational reasons.

34. Prognostic factors
•
•
•
•
•
Visual acuity,
Central foveal thickness,
Presence of a macular pseudohole,
Cystoid macular edema, and
Location, thickness and degree of opacification of the
membrane.
• IS-OS junction (photoreceptor inner and outer
segments), intact, it is strongly suggestive of viable
photoreceptors
• SLO based association between structural abnormalities
of photoreceptors (microfolds) and symptoms of
metamorphopsia.
• Cone outer Segment tips (COST)

35. AO-SLO
• Structural abnormalities in individual
photoreceptor cells in patients with idiopathic
ERM
• IS/OS disruption is not specific to eyes with
ERM

36. Focal macular ERG (FmERG)
• Oscillatory potentials, “b” wave and “a” wave
are all reduced in patients with ERM.
• Reduced b : a wave ratio appears to be a sign
of early disease with a reduction in the a-wave
amplitude being correlated with poor
postoperative visual acuity.

37. Cone Outer Segment Tips (COST)
(Verhoeff membrane)
• 3 groups
– Group A, with a continuous IS/OS and COST line
– Group B, with a continuous IS/OS but disrupted COST
line
– Group C, with a disrupted IS/OS and COST line
• At 6 months, Group A showed a significantly
better BCVA than Group B ( P < .005), and poorer
BCVA was noted in Group C
• Status of the COST line, in conjunction with the
IS/OS junction, is a useful prognostic factor after
ERM surgery

38. • Hierarchy of vulnerability among the 3 lines;
– COST line, (ERM)
– IS/OS junction (Macular Hole)
– ELM (Retinal Detachment)
• Can be disrupted when mild, moderate, and
severe photoreceptor damage respectively is
caused

39. Differential Diagnosis

40. Surgery
Machemer developed the concept of
membrane peeling in 1972

41. ERM Peeling
• Vital dyes to assist visualization and removal,
particularly over the macular area
• Indocyanine Green (ICG)
• Infracyanine Green(IFCG),
• Trypan Blue4 (TB) and
• Triamcinolone accetonide (TA)
• Brilliant Blue G (BBG)
• Chicago Blue
• Bromophenol blue,
• Patent blue (PB).

42. ICG
IfcG
TB
TA
PB
BrB
FMA
BBG
Mol wt
774
774
961
434
582
670
418
854
Chemical gr
Tricar Tricar Diazo
bo
bocy
cyanin anine
e
Steroid Triyl
methane
Triylmetha Steroid
ne
Triylmeth
ane
1st
publication
2000
2002
2003
2003
2006
2006
2007
2006
ILM affinit
High
High
Low
Low
Low
Mod
Unkno
wn
High
ERM affinity
Low
Low
High
Low
Mod
Mod
Unkno
wn
unknown
Vit affinity
Low
Low
Low
High
Mod
Unknown
Low
Unknow
n
Retina
toxicity
Mod
Low
Mod
Mod
Low
Unknown
Low
Nil
RPE toxicity
Mod
Low
Mod
Mod
Low
Unknown
Unkno
wn
Unknow
n

43. Double Staining
Stalmans and colleagues both TB (for ERM)
and IfCG (for ILM) in the treatment of
macular pucker.
•
•
Overlying ERM, which does not stain, but is
visible against a surrounding blue-stained ILM.
Non-stained ERM is first peeled off, and then
BBG dye is injected a second time to stain the
unstained ILM.

44. • Standard pars plana vitrectomy,
• Degree of vitreous clearance is surgeon
dependent
– should avoid any risk of lens trauma or retinal breaks.
• Most cases a PVD will be present at the start of
surgery.
• If posterior hyaloid is attached, PVD attempted
carefully due to the presence of ILM attachments
through the vitreous.

45. PVD
• Deactivate cutting mode reach optic nerve
head (Preferably nasal edge) and perform
suction to grasp posterior hyaloid membrane
and swing vitrectome horizontally.
• Once posterior hyaloid detached complete
halfway down

46. • Observe the macula
– Whether to use dye
– Whether to use macular lenses
• Dyes
– Loaded in 2CC syrringe connected with silicone
tipped cannula
– Pinch infusion line to decrease turbulence when
valved cannulas are not used

47. • Magnifying contact lens
– Microscope head should be moved to lower
setting
– Drastic reduction in field

48. Engaging and Peeling ERMs
• Edge of the ERM
– Clearly visible engaged directly with end-grasping
forceps
– Cannot be clearly identified, created prior to
peeling using a
•
•
•
•
23 G Needle Machemer
surgical pick (rounded tip instrument) O Malley
Diamond dusted scraper Tano
End grasping forceps Charles

53. Technique of ERM peeling
• Outside in membrane peeling – Machemer
• Inside out membrane peeling - Charles

54. • Try to look for area of membrane which is
thicker (contraction center) or near or over
macular vessel
• Pinch the membrane and peel it back until it
gives a flap
• Peel tangentially over the retina centripetally
• Observe both the point of membrane being
peeled and head of forceps

55. • Cystic fovea (prevent Deroofing)
– Strict centripetal peeling
– Membrane dissected from perifoveal retina and at
the end cut at fovea with vitrectome

57. Very Adherent ERM
• No clearly defined tissue planes
• Membrane peeling leaving areas of retinal
whitening underneath.
• Finding an alternative edge and peeling this
toward the adherent area.
• Repeated until only the adherent area
remains,
• Gently peeled without exerting traction on
surrounding areas of retina.

58. Internal limiting
Membrane
• Potential benefit of completing an ILM peel
following the removal of ERM.
• Removes the scaffold for myofibroblast
proliferation and any residual microscopic
ERM, thus reducing the risk of recurrence as
well as improving visual outcomes**
**Bovey EH, Uffer S, Achache F. Surgery for epimacular membrane: impact of
retinal internal limiting membrane removal on functional outcome. Retina
2004;24:728–35.
Park DW, Dugel PU, Garda J, et al. Macular pucker removal with and without
internal limiting membrane peeling: pilot study. Ophthalmology 2003;110: 62–4.

60. Result
• Following surgery there is often a period of several
weeks without any noticeable visual improvement.
• Patients can expect a visual improvement of two or
more lines in 60–85% of cases 6–12 months after
surgery,
• 44–55% achieving a visual acuity of 20/50 or better.
• Patients with a higher preoperative visual acuity tend
to have a higher final acuity even though the
percentage improvement may be less.
• Both idiopathic and secondary ERMs appear to benefit
to an equal extent from surgery,

61. Result
• Following successful ERM surgery
– Macular thickness and foveal contour tend to
improve on OCT,
– Although neither returns to normal
• IVB injection therapy provided no beneficial
effects on CMT or visual acuity improvement
for eyes with persistent macular edema after
idiopathic macular ERM removal*.
*J Ocul Pharmacol Ther. 2011 Jun;27(3):287-92. doi: 10.1089/jop.2010.0166. Epub 2011 Mar 23.
Intravitreal bevacizumab injection therapy for persistent macular edema after idiopathic macular epiretinal membrane surgery.
Chen CH, Wu PC, Liu YC.

62. Intraoperative Complication
• Small petechial hemorrhages 19%
• Preretinal hemorrhages selflimiting
• Peripheral retinal breaks
– 4–9% following 20 G vitrectomy
– 1% with 23 G vitrectomy
– EL or Cryo with air gas tamponade
• Lens touch

63. Postoperative complication
• Cataract
– incidence of cataract within the first year ranges from
30% to 65%
– alterations in oxygen tension and glucose
concentrations,
– Disruption of the anterior vitreous in the retrolental
area and
– Orientation of the infusion cannula at the time of
surgery.

64. Postoperative Complication
• Retinal detachment
– 2–14% of eyes.
– Unidentified entry site breaks at the time of surgery
– careful search for retinal tears using scleral
indentation at the end of surgeryRecurrence
• Recurrence of ERM less than 20% of patients
higher in younger patients (25%).
• Retinal toxicity vital dyes
• Phototoxicity