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Evaluation and
Management of
Epiretinal Membranes
DR TEHREEM TANVEER
DEFINITION
An Epiretinal membrane (ERM) is a transparent, avascular,
fibrocellular membrane on the inner retinal surface.
It adheres to and covers the internal limiting
membrane(ILM) of the retina and can produce varying
degrees of retinal distortion.
Cellophane Maculopathy, Macular Pucker, Premacular
Fibrosis, Epimacular Membrane.
EPIDEMIOLOGY
Beaver Dam Eye Study (Wisconsin, USA)
The Blue Mountains Eye Study (Sydney, Australia)
The prevalence of ERM in people aged 49 years or older
was reported to be 7-12%, with a 5 year incidence of 5.3%.
Idiopathic ERMs were bilateral in 20-31% of cases, and the
5-year incidence of second eye involvement was 13.5%
Age was a significant risk factor for ERM with the
prevalence peaking at 12% between the ages of 70–79
years, and ERMs being uncommon before the age of 60.
EPIDEMIOLOGY
Strong association of PVD with ERM formation.
Higher prevalence of ERM in older patients than in younger
population.
ERMs are uncommon in children and young adults in the
absence of predisposing conditions such as uveitis or trauma.
Both genders appear to be affected equally.
Higher prevalence of ERMs in patients by three years
following cataract surgery. The acceleration of PVD formation
by cataract surgery is considered the most likely contributing
factor.
PREVALENCE OF ERM IN SUBCONTINENT
CLASSIFICATION
Idiopathic ERM ( No identifiable etiology), 90-95% are
associated with PVD.
 Secondary ERM (Pre-existing/Co-existing ocular pathology e.g
uveitis, trauma, diabetic retinopathy, BRVO etc)
 Iatrogenic ERM (Occurs following a surgical or medical
intervention e.g cataract surgery, RD surgery)
PATHOGENESIS
ERM development has long been linked to the presence of
a PVD. PVD has been described in up to 95% of cases of
idiopathic ERM.
According to the classic hypothesis, tractional forces at the
vitreoretinal interface during a PVD cause breaks in the
internal limiting membrane (ILM) through which glial cells
from the inner layers of the retina migrate onto the retinal
surface leading to the formation of an ERM.
Glial cells(microglia, astrocytes, muller cells), retinal
pigment epithelium(RPE), and hyalocytes proliferate at the
vitreoretinal interface, along with secretion of extracellular
matrix cause formation of ERM.
These cells differentiate into fibroblasts and myofibroblasts
having contractile properties & lead to contraction of ERM.
Contraction of ERM causes distortion and thickening of the
retina, resulting in visual impairment.
OCULAR MANIFESTATIONS
Depend on the degree of opacification and the extent to
which an ERM has undergone shrinkage or contraction
causing distortion of retinal surface.
Cellophane Maculopathy
Macular Pucker
Advanced ERM
CELLOPHANE MACULOPATHY
Early ERM
Thin and translucent
Abnormal glistening reflex
Best detected using red-free filter
Mostly asymptomatic
MACULAR PUCKER
Membrane thickens and contracts
Inner retinal striae radiate from the edge of ERM
Cause folds in the retina and distortion of the macula
Mild traction on the retinal vessels
Metamorphopsia, blurred vision
ADVANCED ERM
Thicker , white fibrotic appearence
May obscure underlying structures
Severe distortion of blood vessels
Marked retinal wrinkling and striae formation
More severe degree of macular dysfunction
Significant visual loss, central photopsia,
binocular diplopia, macropsia
ASSOCIATED FINDINGS
ERMs may have associated findings of
 Cystoid macular edema,
Pre-retinal/ intraretinal hemorrhage,
Foveal ectopia,
Macular pseudohole or TRD
DIAGNOSIS
Clinical based on slit lamp examination,
with red-free light
Amsler Grid, shows distortion
Spectral domain OCT is a highly
sensitive and routine method used to
diagnose ERM
FFA sometimes indicated to find cause
of ERM e.g prior RVO
OCT FINDINGS
On OCT, ERM appears as a hyperreflective layer on the inner surface of the retina, usually adherent
across the retina.
The inner retina is thrown into folds, with thickening of the macula & associated cystoid spaces in
various retinal layers.
MANAGEMENT:
1. OBSERVATION
2. SURGERY
Observation
Majority of ERMs are non progressive, remain relatively stable and donot require surgery.
Keep the patient on observation with regular followups.
Educate the pts regarding signs and symptoms of progression and advise them to regularly
assess their monocular central vision for worsening VA, metamorphopsia or central scotoma.
Surgery
PROCEDURE: PPV AND PEELING OF ERM
INDICATIONS:
Significant visual loss
Intolerable Binocular diplopia
Severe metamorphopsia
GOAL OF TREATMENT:
To eliminate or reduce most common mechanisms of visual
loss including macular distortion, TRD and foveal ectopia
STEPS OF SURGERY
Initiate standard 3-port PPV
Induce PVD
Instill the dye for 30 sec - 1 min to stain ERM. (ICG, Trypan blue)
Place macular contact lens
Peel the ERM with intraocular microforceps
Remove the debris
Create tamponade ( fluid/air, gas/oil)
Remove cannulas/ports, suture if leakage.
Antibiotics/steroids post operatively
EPIRETINAL MEMBRANE SURGERY
PROGNOSIS
Main benefit is the elimination of metamorphopsia
More than 75% patients have improved visual acuity
 Atleast 2 lines
Predictors of better visual outcome
 Preoperative visual acuity bettern than 20/100
 Shorter duration of symptoms
 Absense of tractional retinal deatchment
Preoperative cystoid macular edema may be a poor prognostic sign
COMPLICATIONS
Progressive sclerotic catarct – most common – 60-70% in 2 years
Retinal breaks
Retinal Detachment
Phototoxicity
Dye toxicity
Endophthalmitis
Recurrence
THANKYOU

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Evaluation and management of epiretinal membranes

  • 1. Evaluation and Management of Epiretinal Membranes DR TEHREEM TANVEER
  • 2. DEFINITION An Epiretinal membrane (ERM) is a transparent, avascular, fibrocellular membrane on the inner retinal surface. It adheres to and covers the internal limiting membrane(ILM) of the retina and can produce varying degrees of retinal distortion. Cellophane Maculopathy, Macular Pucker, Premacular Fibrosis, Epimacular Membrane.
  • 3.
  • 4. EPIDEMIOLOGY Beaver Dam Eye Study (Wisconsin, USA) The Blue Mountains Eye Study (Sydney, Australia) The prevalence of ERM in people aged 49 years or older was reported to be 7-12%, with a 5 year incidence of 5.3%. Idiopathic ERMs were bilateral in 20-31% of cases, and the 5-year incidence of second eye involvement was 13.5% Age was a significant risk factor for ERM with the prevalence peaking at 12% between the ages of 70–79 years, and ERMs being uncommon before the age of 60.
  • 5. EPIDEMIOLOGY Strong association of PVD with ERM formation. Higher prevalence of ERM in older patients than in younger population. ERMs are uncommon in children and young adults in the absence of predisposing conditions such as uveitis or trauma. Both genders appear to be affected equally. Higher prevalence of ERMs in patients by three years following cataract surgery. The acceleration of PVD formation by cataract surgery is considered the most likely contributing factor.
  • 6. PREVALENCE OF ERM IN SUBCONTINENT
  • 7. CLASSIFICATION Idiopathic ERM ( No identifiable etiology), 90-95% are associated with PVD.  Secondary ERM (Pre-existing/Co-existing ocular pathology e.g uveitis, trauma, diabetic retinopathy, BRVO etc)  Iatrogenic ERM (Occurs following a surgical or medical intervention e.g cataract surgery, RD surgery)
  • 8.
  • 9. PATHOGENESIS ERM development has long been linked to the presence of a PVD. PVD has been described in up to 95% of cases of idiopathic ERM. According to the classic hypothesis, tractional forces at the vitreoretinal interface during a PVD cause breaks in the internal limiting membrane (ILM) through which glial cells from the inner layers of the retina migrate onto the retinal surface leading to the formation of an ERM.
  • 10. Glial cells(microglia, astrocytes, muller cells), retinal pigment epithelium(RPE), and hyalocytes proliferate at the vitreoretinal interface, along with secretion of extracellular matrix cause formation of ERM. These cells differentiate into fibroblasts and myofibroblasts having contractile properties & lead to contraction of ERM. Contraction of ERM causes distortion and thickening of the retina, resulting in visual impairment.
  • 11.
  • 12. OCULAR MANIFESTATIONS Depend on the degree of opacification and the extent to which an ERM has undergone shrinkage or contraction causing distortion of retinal surface. Cellophane Maculopathy Macular Pucker Advanced ERM
  • 13. CELLOPHANE MACULOPATHY Early ERM Thin and translucent Abnormal glistening reflex Best detected using red-free filter Mostly asymptomatic
  • 14. MACULAR PUCKER Membrane thickens and contracts Inner retinal striae radiate from the edge of ERM Cause folds in the retina and distortion of the macula Mild traction on the retinal vessels Metamorphopsia, blurred vision
  • 15. ADVANCED ERM Thicker , white fibrotic appearence May obscure underlying structures Severe distortion of blood vessels Marked retinal wrinkling and striae formation More severe degree of macular dysfunction Significant visual loss, central photopsia, binocular diplopia, macropsia
  • 16. ASSOCIATED FINDINGS ERMs may have associated findings of  Cystoid macular edema, Pre-retinal/ intraretinal hemorrhage, Foveal ectopia, Macular pseudohole or TRD
  • 17. DIAGNOSIS Clinical based on slit lamp examination, with red-free light Amsler Grid, shows distortion Spectral domain OCT is a highly sensitive and routine method used to diagnose ERM FFA sometimes indicated to find cause of ERM e.g prior RVO
  • 18. OCT FINDINGS On OCT, ERM appears as a hyperreflective layer on the inner surface of the retina, usually adherent across the retina. The inner retina is thrown into folds, with thickening of the macula & associated cystoid spaces in various retinal layers.
  • 19.
  • 21. Observation Majority of ERMs are non progressive, remain relatively stable and donot require surgery. Keep the patient on observation with regular followups. Educate the pts regarding signs and symptoms of progression and advise them to regularly assess their monocular central vision for worsening VA, metamorphopsia or central scotoma.
  • 22. Surgery PROCEDURE: PPV AND PEELING OF ERM INDICATIONS: Significant visual loss Intolerable Binocular diplopia Severe metamorphopsia GOAL OF TREATMENT: To eliminate or reduce most common mechanisms of visual loss including macular distortion, TRD and foveal ectopia
  • 23. STEPS OF SURGERY Initiate standard 3-port PPV Induce PVD Instill the dye for 30 sec - 1 min to stain ERM. (ICG, Trypan blue) Place macular contact lens Peel the ERM with intraocular microforceps Remove the debris Create tamponade ( fluid/air, gas/oil) Remove cannulas/ports, suture if leakage. Antibiotics/steroids post operatively
  • 25. PROGNOSIS Main benefit is the elimination of metamorphopsia More than 75% patients have improved visual acuity  Atleast 2 lines Predictors of better visual outcome  Preoperative visual acuity bettern than 20/100  Shorter duration of symptoms  Absense of tractional retinal deatchment Preoperative cystoid macular edema may be a poor prognostic sign
  • 26. COMPLICATIONS Progressive sclerotic catarct – most common – 60-70% in 2 years Retinal breaks Retinal Detachment Phototoxicity Dye toxicity Endophthalmitis Recurrence