Epiretinal Membrane

The internal limiting membrane is the innermost retinal layer, forming the interface between the retina and vitreous. Normally this surface is smooth and unobstructed. Epiretinal membrane (ERM) is a fibrocellular, semi-translucent membrane that proliferates on this inner retinal surface, most often over the macula, most commonly as an idiopathic, age-related process linked to posterior vitreous detachment.

Following PVD, glial cells (astrocytes and Müller cells) migrate through small internal limiting membrane defects onto the retinal surface, proliferate, and acquire contractile, myofibroblast-like properties.¹ Membrane contraction produces tangential traction, causing retinal wrinkling, thickening, and distorted foveal contour. Lamellar hole-associated epiretinal proliferation (LHEP) is a related but distinct entity with thicker, less contractile tissue and different surgical implications.²

Mild ERM is often asymptomatic, found incidentally. Symptomatic patients report metamorphopsia, decreased visual acuity, and sometimes monocular diplopia, related to the degree of foveal traction.

Key differentials: macular hole (full-thickness defect on OCT, not a surface membrane), vitreomacular traction (partial separation without a true proliferative membrane), LHEP (distinct tissue and prognosis)², and cystoid macular edema from other causes that can coexist with or mimic ERM symptoms.

OCT is the key diagnostic and staging tool, demonstrating the membrane, its effect on foveal contour, and associated retinal thickening. OCT also distinguishes classic ERM from LHEP, which appears as a thicker, non-contractile, band-like structure with different treatment considerations.²

Most idiopathic ERMs are mild, stable, and minimally symptomatic, and can be safely observed with periodic monitoring, since progression is variable.¹ Surgery — pars plana vitrectomy with ERM peeling, usually combined with internal limiting membrane peeling to reduce recurrence — is reserved for visually significant metamorphopsia, progressive vision loss, or substantial distortion. Outcomes tend to be better when surgery is performed before longstanding, severe distortion becomes established.¹ Surgical decision-making in LHEP may differ from classic ERM given its distinct tissue characteristics.²

• Idiopathic ERM is strongly linked to PVD via glial cell migration through ILM defects¹
• Most ERMs are mild and stable; observation is appropriate for asymptomatic cases
• OCT is central to diagnosis, staging, and surgical decision-making
• Earlier surgery in visually significant, progressive cases tends to produce better outcomes than waiting¹
• Common pitfall: recommending surgery for asymptomatic ERM without observation first
• Common pitfall: misdiagnosing an ERM pseudohole as a true macular hole