Epiretinal Membrane

Overview

Epiretinal membrane (ERM) is a fibrocellular, semi-translucent membrane that proliferates on the inner surface of the retina, most commonly over the macula. Most ERMs are idiopathic and related to posterior vitreous detachment, though they can also be secondary to other retinal conditions. Contraction of the membrane exerts tangential traction on the underlying retina, causing macular distortion.

Epidemiology & Risk Factors

Idiopathic ERM is strongly age-related, becoming increasingly common with advancing age, and is closely linked to posterior vitreous detachment (PVD), during which microscopic defects in the internal limiting membrane allow glial cells to migrate onto the retinal surface and proliferate.¹ Secondary ERM can occur in association with retinal vascular disease (diabetic retinopathy, retinal vein occlusion), uveitis, prior retinal detachment or its repair, and retinal breaks.

Pathophysiology

Following PVD, glial cells (astrocytes and Müller cells) migrate through small defects in the internal limiting membrane onto the retinal surface, where they proliferate and acquire contractile, myofibroblast-like properties. As the membrane contracts, it produces tangential traction on the retina, leading to retinal wrinkling, thickening, and distortion of the normal foveal contour. A related but distinct entity, lamellar hole-associated epiretinal proliferation (LHEP), arises in association with lamellar macular holes and has a different, thicker, less contractile tissue composition than classic ERM, with correspondingly different surgical implications.²

Clinical Presentation

Many patients with mild ERM are asymptomatic, with the membrane discovered incidentally on routine fundus exam or OCT. Symptomatic patients typically report metamorphopsia (visual distortion, such as straight lines appearing wavy), decreased visual acuity, and sometimes monocular diplopia or difficulty with stereopsis, all related to the degree of foveal traction and distortion.

Exam Findings

• A glistening, cellophane-like sheen on the retinal surface on fundus exam, in mild cases
• Retinal striae radiating from the membrane, and in more advanced cases, macular pucker with visible retinal wrinkling and vascular tortuosity
• Thickened, distorted foveal contour on OCT, the most sensitive tool for detecting and staging ERM severity
• Pseudohole appearance in advanced cases, mimicking a macular hole but without a true full-thickness retinal defect
• On OCT, findings suggestive of LHEP (a thicker, non-contractile band-like structure) should be distinguished from classic ERM given differing prognosis and surgical technique²

Differential Diagnosis

• Macular hole (distinguished by OCT showing a full-thickness retinal defect rather than a surface membrane)
• Vitreomacular traction (partial vitreous separation causing distortion without a true proliferative membrane)
• Lamellar hole-associated epiretinal proliferation (a related but histologically and prognostically distinct entity)²
• Cystoid macular edema from other causes (diabetic, post-surgical, uveitic), which can coexist with or mimic some visual symptoms of ERM

Management

Diagnosis and staging rely primarily on OCT, which demonstrates the membrane, its effect on foveal contour, and associated retinal thickening. Most idiopathic ERMs are mild, stable, and minimally symptomatic, and can be safely observed with periodic monitoring, since progression is variable and many cases remain stable for years.¹

Surgery — pars plana vitrectomy with epiretinal membrane peeling, usually combined with internal limiting membrane peeling to reduce recurrence — is reserved for eyes with visually significant metamorphopsia, progressive vision loss, or substantial macular distortion. Timing of surgical referral should balance visual symptom severity against surgical risk, since outcomes tend to be better when surgery is performed before longstanding, severe distortion becomes established.¹ In LHEP specifically, surgical decision-making may differ from classic ERM given its distinct tissue characteristics and the frequent presence of an underlying lamellar hole.²

Complications

• Progressive metamorphopsia and vision loss if left untreated in visually significant cases
• Recurrence of the membrane after surgical peeling, more common when internal limiting membrane peeling is not performed concurrently
• Cystoid macular edema secondary to chronic traction
• Development of a secondary full-thickness macular hole in eyes with severe traction (uncommon but recognized)

Clinical Pearls

• Idiopathic ERM is strongly linked to posterior vitreous detachment — glial cell migration through internal limiting membrane defects during PVD is the presumed mechanism¹
• Most ERMs are mild and stable; observation is appropriate for asymptomatic or minimally symptomatic cases
• OCT is the key tool for diagnosis, staging, and surgical decision-making
• Earlier surgical intervention in visually significant, progressive cases tends to produce better outcomes than waiting until distortion is longstanding and severe¹
• Distinguish LHEP from classic ERM on OCT, since it has different tissue characteristics and treatment considerations²

Common Pitfalls

• Recommending surgery for asymptomatic or minimally symptomatic ERM without appropriate observation first
• Misdiagnosing a pseudohole (from advanced ERM) as a true macular hole, leading to inappropriate management
• Omitting internal limiting membrane peeling during surgery, increasing recurrence risk
• Failing to distinguish LHEP from classic ERM on OCT, potentially leading to a surgical approach mismatched to the underlying pathology
• Delaying referral until distortion is longstanding and severe, when earlier intervention may have produced better visual outcomes