Background
Epimacular membranes (EMMs) are collections of collagenous cells that occur on the inner surface of the central retina. These membranes have contractile properties and can lead to visual changes and metamorphopsia because of their effect on the underlying retina.
Very dense epimacular membrane with associated macular distortion. This ocular pathology was first described by Iwanoff in 1865, and it has been shown to be a relatively common entity, occurring in about 7% of the population. EMMs have been called a variety of names, including epiretinal membranes, cellophane maculopathy, preretinal macular gliosis, preretinal macular fibrosis, macular pucker, preretinal vitreous membranes, epiretinal astrocytic membranes, surface wrinkling maculopathy, internoretinal fibrosis, and silk-screen retinopathy; all of which pertain to clinico-anatomic descriptions of pathologic findings produced by EMMs of varying severity and differing morphologic characteristics.
EMMs can be associated with a variety of ocular conditions, such as posterior vitreous detachments (PVD), retinal tears, retinal detachments, retinal vascular occlusive diseases, ocular inflammatory diseases, and vitreous hemorrhage. However, a large proportion does not occur in the context of any associated disease or known history and therefore are classified as idiopathic epimacular membranes (IEMM). Idiopathic and postdetachment membranes are the most common EMMs and, as such, will be the focus of this article.
Pathophysiology
EMMs are avascular, fibrocellular membranes that proliferate on the surface of the retina and can lead to varying degrees of visual impairment. These cells, once in contact and attached to the retina, may proliferate and form sheets of membranes over the surface of the retina. Through their contractile properties, the underlying retina is, in turn, distorted. The effect on vision is variable and determined by the severity of the distortion, the location, and other secondary effects on the retina.
The source of the cells producing these membranes has been the source of great debate. Earlier reports proposed that glial cells (primarily fibrous astrocytes) from the inner layers of the neurosensory retina proliferated through breaks in the internal limiting membrane (ILM) produced after a retinal tear or a posterior vitreous detachment. Modern vitrectomy specimens have shown that epiretinal membranes comprise glial cells, retinal pigment epithelial cells, macrophages, fibrocytes, and collagen cells. These cells are found in varying proportions in accordance with the etiology of the membrane. Membranes associated with retinal breaks, previous retinal detachments, or cryopexy are composed mainly of dispersed RPE cells, while cells of glial origin predominate in the IEMM. Furthermore, these cells also possess the ability to change into cells with similar appearance and function.
The incidence of associated PVD in cases of IEMM range from 75-93%, and PVD is present in virtually all eyes with retinal breaks or retinal detachments and subsequent EMM formation. It has been suggested that PVD may contribute to EMM formation in many ways. PVD can lead to retinal breaks that may liberate RPE cells that initiate membrane formation. Small breaks in the ILM after PVD also may provide retinal astrocytes access to the vitreous cavity, where they may subsequently proliferate. Finally, vitreous hemorrhage, inflammation, or both associated with a PVD also may stimulate EMM formation.
EMM formation without PVD may predispose patients to vitreomacular traction syndrome (VMT). Chang et al evaluated patients with VMT using a spectral-domain ocular coherence tomography (SD-OCT) and ultrastructural correlation using samples obtained during surgery.[1] They were able to document fibrocellular proliferation between the inner surface of the retinal and posterior surface of the vitreous, resulting in increased vitreoretinal adhesion.[1]
Bovey and Uffer observed a phenomenon of ILM tearing associated with EMM.[2] They hypothesize that the presence of ILM tears and folds are more likely when the EMM forms prior to a posterior vitreous detachment, resulting in the subsequent cleavage plane being between the ILM and the inner retina rather than at the ILM surface.[2]
Epidemiology
Frequency
United States
The frequency at which EMMs occur varies according to the underlying disease. The idiopathic variety of EMMs has been shown to be present in up to 7% of the population. Bilateral cases have been seen in as much as 30% of the population.
Clinically significant EMMs occur in 3-8.5% of eyes after successful primary retinal detachment surgery. Patients noted to be at the greatest risk for EMMs are those with preoperative signs of proliferative vitreoretinopathy, including rolled retinal edges, star folds, and equatorial ridges.
One study noted no significant difference in the frequency of EMMs in eyes that underwent subretinal fluid drainage compared to those that had nondrainage procedures. The possible risk of epimacular development in eyes that have undergone cryotherapy or laser photocoagulation for retinal tears is difficult to quantify because it is almost impossible to determine whether the cellular dispersion was caused by the retinal tear itself or the subsequent therapy for it.
The incidence of EMM formation associated with other ocular pathologies, such as retinal vascular occlusive disease, ocular inflammation, or vitreous hemorrhage, is unknown.
Mortality/Morbidity
The visual loss depends on the severity of the distortion of the retina, the location of the wrinkling of the retina, and any other secondary effects of the membrane on the retina (eg, edema, hemorrhage).
Sex
Both sexes appear to be affected in relatively equal percentages.
Age
EMMs occur more frequently in the older population with postmortem studies showing 2% prevalence in individuals aged 50 years and as much as 20% prevalence in individuals aged 75 years.
Chang LK, Fine HF, Spaide RF, et al. Ultrastructural correlation of spectral-domain optical coherence tomographic findings in vitreomacular traction syndrome. Am J Ophthalmol. Jul 2008;146(1):121-7. [Medline].
Bovey EH, Uffer S. Tearing and folding of the retinal internal limiting membrane associated with macular epiretinal membrane. Retina. Mar 2008;28(3):433-40. [Medline].
Gupta P, Sadun AA, Sebag J. Multifocal retinal contraction in macular pucker analyzed by combined optical coherence tomography/scanning laser ophthalmoscopy. Retina. Mar 2008;28(3):447-52. [Medline].
Gupta OP, Ho AC, Kaiser PK, et al. Short-term outcomes of 23-gauge pars plana vitrectomy. Am J Ophthalmol. Aug 2008;146(2):193-197. [Medline].
Gupta OP, Weichel ED, Regillo CD, et al. Postoperative complications associated with 25-gauge pars plana vitrectomy. Ophthalmic Surg Lasers Imaging. Jul-Aug 2007;38(4):270-5. [Medline].
Charles S. Epimacular Membranes. In: Guyer DR, Yannuzzi LA, Chang S, et al. Retina-Vitreous-Macula. Vol 2. Philadelphia, Pa: WB Saunders Co; 1999:230-7.
Haritoglou C, Gandorfer A, Gass CA, et al. The effect of indocyanine-green on functional outcome of macular pucker surgery. Am J Ophthalmol. Mar 2003;135(3):328-37. [Medline].
Hillenkamp J, Saikia P, Herrmann WA, et al. Surgical removal of idiopathic epiretinal membrane with or without the assistance of indocyanine green: a randomised controlled clinical trial. Graefes Arch Clin Exp Ophthalmol. Jul 2007;245(7):973-9. [Medline].
Garweg JG, Bergstein D, Windisch B, et al. Recovery of visual field and acuity after removal of epiretinal and inner limiting membranes. Br J Ophthalmol. Feb 2008;92(2):220-4. [Medline].
Gass JDM. Macular dysfunction caused by epiretinal membrane contraction. In: Stereoscopic Atlas of Macular Diseases: Diagnosis and Treatment. Vol 2. 4th ed. St. Louis, Mo: Mosby; 1997:938-950.
Haritoglou C, Gandorfer A, Schaumberger M, et al. Trypan blue in macular pucker surgery: an evaluation of histology and functional outcome. Retina. Aug 2004;24(4):582-90. [Medline].
Marghero RR. Epiretinal macular membranes. In: Albert DM, Jakobiec FA, eds. Principles and Practice of Ophthalmology. Vol 2. Philadelphia, Pa: WB Saunders Co; 1994:919-925.
McDonald HR, Schatz H, Johnson RN. Introduction to epiretinal membranes. In: Ryan SJ, ed. Retina. Vol 2. 2nd ed. St. Louis, Mo: Mosby; 1994:1819-1825.
Russell SR, Crapotta JA. Macular epiretinal membranes. Ophthalmol Clin North Am. June 1993;6(2):239-45.
Sjaarda RN, Michels RG. Macular pucker. In: Ryan SJ, ed. Retina. Vol 3. 2nd ed. St. Louis, Mo: Mosby; 1994:2301-2312.
Ting FS, Kwok AK. Treatment of epiretinal membrane: an update. Hong Kong Med J. Dec 2005;11(6):496-502. [Medline].
Wong JG, Sachdev N, Beaumont PE, et al. Visual outcomes following vitrectomy and peeling of epiretinal membrane. Clin Experiment Ophthalmol. Aug 2005;33(4):373-8. [Medline].
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