Epiretinal Membranes


Gass classification of ERM

Grade 0: Cellophane Maculopathy-translucent with no distortion of retina; cellophane light reflex

Grade 1: Crinkled Cellophane Maculopathy-irregular retinal folds and light reflex, radiating retinal folds; visual acuity >20/40, ±metamorphopsia, insidious onset

Grade 2: Macular Pucker-grayish membrane; marked retinal crinkling and puckering of macula; PVD in 90%; may see edema, retinal heme, CWS, SRD, and leakage viewed by FA; VA 20/200 or less, insidious to sudden onset, usually with metamorphopsia

OCT classification of ERM (Fig. 10.1)

Typical membranes (tractional membranes): In OCT thin hyperreflective structure situated inner to the internal limiting membrane and visibly separated from it

Atypical membranes (dense membranes, thickened membranes, lamellar hole–associated epiretinal proliferation): in OCT hyperreflective line and moderately reflective structure filling the space between the line and retinal nerve fiber layer

Etiopathogenetic classification of ERM and non-full-thickness macular holes

Idiopathic (Figs. 10.5 and 10.6)

Secondary (vascular diseases, retinal detachment, age related macular degeneration) (Fig. 10.7)

Morphologic classification of non-full-thickness macular holes SD-OCT (Fig. 10.5)

Macular pseudoholes

Paralamellar macular holes

Pseudoholes with a lamellar defect

Lamellar macular holes


CWS cotton wool spot, ERM epiretinal membranes, FA fluorescein angiography, PVD posterior vitreous detachment, OCT optical coherence tomography, SRD serous retinal detachment, SD-OCT spectral domain optical coherence tomography, VA visual acuity



A370308_1_En_10_Fig1_HTML.gif


Fig. 10.1
(a) Typical: tractional epiretinal membrane (thin hyperreflective structure situated inner to the internal limiting membrane and visibly separated from it (arrow). (b) Atypical: dense epiretinal membrane (hyperreflective line and moderately reflective structure filling the space between the line and retinal nerve fiber layer [arrow])


In epiretinal membrane cases, we recently confirmed that a preoperative decrease in visual acuity is associated with progressing deformation of the plexiform layers (Fig. 10.2) [9]. Photoreceptor defects and central retinal thickness were also confirmed by many studies to be associated with visual acuity, but their progression during the follow up was not often observed.

A370308_1_En_10_Fig2_HTML.gif


Fig. 10.2
Epiretinal membranes in a 67-year-old woman. (a) Initial visit. Visual acuity is 1.0 Snellen. An epiretinal membrane is visible. Slight deformation of the outer plexiform layer in the form of hyperreflective striae is visible (arrow). (b) One year later. Visual acuity is 0.5 Snellen. No new photoreceptor defects were noted. The outer plexiform layer is wavy (arrow)

Epiretinal membranes may either precisely adhere to the inner retinal layers (Fig. 10.3a) or have many junction spots (Fig. 10.3b). It was proposed that in eyes in which there are many adhesion spots between the epiretinal membrane and retina, the epiretinal membrane may be easier to peel [10]. All data acquired with SD-OCT have been confirmed with Swept Source OCT (SS-OCT).

A370308_1_En_10_Fig3_HTML.gif


Fig. 10.3
(a) Epiretinal membrane with multiple adhesion spots to the retina (black stars) in a 68-year-old man. Visual acuity was 0.15. His final visual acuity one year after phacoemulsification combined with vitrectomy with epiretinal membranes removal and ILM peeling was 0.5. (b) Epiretinal membrane flat adhering to the retinal surface in a 72-year-old man. Visual acuity 0.1. His final visual acuity one year after phacoemulsification combined with vitrectomy with epiretinal membranes removal and ILM peeling was 0.3



10.2 Epiretinal Membranes Alter the Choroid


SS-OCT enables simultaneous visualization of the vitreous, retina, and choroid, and therefore may add a lot to our understanding of the pathomechanism of visual acuity loss associated with the epiretinal membrane.

Choroidal thickness has a very high intra-individual variability. It decreases in glaucoma or in nicotine abuse, and with age and refractive error [11]. It also depends on systemic vascular disease and caffeine or “energy drink” uptake. To make the measurements as reliable as possible, and thus useful for comparisons, they should be acquired at exactly the same time of the day. However, all choroidal thickness measurements should be evaluated very carefully. There is some primary data suggesting that choroidal thickness might slightly decrease three to 6 months after vitrectomy with ILM peeling for epiretinal membranes, which is not the case if vitrectomy is performed for other macular diseases [12]. The mechanism is not completely clear. It may be that choroidal thickness is slightly increased in the presence of epiretinal membranes and returns to normal values after surgery. It is not likely that vitrectomy causes choroidal thinning, as it was not confirmed for other diseases such as macular holes [13]. Thinning is not progressive, and was observed only three to 6 months after surgery. It must be considered, however, that those changes are very subtle.

A new finding observed with SS-OCT is that it is possible to visualize two lines at the choroidoscleral boundary, an upper, hyperreflective line and a lower, hyporeflective line. Together, the lines delineate the suprachoroidal layer (Fig. 10.4) [14]. The suprachoroidal layer is approximately 10–15 μm thick and is situated on the outer choroidoscleral boundary (CSB). It consists of five to ten layers of giant melanocytes interspersed between flattened processes of fibroblastic cells. As this layer was only recently recognized, little is known about its meaning. In idiopathic epiretinal membranes three factors were recognized, by multiple regression analysis, as being independently associated with the visibility of the suprachoroidal layer. First, this layer is more often visible in eyes with epiretinal membranes in which the outer plexiform layer forms waves on its outer surface, when compared to eyes with solely hyperreflective striae at the outer surface of the outer plexiform layer (Fig. 10.2). Second, it is associated with multiple adhesion points to the retina, and third, it correlates with central retinal thickness before surgery [13]. This might suggest that the suprachoroidal layer is more often visible in eyes with more prominent vitreoretinal traction and tangential traction between the epiretinal membrane and the retina.

A370308_1_En_10_Fig4_HTML.jpg


Fig. 10.4
Suprachoroidal layer (SCL) and suprachoroidal space (SCS) (enlarged box) visible in an eye with idiopathic epiretinal membrane


10.2.1 Epiretinal Membranes and Non-Full-Thickness Macular Holes


Since epiretinal membranes are reported to be present in most, if not in all, cases of non-full-thickness macular holes, they also need to be mentioned in this chapter [7, 15]. Before and early in the history of OCT two types of non-full-thickness macular holes were distinguished: macular pseudoholes (Fig. 10.5a) and lamellar macular holes (Fig. 10.6). Originally, lamellar macular holes were described by Gass, in 1975, as an abortive process of full-thickness macular hole-formation resulting from the de-roofing of cystoid macular edema, and macular pseudoholes were described as attributable to centripetal contraction of epiretinal membranes [16]. New developments in retinal imaging enabled a new classification to be proposed (Table 10.1).

Only gold members can continue reading. Log In or Register to continue

Stay updated, free articles. Join our Telegram channel

Oct 16, 2017 | Posted by in OPHTHALMOLOGY | Comments Off on Epiretinal Membranes

Full access? Get Clinical Tree

Get Clinical Tree app for offline access