Epimacular membranes and vitreomacular traction syndromes

Published on 08/03/2015 by admin

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CHAPTER 65 Epimacular membranes and vitreomacular traction syndromes

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Epimacular membranes represent avascular cellular layers which grow on the retinal surface in the area of the macula. Due to transformation of the cells these membranes can be associated with more or less severe tractional forces to the underlying neurosensory retina. Depending on the severity of the diseases this may result in either a wrinkling of only the inner retinal layers, a distortion of all retinal layers, or even a localised tractional retinal detachment. In typical epimacular membranes the vitreous is already detached in most cases. However, in some patients a contraction of the posterior vitreous cortex with strong adherences in the area of the macula can be observed. This condition is referred to as vitreomacular traction syndrome.

Epidemiologic considerations and terminology

Idiopathic, primary epimacular membranes are a quite common finding, especially in elder people. The prevalence ranges between 2 and 20% in patients aged 70–80 years1. It is hypothesized that this type of epimacular membrane is the result of glial cell migration and proliferation through small breaks of the internal limiting membrane (ILM), which represent a sequelae of posterior vitreous detachment2. Other, secondary, pathomechanisms include retinal breaks, laser coagulation or cryotherapy of the retina, inflammation, and vascular diseases3. An association with macular holes has been described4.

A variety of names are used to describe this entity, mainly based on the heterogeneous clinical appearance: cellophane maculopathy, surface wrinkling retinopathy, macular pucker, or premacular gliosis. However, there is no standardized nomenclature and therefore the term epimacular membrane is used, as it covers all types of epiretinal proliferations over the macula.

Clinical features, diagnosis, and differential diagnoses

The diagnosis of epimacular membranes can be very well established using clinical examination techniques such as slit-lamp biomicroscopy with a 78 or 90 diopter lens to assess the macula. As mentioned above, the clinical features and findings can vary considerably and are dependent on the extent of the epimacular proliferation. Using biomicroscopy one may see a translucent, glistening reflex over the macula, wrinkles of the retinal surface potentially associated with a distortion of the adjacent vasculature in more pronounced cases of traction, or even an opaque sheet of tissue covering the retinal surface associated with full-thickness retinal folds and localized tractional retinal detachment (Fig. 65.1). The contraction of such membranes forming a macular pseudohole may be misinterpreted as a full-thickness macular hole in some cases. Secondary tissue alterations are the result of tractional forces and include macular edema, which can also be noted during fluorescein angiography, and small retinal hemorrhages.

New and high resolution imaging techniques such as optical coherence tomography (OCT) allow for a better insight into the morphological retinal changes due to localized tractional forces and the interaction of the vitreous with the retinal surface in this disease. OCT can be of great value to detect anomalous posterior vitreous detachment (PVD) such as vitreoschisis before surgery and differentiate epimacular membranes from vitreomacular traction syndromes. The latter is sometimes difficult to diagnose by using biomicroscopy alone.

Anatomical considerations

The most common cellular components of epimacular membranes are fibrous astrocytes, retinal pigment epithelial cells, fibrocytes, myofibroblasts, and macrophages. Myofibroblasts were also identified as the predominant cell type in vitreomacular traction syndrome5. The predominance of myofibroblasts may help to explain the high prevalence of cystoid macular edema and progressive vitreomacular traction characteristic of this disorder. Müller cells may also play a relevant role. A very important aspect of the pathogenesis of epimacular membranes is the anomalous PVD or splitting of the vitreous cortex (vitreoschisis) where collagen fibers are left adherent to the inner surface of the retina. These collagen fibers serve as a scaffold for cellular proliferations. Histological studies revealed that the cellular layers, which may vary from single cells to single sheet or multi-sheet layers, may grow either directly on the ILM or on a collagen layer being interspersed between the ILM and the cellular proliferation6 (Fig. 65.2). Similar observations were made in patients with vitreomacular traction syndrome5, where two distinct clinicopathologic features were identified suggesting different forms of epiretinal fibrocellular proliferation, with epiretinal membranes being interposed in native vitreous collagen and single cells or a cellular monolayer proliferating directly on the ILM. These histological findings have implications for surgery, as in one type the vitreoretinal surgeon will remove fragments of the ILM along with the epiretinal proliferation in many cases, whereas in the other type the epiretinal proliferation will be removed without the ILM, as the plane of dissection is within the collagen layer. As a consequence, parts of the collagen fibers and the ILM will remain in place. The surgeon needs to consider that in the first type only one membrane is to be removed, whereas in the second type two are to be removed.

These findings also indicate the important role of the ILM in the treatment of epimacular membranes. The understanding of the clinical relevance of the ILM for macular surgery emerged in the 1980s, when histopathological examinations of removed epiretinal membranes disclosed fragments of the ILM to be a common feature of these membranes and no functional deficits were noted in these patients7,8. It took years to transfer these findings into clinical consequences. The topic of intentional ILM removal returned to the focus of attention following the presentation of the Gass’ classification of macular holes coinciding with the first report on successful vitrectomy for macular hole closure by Kelly and Wendel in 19919,10. Intentional ILM removal was then first described by Morris et al. in patients with Terson syndrome where ILM peeling led to excellent functional results even in the long term; as a consequence, ILM peeling was then suggested for other ‘traction maculopathies’11.

Indications for surgery

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