Ординатура / Офтальмология / Английские материалы / Retinal and Vitreoretinal Diseases and Surgery_Boyd, Cortez, Sabates_2010

Different etiologies of ERM may also show as different patterns in OCT, as has been recently shown by Mori et al. Secondary ERM are more likely to be characterized by focal retinal adhesion than are primary ERM, which tend to be globally adherent.(29)

The exact composition of the extracellular matrix and the pathogenesis of ERM may be different and dependent upon the etiology of the membrane. The presence of collagens, type I-IV, laminin, and fibronectin have been shown by means of immunofluorescence techniques.(30) Glial cells and newly formed collagen may play an important role in ERM and macular hole formation as well as in the healing of the retinal defects. Indeed, pars plana vitrectomy with peeling of an ERM, and/or the ILM may induce direct glial cell proliferation and migration.(31)

The role of posterior vitreous detachment (PVD) in the genesis of ERM is not clear. PVD is observed in 80-95% of the cases of ERM. It has been postulated that ERM may be the result of anomalous PVD with vitreoschisis, leaving the outermost layer of posterior vitreous cortex attached to the macula.(32) The adherent posterior vitreous may play an inhibiting role on the cellular proliferation. The possibility that the traction temporarily exerted by the partially detached posterior hyaloid may stimulate the migration and proliferation of glial cells over the retinal surface has been suggested. It has been considered that remnants of vitreous cortex may remain adhered to the surface of retina once the PVD has been completed giving rise to a cellular proliferation leading to the appearance of the ERM.(33)

Multiple pathological studies have been carried out about the composition of ERM. Most of these works agree that the cells forming the ERM have a retinal origin, most probably from the glia. However, the origin of these cells remains controversial.(34) More recent works have identified cells from the retinal pigment epithelium (RPE),(35) fibroblasts,(36) hyalocytes,(37) and pericytes.(38)

Natural History

VA usually stabilizes after ERM formation and only 10% to 25% of patients lose one or two lines of vision when followed for a 2-year period.(39,40) Most of the ERM usually remain unchanged after an initial period of growth. Occasionally, idiopathic ERM may induce slow and progressive vision loss throughout the years. If the vision goes worse the occurrence of other ocular diseases, such as cataracts or age macular degeneration, should be considered.

PVD is reported in up to 90% of the patients with idiopathic ERM.(39,41) However, PVD does not seem to be a prerequisite for the appearance of ERM, and VA may be poorer and the risk of cystoid macular oedema be higher in eyes with posterior vitreomacular traction than in eyes with PVD.

ERM have been reported to resolve spontaneously, especially among younger patients in association with PVD.(42-47) This finding is more frequent among eyes with incomplete PVD when the vitreous becomes completely detached, though it may also occur in eyes with previous complete PVD.(48)

ERM may also be associated with RPE defects either as a consequence of the ERM or related to the primary cause of the ERM, such as intraocular inflammation, retinal detachment, trauma or surgery. RPE defects are considered to be related to a poorer visual outcome.

Clinical Findings

Most of the patients do not present symptoms and may have a normal vision. Symptomatic cases may present a variable amount of visual involvement, from mild metamorphopsia in the early stages to a marked decrease of VA in well advanced cases. The onset of symptoms may be slow and hardly noticeable in some patients, yet many are acutely aware of a change in vision. Central diplopia, photopsia and macropsia can appear, as well as blurred vision, distortion, diplopia, and even profound central visual loss.

VA among patients with ERM is 20/70 or better in most of the cases.(49) and less than 5% have vision worse than 20/200.

The diagnosis of ERM is based on clinical findings (Figures 1 and 2). Bio microscopically it is characterised by an increased brightness on the ILM which does not affect the course of the retinal vessels in the early stages, and is better appreciated by contact bio microscopy. The limits of these cellophane membranes are usually poorly defined. The contraction of the ERM may cause tiny folds on the ILM or the retina following a radial pattern. In more advanced cases it may show a white-

gray membrane distorting the retinal vessels with dilated veins and eventually macular oedema. As in other conditions affecting the vitreo-retinal interface, bio microscopy may not completely show the adherence of the posterior hyaloid to the retina.

The amount of retinal involvement may be better appreciated by fluorescein angiography (FA) which reveals vascular distortion and an increased vascular permeability caused by the traction exerted by the ERM giving rise to a macular oedema (Figure 2). The presence of retinal vascular tortuosity and tethering is useful in assessing the extent of retinal wrinkling caused by the membrane. Foveal ectopia causing diplopia can be appreciated as a distortion of the perifoveal capillary net.

Multiple small round haemorrhages may appear on the inner retina which may be associated with microaneurysms and irregular dilation of the retinal capillaries and cotton wool spots caused by blockade of axoplasmic flow. In these cases stretching of the inner retina seems to play a role in the retinal distortion.(50)

Occasionally, and more frequently following retinal detachment surgery ERM may be opaque and thick creating dense retinal folds which may detach the fovea from the RPE and induce xantophyll pigment migration, markedly reducing central VA. In other cases contraction of ERM and ILM in the perifoveal area may increase the foveal depression which will appear darker and surrounded by a greyish tissue looking like a macular hole.

B scan may show the presence of macular thickening in those more advanced cases of ERM exerting greater traction on the macula. Perrenaud et al reported identification of ERM and condition of the posterior hyaloid using B scan and compared it with OCT. Preoperative ultrasonography allowed an excellent evaluation of both the peripheral and the posterior vitreous and showed the membrane, permitting visualization of the retinal thickening and the retinal folds. Fol-

lowing surgery, both methods were able to detect membrane remnants. Furthermore, B scan is the only imaging procedure that can be useful when the ocular media are not transparent and allows an excellent global analysis of the anterior and posterior vitreous, which is very useful for the surgeon.(51)

OCT is probably the most useful diagnostic tool to identify ERM (Figures 3-5). ERM visualization improves when a flat detachment

from the retinal surface with focal points of attachment is present, which is estimated to occur in up to 30% of the patients.(52) According to this series, ERM was undetectable on OCT in 12/186 eyes. Mean central macular thickness measured with OCT correlates well with VA. Quantitative measurements and the assessment of membrane adherence with OCT may be useful in characterizing the surgical prognosis of eyes with ERM.

Posterior hyaloid appears in OCT as a reflective membrane somewhat similar to ERM, though some differences exist:

-ERM is thicker than the posterior hyaloid.

-ERM presents a higher and more homogeneous hyper reflectivity, whereas posterior hyaloid usually shows hyper reflective areas.

-Posterior hyaloid is usually more detached from the retina than the ERM.

Treatment

The aim of vitreoretinal surgery is to remove ERM causing significant vision loss. The indications for surgery may vary individually but it is usually reserved for those cases in which VA has decreased at the level of 20/60.(53-56) Occasionally, patients with VA 20/50 or better may undergo surgery when incapacitating metamorphopsia or monocular

diplopia occur or the patient requires VA improvement to continue working.

The usual procedure for ERM is threeport 20G vitrectomy which is presently being replaced by 25G and 23 G procedures under peribulbar (more rarely, topical) anaesthesia with sedation (Figures 6-7).

Following central core vitrectomy, a posterior hyaloid detachment is induced by aspiration of the posterior hyaloid in the area surrounding the optic disk with an extrusion cannula or the vitrectomy probe. Triamcinolone acetonide has been used to aid in the complete dissection of the posterior hyaloid.(57-60)

In order to facilitate the visualization and removal of ERM, different vital dyes have been used. There is a consensus that the application of vital dyes facilitates the delicate removal of intraocular membranes during vitreoretinal surgery. Controversy still remains around various issues, mainly concentration and potential toxicity and safety.

Due to its availability, indocyanine green (ICG) was the first dye used. Burk performed ILM stain in cadaveric eyes using a 0.5% ICG solution injected into the posterior vitreous cavity over the macula, allowing the dye to settle for 5 minutes and removing it by mechanical aspiration. Bright green staining of the ILM resulted from this procedure which greatly facilitated ILM peeling by improving direct visualization of the membrane.(61)