Clinicians and retinal specialists owe great debt to OCT for transforming understanding of CME

Clinicians and retinal specialists owe  great debt to OCT for  transforming understanding of CME
Arthur Cummings
Published: Thursday, September 17, 2015

Clinicians and retinal specialists owe a great debt to optical coherence tomography (OCT) for completely transforming our understanding of cystoid macular oedema (CME) and other pathologies of the macula, said Alain Gaudric MD, who delivered this year’s EURETINA Lecture.

Dr Gaudric, Professor and Chairman of the Department of Ophthalmology, at the Lariboisiere Hospital, University of Paris 7 Denis Diderot, France, told delegates that OCT has definitively changed the diagnosis paradigm of CME.

“Thanks to OCT we know that CME is not limited to the blood retinal barrier (BRB) breakdown, as was once believed, but includes a broad range of cystoid maculopathies including retinal vein occlusion, chronic central serous choroidopathy, epiretinal membrane, vitreomacular traction and bestrophinopathy, among others,” he said.

OCT has enhanced our understanding of cystoid macular changes at many different levels, said Dr Gaudric.

“Because of OCT we know that leakage is not always associated with macular thickening, that CME is not always associated with leakage and that cystoid cavities are associated with variable retinal tissue loss. Furthermore, cystoid changes are not always associated with macular thickening, nor is leakage always associated with macular thickening,” he said.

It is now well known that leakage may occur without resulting in CME, and therefore, although the BRB breakdown may be necessary, it is not sufficient to cause CME, noted Dr Gaudric.

“On the other hand, when faced with a typical CME, it is not always easy to tell which is due to a BRB breakdown and which is not, and what is its etiology,” he said.

While an oedema is usually defined as an abnormal accumulation of fluid in the interstitium, this definition does not exactly apply to the retina because the retina is usually devoid of interstitial fluid compartments, explained Dr Gaudric.

“The retinal tissue is protected by a BRB at the vascular endothelium and at the retinal pigment epithelium. Once the BRB is impaired, fluid may accumulate within the retina, and is subject to Starling's law. However, even in normal conditions and intact BRB, there is a permanent transport of water through the retina, from the vitreous to the choroid, and it is well known that Muller cells play a major role in this transport, as well as the active pump of the RPE,” he said.

The history of CME is closely linked to BRB studies and to the advent of fluorescein angiography at the end of the 1960s, said Dr Gaudric.

“For years CME has been synonymous with dye pooling in cystoid spaces on late phase angiograms. At the end of the 1980s, however, we saw the first attempts to correlate macular thickness with visual acuity using a retinal thickness analyser,” he said.

This eventually paved the way for OCT imaging technology in the mid-1990s, which made it possible to routinely measure macular thickness.

“It is noteworthy that the quantitative assessment of macular oedema was the subject of the first publication on the use of OCT in macular oedema,” Dr Gaudric added.

In the future, treatment strategies will probably be oriented towards earlier treatment of chronic CME acting on the restoration of the BRB, but possibly also on the restoration of Muller cell function and cell-to-cell adherence, concluded Dr Gaudric.

 

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