**4. Macular edema**

Macular edema is the main pathologic feature of diabetic maculopathy. According to ETDRS, it is defined as any detectable retinal thickening due to fluid accumulation. It may be localized in a sector of the macular region (focal) or it may be diffused. Persistent macular edema leads to the necrosis of Muller cells with subsequent formation of cystoid cavities localized mainly in the outer retinal layers (Henle's fiber, external plexiform) and sometimes in the inner plexiform layer too. In more advanced stages, the cavities may coalesce centrally forming a large hyporeflective cavity that accounts for the significant increase of foveal thickness. By consequence, beside increase of macular thickness (which is the most important OCT sign) in DME appear: large intraretinal spaces of reduced reflectivity, loss of the normal layered retinal structure and flattening of the central foveal depression. Sometimes fluid can be seen under the neurosensory retina. Hard exudates and hemorrhages are typical landmarks for DR and they appear on OCT images as small hyperreflective deposits with posterior shadowing [6].

The cysts that develop in the retina during DME vary in size. According to their size, a classification of cystoid edema was proposed by Koleva-Georgieva into mild, moderate and severe. In mild edema, cysts are small and predominantly located in the outer retinal layers. In the intermediate and severe forms, cysts are located in the outer layers, especially in the fovea. If cysts continue to increase, they occupy the whole thickness of the retina, leading to macular atrophy and profound visual loss. In mild edema, the cysts have a horizontal diameter below 300 μm, in intermediate edema the horizontal diameter of the cysts is between 300 and 600 μm and in the severe one the horizontal diameter of the cysts is above 600 μm or large confluent cavities with retinoschisis appearance are identified [6–8].

It has been shown that the status of the outer retinal layers is important for the visual outcome in patients with DME. Yohannan et al. proved that disruption of the IS/OS junction correlates well with a significant decrease of point sensitivity in patients with DME. Also, the integrity of ELM and IS/OS junctions correlates positively with visual acuity. Therefore, OCT evaluation of the outer retinal layers in patients with DME is important in predicting visual outcome [6].

Vitreo-retinal interface is very important in diabetic patients. It is known that diabetics have higher than normal vitreo-retinal adherence and that vitreo-macular traction is one of the factors explaining DME. OCT identifies various aspects: incomplete posterior vitreous detachment (PVD), epiretinal membranes (ERM) [6, 7]. OCT identifies vitreo-macular interface disorders from the preclinical stage. If posterior hyaloid is thin and partly detached from the macula, this aspect cannot be seen on biomicroscopy, but it is easily detectable on OCT. The same is true regarding the thin ERM. Thus, OCT is a very useful tool that establishes the best therapeutic option in these cases: vitrectomy with release of vitreo-macular traction/dissection of ERM, from the early stages, when the chances for a good functional outcome are the highest. Assessment of vitreo-macular interface is an important step in evaluating diabetic patients. Not only does OCT indicate the moment for vitrectomy in these patients, but it also monitors the postoperative morphological outcomes: favorable evolution (decrease of macular thickness), development of ERM or of lamellar macular hole [6].

distance between the vitreo-retinal interface and the anterior surface of the RPE is generally comprised between 200 and 275 μm; the foveal depression ranges from 170 to 190 μm and the

Macular edema is the main pathologic feature of diabetic maculopathy. According to ETDRS, it is defined as any detectable retinal thickening due to fluid accumulation. It may be localized in a sector of the macular region (focal) or it may be diffused. Persistent macular edema leads to the necrosis of Muller cells with subsequent formation of cystoid cavities localized mainly in the outer retinal layers (Henle's fiber, external plexiform) and sometimes in the inner plexiform layer too. In more advanced stages, the cavities may coalesce centrally forming a large hyporeflective cavity that accounts for the significant increase of foveal thickness. By consequence, beside increase of macular thickness (which is the most important OCT sign) in DME appear: large intraretinal spaces of reduced reflectivity, loss of the normal layered retinal structure and flattening of the central foveal depression. Sometimes fluid can be seen under the neurosensory retina. Hard exudates and hemorrhages are typical landmarks for DR and they appear on OCT images as small hyperreflective deposits with

The cysts that develop in the retina during DME vary in size. According to their size, a classification of cystoid edema was proposed by Koleva-Georgieva into mild, moderate and severe. In mild edema, cysts are small and predominantly located in the outer retinal layers. In the intermediate and severe forms, cysts are located in the outer layers, especially in the fovea. If cysts continue to increase, they occupy the whole thickness of the retina, leading to macular atrophy and profound visual loss. In mild edema, the cysts have a horizontal diameter below 300 μm, in intermediate edema the horizontal diameter of the cysts is between 300 and 600 μm and in the severe one the horizontal diameter of the cysts is above 600 μm or large

It has been shown that the status of the outer retinal layers is important for the visual outcome in patients with DME. Yohannan et al. proved that disruption of the IS/OS junction correlates well with a significant decrease of point sensitivity in patients with DME. Also, the integrity of ELM and IS/OS junctions correlates positively with visual acuity. Therefore, OCT evaluation of the outer retinal layers in patients with DME is important in predicting

Vitreo-retinal interface is very important in diabetic patients. It is known that diabetics have higher than normal vitreo-retinal adherence and that vitreo-macular traction is one of the factors explaining DME. OCT identifies various aspects: incomplete posterior vitreous detachment (PVD), epiretinal membranes (ERM) [6, 7]. OCT identifies vitreo-macular interface disorders from the preclinical stage. If posterior hyaloid is thin and partly detached from the macula, this aspect cannot be seen on biomicroscopy, but it is easily detectable on OCT. The same is true regarding the thin ERM. Thus, OCT is a very useful tool that establishes the best

confluent cavities with retinoschisis appearance are identified [6–8].

thickness of the peripheral retina is between 220 and 280 μm [5].

**4. Macular edema**

44 OCT - Applications in Ophthalmology

posterior shadowing [6].

visual outcome [6].

The detached posterior vitreous face appears on OCT scans as a thin horizontal or oblique line with low/medium reflectivity in the nonreflective vitreous, above or inserting into the retina. If PVD is incomplete, it may adhere to the foveal or peripapillary region. ERM appears on OCT as a hyperreflective line on the surface of the retina. Its presence leads to retinal modifications: increase of macular thickness, loss of foveal depression, formation of intraretinal cysts and pseudoholes. The difference between PVD and ERM is made according to their reflectivity (low in PVD, high in ERM). OCT provides other details related to ERM (degree of opacity, thickness, and distance from the macula) and to its effects on the underlying retina: distortion, edema, neurosensory detachment [6].

OCT is a very reliable and reproducible method to assess and monitor macular thickness following various treatments for DME: intravitreal injections with anti-VEGF and steroids, laser photocoagulation, vitrectomy. OCT also identifies macular atrophy which explains functional failure despite resolution of edema. Monitoring patients with DME must include two major parameters: functional (visual acuity) and anatomical (OCT) [5, 6].

Cystoid macular edema (CME) appears like large ovoid spaces of low reflectivity separated by hyperreflective septae that represent intraretinal cystoid-like cavities. Posterior hyaloid traction (PHT) appears like a highly reflective band on the surface of the retina. Serous retinal detachment (SRD) appears as a dark accumulation of subretinal fluid beneath the high reflective and dome-like elevation of detached retina. The highly reflective band which represents the outer surface of the retina helps differentiating subretinal fluid from the intraretinal fluid. Tractional retinal detachment (TRD) is identified as the area of low signal underlying the highly reflective border of detached retina. It often takes the appearance of a pick-shaped configuration [5, 6].

The most common finding in diabetics is diffuse retinal thickening (DRT) [6].

There is a correlation between macular thickness and visual acuity in patients with DME. The OCT pattern that was associated with worse visual outcome is CME [6].

In DME OCT technology has significant impact at various levels: it elucidates the pathogenic mechanisms of DME; it has a major contribution in identifying hyaloid-macular traction; it identifies the subclinical DME allowing early treatment; it makes it possible to correlate macular thickness with visual acuity; it monitors the evolution of DME following treatment [5–7].
