Focal Macular Edema Research Articles

Morphofunctional changes of macular area in diabetic macular edema

Abstract Purpose To investigate the electrogenesis in the L‐ and S‐cone system of the retina and their role in diagnosis of focal and diffuse macular edema (ME) in diabetic retinopathy (DR). Methods 30 patients with diabetes mellitus type II were tested. All patients had ME: focal – 24 eyes, diffuse – 21. ISCEV Standard electroretinography (ERG) tests and additional chromatic macular ERG (M‐ERG) were used. Psychophysical test was presented by screening a topography of contrast and color sensitivity of the cone system. OCT was used to confirm macular edema that was found ophthalmoscopically. Results In focal and diffuse ME a similar decrease of amplitude (?=6 mv; norm M=18 mv) and prolonged latency of b‐wave (M=58 ms; norm M=54 ms) to red stimuli were registered. M‐ERG to blue stimuli was subnormal in all cases: b‐wave amplitude in focal ME was M=23 mv, in diffuse M=26 mv (norm ?=62 mv). The b‐wave latency of M‐ERG to blue (norm ?=62 mv) was prolonged mostly in focal (M=80 ms) than in diffuse ME (M=76 ms). Campimetry for color sensitivity to red and blue stimuli revealed significant changes in all patients, dark channels affected earlier than light. Conclusion In focal and diffuse ME similar changes of chromatic M‐ERG to red and blue stimuli are an evidence of cone function suppression. Prolonged b‐wave latency is due to excitation delay from photoreceptors to ganglion cells as a result of neuronal damage. Decreased sensitivity of dark and light channels with dominant localization of pathological process in macular area were found. The functionally revealed changes in focal ME may reflect the extensiveness and prevalence of retinal damage unlike the clinical picture.

Non surgical approach in diabetic macular edema : the future ?

Abstract Purpose To present the different non surgical therapeutical options of diabetic macular edema Methods The pathogenesis of diabetic macular edema is multifactorial. Hyperglycemia and poor systemic factor balance are major risk factors. Laser treatemnts and antiagiogenic treatments represent the main non surgical options to treat macular edema. Results Focal macular edema remains the best indication of laser treatment. Laser remains also the standard of care of diffuse macular edema but some edemas remain resistant. Several therapeutic options have been proposed : Steroid intravitreal injection and antiVEGF therapy (either PKC inhibitors, VEGF aptamers or VEGF antibodies) represent the future alternative treatments as well as their potential combination. Conclusion Laser remains the main treatment of diabetic macular edema. However, steroids and antiangiogenic agents either isolated or combined represent the main alternative treatment for non responding diffuse macular edema.

Intravitreal steroids in the management of macular oedema

The use of intravitreal corticosteroids in the management of macular oedema has recently gained widespread acceptance. New long-acting steroid preparations and methods of delivery have facilitated the use of these new modalities. This review describes the various types of macular oedema for which this therapeutic option is used and the results.

STEREOSCOPIC FLUORESCEIN ANGIOGRAPHY IN DIABETIC MACULOPATHY

To explore the possible differences in the depth location of microaneurysms in focal as well as diffuse diabetic macular edema. The density of superficial and deep retinal microaneurysms was assessed using a stereoscopic fluorescein angiographic method. The density of deep retinal microaneurysms was nearly identical in the group with diffuse macular edema (89.9 +/- 28.5 microaneurysms/test grid) and the group with focal macular edema (90 +/- 65.4 microaneurysms/test grid). The density of superficial retinal microaneurysms was significantly lower in the group with diffuse macular edema (22.8 +/- 12.5) than in the group with focal macular edema (47.9 +/- 30.6). The density fraction of superficial retinal microaneurysms was lower in the group with diffuse macular edema (0.19 +/- 0.07) than in the group with focal macular edema (0.36 +/- 0.14). In the group with focal macular edema, areas without edema had a significantly lower density of superficial (6.1 +/- 2.8) and deep (15.6 +/- 7.8) retinal microaneurysms than did areas with edema (superficial: 47.9 +/- 30.6; deep: 90.0 +/- 65.4). In the group with focal macular edema, the density fraction of superficial retinal microaneurysms was nearly identical in areas with (0.36 +/- 0.14) and areas without (0.30 +/- 0.10) edema. The development of focal macular edema might be linked to the density of microaneurysms. Diffuse macular edema might be a result of some unknown effect on the deeper retina and/or the choroid.

Risk factors for diffuse and focal macular edema

Objective: The epidemiological risk factors for the different forms of diabetic macular edema (focal or diffuse) are not differentiated in the literature. In the present study, the objective was to determine which risk factors influence the appearance of focal or diffuse macular edema. Research, Design, and Methods: A 4-year prospective study in a population of Type II diabetic patients (NIDDM) in three groups, the first with 29 patients with diffuse diabetic macular edema (Group A), the second with 32 patients with focal macular edema (Group B), and the third with 32 patients with diabetic retinopathy but without diabetic macular edema (Group C); the three groups were selected on the basis of sex, age, and duration of diabetes with similar patterns. We studied the following risk factors: treatment of diabetes mellitus by insulin, presence of diastolic blood hypertension, presence of microalbuminuria or diabetic nephropathy, levels of HbA 1c, type of diabetic retinopathy, presence of previous panretinal photocoagulation, and levels of triglycerides and fractions of cholesterol. Results: In discriminant analysis and in order of importance, the epidemiological risk factors for Group A were the following: presence of panretinal laser, diastolic blood hypertension, diabetic nephropathy, and insulin treatment; for group B, the risk factors were the following: insulin treatment, presence of diastolic blood hypertension, and high levels of glycated haemoglobin (HbA 1c); and for group, C the risk factors were the following: diastolic blood hypertension, insulin treatment of diabetes, and high levels of HbA 1c. Conclusions: In the present study, the group of patients with focal macular edema were epidemiologically similar to the group of patients with diabetic retinopathy without macular edema, the group of patients with diffuse macular edema were epidemiologically different.

Laser management of diabetic retinopathy

The UK National Service Framework for Diabetes recommends nationwide screening of people with diabetes for development of sight-threatening retinopathy.1 All health workers who provide diabetes care require an understanding of the common ophthalmic treatments that can be offered for such disease. The principal conditions to consider are diabetic maculopathy and proliferative retinopathy. In diabetic maculopathy, central vision may be compromised by macular (central retinal) oedema with varying degrees of ischaemia. The oedema may respond to laser therapy, ischaemia does not. Therapy takes the form of ‘focal’ (Figure 1) or ‘grid’ (Figure 2) macular laser, consisting of up to 200 small (e.g. 100 μm) gently applied burns to areas of central retinal thickening. This tends to encourage resolution of thickening. Figure 1 Focal macular laser therapy for focal macular oedema. Fluorescein angiography reveals focal leakage from diabetic microvascular abnormalities (white arrow). Laser burns (white spots) are placed on the area of thickened retina. Colour version available ... Figure 2 Grid macular laser therapy for diffuse macular oedema. Fluorescein angiography reveals diffuse leakage from diabetic microvascular abnormalities (white arrows). Laser burns (spots) are placed on the area of thickened retina. Colour version available ... In proliferative retinopathy, central and peripheral vision may be compromised by bleeding from new vessels arising on the optic disc (NVD) or elsewhere in the retina (NVE). These vessels typically bleed because of the tendency of the overlying vitreous gel, to which the new vessels are attached, to retract, stretching vessels between vitreous and retina. Therapy takes the form of panretinal photocoagulation, in which perhaps 2000 large (e.g. 500 μm) burns, of greater intensity than employed in macular laser, are applied to retina outside the central thirty-degree zones (Figure ​(Figure3a3a​3a3b). 3b). This tends to encourage a reduction in the calibre of new vessels. Figure 3a Panretinal photocoagulation for proliferative retinopathy. Laser burns (spots) are placed outside central retina (a) as can be seen in the fluorescein angiogram Figure 3b Panretinal photocoagulation for proliferative retinopathy. Laser burns (spots) are placed outside central retina (b). Colour version available on [www.jrsm.org]

Plasma level of interleukin-6 is an indicator for predicting diabetic macular edema.

To find a predictor in the pathogenesis of macular edema, we investigated ocular and systemic risk factors. One hundred and fifty-nine patients with mild diabetic retinopathy who showed one or more soft exudates were recruited. We selected the possible predictors on the basis of relevant factors, including concentration of vascular endothelial growth factor, interleukin-6 (IL-6), transforming growth factor (TGF)-beta(1), tumor necrosis factor (TNF)-alpha, and lipoprotein(a) in plasma, and serum level of von Willebrand factor and thrombomodulin. Macular edema was not detected in 94 eyes; focal macular edema was detected in 46 eyes; diffuse macular edema was detected in 18 eyes; and cystoid macular edema was present in 1 eye. The plasma level of IL-6 concentration and the state of the posterior vitreous detachment (PVD) correlated significantly with the severity of macular edema (odds ratios = 3.68, 1.70, respectively). Other risk factors were not significantly associated with macular edema. We estimated the probability of macular edema according to the IL-6 level in plasma and the state of the PVD, and were able to predict the probability of macular edema. The results of the present study indicate that IL-6 concentration in plasma and the state of the PVD can be predictors of macular edema.

La maculopathie diabétique: aspects cliniques, facteurs de risque et possibilités thérapeutiques

Edema of the macula is a frequent component of diabetic retinopathy, as well as a common cause of visual impairment in this disorder. It is strongly associated with high blood pressure and the presence of proteinuria. Correction of these risk factors may reduce macular edema and should be included as part of the total management of patients with diabetic maculopathy. The benefit of a focal treatment for focal macular edema has been established but the results are not so good when a grid treatment for diffuse macular edema is performed.

Laser photocoagulation control of diabetic macular oedema without fluorescein angiography.

This study included 40 eyes in 22 diabetic patients with focal macular oedema. Laser photocoagulation was directed at decompensated or leaking microvascular lesions clinically detected without using pretreatment fluorescein angiograms. Post-treatment fluorescein angiograms performed after adequate clinical control of disease showed complete resolution of the macular oedema in 25 eyes (62.5%), whereas persistent leakage from microvascular lesions closer than 500 microns from the centre of the foveola was noted in 15 eyes (37.5%). These were clinically detected during the pretreatment examination and were found not to impair or threaten the patient's vision. Our data confirm the clinical impression that fluorescein angiography is not necessary for effective treatment and should be used only if necessary.

Classification of proliferative diabetic retinopathy.

Using panretinal fluorescein angiography, three patterns (A, B, C) of capillary nonperfusion were identified in 308 eyes with proliferative diabetic retinopathy. Statistical analysis showed that there was a significant association with different retinal complications and clinical parameters. Pattern A (83.7%: midperipheral location of capillary nonperfusion) occurs in type I and II diabetes and is associated with early retinal neovascularization and focal macular edema. Pattern B (8.1%: capillary exclusions disseminated on the whole retina) is typical of young type-I diabetics and is complicated by early disc new vessels and ischemic maculopathy. Pattern C (8.1%: capillary nonperfusion confined to the peripheral retina) is observed in type-I diabetic females and associated with multiple, retinal new vessels, without maculopathy. This study also demonstrated that eyes with pattern B retinal ischemia respond less well to laser treatment than eyes with other pattern types. Various pathogenetic factors could lead to these three distinct types of proliferative diabetic retinopathy.

Diabetic Maculopathy: A Critical Review Highlighting Diffuse Macular Edema

Retinal ischemia and edema are the two major intraretinal components of diabetic maculopathy. Focal macular edema is caused by focal leakage from retinal microaneurysms and dilated capillary segments; diffuse edema is caused by leakage from diffusely dilated retinal capillaries throughout the posterior pole. Diffuse macular edema may be exacerbated by systemic factors such as cardiac or renal failure, and hypertension. It is postulated that dysfunction of the retinal pigment epithelial barrier and transport functions might contribute to the problem of diffuse macular edema. Newer techniques of laser grid photocoagulation for diffuse edema have been proposed. It is postulated that photocoagulative debridement of a disordered retinal pigment epithelium could be a mechanism of action of this treatment.