Diabetic macular edema: Evidence-based management

Abstract

Diabetic macular edema (DME) is the most common cause of vision loss in patients with diabetic retinopathy with an increasing prevalence tied to the global epidemic in type 2 diabetes mellitus. Its pathophysiology starts with decreased retinal oxygen tension that manifests as retinal capillary hyperpermeability and increased intravascular pressure mediated by vascular endothelial growth factor (VEGF) upregulation and retinal vascular autoregulation, respectively. Spectral domain optical coherence tomography (SD-OCT) is the cornerstone of clinical assessment of DME. The foundation of treatment is metabolic control of hyperglycemia and blood pressure. Specific ophthalmic treatments include intravitreal anti-VEGF drug injections, intravitreal corticosteroid injections, focal laser photocoagulation, and vitrectomy, but a substantial fraction of eyes respond incompletely to all of these modalities resulting in visual loss and disordered retinal structure and vasculature visible on SD-OCT and OCT angiography. Efforts to close the gap between the results of interventions within randomized clinical trials and in real-world contexts, and to reduce the cost of care increasingly occupy innovation in the social organization of ophthalmic care of DME. Pharmacologic research is exploring other biochemical pathways involved in retinal vascular homeostasis that may provide new points of intervention effective in those cases unresponsive to current treatments.

Keywords: Diabetes; diabetic retinopathy; macular edema.

Figure 1

A macular lipid star is a common fundus sign in diabetic macular edema and indicates that the center of the macula is a preferential site for accumulation of extracellular fluid

Figure 2

Schematic summarization of the mechanisms of action of the various treatments for diabetic macular edema. The color-filled blocks represent different treatment modalities for diabetic macular edema

Figure 3

Images of a 77-year-old man with type 2 diabetes mellitus, who developed diabetic macular edema of the left eye that reduced visual acuity to 20/63. (a) Red free fundus photography shows microaneurysms and one large blot hemorrhage above the fovea. Fluorescein angiography shows multiple hyperfluorescent microaneurysms in the mid-phase, and late leakage above the fovea in the late frame. (b) The spectral domain-optical coherence tomography on November 30, 2017 shows center-involved diabetic macular edema and subfoveal fluid. After 5 monthly aflibercept injections, the edema has decreased, but persistent edema is present. An ellipsoid zone defect (yellow arrow) is apparent

Figure 4

Images of the left eye of a 21-year-old woman with type 1 diabetes mellitus with proliferative diabetic retinopathy and center-involved diabetic macular edema. Her best corrected visual acuity was 20/40. Because of documented poor adherence to scheduled clinic visits, vitrectomy rather than serial anti-VEGF injection therapy was chosen. (a) New vessels were present on the disc and in the midperiphery of all quadrants with a preretinal hemorrhage superiorly. (b) Fluorescein angiography shows leakage from new vessels and areas of capillary nonperfusion in the midperiphery. (c) Spectral domain-optical coherence tomography shows center-involved intraretinal fluid and subfoveal fluid. The ellipsoid zone is intact (yellow arrow)

Figure 5

Postoperative images from the same patient shown in Fig. 4. (a) Following a single preoperative bevacizumab injection (to limit intraoperative bleeding), vitrectomy, internal limiting membrane peeling, and panretinal photocoagulation, the new vessels have regressed. (b) Five years later the center-involved diabetic macular edema remains resolved with no subsequent treatments. The best corrected visual acuity was 20/25.