DME results from a hyperglycemia-induced breakdown of the blood–retina barrier, which leads to fluid extravasation from retinal vessels into the surrounding neural retina (Fig 5-9). A diagnosis of DME is made when retinal thickening that involves the macula is present. DME may be associated with hard exudates, which are precipitates of plasma lipoproteins. Central subfield–involved DME that affects the fovea is a common cause of vision loss in diabetic patients. In contrast, non–center-involved DME is unlikely to affect vision unless it progresses to center involvement. Although DME is increasingly common among eyes with more advanced diabetic retinopathy, DME can be present in any severity level of diabetic retinopathy. Even eyes with mild NPDR can have substantial vision loss from highly thickened retinas.
FA is useful in demonstrating the breakdown of the blood–retina barrier by showing local areas of retinal capillary leakage. However, leakage shown on the angiogram may occur in the absence of macular retinal thickening and is thus not considered macular edema. Examination with OCT or slit-lamp biomicroscopy are the most appropriate methods to evaluate eyes for the presence or absence of macular thickening.
Classification of Diabetic Macular Edema
Current algorithms for pharmacologic intervention in DME use a simple, OCT-based definition to classify DME as center-involved or non–center-involved. In center-involved DME, the central retinal subfield appears thickened on OCT scans. DME that does not affect the central subfield is termed non–center-involved (Fig 5–10; Activity 5-1).
ACTIVITY 5-1 OCT Activity: OCT of diabetic macular edema.
Courtesy of Colin A. McCannel, MD.
Access all Section 12 activities at www.aao.org/bcscactivity_section12.
The ETDRS was the first prospective, randomized clinical trial of photocoagulation in diabetic patients with less than high-risk PDR in order to establish standard treatment paradigms for managing DME (see Clinical Trial 5-3). It defined clinically significant diabetic macular edema (CSME) as the indication for focal laser photocoagulation treatment in the following settings:
-
retinal thickening located at or within 500 μm of the center of the macula
-
hard exudates at or within 500 μm of the center if associated with thickening of adjacent retina
-
a zone of thickening larger than 1 disc area, if located within 1 disc diameter of the center of the macula
CSME is an older term that predates diagnoses made with OCT technology. Now that anti-VEGF treatment has supplanted macular laser photocoagulation as the first-line therapy for DME, the CSME diagnosis, which is made clinically, is much less frequently used.
Regardless of whether it is center-involved or non–center-involved, DME may manifest as focal or diffuse retinal thickening. Focal macular edema is characterized by areas of local fluorescein leakage from specific capillary lesions, such as microaneurysms (Fig 5-11A). Diffuse macular edema is characterized by extensive retinal capillary leakage and widespread breakdown of the blood–retina barrier, often accumulating in a cystoid configuration in the perifoveal macula (cystoid macular edema) (Fig 5-11B). Studies have not demonstrated any difference in treatment response corresponding to the pattern of macular edema, whether focal, diffuse, or a combination of these.
Excerpted from BCSC 2020-2021 series: Section 10 - Glaucoma. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.