This occurs most prominently in the macula, threatening central acuity. Retinal edema is slowly toxic to the neurosensory retina, and associated lipid hard exudate is very damaging to photoreceptors. Without treatment, the course of diabetic maculopathy tends to be progressive. The goal of DME management is to limit DME's development and to reduce its damage during the active phase of the disease. Clinically significant DME is defined as retinal thickening within 500 microns of the foveal center, hard exudate within 500 microns of the foveal center associated with retinal thickening, or 1 disc diameter of retinal thickening with at some part within 1 disc diameter of the foveal center.
Diagnosis requires binocular, stereoscopic examination.
Fluorescein angiography can detect leakage, but it can not demonstrate retinal thickening unless stereoscopic angiography is performed. Several therapeutic interventions can reduce DME and spare central visual acuity. Control Several studies have demonstrated that glucose control improves the prognosis for diabetic maculopathy. Among patients without retinopathy at baseline, those with tight glucose control group had a markedly reduced rate of developing retinopathy. Also, among patients with mild retinopathy at baseline, the tight glucose group experienced less progression of retinopathy.