Practice Essentials
Macular edema in diabetes, defined as retinal thickening within 2 disc diameters of the center of the macula, results from retinal microvascular changes that compromise the blood-retinal barrier, causing leakage of plasma constituents into the surrounding retina and, consequently, retinal edema.
Focal edema is associated with hard exudate rings caused by leakage from microaneurysms. Diffuse edema is caused by leakage from microaneurysms, retinal capillaries, and arterioles.
Diabetes is the leading cause of new blindness in the United States, with clinically significant macular edema (CSME) contributing greatly to this vision loss.
Signs and symptoms
The following findings indicate the presence of clinically significant macular edema (CSME), as defined by the Early Treatment Diabetic Retinopathy Study (ETDRS):
Retinal thickening within 500 µm of the center of the fovea
Hard, yellow exudates within 500 µm of the center of the fovea with adjacent retinal thickening
At least 1 disc area of retinal thickening, any part of which is within 1 disc diameter of the center of the fovea
See Clinical Presentation for more detail.
Diagnosis
Diabetic macular edema (DME) is diagnosed by funduscopic examination. The following studies can also be performed, to provide information for treatment and follow-up:
Optical coherence tomography (OCT): Captures reflected light from retinal structures to create a cross-sectional image of the retina, which is comparable to histologic sections as seen with a light microscope; it can demonstrate 3 basic structural changes of the retina from diabetic macular edema: retinal swelling, cystoid edema, and serous retinal detachment
Fluorescein angiography: Distinguishes and localizes areas of focal versus diffuse leakage, thereby guiding the placement of laser photocoagulation
Color stereo fundus photographs: Can be used to evaluate long-term changes in the retina
Visual acuity should also be measured. Although it does not aid in the diagnosis of CSME—initially, at least, patients may have a visual acuity of 20/20—it is an important parameter in following the progression of macular edema.
Laboratory studies
Protein levels: Proteinuria is a good marker for the development of diabetic retinopathy; thus, patients with diabetic nephropathy should be observed more closely
Lipid and triglyceride levels: Elevated triglyceride and lipid levels increase the risk of retinopathy, while normalization of lipid levels reduces retinal leakage and deposition of exudates
See Workup for more detail.
Management
Pharmacologic treatment
Intravitreal treatments for macular edema include the following:
Triamcinolone acetonide: Significantly reduces macular edema and improves visual acuity, particularly when the macular edema is pronounced
Ranibizumab: Recombinant humanized antibody fragment that is active against all isoforms of vascular endothelial growth factor (VEGF) ̶ A (a protein that causes breakdown of the blood-retina barrier)
Fluocinolone intravitreal implant: Significant improvement in visual acuity maintained for 36 months
Laser treatment
Laser photocoagulation is a well-proven therapy to reduce the risk of vision loss from diabetic macular edema. Treatments include the following:
Focal treatment: Addresses leaking microaneurysms
Grid pattern photocoagulation: Used for diffuse leakage
See Treatment and Medication for more detail.