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.
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.
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.
Intravitreal treatments for macular edema include the following:
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 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
The Early Treatment Diabetic Retinopathy Study (ETDRS) set the guidelines for the treatment of diabetic macular edema (DME). Since that time, the standard of treatment for diabetic macular edema has been glycemic control as demonstrated by the Diabetes Control and Complications Trial (DCCT), optimal blood pressure control as demonstrated by the United Kingdom Prospective Diabetes Study (UKPDS), and macular focal/grid laser photocoagulation.
In ETDRS, laser photocoagulation reduced the risk of moderate visual loss from diabetic macular edema by 50% (from 24% to 12% 3 years after initiation of treatment).  Nevertheless, some patients suffer permanent visual loss even after intensive treatment.
Over the past few years, research has started to focus on the use of anti-vascular endothelial growth factor (VEGF) therapy to treat DME. As new and promising treatment options emerge, these treatments will need to be reevaluated.
It is imperative for patients with diabetes to understand that a healthy lifestyle and compliance with medical care can greatly reduce the development and progression of complications of their disease, in the eyes as well as other organs.
Diabetic macular edema results from retinal microvascular changes. Thickening of the basement membrane and reduction in the number of pericytes are believed to lead to increased permeability and incompetence of the retinal vasculature. This compromise of the blood-retinal barrier leads to the leakage of plasma constituents into the surrounding retina, with subsequent retinal edema.  Hypoxia produced by this mechanism can also stimulate the production of vascular endothelial growth factor (VEGF). There is evidence that VEGF is up-regulated in diabetic macular edema and proliferative diabetic retinopathy. 
A study suggests that the pathogenesis of diabetic macular edema is not only related to VEGF dependency but also to other inflammatory and angiogenic cytokine levels that can be suppressed by corticosteroids. 
Diabetes is the leading cause of new blindness in the United States, and clinically significant macular edema (CSME) contributes greatly to this vision loss. In the absence of ophthalmologic treatment, persons with diabetes have a 25-30% risk of moderate vision loss. With treatment, the risk drops by 50%. According to 2007 data, 23.6 million people in the United States have diabetes, but only 17.9 million have been diagnosed.  . About 50% of those with diagnosed diabetes do not receive appropriate eye care. The World Health Organization estimates that worldwide, more than 150 million people have diabetes.
Although diabetes is more common in Hispanics, African Americans, and Native Americans than in whites, no data describe a greater risk of developing macular edema among diabetic patients of any one racial group. Likewise, no data describe a difference in risk of diabetic macular edema between the sexes.
Diabetic retinopathy, not specifically diabetic macular edema, generally occurs in persons older than 40 years. It rarely occurs before puberty.
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