Diabetic macular edema (DME) is the leading cause of significant visual impairment in people with diabetes. Analysis shows that somewhere between four to nine percent of patients over the age of 40 in the U.S. have DME.1
Risk factors for DME include a longer duration of diabetes and higher mean blood glucose levels as reflected by glycosylated hemoglobin (HbA1c)—an effect especially heightened with poor blood pressure control, African-American race, elevated serum triglycerides insulin use, and possibly sleep apnea.2-4
Treatment with vascular endothelial growth factor inhibitors (anti-VEGF) has become the most important tool for treating “center-involved” DME when patients suffer loss of visual acuity. Center-involved DME is defined as retinal thickening demonstrable on SD-OCT within the central macular subfield.
Previously from Dr. Chous: The OD’s role with new diabetes drugs
The potential benefits of pre-emptively treating center-involved DME patients who have good visual acuity with anti-VEGF therapy remains an open question and is currently being investigated by the Diabetic Retinopathy Clinical Research Network’s Protocol AA.5
Not all DME involves the foveal center, but these patients have about a three-fold increased risk of developing foveal involvement over time.6 Is there anything else that can be done to improve patients’ visual function and retinal health prior to worsening macular edema or vision?
I present a case demonstrating the potential benefit of a novel intervention for one such patient.
TR is a 27-year-old man who has had type 1 diabetes for 16 years. He wears an insulin pump and has Hashimoto’s disease—a common auto-immune thyroiditis that may accompany type 1 diabetes.
TR reported he checks his blood glucose about four times each day, and his blood sugars range from 50 to 280 ng/ml with an HbA1c of 7.2 percent at his last visit with the endocrinologist (estimated mean blood glucose of 170 mg/dl).
Chart review showed TR’s HbA1 ranged between 6.4 percent and 8.1 percent over the last five years. TR denied any history of nephropathy or neuropathy when asked, and serum microalbumin testing was normal within the previous six months.
TR reported good sleep quality and had no symptoms or signs of obstructive sleep apnea. A recent analysis has shown a very high prevalence of asymptomatic sleep apnea—30 to 60 percent in type 1 diabetes patients.7
TR’s best corrected vision was 20/20 in each eye. However, his contrast sensitivity was reduced at multiple spatial frequencies in each eye, and he had a blue-yellow color vision defect, OD worse than OS. Macular pigment was low at 0.18 DU. Slit lamp examination and intraocular pressures were normal (16 mm Hg/18 mm Hg by applanation), but his dilated retinal exam showed scattered microaneurysm formation in each eye. TR had associated hard exudate about 600 µm from the foveal center OS only (Figure 1).
I could not detect retinal thickening in either macula, but OCT was performed and showed thinning of the inner retina in both eyes with subtle perifoveal cystic DME OD only.