Diagnosing and treating diabetic macular edema (DME) can pose a challenge for ODs. A. Paul Chous, OD, MA, FAAO, CDE, examines a case of non-center involved DME and the challenges he faced when treating one patient.
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.
TR and I discussed the clinical findings, and I suggested that he get a continuous glucose monitoring system (CGMS) to better assess blood glucose patterns at various times of day and guard him against acute hypoglycemia. My goal was to minimize TR’s post prandial blood sugar spikes and reduce his HbA1c by 10 percent.
I asked TR to minimize the duration of post meal hyperglycemia as much as possible via 15-minute pre-prandial insulin delivery, moderation of carbohydrate intake, and intramuscular injection of insulin when blood glucose levels are above 200 mg/dl.
In addition, I recommended that TR take a multi-component nutritional supplement (EyePromise DVS, ZeaVision). This formula has been shown to improve visual function (contrast sensitivity, color perception, and visual field sensitivity), blood lipids, hsCRP, and macular pigment as shown in a 6-month randomized control trial of adult diabetes (both type 1 and type 2) patients both with and without diabetic retinopathy, and without affecting HbA1c levels.8
TR was asked to return in six months to assess his DME.
TR’s color vision and contrast sensitivity improved in each eye. His last HbA1c value was 6.9 percent, and he reported high satisfaction with his CGMS. In particular, he reports less frequent acute hypoglycemia thanks to the CGMS alarm feature and fewer episodes of blood sugar levels >200 mg/dl.
He has taken the recommended vitamin twice per day since his last visit, and his vision remains at 20/20 in each eye. Dilated fundus exam shows total resolution of hard exudate OD (Figure 2) with resolution of the subtle cystic DME on SD-OCT.
TR will continue to be followed every six months for now.
1. Varma R, Bressler NM, Doan QV, Gleeson M, Danese M, Bower JK, Selvin E, Dolan C, Fine J, Colman S, Turpcu A. Prevalence of and Risk Factors for Diabetic Macular Edema in the United States. JAMA Ophthalmol. 2014 Nov;132(11):1334-40.
2. Zhang J, Ma J, Zhou N, Zhang B, An J. Insulin Use and Risk of Diabetic Macular Edema in Diabetes Mellitus: A Systemic Review and Meta-Analysis of Observational Studies. Med Sci Monit. 2015; 21: 929–936.
3. Chung YR, Park SW, Choi SY, Kim SW, Moon KY, Kim JH, Lee K. Association of statin use and hypertriglyceridemia with diabetic macular edema in patients with type 2 diabetes and diabetic retinopathy. Cardiovasc Diabetol. 2017 Jan 7;16(1):4.
4. Mason RH, West SD, Kiire CA, Groves DC, Lipinski HJ, Jaycock A, Chong VN, Stradling JR. High prevalence of sleep disordered breathing in patients with diabetic macular edema. Retina. 2012 Oct;32(9):1791-8.
5. Diabetic Retinopathy Clinical Research Network. Protocol. Available at: http://drcrnet.jaeb.org/Studies.aspx. Accessed 12/19/17.
6. Bhavsar KV, Subramanian ML. Risk factors for progression of subclinical diabetic macular oedema. Br J Ophthalmol. 2011 May;95(5):671-4.
7. Banghoej AM, Nerild HH, Kristensen PL, Pedersen-Bjergaard U, Fleischer J, Jensen AEK, Laub M, Thorsteinsson B, Tarnow L. Obstructive sleep apnoea is frequent in patients with type 1 diabetes. J Diabetes Complications. 2017 Jan;31(1):156-161.
8. Chous AP, Richer SP, Gerson JD, Kowluru RA. The Diabetes Visual Function Supplement Study (DiVFuSS). Br J Ophthalmol. 2016 Feb;100(2):227-34.