Using OCT with your diabetes patients

Patients with diabetes may present a variety of interesting findings best unveiled by use of spectral domain optical coherence tomography (SD-OCT). OCT is one of the best way to assess patients for the presence of diabetic macular edema (DME). It is extremely useful for monitoring responses to treatments such as anti-VEGF injections, grid or focal laser, intravitreal steroids, or any combination thereof in patients with DME involving or threatening the fovea (center-involved DME).

However, detecting and monitoring increased retinal thickness associated with diabetes is not the only relevant anatomical feature best visualized and appreciated with OCT.

Let’s consider a few cases showing multiple OCT presentations that might be encountered in patients who have diabetes.

Previously from Dr. Chous: Fasting regimens may be key in treating type 2 diabetes

The case of the epiretinal membrane (ERM)

Jim is a 58-year-old man with type 2 diabetes diagnosed three years ago. He takes his diabetes medications, which include combination canigliflozin with metformin (Invokamet XR, Janssen), lisinopril (Prinivil, Merck), simvastatin (Zocor, Merck), and 81 mg of aspirin.

His last HbA1c was 6.2 percent, and his last dilated eye examination was two years earlier at another office. He has recently experienced visual distortion in the right eye and was referred to me for evaluation by his endocrinologist.

Jim’s vision is 20/40 in the right eye and 20/20 in the left. His anterior segment exam and intraocular pressures (IOP) are normal, and his dilated exam shows no evidence of retinopathy or macular edema. However, SD-OCT shows a significant epiretinal membrane (ERM) on the right side with loss of the foveal depression (see Figure 1).

Though ERM is a common condition, it may be up to twice as likely in people with diabetes and is a known complicating risk factor for macular edema.^1,2 Jim was offered a consultation with a vitreo-retinal specialist who recommended his condition be monitored for progression or development of DME. 

The case of the thinning central retina

Kathy is a 38-year-old woman who has had type 1 diabetes for 18 years. She wears an insulin pump with a continuous glucose monitor (CGM). Her HbA1c ranged from 6 percent to 7.2 percent for the entirety of her diagnosis to date.

She has 20/20 vision and no ophthalmoscopic evidence of diabetic retinopathy or macular edema. She also shows no signs of diabetic kidney disease. Her diabetic peripheral neuropathy, intermittent “pins and needles” sensation in her toes, is mild to moderate. A baseline SD-OCT was performed and shows significant thinning of the central retina, particularly the parafoveal regions of each eye (see Figure 2). 

A report shows that diabetes, both with and without retinopathy, is associated with decreased retinal thickness in general. Both her decreased retinal nerve fiber layer (RNFL) and her inner plexiform layer (ganglion cell complex) thickness in particular were impacted. Diabetic retinopathy (DR) is now widely considered a “neurovascular” disease that affects neural components of the retina prior to capillary damage that results in the vascular lesions we typically associate with DR.³

Recent analysis suggests that loss of inner retina seen in diabetes is more highly associated with peripheral neuropathy than with vascular retinopathy^4,5. Retinal thinning shows signs in type 1 diabetes more commonly than in type 2 diabetes-presumably due to delayed diagnosis of the latter resulting in capillary leakage that masks thinning of the neural retina.⁶

This patient also has diminished color perception (moderate tritan defect with ColorDx, Konan) and contrast sensitivity (SmartSystem CSF, M&S Technology). She was offered a multi-component nutritional supplement shown to improve these symptoms as well as symptoms of diabetic peripheral neuropathy in an RCT (EyePromise DVS, ZeaVision).⁷

Related: What’s new for diabetes management and prevention

The case of the worsening DME

Armando is a 60-year-old man who has had type 2 diabetes for 20 years, an HbA1c of 8 percent, and center-involved DME. He has been treated the last four years with all three commonly used anti-VEGFs-Avastin (bevacizumab, Genentech), Lucentis (ranibizumab injection, Genentech), Eylea (aflibercept, Regeneron)-(roughly a dozen injections per eye at last count), focal macular laser, and intravitreal steroids.

He is on insulin therapy (Levemir plus NovoLog, Novo Nordisk) and has sleep apnea treated with continuous positive airway pressure (CPAP).

His best corrected vision is 20/30 in the right eye and 20/60 in the left. Armando complains of great difficulty seeing colors and driving at night. He also has a severe tritan color defect in each eye, and his contrast sensitivity is abnormal. His OCT scans show his DME over the last year has worsened despite monthly treatment by retinology (Figure 3).

This case represents classic use of OCT to monitor response to treatment in a patient with DME. We know that poor blood glucose control, inadequately treated sleep apnea, and delayed initiation of intravitreal anti-VEGF drugs are all risk factors for poor response to treatment.

Recent analysis suggests that disorganization of the retinal internal layers (DRIL) predicts poor response to anti-VEGF therapy for DME⁸, as does damage to the deep capillary plexus (vessels within the outer plexiform layer) as imaged by OCT angiography.⁹ I stressed to him the importance of improving blood glucose control, consistent use of CPAP and following up with the retinal specialist.

I suggested oral minocycline, an inexpensive and easily accessible medication that is showing some promise as adjunctive therapy for DME,¹⁰ as well as Pycnogenol (French maritime pine bark extract, Horphag), widely used for retinal capillary leakage in Europe, and macular carotenoids to improve visual function.

I also equipped him with an updated prescription with impact-resistant lenses and referred him to an endocrinologist (to improve glucose control, assess for kidney disease and thyroid dysfunction associated with sight-threatening retinopathy), a dentist (to assess for periodontal disease common in diabetes), a pharmacist (to review medications, dosages, and timing), and a podiatrist (to assess a “sore” on his big toe).

Remember that diabetes-related eye disease does not occur in a vacuum, and patients are well served by a multi-disciplinary, team approach.

Patients with diabetes may present with a number of interesting and important OCT findings. These may include retinal thickening-as in DME, and retinal thinning-a potential early biomarker for both retinal and visual dysfunction, as well as diabetic peripheral neuropathy. Vitreo-retinal interface conditions like epiretinal membrane, vitreomacular traction, and macular hole formation are also a concern.

With the availability of wide-field OCT and OCT angiography, in tandem, with an explosion of knowledge resulting from clinical studies, this technology will likely become even more useful to primary eyecare providers and specialists alike.

Related: How diabetes affects contact lens wear

References

1. Ng CH, Cheung N, Wang JJ, Islam AF, Kawasaki R, Meuer SM, Cotch MF, Klein BE, Klein R, Wong TY. Prevalence and Risk Factors for Epiretinal Membranes in a Multi-Ethnic United States Population. Ophthalmology. 2011 Apr;118(4):694-699.

2. Akbar Khan I, Mohamed MD, Mann SS, Hysi PG, Laidlaw DA. Prevalence of vitreomacular interface abnormalities on spectral domain optical coherence tomography of patients undergoing macular photocoagulation for centre involving diabetic macular oedema. Br J Ophthalmol. 2015 Aug;99(8):1078-81.

3. Jindal V. Neurodegeneration as a primary change and role of neuroprotection in diabetic retinopathy. Mol Neurobiol. 2015;51(3):878-84.

4. Kim K, Yu SY, Kwak HW, Kim ES.  Retinal Neurodegeneration Associated With Peripheral Nerve Conduction and Autonomic Nerve Function in Diabetic Patients. Am J Ophthalmol. 2016 Oct;170:15-24.

5. Shahidi AM, Sampson GP, Pritchard N, Edwards K, Vagenas D, Russell AW, Malik RA, Efron N. Retinal nerve fibre layer thinning associated with diabetic peripheral neuropathy. Diabet Med. 2012 Jul;29(7):e106-11.

6. Chen Y, Li J, Yan Y, Shen X. Diabetic macular morphology changes may occur in the early stage of diabetes. BMC Ophthalmology. 2016 Jan;16:12. doi:10.1186/s12886-016-0186-4.

7. Chous AP, Richer SP, Gerson JD, Kowluru RA. The Diabetes Visual Function Supplement Study (DiVFuSS). The British Journal of Ophthalmology. 2016 Feb;100(2):227-234.

8. Sun JK, Lin MM, Lammer J, Prager S, Sarangi R, Silva PS, Aiello LP. Disorganization of the Retinal Inner Layers as a Predictor of Visual Acuity in Eyes With Center-Involved Diabetic Macular Edema. JAMA Ophthalmol. 2014 Nov;132(11):1309-1316.

9. Lee J, Moon BG, Cho AR, Yoon YH. Optical Coherence Tomography Angiography of DME and Its Association with Anti-VEGF Treatment Response. Ophthalmology. 2016 Nov;123(11): 2368-75.

10. Cukras CA, Petrou P, Chew EY, Meyerle CB, Wong WT. Oral minocycline for the treatment of diabetic macular edema (DME): results of a phase I/II clinical study. Invest Ophthalmol Vis Sci. 2012 Jun;53(7):3865-3874. 

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