DIABETIC RETINOPATHY

Diabetic retinopathy is one of the most common complications of diabetes and remains a leading cause of preventable vision impairment amongst working-age adults worldwide (1). The condition develops when the complex pathophysiology of diabetes, compounded by long duration of the disease or suboptimal blood glucose control, damages the delicate blood vessels that supply the retina, the light-sensitive tissue lining the back of the eye (2,3). Although diabetic retinopathy may initially cause no noticeable symptoms, progressive retinal damage can result in irreversible vision loss if left undetected or untreated(4-7).

Importantly, the presence of diabetic retinopathy does not necessarily indicate poor management of diabetes. Even individuals who are highly motivated and actively engaged in their healthcare may develop retinal complications over time. Factors such as disease duration, blood glucose control, blood pressure, cholesterol levels, genetics and overall vascular health all influence the risk of retinal damage (8-11). Consequently, regular eye examinations, involving dilation of the pupils and retinal scans, form an essential component of comprehensive diabetic healthcare regardless of how well diabetes appears to be controlled.

  • The retina is one of the most metabolically active tissues within the body and relies upon a highly specialised network of blood vessels to maintain its function (12). In diabetic retinopathy, chronic vascular injury may cause these vessels to weaken, leak fluid or blood, become obstructed, or develop abnormal new vessel growth. The earliest stages of disease are often characterised by microaneurysms, retinal haemorrhages and lipid deposits within the retina. As these changes progress, the risk of visual impairment increases significantly(6,7,10,13).

    One of the most vision-threatening complications of diabetic retinopathy is diabetic macular oedema. This condition occurs when fluid accumulates within the macula, the central region of the retina responsible for detailed vision. Because the macula is essential for reading, driving, recognising faces and many occupational tasks, swelling within this region can substantially affect visual function and quality of life (14-16). Advanced diabetic retinopathy may also result in retinal bleeding, scar tissue formation, retinal detachment and other complications capable of causing severe and permanent vision loss(17).

    The relationship between diabetes and ocular health continues to evolve as new treatments become available. Modern diabetic medications have contributed substantially to improved systemic disease management and may positively influence long-term vision outcomes. Nevertheless, some ocular complications of these medications have been reported, and ongoing retinal monitoring remains essential because individual responses to treatment and disease progression can vary considerably between patients(18-20).

    At Onèj Optometry, we are committed to helping patients understand the relationship between diabetes and vision. Comprehensive diabetic retinal assessment involves careful evaluation of retinal health using advanced imaging technologies capable of detecting subtle retinal changes that may not be visible through conventional testing techniques. These examinations provide valuable information regarding both current ocular health and future risk, allowing management decisions to be made with greater confidence.

    If you have diabetes, we encourage you to learn more about comprehensive diabetic eye examinations and the role they play in preserving long-term ocular health. Our dedicated Diabetic Eye Test page provides further information regarding diabetic retinal assessment, retinal imaging and recommended examination intervals. Through regular monitoring, clear communication and collaborative care with your broader healthcare team, it is often possible to detect retinal changes early and support the preservation of vision throughout life.

References

  1. Vision Loss Expert Group of the Global Burden of Disease Study. (2024). Global estimates on the number of people blind or visually impaired by diabetic retinopathy: a meta-analysis from 2000 to 2020. Eye, 38(11), 2047. 

  2. Estaji, M., Hosseini, B., Bozorg-Qomi, S., & Ebrahimi, B. (2023). Pathophysiology and diagnosis of diabetic retinopathy: a narrative review. Journal of Investigative Medicine, 71(3), 265-278. 

  3. Kusuhara, S., Fukushima, Y., Ogura, S., Inoue, N., & Uemura, A. (2018). Pathophysiology of diabetic retinopathy: the old and the new. Diabetes & metabolism journal, 42(5), 364. 

  4. Sedova, A., Hajdu, D., Datlinger, F., Steiner, I., Neschi, M., Aschauer, J., ... & Pollreisz, A. (2022). Comparison of early diabetic retinopathy staging in asymptomatic patients between autonomous AI-based screening and human-graded ultra-widefield colour fundus images. Eye, 36(3), 510-516. 

  5. Bailey, C. C., & Sparrow, J. M. (2001). Visual symptomatology in patients with sight‐threatening diabetic retinopathy. Diabetic medicine, 18(11), 883-888. 

  6. Mohamed, Q., Gillies, M. C., & Wong, T. Y. (2007). Management of diabetic retinopathy: a systematic review. Jama, 298(8), 902-916. 

  7. Lee, R., Wong, T. Y., & Sabanayagam, C. (2015). Epidemiology of diabetic retinopathy, diabetic macular edema and related vision loss. Eye and vision, 2(1), 17. 

  8. Bryl, A., Mrugacz, M., Falkowski, M., & Zorena, K. (2022). The effect of hyperlipidemia on the course of diabetic retinopathy—literature review. Journal of clinical medicine, 11(10), 2761. 

  9. Zhang, M., Wu, J., Wang, Y., Wu, J., Hu, W., Jia, H., & Sun, X. (2023). Associations between blood pressure levels and diabetic retinopathy in patients with diabetes mellitus: A population-based study. Heliyon, 9(6). 

  10. Lundeen EA, Burke-Conte Z, Rein DB, et al. Prevalence of Diabetic Retinopathy in the US in 2021. JAMA Ophthalmol. 2023;141(8):747–754. 

  11. Abhary, S., Hewitt, A. W., Burdon, K. P., & Craig, J. E. (2009). A systematic meta-analysis of genetic association studies for diabetic retinopathy. Diabetes, 58(9), 2137-2147. 

  12. Archer, D. B., Gardiner, T. A., & Stitt, A. W. (2007). Functional anatomy, fine structure and basic pathology of the retinal vasculature. In Retinal vascular disease (pp. 3-23). Berlin, Heidelberg: Springer Berlin Heidelberg. 

  13. Fong, D. S., Ferris III, F. L., Davis, M. D., Chew, E. Y., & Early Treatment Diabetic Retinopathy Study Research Group. (1999). Causes of severe visual loss in the early treatment diabetic retinopathy study: ETDRS report no. 24. American journal of ophthalmology, 127(2), 137-141. 

  14. McAllister, M., Ko, S., Bawa, K., Mearns, E., Tabano, D., Martinez, A., ... & Lim, J. I. (2025). Clinical practice guidelines for the treatment and management of diabetic macular oedema: a systematic review. Eye, 39(17), 3121-3128. 

  15. Yuen, Y. S., Gilhotra, J. S., Dalton, M., Aujla, J. S., Mehta, H., Wickremasinghe, S., ... & Broadhead, G. K. (2023). Diabetic macular oedema guidelines: an Australian perspective. Journal of Ophthalmology, 2023(1), 6329819. 

  16. Liu, E., Craig, J. E., & Burdon, K. (2017). Diabetic macular oedema: clinical risk factors and emerging genetic influences. Clinical and Experimental Optometry, 100(6), 569-576. 

  17. Crabtree, G. S., & Chang, J. S. (2021). Management of complications and vision loss from proliferative diabetic retinopathy. Current diabetes reports, 21(9), 33. 

  18. Wong, T. Y., Sun, J., Kawasaki, R., Ruamviboonsuk, P., Gupta, N., Lansingh, V. C., ... & Taylor, H. R. (2018). Guidelines on diabetic eye care: the international council of ophthalmology recommendations for screening, follow-up, referral, and treatment based on resource settings. Ophthalmology, 125(10), 1608-1622. 

  19. Luo, Y., Xia, Y., Gong, X. et al. GLP-1 receptor agonists in eye disease: a comprehensive review of current research and future potential. BMC Ophthalmol 26, 12 (2026). 

  20. Saw, M., Wong, V. W., Ho, I. V., & Liew, G. (2019). New anti-hyperglycaemic agents for type 2 diabetes and their effects on diabetic retinopathy. Eye, 33(12), 1842-1851.