Diabetic macular oedema: pathophysiology, management challenges and treatment resistance

Diabetologia. 2016 Aug;59(8):1594-608. doi: 10.1007/s00125-016-3974-8. Epub 2016 May 14.

Abstract

Diabetic macular oedema (DMO) is the leading cause of vision loss in patients living with diabetes. DMO results from hyperglycaemia-induced activation of pathways that lead to oxidative stress and release of cytokines, impairing the inner and outer blood-retinal barriers. Improved understanding of the pathophysiological mechanisms leading to DMO have led to the development of effective therapies, including vitreoretinal surgery, laser photocoagulation, intravitreal anti-vascular endothelial growth factor drugs and corticosteroids. Advances in imaging, including fluorescein angiography and optical coherence tomography, have also enhanced diagnosis and management of the condition. Despite these advances, there remain patients who do not respond completely to therapy, reflecting the complex pathophysiology of DMO. These patients may be considered treatment-resistant. In this review, we summarise the pathophysiology of DMO, as well as the available treatments and their mechanism of action. Additionally, we focus on treatment-resistant disease and review the literature on potential options for managing this complication of diabetes.

Keywords: Anti-vascular endothelial growth factor; Diabetic macular oedema; Intravitreal corticosteroids; Laser photocoagulation; Review; Treatment resistance; Vitrectomy.

Publication types

  • Review

MeSH terms

  • Animals
  • Diabetic Retinopathy / metabolism
  • Diabetic Retinopathy / physiopathology
  • Humans
  • Hyperglycemia / drug therapy
  • Macular Edema / metabolism
  • Macular Edema / physiopathology*
  • Vascular Endothelial Growth Factor A / antagonists & inhibitors
  • Vascular Endothelial Growth Factor A / metabolism

Substances

  • Vascular Endothelial Growth Factor A