Diabetic Macular Edema (DME) it is a complication associated with DR and the main cause of vision loss in diabetic patients. It represents the main cause of blindness in the active population in industrialized countries, and presents a prevalence of around 7.5% of diabetic patients (1). In Europe there are 4 million people with DME and in Spain, approximately 300,000 patients.
DME affects the macula, which is the central region of the retina where there is the highest concentration of photoreceptors and is where the central vision is generated and in greater detail.
Traditionally it has been defined as a clinical picture characterized by the existence of a thickening of the retina in the macular area (in an area of 2 papillary diameters from the center of the macula) that occurs as a result of the appearance of microvascular changes that compromise to the blood-retinal barrier, which separates the blood from the retina (2).
In most cases, the DME is a pathology that requires interventions and continued treatment. Laser, which has traditionally been considered the treatment of choice in these patients, has been replaced, in many cases, by pharmacotherapy to the point where different treatment options are available today. The key to success lies in knowing how to choose the most appropriate for each specific case.
The pathogenesis of this disease varies with time and between patients. In early stages, DME is mainly mediated by the angiogenic factor VEGF (Vascular Endothelial Growth Factor), which is induced due to the hypoxia suffered by the tissue of the retina and which favors the accelerated and abnormal growth of blood vessels of poor quality. that contribute to the filtration of plasma components in the retina and the consequent appearance of inflammation and edema. At this time it is convenient to block the action of VEGF by intravitreal anti-VEGF drugs.
But as the disease progresses and, in turn, the degree of severity of DR increases, VEGF levels remain relatively constant while the levels of other pro-inflammatory cytokines increase exponentially (3). In this phase, which can reach, with high interindividual variability, between 1 and 2 years after diagnosis, it may be necessary to treat with an anti-inflammatory drug (4), (5).
Intravitreal corticosteroids have shown in numerous studies that, in addition to blocking numerous pro-inflammatory cytokines, they also have a known anti-angiogenic effect (6). Thus, in this phase of the disease, anti-VEGF are not as suitable since they have effect only against VEGF and conversely, corticoids can do much better treatment of this multifactorial disease. Currently, there are 2 options of corticosteroid for the treatment of DME: a short-acting one that requires reinjections every 3-6 months and a long-acting one, which has shown a duration of effect of 3 years.
The diagnosis and assessment of edema should be carried out by an expert ophthalmologist and in the follow-up should always take into account: best corrected visual acuity (BCVA), biomicroscopic examination and OCT (optical coherence tomography), non-invasive test with which the thickness of the enlarged macula can be measured quantitatively, one of the signs that there is edema (thickening in the macular area) (2).