Results of intravitreal injection in the treatment of diabetic macular edema

Diabetic macular edema (DME) is the most common cause of visual impairment in patients with diabetes mellitus. DME occurs as a result of disruption of the blood–retinal barrier, by accumulation of fluid within the intraretinal layers of the macula. Hypoxia and inflammation due to diabetes related vasoconstriction and capillary loss leads to up-regulation in expression of vascular endothelial growth factor (VEGF) and increases vascular permeability. Although laser photocoagulation is the standard care of-treatment, it was not curable. As pathophysiology of DME consists of a variety of factors and biochemical pathways, many different modalities are being used in its treatment. Ranibizumab (Lucentis®) is an intravitreal agent that is currently licensed for the treatment of visual impairment due to DME. Ranibizumab selectively inhibits the binding of active isoforms of human vascular endothelial growth factor A (VEGF-A) to its receptors. It is suggested that dexamethasone intravitreal implant (Ozurdex®) may be an effective and safe alternative in treatment of chronic DME nonresponsive to regular intravitreal anti-VEGF injection. In our study, at least 3 doses of intravitreal ranibizumab, at least one dose of dexamethasone intravitreal implant and 3 doses of intravitreal ranibizumab were considered to be resistant to treatment with diabetic macular edema, and we aim to compare the efficacy and safety of treatment with dexamethasone intravitreal implant in a short time and compare it's effects to visual acuity, retinal thickness,intra ocular pressure (IOP). The files of the patients who were diagnosed with diabetic retinopathy between January 2014 and August 2016 were retrospectively reviewed in the retina unit of Department of Ophthalmology, Akdeniz University Medical Faculty. The disease was diagnosed with fundus examination, OCT and FFA. The records of 475 eyes of 365 patients diagnosed with DME were reviewed. However, due to follow-up and / or data insufficiency; 350 eyes of 250 patients were included in the study. There were 287 eyes in group 1, 32 eyes in group 2 and 31 eyes in group 3. In the visual evaluation of the patients; Mean best corrected visual acuity before injection was 0.64 ± 0.36 logMAR in group 1, 0.76 ± 0.41 logMAR in group 2 and 0.65 ± 0.35 logMAR in group 3 respectively. After treatment, group 1 was found to be 0,45 ± 0,33 logMAR after best corrected visaul acuity, 0,40 ± 0,29 and 0,43 ± 0,35 logMAR in group 2 and 3, respectively. In all groups, best corrected visaul acuity values were significantly higher than before treatment. (p <0,01). When best corrected visaul acuity was evaluated before and after treatment between groups, the most change was observed in group 2 (p <0,01). Mean macular thickness was assessed by OCT in all groups. Mean macular thickness value after injection was significantly lower than mean macular thickness before injection. (p <0,01) When the groups were evaluated in terms of macular changes, it was found that the change in macular thickness was significantly higher in the group 2 treatment group (p <0.01). There was a statistically significant increase in intraocular pressure values in groups 2 and 3. (P & lt; 0.05). No significant adverse effects due to injections were observed in all treatment groups. As a result, there is an increase in visual acuity with a decrease in diabetic macular edema in the treatment groups in the short term. Combinations of anti-VEGF and steroids are promising in refractory diabetic macular edema. Key words: Ranibizumab, Dexamethasone implant, dexamethasone implant in Ranibizumab resistant cases, mean macular thickness, diabetic macular edema, intraocular pressure, best corrected visual acuity