Abstract
Purpose :
Intravitreal dexamethasone implant (Ozurdex®) is an effective alternative treatment for diabetic macular edema (DME). The pathophysiology of DME involves both intracellular swelling of Muller cells and extracellular fluid accumulation. The clinical efficacy of Ozurdex® on reducing fluid accumulation in different retinal layers, i.e. histopathologic sections of DME, is not well understood.
Methods :
We analyzed spectral-domain optical coherence tomography (SD-OCT) data of 12 recalcitrant DME cases at the Drexel Eye Clinic from July 2015 to September 2017. All patients received an SD-OCT at the time of the first Ozurdex® and a follow up SD-OCT 1-4 months later. The small sample size of the current study was the result of stringent requirements on SD-OCT image quality. First, overlay analysis using identifiable foveal architectural elements was performed on each SD-OCT scan. Second, a self-designed software protocol was used to compensate for errors in layer segmentation from edematous macula. The thickness of each layer of the central retina belt between the 1mm and 3mm circles was then averaged. Two-tailed t-tests were used to assess two group comparisons. Multi-group comparisons were analyzed with one-way ANOVA. P-values less than 0.05 were considered statistically significant.
Results :
Central subfield foveal thickness (CSFT) decreased after Ozurdex implant from 380µm to 299µm (p=0.02). The mean thickness of individual parafoveal layers changed as follows - retinal nerve fiber layer: 117µm to 81µm (p=0.03), ganglion cell layer: 54µm to 43µm (p=0.06), inner plexiform layer: 41µm to 38µm (p=0.07), inner nuclear layer (INL): 45µm to 40µm (p=0.0006), outer plexiform layer (OPL): 37µm to 36µm (p=0.58). One-way ANOVA showed significant differences between the reduced CSFT and the decreased INL (p = 0.0105) as well as the reduced CSFT and the decreased OPL (p=0.0067), respectively.
Conclusions :
The inner nuclear layer, containing Muller cell somas, had the most statistically significant reduction in parafoveal thickness. This suggests that a decrease in intracellular swelling of Muller cells is a major mechanism for intravitreal dexamethasone. In addition, the decreases in CSFT and thickness of OPL were significantly correlated, suggesting there is an additional mechanism of intravitreal dexamethasone on extracellular edema.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.