Abstract
Purpose: :
The aim of the current study was to examine the effect of intravitreal triamcinolone acetonide on patients with diabetic macular edema. Previously, we have proposed a mathematical model that relates pressure attenuation in retinal arterioles to the length and caliber of vessels. The development of macular edema or any exudative fluid collection requires two preexisting conditions: increased vascular permeability and sufficient hydrostatic pressure to drive fluid out of the vasculature. We hypothesized that the mechanism of action of triamcinolone acetonide in the resolution of macular edema is through a reduction of perfusion within the arterioles.
Methods: :
In the current study, we tested the effect of intravitreal triamcinolone acetonide in 7 patients with macular edema related to diabetes mellitus. To test our hypothesis that triamcinolone acetonide acts by reducing perfusion within retinal arterioles, we measured retinal vessel caliber pre– and several weeks post– injection.
Results: :
Preliminary results (n=7) show no statistically significant reduction in vessel caliber post triamcinolone injection, suggesting that modification of vascular permeability may be the primary mechanism for resolution of macular edema. Complete results from this study will be presented.
Conclusions: :
Injection of triamcinolone acetonide resulted in a resolution of macular edema although retinal arteriolar caliber was unaltered pre– and post– injection. These findings are inconsistent with the hypothesis that triamcinolone acetonide reduces perfusion within arterioles and rather they support a view that triamcinolone acetonide acts by decreasing vascular permeability.
Keywords: corticosteroids • diabetes • macula/fovea