Session Title: Quick Fire Free Paper 1
Session Date/Time: Thursday 11/09/2014 | 08:00-10:00
Paper Time: 08:45
Venue: Boulevard D
First Author: : K.Xue UK
Co Author(s): : E. Yang V. Chong
The pathogenesis of diabetic macular oedema (DMO) is not fully understood. The angiogenic cytokine, vascular endothelial growth factor (VEGF), is thought to be one of the contributing factors. The anti-VEGF drug, ranibizumab, has been shown to be effective in the treatment of DMO, but it is unclear whether subgroups of DMO patients respond more to treatment than others. Our aim is to distinguish different mechanisms of DMO based on clinical imaging techniques, and attempt to predict differential responses to anti-VEGF treatment based on these findings.
A retrospective analysis of images and clinical data derived from a consecutive cohort of patients who received intravitreal ranibizumab treatment for DMO in accordance with National Institute of Clinical Excellence (NICE) guidelines at the Oxford Eye Hospital, United Kingdom.
DMO patients with central retinal thickness (CRT) greater than 400 μm on OCT underwent Heidelberg ultra-widefield fundus fluorescein angiography (FFA) prior to receiving monthly intravitreal ranibizumab therapy. Follow-up with best-corrected visual acuity (BCVA) and OCT were carried out at monthly intervals up to a period of six months. FFA and OCT images were analysed by two independent assessors to determine different mechanisms of DMO. Mechanistic findings were correlated with responses to ranibizumab treatment.
Ultra-widefield FFA and OCT of 63 eyes of 45 patients with DMO were analysed. DMO appeared to be driven by three predominant mechanisms based on ultra-widefield FFA findings: (A) local leakage from microaneuryms (51%), (B) adjacent areas of retinal ischaemia demonstrating capillary non-perfusion (35%), (C) presence of active new vessels showing leakage (14%). DMO associated with mechanisms B and C (but not A) showed significantly greater probability of fluid extension beyond the macula region on OCT (Chi-square 7.02, p = 0.03). There was however no significant difference in CRT or area of DMO between the three groups. Following three months of ranibizumab treatment, DMO associated with mechanisms A and B achieved mean reductions in CRT of 130 μm (standard deviation 66) and 358 μm (SD 215) respectively, whereas those associated with mechanism C showed no significant reduction in CRT.
DMO has heterogeneous pathogenesis based on ultra-widefield FFA, varying from focal vascular leakage from clusters of microaneurysms within the macula to generally increased vascular permeability driven by VEGF derived from ischaemic peripheral retina. The latter mechanism should be suspected when DMO appears to extend beyond the macular region on OCT. DMO associated with microaneurysms or areas of capillary drop-out on ultra-widefield FFA appear to respond more favourably to anti-VEGF therapy than those associated with frank new vessels. The findings would support the use of ultra-widefield FFA prior to anti-VEGF therapy when OCT shows DMO extending beyond the macula. This would help to rule out active new vessels which would be more effectively treated with laser retinal photocoagulation.