Type of publication:
Conference abstract
Author(s):
*Rao P.; *Zaw S.-N.; Garikapati N.; *Godbole K.; Veeramani P.; *Perera L.
Citation:
Eye (Basingstoke). Conference: The Royal College of Ophthalmologists Annual Congress 2025. Liverpool United Kingdom. 39 (pp 244-245), 2025. Date of Publication: 01 Jun 2025.
Abstract:
Introduction: With emergence of new imaging technology adult vitelliform macular degeneration (AVMD) is being diagnosed with increasing frequency over the last two decades. The condition is often mistaken for wet age-related macular degeneration (ARMD) when the vitelliform material starts scrambling showing pseudo fluid in optical coherence tomography (OCT) scans. In addition, in some AVMD patients the vitelliform lesions in fact do develop choroidal neovascularisation (CNV) requiring urgent intravitreal injections. We aim to highlight the prevalence, natural progression and treatment options for patients presenting with AVMD. Method(s): We have retrospectively analysed 123 eyes of 82 patients of AVMD presented to this department over the last 4 years. Result(s): We identified 44 females and 38 males, 41 patients with bilateral involvement at presentation. The clinical findings varied from a classical sub foveal yellow lesion to partial empty spaces within the lesion, to complete atrophic scar following resorption of all the colloid material. The presenting Visual acuity in the worse eye also varied from 6/9 to HM according to the stage of degeneration they presented with. Thirty-nine patients were asymptomatic and AVND was an incidental finding in one of their eyes. We have obtained serial optical coherence tomography (OCT) scan to monitor the progress whenever possible. All patients had OCT, optical coherence tomographic angiography (OCTA), and fundus autofluorescence (FAF). Some patients in addition underwent fundus fluorescein angiography (FFA) and indocyanine green angiography (ICG) when a choroidal neovascular membrane (CNVM) was suspected. Sixty nine of 82 patients did not need any active interventions. Fourteen patients were already taking antioxidant supplementations. Thirteen patients have developed significant subretinal fluid (SRF) and were treated with intravitreal anti-vascular endothelial growth factor (VEGF) injections. On further reviewing of the OCTA scans and FFA only 10 of 13 showed active CNVM. The other 3 patients only had passive subretinal fluid with no evidence of CNVM. Therefore only 12 % of AVMD patients seem to have developed wet ARMD in our series. Response to the anti-VEGF injections was suboptimal in AVMD patients with CNV compared to a case of conventional wet ARMD. This unfavourable response was most likely due to pre-existing long standing atrophic and degenerative changes. Contrary to earlier publications, based on family history alone we did not find any strong evidence of autosomal dominance inheritance therefore we prefer to call it a degenerative rather than dystrophic condition. Conclusion(s): With increasing use of OCT imaging by optometrists and primary care physicians more patients are being diagnosed with macular pathology, AVMD is one such condition. Most of these patients do not need any active interventions or long term follow ups in hospital clinics. Our study shows only 12% of AVMD patients go on to develop CNV requiring intravitreal anti-VEGF injections. As our cohort shows it may not be unusual to mistake passive fluid lakes within vitelliform lesions for active wet ARMD. It is important for clinicians to be aware of the possibility of AVMD with passive subretinal fluid and not to resort to unnecessary long term intravitreal anti-VEGF injections. As we have shown even in cases of AVMD with secondary CNV the prognosis is poor for long term retention of central vision.
DOI: 10.1038/s41433-025-03831-0
