Posters

Drusen ooze: A novel hypothesis in geographic atrophy

Poster Details

First Author: J.Monés SPAIN

Co Author(s):    M. Garcia   M. Biarnes   A. Lakkaraju   L. Ferraro                    

Abstract Details



Purpose:

To describe a subgroup of subjects with soft drusen associated with geographic atrophy (GA) and novel spectral-domain optical coherence tomography (SD-OCT) findings consistent with presumed drusen leakage. We also propose a mechanism leading to GA progression in these patients.

Setting:

Institut de la Màcula, and Barcelona Macula Foundation, Barcelona

Methods:

A retrospective, observational cohort study. Forty-eight eyes of 33 patients with soft drusen secondary to age-related macular degeneration (AMD). Drusen were evaluated with SD-OCT and retinal imaging to characterize the development of atrophy-associated drusen regression (drusen collapse) over a follow-up period of at least 18 months. Main outcomes were presence of isoreflective dots at the outer retinal layers associated with retinal pigment epithelium (RPE) defects. Previously reported rates of hyper-reflective RPE, and hyper-reflective dots (HRD) were also determined.

Results:

Nineteen (19) of 48 eyes (39.6%) showed a collapse of at least one drusen during the follow-up period. Thirty-four foci of collapsed drusen were found to be associated with either isoreflective dots associated with RPE defects (32.4%), hyper-reflectivity of the RPE (91.2%), or HRD (79.4%). A post-hoc showed the adjusted odds ratio of drusen collapse for isoreflective dots (65.8), for HRD (6.0) or both (12.1).

Conclusions:

In soft drusen progressing to subsequent atrophy, approximately 33% were associated with isoreflective dots and RPE defects. In addition, overlying hyper-reflectivity of the RPE and HRD were noted with high frequency. Presence of isoreflective dots, with or without HRD, was associated with a strong risk of developing atrophy compared to drusen without these findings. We hypothesize that these isoreflective dots associated with RPE defects may be debris extruded from the soft drusen into the subretinal space, which we have termed 'drusen ooze'. Drusen ooze may activate the RPE apical surfaces, leading to a marked increase in phagocytosis/endocytosis of extracellular debris that eventually overwhelms the RPE capacity, and leads to RPE death, subsequent release of intracellular RPE material and thereby propagate a cycle of cellular death resulting in GA development and progression. Therapeutic targeting of drusen material, prior to its extrusion into the subretinal space and prior to irreversible damage to the RPE, might prevent or delay onset and progression of GA.

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