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To describe the frequency and characteristics of intraretinal and subretinal fluid in nonarteritic anterior ischemic optic neuropathy (NAAION) and to assess the influence on the visual deficit and optic nerve fiber/ganglion cell loss. A retrospective, single-center study. Thirty-two patients with NAAION referred to our Neuro-ophthalmology Department between 2014 and 2021. The study was carried out at the University Hospital of Liège, Belgium. For participants in whom subretinal fluid was identified on standard OCT (Carl Zeiss Meditec) an additional macular OCT (Spectralis Heidelberg) had been performed. The pattern and the maximal height of the retinal fluid were determined manually, and thicknesses of retinal layers were obtained using the OCT protocol analysis. The mean age of the cohort was 60 years (standard deviation, ±12.5; range, 22–88 years), and 65.6% were male. In the 21 eyes (46.7%) in which retinal fluid was observed, macular OCT findings were categorized according to fluid localization: 19 cases had parafoveal fluid (of whom 9 also had subfoveal fluid). One patient had subfoveal fluid alone, and 1 patient had peripapillary subretinal fluid alone. Specific patterns of optic disc (OD) swelling were associated with the occurrence and distribution of retinal edema. Visual acuity, visual field loss, and foveal thresholds were stable over the period of observation (P = 0.74, P = 0.42, and P = 0.36, respectively). No difference was found in visual function at 6 months between patients with retinal fluid treated (n = 10) or not treated (n = 11) with corticosteroids (visual acuity, P = 0.13; foveal threshold, P = 0.59; mean deviation, P = 0.66). Subretinal fluid is found in a high proportion of cases of NAAION. Visual function remained largely stable from presentation in this cohort. Corticosteroid intake at presentation did not influence visual recovery or timing of the resorption of tissue edema. Our findings do not support treatment of NAAION with corticosteroids with or without evidence of subretinal fluid acutely. With regard to pathogenesis, we propose that the volume of transudate generated at the OD is the critical factor rather than dysfunction of retinal mechanisms subserving reabsorption. Proprietary or commercial disclosure may be found in the Footnotes and Disclosures at the end of this article. [ABSTRACT FROM AUTHOR]