RPE microrips within pigment epithelial detachments colocalise with focal leakage in acute central serous chorioretinopathy: pathophysiology and therapeutic implications.

内容摘要

To determine the prevalence of retinal pigment epithelium (RPE) microrips within serous pigment epithelial detachments (PEDs) in first-episode acute central serous chorioretinopathy (CSCR) and to assess their spatial relationship with focal angiographic leakage using multimodal imaging. Retrospective observational case series. Thirty-nine eyes of 39 patients with acute CSCR (symptom duration <3 months). All eyes underwent spectral-domain OCT, fluorescein angiography, and indocyanine green angiography (ICGA). Imaging biomarkers at leakage sites included PEDs, RPE microrips, outer retinal erosion and outer retinal pinching, pachyvessels, midphase ICGA hyperfluorescent plaques, and subfoveal choroidal thickness. Clinical outcomes included best-corrected visual acuity, subretinal fluid (SRF) resolution, recurrence, and progression to chronic disease. Mean age was 44.5 &#xb1; 10.0 years, and 61.5% of patients were male. PEDs colocalized with the focal leakage site in all eyes, whereas RPE microrips colocalized with the site of focal angiographic leakage in 66.7% of eyes, with good interobserver agreement (&#x3ba;&#x202f;=&#x202f;0.79) observed. Outer retinal erosion and outer retinal pinching were observed in 38.5% and 12.8% of eyes, respectively. Midphase ICGA hyperfluorescent plaques were observed in 56.4% and pachyvessels in 46.2% of cases. Mean best-corrected visual acuity improved from 0.24 &#xb1; 0.25 (20/34 Snellen) to 0.10 &#xb1; 0.17 logMAR (20/25 Snellen) at final follow-up, with complete SRF resolution in 68.4%. Baseline subfoveal choroidal thickness correlated with SRF height (P&#x202f;=&#x202f;0.018), but no baseline imaging biomarkers predicted final visual or anatomical outcomes. RPE microrips within serous PEDs frequently are observed and precisely colocalise with focal leakage in acute CSCR, supporting a mechanical model of focal RPE dehiscence driven by increased choroidal pressure. These findings provide insight into CSCR pathophysiology and may inform therapeutic strategies.