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RPE microrips within pigment epithelial detachments colocalize with focal leakage in acute central serous
Mostafa Mafi1, Elodie Bousquet2, Alessandro Feo3
1Flaum Eye Institute, University of Rochester Medical Center, Rochester, NY; Stein Eye Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA.
Objective:
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.
Design:
Retrospective observational case series.
Participants:
Thirty-nine eyes of 39 patients with acute CSCR (symptom duration <3 months).
Methods:
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.
Results:
Mean age was 44.5 ± 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 (κ = 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 ± 0.25 (20/34 Snellen) to 0.10 ± 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 = 0.018), but no baseline imaging biomarkers predicted final visual or anatomical outcomes.
Conclusions:
RPE microrips within serous PEDs frequently are observed and precisely colocalize 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.
Insights
Retinal pigment epithelium (RPE) microrips are common in serous pigment epithelial detachments (PEDs) in acute central serous chorioretinopathy (CSCR). These microrips precisely align with leakage sites, suggesting a mechanical cause related to choroidal pressure.
Area of Science:
- Ophthalmology
- Retinal Imaging
- Chorioretinopathy Research
Background:
- Central serous chorioretinopathy (CSCR) is characterized by fluid accumulation under the retina.
- The role of retinal pigment epithelium (RPE) abnormalities in CSCR pathophysiology requires further elucidation.
- Serous pigment epithelial detachments (PEDs) are common findings in acute CSCR.
Purpose of the Study:
- To determine the prevalence of RPE microrips within serous PEDs in acute CSCR.
- To assess the spatial relationship between RPE microrips and focal angiographic leakage.
- To investigate the association of imaging biomarkers with clinical outcomes in CSCR.
Main Methods:
- Retrospective observational case series of 39 eyes with acute CSCR.
- Multimodal imaging including spectral-domain OCT, fluorescein angiography, and ICGA.
- Analysis of imaging biomarkers at leakage sites and correlation with visual acuity and fluid resolution.
Main Results:
- RPE microrips colocalized with focal leakage in 66.7% of eyes with PEDs.
- Outer retinal erosion and pinching were observed in 38.5% and 12.8% of eyes, respectively.
- Visual acuity improved significantly, and subretinal fluid resolved in 68.4% of cases; no baseline biomarkers predicted outcomes.
Conclusions:
- RPE microrips within serous PEDs are frequent and align with focal leakage in acute CSCR.
- Findings support a mechanical model of RPE dehiscence due to increased choroidal pressure.
- Understanding these mechanisms may guide future therapeutic strategies for CSCR.
