Abstract
Purpose:
To investigate the intrachoroidal structure in eyes with acute or chronic central serous chorioretinopathy (CSC) using spectral-domain optical coherence tomography (SD-OCT).
Methods:
This retrospective observational case series involved 53 eyes of 51 patients (11 eyes of 11 females and 42 eyes of 40 males; mean age: 53.9 years) with CSC which had serous retinal detachment at the fovea. The clinical diagnosis of acute CSC was based on the duration of symptoms less than 6 months and the clinical findings on fluorescein angiography showing the typical pattern for one or several leakage points at the level of the retinal pigment epithelium. CSC cases other than acute CSC were categorized as chronic CSC. Eyes with a history of any other retinal diseases, a history of intraocular surgery or photodynamic therapy, a history of taking systemic corticosteroids, or high myopia (spherical equivalent less than minus 6 diopters or axial length longer than 26.5 mm) were excluded. The SD-OCT images of each case were evaluated for intrachoroidal structure; i.e., choroidal thickness (CT), thickness of the choriocapillaris with Sattler`s layer (CS), and thickness of the Haller`s layer (HL). The CT, CS, and HL were measured by 2 independent observers at the fovea, 1-mm nasal and temporal to the fovea on the horizontal cross-sectional image.
Results:
Twenty-two eyes of 21 patients with acute CSC and 31 eyes of 30 patients with chronic CSC were included. The mean CT in the eyes with acute CSC was significantly thicker than in those with chronic CSC, even after adjusting for age and spherical equivalent (423 μm vs. 359 μm, p=0.01). The mean HL in the eyes with acute CSC was significantly thicker than in those with chronic CSC (314 μm vs. 246 μm, p<0.01). The difference in mean CS between the eyes with acute CSC and those with chronic CSC was not statically significant (109 μm vs. 113 μm, p=0.45).
Conclusions:
The eyes with acute CSC had a significantly thicker choroid and thicker Haller`s layer compared to those with chronic CSC. This result suggests that the contribution of the choroid, especially the HL, to the pathogenesis of CSC may differ at each phase of the disease.