Uveal effusion may be caused by hypotony, ocular inflammation, infection, trauma, nanophthalmos, medications, vascular malformations, or circulatory abnormalities. In these conditions excessive leakage from the choroidal vasculature, driven by increased flow, pressure, or decreased vascular competence, leads to the accumulation of choroidal fluid, typically in the equatorial and pre-equatorial regions of the eye. While the accumulation of fluid can occur anywhere in the thickness of the choroid, prominent collections accumulate in the outer choroid, typically in the suprachoroidal space, a region where there is a sparse collection of linking fibers. Central serous chorioretinopathy is a condition presumed to occur secondary to choroidal hyperpermeability as first proposed by Gass. Multifocal areas of hyperpermeability in the posterior pole were found decades later when angiography using indocyanine green became possible. The idea was that the hyperpermeability caused the choroid hydrostatic pressure to increase, leading to detachments of the retinal pigment epithelium (RPE) and hyperbaric defects in the RPE monolayer, seen as “leaks” under the retina. If the pressure increased within the choroid in central serous chorioretinopathy, one would expect the choroid to be thickened. Indeed, thickening of the choroid was found using enhanced depth imaging (EDI) optical coherence tomography (OCT). However, the nature of the thickening of the choroid remains undefined; it is possible that fluid accumulates in the posterior choroid in central serous chorioretinopathy as it does in other forms of uveal effusion. Evaluation of the nature of any possible accumulation may give further clues as to the pathophysiology of the disease and suggest additional modalities of treatment.

Methods

This retrospective study was approved by the Western Institutional Review Board (Puyallup, Washington, USA) and complied with the Health Insurance Portability and Accountability Act of 1996. The patients in this study were evaluated in a community-based retinal practice in New York during the past 2 years by one of the authors (R.F.S.) and from a community-based retinal practice in Minnesota (by author E.H.R.). Patients with a diagnosis of central serous chorioretinopathy were included whether or not they had active disease at the time of study entry. The diagnosis of central serous chorioretinopathy was based on the appearance of subretinal fluid caused by leaks from the level of the retinal pigment epithelium as diagnosed by fluorescein angiography in the absence of accelerated hypertension, inflammation, or infiltration. Patients with choroidal neovascularization or a history of photodynamic therapy or those with ocular media problems limiting fundus imaging were excluded. The patients had macular OCT evaluations using the Heidelberg Spectralis HRA+OCT (Heidelberg Engineering, Heidelberg, Germany) to include EDI OCT scans over a 30 × 5 degree region with 100 images averaged using 7 sections in New York. In Minnesota a number of scan variations were done with the EDI technique using the same OCT instrument. The scan width varied between 15 and 30 degrees. The section through the fovea was used to measure the choroidal thickness, which was the distance between the outer edge of the reflection caused by the retinal pigment epithelium/Bruch membrane complex to the inner border of the sclera. Some patients were also imaged using a prototype swept source OCT instrument (Atlantis OCT; Topcon Medial Systems, Oakland, New Jersey, USA), which has a light source with center wavelength of 1050 nm and a bandwidth of 100 nm; the instrument scans at 100 000 A-scans per second and, depending on the scan protocol, can average images. The choroid was evaluated for the presence of hyporeflective extravascular spaces greater than 250 μm in smallest diameter. These were presumed to represent posterior loculations of fluid. These were subclassified as interdigitated, in which the dark extravascular spaces extended between and behind the larger choroidal vessels in the posterior choroid ( Figure 1 ). A second subtype was termed dissociated and represented isolated collections of fluid posterior to the larger choroidal vessels. Data were analyzed with descriptive statistics and to evaluate relationships between the vitreous anatomic findings and age-generalized estimating equations were used. A P value less than or equal to .05 was considered significant. The IBM SPSS version 21 statistical package was used (IBM Corporation, Armonk, New York, USA).

Drawing showing the possible patterns of accumulation of choroidal fluid graded in this study of eyes with central serous chorioretinopathy. (Top) A schematic representation of a normal choroid showing the choriocapillaris and Sattler’s and Haller’s layers. (Middle) The choroid is drawn to be approximately 50% thicker, as is common to see in central serous chorioretinopathy. In this drawing there is an accumulation of fluid in the outer choroid, but the boundary between the fluid and the choroidal stroma is not well demarcated. The fluid extends up between the larger choroidal vessels; this type of appearance was called “interdigitated.” Bottom. The choroid in this drawing is also thicker, but there is a well-defined separation between the fluid collection and the rest of the choroid.