Central serous chorioretinopathy (CSCR) is a maculopathy characterized by the separation of the neurosensory layer as a result of fluid accumulation between the retinal pigment epithelium (RPE) and the photoreceptor layer. Classically it is classified as acute and chronic forms. When the disease lasts longer than 4-6 months, it is called a chronic form and comprises 15% of all CSCR cases. Although the exact etiology is unknown; studies emphasize changes in choroidal circulation causing choroidal ischemia and vascular hyperpermeability as well as subretinal fluid accumulation due to deterioration pump function of RPEs. Subretinal fluid accumulation can lead to photoreceptor dysfunction and loss of vision. Classical findings in patients are a decrease in visual acuity, blurred vision, metamorphopsia, micropsia, disturbance in color vision and dark adaptation, and scotomas. Diagnosis and follow-up depend on fundoscopy as well as imaging. Optical coherent tomography is the primary method. Fundus autofluorescence (FAF) is useful in defining RPE changes noninvasively. Fundus fluorescein angiography (FFA) shows the source of leakage. In recurrent, unresolved and chronic cases, OCT, FAF, FFA, and indocyanine green angiography can be used all together to manage the disease, to follow-up its extension, and to diagnose possible neovascular as well as polypoidal component. For the treatment of chronic CSCR patients, besides medical treatments such as carbonic anhydrase inhibitors, mineralocorticoid receptor, and glucocorticoid antagonists and intravitreal vascular endothelial growth factor antagonist (Anti-VEGF) injections, half-dose photodynamic therapy and subthreshold micropulse laser treatment are used. Prospective, controlled trials with large series for the treatment of chronic CSCR warranted.
The association between visual function and retinal structure in chronic central serous chorioretinopathy
