Central serous chorioretinopathy: an update on pathogenesis and treatment

Central serous chorioretinopathy (CSC) is a chorioretinal disease, incompletely understood with systemic associations, a multifactorial aetiology, and a complex pathogenesis. Increased permeability from the choriocapillaris leads to focal or diffuse dysfunction of the retinal pigment epithelium causing a detachment of the neurosensory retina. CSC has been described in patients with endogenously high levels of corticosteroids as well as in patients with hypercortisolism due to the treatment of ocular or systemic diseases. It is therefore the only ‘inflammatory’ choroiditis, not proven to be associated with infection that is precipitated or worsened by glucocorticoids. Foveal attenuation, chronic macular oedema, and damage of the foveal photoreceptor layer have been reported as causes of visual loss in CSC. Photoreceptor atrophy in the fovea, despite successful retinal reattachment, typically occurs after a duration of symptoms of approximately 4 months. Treatment should therefore be considered after 3 months if there is angiographic evidence of ongoing foveal leakage in recurrent chronic CSC or in a single CSC episode accompanied by signs of chronic CSC alterations. Based on results of trials conducted so far, it appears that photodynamic therapy with verteporfin is effective and safer than argon laser treatment and should be considered as the treatment of choice, whereas micropulse diode laser photocoagulation seems to be an effective alternative. Glucocorticoid inhibitors are an interesting alternative treatment. Clinical trials are ongoing to test their efficacy. In addition, it is important, where possible, to discontinue any corticosteroid treatment. The possible association of CSC with stress should also be discussed with patients.