Central serous chorioretinopathy

Abstract

ABSTRACT.Central serous chorioretinopathy (CSC) is a disease of the retina characterized by serous detachment of the neurosensory retina secondary to one or more focal lesions of the retinal pigment epithelium (RPE). CSC occurs most frequently in mid-life and more often in men than in women. Major symptoms are blurred vision, usually in one eye only and perceived typically by the patient as a dark spot in the centre of the visual field with associated micropsia and metamorphopsia. Normal vision often recurs spontaneously within a few months. The condition can be precipitated by psychosocial stress and hypercortisolism. Ophthalmoscopic signs of CSC range from mono-or paucifocal RPE lesions with prominent elevation of the neurosensory retina by clear fluid -typical of cases of recent onset -to shallow detachments overlying large patches of irregularly depigmented RPE. The spectrum of lesions includes RPE detachments. Granular or fibrinous material may accumulate in the subretinal cavity. Serous detachment often resolves spontaneously. From first contact, counselling about the potential relation to stress and glucocorticoid medication is warranted. After 3 months without resolution of acute CSC or in chronic CSC, treatment should be considered. Resolution of detachment can usually be achieved in acute CSC by focal photocoagulation of leaking RPE lesions or, in chronic CSC, by photodynamic therapy. The effect of therapy on long-term visual outcome is insufficiently documented. Reattachment within 4 months of onset is considered a relevant therapeutic target because prolonged detachment is associated with photoreceptor atrophy. This suggests that the value of treatment depends upon proper selection of cases that will not resolve without therapy. Chronic CSC may be difficult to differentiate from occult choroidal neovascularization secondary to CSC. Patients with chronic CSC who receive glucocorticoid treatment for systemic disease can often be managed without having to discontinue this medication.

MEK inhibitor-associated retinopathy (MEKAR) in metastatic melanoma: Long-term ophthalmic effects

“…Venous occlusion and macular oedema occur in the inner retinal layers due to the dysfunction of the retinal vessels forming the inner blood-retinal barrier, while the pigment epithelium maintains the blood-retinal barrier to the choroid [30]. Classic central serous chorioretinopathy is thought to be primarily due to pathological changes in the choroid circulation, associated with a marked measurable thickening, and to hormonal influences [16].…”

“…However, drug-related adverse events typical for MEK inhibitors, including retinal events, persist [8][9][10]. Some clinical features of MEK inhibitor-associated retinopathy, resembling to the well-known central serous chorioretinopathy [16], have been described in two studies with about 30 patients and in three small case series [15,[17][18][19][20]. At present, no long-term data is available.…”

Central serous chorioretinopathy due to low dose exogenous corticosteroid administered for a bee sting: a complication or coincidence?

“…Many studies have demonstrated that CSs are a risk factor for acute CSCR [2][3][4][5]. CSs can damage the retina pigment epithelium (RPE) or the tight connection between the retina pigment epithelium (RPE) cells and delay RPE healing.…”

“…The etiopathogenesis of CSCR has not been fully elucidated but there are some well-defined risk factors that cause the disorder. These include type A personality, pregnancy, systemic corticosteroid (CS) use and Cushing syndrome [2,3]. There is increased CS in the body in all these conditions and many studies have indicated a relationship between CSs and CSCR pathogenesis [2][3][4][5].…”

“…These include type A personality, pregnancy, systemic corticosteroid (CS) use and Cushing syndrome [2,3]. There is increased CS in the body in all these conditions and many studies have indicated a relationship between CSs and CSCR pathogenesis [2][3][4][5]. Although almost all CS administration routes cause CSCR, a long usage duration and/or high doses of CS are generally required for CSCR development [4].…”