This atypical case of CSC in a pediatric patient resolved promptly on cessation of the topical steroid and administration of Bromfenac eye drops.
The pathophysiology of CSC is poorly understood. Guyer and colleagues suggested that the pathogenesis of CSC may be choroidal vascular hyperpermeability. They noted diffuse hyperpermeability around active leakage sites seen with indocyanine green videoangiography (ICG-V) but not with fluorescein angiography (FA). Therefore, they concluded that hyperpermeability was at the level of the choroid rather than the RPE.9 An alternative theory suggests that CSC results from dysfunction of the RPE which causes a reverse in fluid movement in a chorioretinal direction.10
CSC induced by the systemic use of steroids was first reported in 1984 in two patients that developed serous macular detachment upon initiation of systemic Betamethasone therapy for retrobulbar neuritis.11 However, the best evidence for an association between corticosteroid use and CSC comes from two large, retrospective case-control studies.12,13 Tittl and colleagues conducted the first of these, studying systemic factors associated with CSC.12 This study included a total of 230 CSC cases and 230 age and sex-matched controls. They found that 21 CSC subjects were using corticosteroid medications, whereas 7 control subjects were using corticosteroids. This difference yielded an odds ratio of 3.2 (95% CI 1.3 to 7.70, P = 0.0063). Carvalho-Recchia et al. published the first report of a consecutive series of patients with acute CSC studied prospectively for an association with corticosteroids.13 They found a statistically significant difference in corticosteroid exposure between study patients and controls.
The mainstay of Atopic Dermatitis treatment is represented by topical corticosteroids, while several routes of steroid administration have been discussed in the literature. These medications reduce inflammation and pruritus primarily by inhibiting the transcriptional activity of various proinflammatory genes. Topical corticosteroids are available in a wide range of potencies, from the least potent Group 1 preparations (e.g. Hydrocortisone 1% ointment), to the most potent Group 7 preparations (e.g. Clobetasol Propionate 0.05% ointment). The greater the potency of topical corticosteroid used, the greater the risk of systemic and local side effects.14 Betamethasone Valerate 0.1% is in group 3 (high potency topical corticosteroids).
Despite that, it was suggested that steroid-induced CSC may be related to an idiosyncratic response in selected vulnerable individuals rather than to a dose-dependent effect, since very low doses can induce CSC episodes.15
CSC has been associated with topical steroid use in several case reports. In 2004, Karadimas and colleagues reported two cases of presumed topical steroid-associated CSC.16 Fernandez and colleagues reported a suspected case of topical steroid-associated CSC, in which a 43-year-old female developed CSC after one month of topical steroid use for lichen planus.17 Ezra and colleagues also reported a case of a 25-year-old male with psoriasis and 15 years of topical steroid use. He experienced a single episode of CSC with resolution upon steroid cessation.18
While CSC has previously been linked to systemic corticosteroid use, it is rarely linked to topical administration.
Idiopathic CSC in children has been reported in a few case reports,5,6,7,8 however this condition has never been linked to topical corticosteroid therapy in young patients.
In light of this, we assume that this may be the first pediatric case of CSC related to transdermal steroid treatment.
Poor imaging is a limitation of this case report, because CSC diagnosis is typically based on a serous retinal detachment described on OCT examination and confirmed by FA, which reveals early-phase localized dye leakage and late-phase dye pooling under the sensory retina. However, we chose not to perform FA on our young patient because OCT scans clearly revealed the diagnosis.