Central serous chorioretinopathy (CSCR) is a retinal condition characterized by fluid accumulation in the subretinal space, resulting in neurosensory detachment or pigment epithelial detachment [1] . CSCR has a wide spectrum of clinical features; some patients have mild symptoms, which recover spontaneously, while others have more chronic retinal dysfunction. We present a case of CSCR in an apparently healthy young man to illustrate the importance of a thorough assessment of underlying risk factors in the management of CSCR.

A 37-year-old Malay policeman with underlying well-controlled hypertension and bronchial asthma presented with sudden onset of bilateral blurring of central vision for 1 day, worse over the left eye. There was no metamorphopsia, floaters, flashes, eye pain, eye redness or history of ocular trauma. Patient does not wear spectacles. He is an active smoker. He has been on Symbicort Turbohaler daily for the past 5 years, and tablet Micardis 40 mg daily. He denies intake of any other medications.

The visual acuity was 6/9 bilaterally. The anterior segment of both eyes was normal. Pupils were 3 mm bilaterally, with no relative afferent pupillary defect. The intraocular pressure was 11 mmHg bilaterally. Examination of the right fundus revealed a dome- shaped swelling inferior to the fovea, while the left fundus showed circular detachment of the neurosensory retina at the macula. The optic disc was pink (Figure 1). Optical coherence tomography revealed right eye pigment epithelial detachment with minimal subretinal fluid at the fovea, and left eye pigment epithelial detachment with neurosensory detachment of the retina involving the fovea (Figure 2). Fundus fluorescein angiography (FFA) showed an ink-blot appearance in the left eye (Figure 3) and a hyperfluorescent spot in the right eye (Figure 4).

He was diagnosed to have bilateral central serous chorioretinopathy and counseled to stop smoking. Upon his next review two months later, his condition was stable.

CSCR is usually a self-limited condition. The duration of retinal detachment is usually

less than 6 months [2] . The spectrum of retinal abnormalities includes pigment migration, cystoid macular edema, and, less commonly, choroidal neovascularization (CNV) [3] .

The pathogenesis of CSCR is postulated to be due to retinal pigment epithelial (RPE) dysfunction and choroidal dysfunction [4] . Another postulated mechanism is autoregulatory changes in choroidal blood flow, associated with choroiditis. This leads to mechanical disruption of the RPE barrier, damage of RPE cells and subretinal fluid accumulation [5] .

The risk factors of CSCR have not been fully elucidated. Among these, type A personality and elevated endogenous cortisol are well-known associations. Gender also plays a role, with a male-to-female ratio of 8:1 among these patients. The association of CSCR with cortisol and the stress response is postulated to be due to transient hypertension and choroidal vasoconstriction, causing loss of choroidal blood flow autoregulation and RPE cell dysfunction [6] [7] . The risk factors of CSCR in this patient were male gender, age, stressful occupation, smoking and chronic use of corticosteroids.

It is important to balance the need for corticosteroids with their risks, as corticosteroid use may perpetuate CSCR. In this case, the patient’s corticosteroids were continued due to the risk of precipitating an attack if they were withheld. The patient was counseled about the risk of CSCR recurrence in future, as well as advised on lifestyle modifications such as smoking cessation.

Most cases of CSCR resolve spontaneously within a few months, with a final visual acuity of 6/9 or better. In our case, patient’s vision on presentation remained at 6/9, so we chose to monitor him while awaiting spontaneous resolution of disease.

In some patients, such as those with high visual requirements, early treatment may be considered. Likewise, in atypical cases such as bilateral or recurrent CSCR with significant effect on vision, laser may be required. Laser treatment may include options like argon laser photocoagulation or photodynamic laser therapy (PDT). Argon laser photocoagulation can speed the resolution of CSCR, but has no effect on the final visual acuity [8] . As for PDT, Maruko et al. demonstrated that PDT reduces the choroidal vascular permeability seen in CSCR via a different mechanism from laser treatment [9] . However, treatment with either argon laser photocoagulation or PDT may place the patient at risk of developing complications like secondary choroidal neovascular membranes [10] [11] .

Another potential treatment option currently being explored is anti vascular endothelial growth factors (anti-VEGF). These agents have been postulated to hasten visual recovery [12] . However, other reports are conflicting; Unlu et al. found that intravitreal anti-VEGF injection has no significant effect on the anatomical outcome of patients with CSCR [13] , while Lim et al. observed that the use of intravitreal anti-VEGF was not associated with earlier remission of disease [14] . As both PDT and anti-VEGF agents may hasten the visual recovery in CSCR, future randomized controlled trials directly comparing these two modalities will be useful.

CSCR is usually a self-limited condition, with good visual outcome. A thorough medical, social and drug history should be obtained, and patients advised to modify their lifestyle to eliminate or reduce risk factors such as smoking, stress and corticosteroid use.

Fhun, L.C., Min, E.T.L., Chong, M.F. and Liza-Sharmini, A.T. (2016) Bilateral Central Scotoma Due to CSCR in an Asthmatic Policeman. Open Journal of Ophthalmology, 6, 240-245. http://dx.doi.org/10.4236/ojoph.2016.64033