Ocular Manifestations

Although unilateral metamorphopsia is the classic symptom of central serous chorioretinopathy (CSC), patients also may present with unilateral blurred vision, micropsia, impaired dark adaptation, color desaturation, delayed retinal recovery time to bright light, and a relative scotoma. Visual acuity ranges from 20/15 (6/5) to 20/200 (6/60), but averages 20/30 (6/9). The visual acuity may improve with hyperopic correction. Symptoms typically resolve after several months, but may linger even after the fluid resolves; only rarely do they persist indefinitely. Permanent sequelae include metamorphopsia, decreased brightness perception, and altered color vision [1,2].

Also, CSC can present as a bullous, inferior nonrhegmatogenous peripheral retinal detachment.

The presence of retinal pigment epithelium atrophic tracts from the macular region to the peripheral detachment, seen best with fluorescein angiography, reveal the true diagnosis and source of the subretinal fluid [13].

A chronic form of CSC exists as well. In about 5% of cases, a diffuse retinal pigment epitheliopathy progresses in conjunction with persistent or intermittent subretinal fluid. The retinal detachments tend to be shallower and more diffuse than in the classic form. The visual prognosis is more guarded.

3.4 Diagnosis

The diagnosis of central serous chorioretinopathy (CSC) is clinical and confirmed with fluorescein angiography. While in most cases the diagnosis can confidently be made without ancillary testing, the information derived from angiography is critical to detect the extent of the retinal abnormalities and to exclude the presence of other pathology.

Biomicroscopically, a transparent blister in the posterior pole between the neural retina and the retinal pigment epithelium (RPE) is observed. This is best seen through a fundus contact lens with a wide light beam, set slightly off axis. Signs that suggest the presence of a retina-RPE separation include beam splitting as the light traverses the serous space, an increased distance between the retinal vessels and their shadows, and an absent foveal reflex. Shallow detachments may be difficult to demonstrate clinically [2].

The subretinal serous fluid within the blister often is transparent. This fluid may have protein and fibrin and be turbid or yellowish, especially in more pigmented individuals or in pregnant women. It is believed that the small dot-like deposits that form on the posterior surface of the retina or on the anterior surface of the RPE cells under the area of the detachment represent precipitates of this protein [2]. This is noted best when the fluid component is resolving. Diffuse deposits of serous proteins can produce a whitish retinal appearance that mimics intraretinal edema. A normal retinal thickness and transparency help to distinguish this from true retinal edema [2].

Oval yellow-gray elevations beneath the detachment also may be seen. These are generally less than one-fourth of a disk diameter in size and are surrounded by a faint grayish halo.

Fluorescein angiography identifies them as retinal pigment epithelial detachments (RPEDs) and frequently demonstrates the focal RPE leaks responsible for the neural retinal detachment within their borders. Since subretinal exudative fluid may track inferiorly in response to gravity, a leaking RPED may lie beyond the superior margin of its retinal detachment. Numerous factors can help differentiate an elevated RPED from a shallow focal retinal detachment [2]:

• an RPED obscures the choroidal pattern (this characteristic may abate as the RPE cells in the RPED atrophy);

• the boundary of the RPED typically is better defined than the edge of the retinal detachment;

and

• an RPED bows the light beam reflex forward toward the observer and prevents visualization of the sub-RPE space.

A large RPED must be differentiated from an amelanotic melanoma or metastatic lesion to the choroid. Both can appear dome-shaped, solid, nontranslucent, and produce an overlying neurosensory detachment [2].

The presence of cystic retinal degeneration, fine RPE mottling, or RPE clumping suggests chronicity of the present episode or a history of a previous CSC episode (Fig.4).

Additional ophthalmoscopic findings, such as lipid or hemorrhage, are rare and should call into question the diagnosis of idiopathic CSC [2]. The fellow eye may show evidence of either concurrent or previously resolved CSC, manifested as focal areas of RPE rarefaction or small asymptomatic RPEDs.

Fluorescein angiography plays an important role in the evaluation of CSC. It is used to exclude the presence of other pathologies that produce neural retinal detachments and yet also confirms the diagnosis. Classically, dye from the choroid leaks through a focal RPE defect and pools in the subretinal space. In over 75% of patients, this pooling occurs within 1 disk diameter of the fovea [14]. Less pooling may be observed in older lesions in which the RPE exudate has become inspissated [2]. When fluorescein angiography is atypical, indocyanine green angiography can help to exclude the presence of other pathology. Indocyanine green angiography of CSC reveals multifocal choroidal hyperfluorescence in affected and unaffected regions of both the active and fellow eyes [15,16].

A new, noninvasive technique of ocular imaging called optical coherence tomography can demonstrate the presence of subretinal fluid. In cases of CSC, optical coherence tomography has been used successfully to quantify the amount and extent of subretinal fluid [17].

Fig.4 Fundus photograph of an eye with resolved central serous

chorioretinopathy showing chronic pigmentary changes.