We thank Takkar and associates for their interest in our article. The hyperpermeability that is seen in central serous chorioretinopathy occurs at the level of the choriocapillaris. This increased permeability has the potential to increase the hydrostatic pressure in the choroid, with distention of the choroid as a result. We previously have shown that the increase in thickness of the choroid persists even after leakage from the level of the retinal pigment epithelium subsides and also in fellow eyes that have not experienced subretinal fluid. Exudation in the more anterior portions of the choroid from other causes produces choroidal detachments but rarely subretinal fluid. These accumulations of fluid seem to occur in the suprachoroidal space and may be amenable to surgical drainage. So a logical question to ask is, does fluid accumulate in the suprachoroidal space in central serous chorioretinopathy?

We examined a large series of patients and found that there is an accumulation of fluid in the outer choroid/suprachoroidal space, particularly if the choroidal thickness exceeds 400 μm. In addition, the suprachoroidal fluid was more likely to be present if there was also subretinal fluid. This is a logical consequence of the proposed pathophysiology. Excessive hyperpermeability would cause increased hydrostatic pressure, which in turn would make both frank leakage from the level of the retinal pigment epithelium and the accumulation of fluid posteriorly more likely. The fluid in each location is related to the third variable, choroidal vascular hyperpermeability, as modulated by other factors such as the specific anatomic differences between the posterior pole and the periphery. Treatment of central serous chorioretinopathy was proposed as a means of targeting hyperpermeability. We showed that photodynamic therapy can stop leakage of subretinal fluid and also that there is a simultaneous decrease in choroidal thickness.

Takkar and associates start by saying subretinal fluid was “inconsistent” between the 2 centers. We are not certain why samples of patients from 2 sites located more than 1500 kilometers apart with populations having differing demographic characteristics should have the same proportions of patients with subretinal fluid. Next Takkar and associates state that posterior accumulation of fluid would be expected to precede leakage from the retinal pigment epithelium and would decrease after a leak forms. Perhaps Takkar and associates should consider where subretinal fluid goes when it is cleared from the subretinal space: it is pumped by the retinal pigment epithelium into the choroid. Thus accumulation of subretinal fluid is not an efficient way to vent choroidal hydrostatic pressure and the amount of subretinal fluid would likely be correlated to the amount of choroidal vascular hyperpermeability, as would the posterior accumulation of fluid in the choroid.

The authors then make the claim that angiography is the modality of choice for monitoring disease activity, without offering either evidence for this statement or a definition of what they mean by disease activity. Fluorescein angiography does not show the choroidal vascular hyperpermeability. Indocyanine green angiography shows areas of choroidal hyperpermeability in eyes with a past history of central serous chorioretinopathy as well as in those with active disease, and even in those with no history of disease. Neither fluorescein nor indocyanine green angiography could show posterior accumulation of fluid in any case. Our study was the first to demonstrate this accumulation of fluid and proposed pathophysiologic mechanisms to explain its presence.