Serous detachments, with bullous elevation of the retina, occur in a variety of disorders including central serous chorioretinopathy (CSC), age related macular degeneration, lupus erythematosus, choroidal ischaemic disorders such as accelerated hypertension and pre-eclampsia, systemic corticosteroid usage, over some choroidal tumours, and in inflammatory disorders such as Harada’s disease. There is little mystery about the appearance of fluid when it overlies a large area of leaky retinal pigment epithelium (RPE), which itself overlies exudative choroidal inflammation or vasculopathy. However, the development and persistence of elevated detachment is rather curious in disorders such as CSC where the region of leakage is very small relative to the area of retina that is detached. Under these conditions, the question of pathophysiological interest is not so much ‘why does fluid enter?’ but ‘why does fluid persist?’

To form a serous detachment, there must be a driving force for fluid entering the subretinal space (for example, a pressure gradient from the choroid acting through an RPE defect) that overcomes retinal adhesive force. But how and why is the detachment maintained? Animal experiments have shown that fluid does not ordinarily persist in the subretinal space (SRS), since it is rapidly transported across the RPE by active and facilitated ionic transport.1-3 Hydrostatic and osmotic forces also drive fluid towards the choroid,45 but are less powerful in a normal eye because they are blocked by the tight junctional barrier of the RPE. It is not surprising, therefore, that when the RPE barrier is damaged (for example, by laser or by an RPE toxin such as sodium iodate), fluid actually leaves the subretinal space faster.67 Removal of the barrier allows a more rapid passive egress of subretinal fluid.

Why, then, do some serous detachments (as in CSC) extend far beyond a focal site of …