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ARTICLES
Year : 1983  |  Volume : 31  |  Issue : 3  |  Page : 129-130

Pathophysiology of central serous retinopathy


Retina Associates, New Delhi, India

Correspondence Address:
Bijyananda Patnaik
Retina Associates, 203, Sethi Bhawan, Rajindra Place, New Delhi
India
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Source of Support: None, Conflict of Interest: None


PMID: 6676196

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How to cite this article:
Patnaik B. Pathophysiology of central serous retinopathy. Indian J Ophthalmol 1983;31:129-30

How to cite this URL:
Patnaik B. Pathophysiology of central serous retinopathy. Indian J Ophthalmol [serial online] 1983 [cited 2015 Aug 1];31:129-30. Available from: http://www.ijo.in/text.asp?1983/31/3/129/29765

The clinical picture of Central Serous Retinopathy is well known. The salient fea­tures are: (i) A well circumscribed elevation of the central retina with fine subretinic precipi­tates (ii) Symptoms related to relative central scotoma (iii) metamorphopsia.

Unfortunately the nature of this elevation of the retina is grossly misunderstood, thanks to outdated information printed in some of our most valuable text books. It is erroneously taken as a macular oedema. (Duke Elder).

Furthermore basing on some dubious evidences a theory of spasm of macular blood vessels has been propounded by Horniker and others and have received widespread attention.

A simple slit lamp fundoscopy clearly shows that the elevation at the centre is due to the detachment and not due to oedema of the neuroretina. Besides in some cases a careful indirect ophthalmoscopy clearly reveales a down ward extension of the macular detach­ment which spreads out at the periphery.

Then the question arises as to what is the pathophysiology of this detachment? It has been observed that the detachment is associated with the leakage of choroidal free fluorescein (the dye in the tissue fluid) through the pig­mented epithelium to the subretinal space, when the dye is injected intravenously. The leakage can be stopped by directing a precise beam of light energy from a photocoagulator (we call it photofomentation) to the leaking point. With the ceasation of leakage there is prompt flattening of the detachment. The be­haviour of fluorescein indicates that of choroi­dal tissue fluid which normally cannot cross the pigment epithelial barrier. When there is a breakdown in this barrier and tissue fluid leak into the subretinal space-a detachment deve­lops. It is maintained as long as the leakage persists.

Further, it has been observed from the fluorescein picture there are at least 2 clinical varieties.

1. A fine point leakage, develops spon­taneously and stops spontaneously apparently with no relation to any treatment. Photo­fomentation can be used to shorten the course of detachment. Corticosteroids do not have any notable effect. The etiology remains obscure.

2. Multiple, often diffuse areas of staining and leakage. These are often bilateral and sometimes associated with pigment epithelial detachments, occasional isolated deep choroi­ditis scars. These cases deteriorate dramatically under adequate steroid therapy. The majority are cured by systemic antitubercular treatment. These seem to be cases of choroiditis with low inflammatory reaction. This subject will be elaborated by my colleague in the next paper.

The possible pathophysiology could be as follows: The low grade inflammation caused by microbial agents like perhaps histoplamosis, tuberculosis or toxoplasmosis could result in break down of blood retinal barrier at the level of pigmented epithelium. This leads to leakage of choroidal tissue fluid to subretinal space, maintaining a disciform detachment. Exudative choroiditis, though damage the pig­ment epithelium do not lead to disciform de­tachment. The products of exudation seem to prevent free leakage, with the use of steroids the exudative process is further depressed­while other choroiditis process associated with these specific organisms-continued. As a results there is an increased facility in the- tissue fluid leakage to subretinal space.

Withdrawal of steroids, helps by releasing the exudative process from supression. This slows the leakage. Specific antimicrobial treatment leads to healing and restoration of P.E. barrier. Photofomentation on or around the leaking spot creates a fresh heat induced exudative reaction which slows the leakage immediately and closes it on healing. However, with specific choroiditis continuing, a recur­rence is to be expected. In the first category use of steroids or vasodilators are unnecessary. But in the second category their use is outright dangerous.




 

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