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ARTICLES |
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Year : 1983 | Volume
: 31
| Issue : 3 | Page : 149-150 |
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Central serous retinopathy and choroiditis
R Kalsi
Retina Associates, New Delhi, India
Correspondence Address: R Kalsi Retina Associates, New Delhi India
Source of Support: None, Conflict of Interest: None | Check |
PMID: 6676202
How to cite this article: Kalsi R. Central serous retinopathy and choroiditis. Indian J Ophthalmol 1983;31:149-50 |
The purpose of this presentation is to describe a clinical picture of a form of central serous retinopathy subsequent to choroiditis and its course under steroid therapy. Evidences will be presented to establish that these cases of choroiditis are due to certain specific organisms-the vast majority being tuberculosis.
Clinical picture: On a conventional examination it is no different than a case of C.S.R. However on careful examination one may note one or more of following features.
1. The macular detachment may be somewhat wider.
2. There may be diffuse pigment changes under the detached retina.
3. There may be one or more patches of pigment epithelial detachments under or away from the disciform detachment.
4. There may be lesions of old healed deep choroiditis in the fundus.
On fluorescein angiography the features are more definite. There are multiple often diffuse patches of dye staining with one or more point of dye leakage. The pigment epithelial detachments stain characteristically.
On adequate dosage (over 40mg of Prednisolon daily) of systemic steroids there is an acceleration of dye leakage with rapid increase in the detachment. The detachment gravitates downwards. The fluid shifts freely with posture. With continued steroid therapy the detachment may become total and even ballooned. Withdrawal of steroids results in slowing of the leakage with flattening of the detachment. In a series of 205 cases with floorescein picture suggestive of specific choroiditis 204 cases showed a positive response to antitubrcular treatment. The detachment completely subsided The areas of dye staining and leakage healed with scarring and pigmentation. The vast majority (88%) showed dramatic clinical improvement within first 2 weeks of treatment. All showed positive response within 3 weeks. The slowing and stoppage of the dye leakage preceeded clinical improvement. The treatment was continued for 2 months beyond the point at which the lesions on the pigmented epithelium could be said to be dried out with no spread of the dye. The longest a patient has been kept on antitubercular treatment was 2 years. Reappearance of dye leakage calls for resumption of treatment. Evidence suggestive of active systemic tuberculosis was the exception rather than the rule. In over 50% of cases the E.S.R. was raised. The Mantoux was positive in 30% of cases.
The initially 30 consecutive cases were treated first with pure antitubercular drugs such as isoniazid, thiacetazone etc. Subsequently the initial treatment has been with streptomycin and Isoniazid. Usually after 40 days, the treatment is changed to Isoniazid and Thiacetazone. Other combination treatment has also been used.
The case which did not respond to antitubercular treatment was showing positive haemagglutination test for toxoplasmosis in significant titre. She did respond to treatment for toxoplasmosis.
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