|Year : 1966 | Volume
| Issue : 6 | Page : 250-252
Maculopathy a corticosteroid side-effect
IS Jain, Kapaimit Singh
Department of Ophthalmology, Institute of Post Graduate Medical Education and Research, Chandigarh, India
|Date of Web Publication||17-Jan-2008|
I S Jain
Department of Ophthalmology, Institute of Post Graduate Medical Education and Research, Chandigarh
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Jain I S, Singh K. Maculopathy a corticosteroid side-effect. Indian J Ophthalmol 1966;14:250-2
Since Horniker's time (1929) it has been assumed that central serous retinopathy is due to vasoconstriction. Almost all the later workers have subscribed to this view. The association of this condition with corticosteroids has not been referred to in literature, though corticoids are known to produce various ocular disturbances e.g. cataract, glaucoma, papilloedema etc. Macular involvement was observed during corticoid therapy in one of our cases, and therefore is being put on record as it is the first case of its kind where such an association has been noticed.
| Case Report|| |
N.R. 42 years Hindu male was admitted in our Institute, Chandigarh on 4-2-1965 as a case of Reiter's syndrome, with the history of pain, in the left side of flank and illiac region for the past ten years, joint pains for the last six months and burning micturition for the past 2 months. Almost all the big joints were involved one after the other. There was history of development of a penile sore a year back, which regressed with the treatment. He also complained of redness of the eyes (conjuctivitis) for two days following the acute attack in joint pains.
| Examination|| |
General physical examination-within normal limits. Respiratory and central nervous systems were normal.
Cardiovascular systems: Soft systolic murmur in parasternal area (left).
Locomotor system -Movements of joints were painful and restricted; left knee and ankle joints were also swollen. Movements of spine were restricted.
Ocular examination: Normal.
Investigations: Haematological examination was normal.
ESR was 40 mm, first hour. Wintrobe. Examination of urine and stools were normal.
Rose Waller: Sheep cell agglutination test 1:2.
Blood for LE cells Negative.
Serum Electrolytes Normal.
Patient had previously received the following treatment.
Decadron tablets-4 daily for 17 days and then 5 tablets for 4 days.
Butazolidine, 3 tablets daily for 15 days.
P-A.M. (Penicillin Aluminium monosferate) daily for 10 days.
After admission to this Hospital on 4-2-1965 he was put on 30 mg/Prednisolone daily with vit. C and B-complex.
The dose of Prednisolone was raised to 50 mg/day on 10-2-65 and 60 mg/day on 12-2-1965.
Streptomycin 1 gm. twice a day from 15-2-1965 for 5 days was also given.
On 8-2-1965 eye examination was normal. On 23-2-1965 he complained of diminution of vision in the left eye, alongwith micropsia and metamorphopsia. Fundus examination revealed macular oedema with reflex ring in the lower part.
Amsler's chart and central fields confirmed the clinical diagnosis.
Blood pressure readings were as follows: [Table - 1]
The retinal oedema cleared when prednisolone was omitted. Later the patient was lost to follow up.
A patient of Reiter's syndrome was admitted and put on Prednisolone. From a dose of 30 mg/day, it was suddenly raised to 50 , mg/day on 10-2-65 and to 60 mg/day on 12-2-65. Blood pressure readings shot up on 13-21965 and came to normal on 24-2-65. On 23-2-1965 he developed central serous retinopathy.
| Discussion|| |
Horniker (1929) assumed functional changes in the calibre of small vessels specially capillaries supplying the macula to be the cause of central serous retinopathy. Because the disease occurred in individuals with vasoneurotic symptoms, he called it retinitis angioneurotica.
Gifford and Marquardt (1939) also came to this conclusion that this condition is due to spasm of smaller retinal arterioles: or capillaries. They used special methods to determine the presence of any functional disturbance in the peripheral vessels. They brought forth evidence for high degree of spasm of peripheral vessels in all but one case. Agarwal and Dayal (1964) considered it as "angiospatic" and grouped it along with solar retinitis, Berlin's eedema and toxic macular oedema. The angisopastic nature was later confirmed by the authors on therapeutic trials by Vasodilators (Khosla et al 1965).
In this case under discussion hypertension occurred first and then as blood pressure came down central serous retinopathy resulted. The rise in blood pressure is well known under corticoid therapy, while central serous retinopathy that occurred in this case also seemed to have resulted from corticoid therapy. Considering the relationship of oedema and blood pressure, with corticoids Gifford (1960) observed that most of the patients who receive large doses of steroids and develop oedema also have a rise in blood pressure. According to him it can be true that there can be rise in blood pressure with administration of large doses of steroids without any detectable cedema. The correlation between salt retention and hypertension is definite. Labram et al (1962) reported that intravascular clumping is more in cases receiving steroids, than in controls of the same age and sex.
Even conjuntival ischaemia has been reported. Beckman (1963) observed that within 10 days of instituting therapy with steroids the blood becomes much more coagulable through the operation of unknown mechanisms. This may predispose to thromboembolic complication. Danko and Schroeder noted purpura, ecchymotic skin lesions and easy brusing in 20% of a group of 75 patients receiving prednisolone for a variety of rheumatic disorders, suggesting action upon either platelets or capillary walls. The macula being the sensitive area, the vascular effects of cortisone have manifested as central serous retinopathy in this case. Whether ischaemia produced, is due to intravascular clumping, or, some other change in the vessels of the nature already described is very difficult to say, but the production of transitory hypertension may be in favour of peripheral vasoconstriction; a change that can manifest as central serous retinopathy also. How exactly the steroids bring about these changes is very difficult to answer. Could this macular lesion be an expression of oedema which is not manifested elsewhere?
| Summary|| |
A case of central serous retinopathy developing during a course of therapy with corticosteroids is described.
The probable nature of the vascular changes involved is discussed.
| References|| |
Aggarwal. L. P.. Dayal. Y. (1964), Oriental Arch. Ophth. 2: 203.
Backman. H. (1963), Pharmacology II nd Ed. W. B. Sanders. Philadalphia, Page 608.
Denko. C. W.. Schroeder, L. R..
(1957), J.A.M.A. 164: 41.
Gifford. R. W. In 'Oedema' mechanism and management. ed. JOHN H. Moyer and Morton Fuchs.
Gifford, S. R..
Marguardt, G. (1939),
Arch. of Ophth. 21: 211.
Horniker. E. (1929),
Arch. of Ophth. 13: 286, 1929.
Ref. by Elwyn. F. (1953) in Diseases of the Retina. IInd Ed., Balkiston Co. Inc. Page 65).
Khosla, P. K. Aggarwal. L. P.; Angra, S. K. (1965) Orient. Arch. Ophth. 3: 193.
Labram, C.. Ryckewaert, A.. Debeyre, N. Kahn. M. F. (1962)
Rev. franc, clin, et. biol. 7: 715. (From Hughe: W. F. Year Book of Ophthal. 1963-64. Year book medical Publishers Chicago. Page 94).
[Table - 1]