Year : 1989 | Volume
: 37 | Issue : 1 | Page : 28--29
Metakelfin toxicity-With pale centered superficial retinal haemorrhages
Gurdeep Singh, Jagmeet Kaur
E-1/100, Area Colony, Bhopal (M.P.) 462 016, India
E-1/100, Area Colony, Bhopal (M.P.) 462 016
An interesting case of acute onset bilateral superficial white-centered retinal haemorrhages probably due to idiosyncrasy to a new antimalarial drug is reported.
|How to cite this article:|
Singh G, Kaur J. Metakelfin toxicity-With pale centered superficial retinal haemorrhages.Indian J Ophthalmol 1989;37:28-29
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Singh G, Kaur J. Metakelfin toxicity-With pale centered superficial retinal haemorrhages. Indian J Ophthalmol [serial online] 1989 [cited 2021 Jun 19 ];37:28-29
Available from: https://www.ijo.in/text.asp?1989/37/1/28/26106
For centuries_ malaria was treated with Cinchona bark and, until fairly recently Chinchona the alkaloid quinine was the most generally employed antimalarial drug.
More recently a combination of Pyrimethamine and Sulphonamide has been advocated which not only increases the efficacy, but is also useful in chloroquine resistant cases as well as for prophylactic treatment.
We had the opportunity to observe a case of acute onset pale centered retinal haemorrhages in an adult following treatment of malaria with Metakelfin a combination of 25 mg. Pyrimethamine and Sulphamethopyrazine 500 mg.
A twenty four year old man was hospitalised with complaints of sudden diminution of vision in both eyes. History revealed that he had fever with chills and rigors one day before, for which he was treated with two tablets of Metakelfin. After taking this, he noticed diminution of vision which deteriorated next day upon which he reported at the hospital. His visual acuity on first examination was CF 1 1/ z metre in the RE and 6/60 in the LE. Examination of the anterior segment did not reveal any abnormality. Fundus examination in both the eyes showed hyperaemic discs with well defined margins. The veins were slightly dilated and the retinal arteries were normal. There were multiple white-centered haemorrhages scattered all over the fundus including the macular area, which was more in the RE with a dull foveal reflex in both eyes.
Laboratory work up including complete blood picture with ESR, blood VDRL, platelet count, sickling Test, presence of immature cells, fasting blood sugar, chest roentgenogram, blood coagulation studies, electro cardiogram and repeated physical examinations did not show any systemic abnormality.
The patient was kept on anti-allergic drug-Incidal 1 BD, capsuleCVP2TDSandCrookesCollosalIodine2BD. His visual acuity improved to 6/60 in the RE and 6/36 in the LE after a week. He was discharged after 3 weeks with visual acuity of 6/18 BE. On his last follow up after about 8 weeks his VA was 6/9 BE with no clinical abnormality in the fundus of both eyes.
Pale centered haemorrhages have been described in a large variety of infectious and non-infective conditions,,
There has been a lot of confusion in the literature regarding the origin of this type of lesion and various mechanisms have been proposed to account for it.
In leukaemia the white centre has been shown histologically to be an infiltrate of leukaemic cells .
In many cases of bacterial endocarditis it has been shown to be a focal accumulation of WBC, polymorphonuclear cells in acute illness and mononuclear cells in chronic illness sub .
In localised or generalised hypoxic states including those associated with septic emboli, collagen vascular disorders, haematological diseases, hypertension and diabetes mellitus the lesion may be a result of haemorrhage around a collection of cytoid bodies.
Other explanations for pale centered haemorrhages include extracellular and/or intracellular oedema predominantly involving the glial cells in the centre of the haemorrhages .
More recently Duane et al  demonstrated that many of the lesions resulting from retinal anoxic insults and/or sudden elevation of venous pressure lead to pale centered haemorrhages in which the pale centered area contained fibrin and platelet aggregates.
In our case the cause of retinal haemorrhage is not clear. An underlying systemic cause was ruled out by clinical and laboratory work up. Furthermore the occurrence of haemorrhages on the day following treatment with Metakelfin suggests that they were related to sonic type of drug idiosyncrasy.
In clinical practice with multiple variables it may not be possible to pinpoint definitely that these ocular symptoms and signs are the result of some drug reaction, however sulphonamides are known to cause retinal haemorrhages and Metakelfin does contain a long acting sulphonamide.
The most probable pathogenic mechanism in our case was acute retinal ischaemia and the lesion presented as a superficial retinal haemorrhage around a collection of cytoid body as suggested previously.
Thus, even as a presumptive diagnosis it would be worth while to keep in mind this drug relationship in treating cases of malaria and it is also necessary to examine the fundus of patients taking antimalarial drugs particularly it a patient complains of any ocular symptoms so that adverse effects get prompt attention.
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