Key result
Stopping digoxin reverses cone-mediated ERG abnormalities and color vision defects in clinical toxicity.
Why the study?
The clinical and electrophysiological features of digoxin retinal toxicity and its resolution after cessation of therapy were studied to understand retinal effects of cardiac glycosides.
Case Report (n=1)
Digoxin toxicity can cause a reversible cone dysfunction syndrome, likely due to inhibition of sodium-potassium ATPase affecting retinal neurons.
Answers are grounded in this paper and cite their sources.
Digoxin toxicity may cause reversible cone dysfunction; single case leaves open need for prospective studies on monitoring.
A 70-year-old man was studied both during and after resolution of clinical digoxin toxicity using color vision tests, ganzfeld electroretinography and electro-oculography. Concomitant administration of quinidine sulfate probably contributed to digoxin toxicity. Abnormalities in color vision and subnormal amplitude and prolonged implicit time for cone-mediated electroretinogram (ERG) responses suggested a cone dysfunction syndrome. The electro-oculographic light-to-dark ratio during clinical toxicity was high for our laboratory, but this is probably normal. Notable improvement was seen in color vision and the ERG after cessation of digoxin therapy. Inhibition of sodium-potassium adenosine triphosphatase by digoxin probably influences normal uptake of extracellular potassium by Müller's cells and other retinal neurons. This mechanism may contribute to subnormal, prolonged cone-mediated ERG responses in retinal toxic reactions from cardiac glycosides.
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Richard G. Weleber (1981) conducted a case report in Digoxin retinal toxicity (n=1). Digoxin vs. Post-cessation of digoxin therapy was evaluated on Color vision and electroretinogram (ERG) responses. Clinical digoxin toxicity was associated with abnormalities in color vision and cone-mediated ERG responses, which notably improved after cessation of digoxin therapy.
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