Digoxin retinal toxicity. Clinical and electrophysiological evaluation of a cone dysfunction syndrome
R. G. Weleber and W. T. Shults
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 Muller's cells and
other retinal neurons. This mechanism may contribute to subnormal,
prolonged cone-mediated ERG responses in retinal toxic reactions from
cardiac glycosides.
