Electrophysiologic and electroretinographic evidence for photoreceptor dysfunction as a toxic effect of digoxin
S. A. Madreperla, M. A. Johnson and K. Nakatani
Department of Ophthalmology, Johns Hopkins University, Baltimore, Md.
PURPOSE: To investigate photoreceptor dysfunction caused by digoxin
toxicity. METHODS: First, a patient who experienced toxic side effects from
digoxin was studied acutely by serial electroretinography and later during
convalescence. Second, the light responses of isolated photoreceptors
exposed to varying amounts of digoxin were studied in vitro. RESULTS:
Electroretinographic amplitudes were reduced and implicit times were
delayed when digoxin levels were elevated and recovered slowly after return
to normal digoxin levels. Isolated photoreceptors exhibited
concentration-dependent reductions in the magnitude of the light response
during digoxin exposure, suggesting reduction in the dark current due to
blockade of the sodium-potassium-adenosine triphosphatase pump. Cones were
about 50-fold more sensitive than rods. CONCLUSIONS: Reversible rod and
cone dysfunction occur during exposure to toxic levels of digoxin.
Photoreceptor dysfunction is probably due to the diminution of the dark
current in response to the sodium-potassium-adenosine triphosphatase
blockade.
