Electrophysiologic and electroretinographic evidence for photoreceptor dysfunction as a toxic effect of digoxin

Arch Ophthalmol. 1994 Jun;112(6):807-12. doi: 10.1001/archopht.1994.01090180105044.


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.

Publication types

  • Case Reports
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Ambystoma
  • Animals
  • Dark Adaptation
  • Digoxin / adverse effects*
  • Digoxin / blood
  • Electrophysiology
  • Electroretinography*
  • Female
  • Humans
  • Middle Aged
  • Photic Stimulation
  • Photoreceptor Cells / drug effects*
  • Photoreceptor Cells / physiopathology*
  • Retinal Diseases / chemically induced
  • Retinal Diseases / physiopathology
  • Sodium-Potassium-Exchanging ATPase / drug effects


  • Digoxin
  • Sodium-Potassium-Exchanging ATPase