Optic nerve amiodarone

A primary lipidosis has been described in human optic nerves affected by amiodarone. One study has shown that intracytoplasmic inclusions may mechanically or biochemically block axoplasmic flow in large optic nerve axons, resulting in optic disc edema and hemorrhage. 

Mansour AM, Puklin JE, O Grady R. Optic nerve ultrastructure following amiodarone therapy. J CUn Neuroophthalmol 1988 8(4) 231-7. 

A 75-year-old female patient with no history of ocular disease was treated with warfarin and amiodarone due to arrhythmias that occurred after aortic valve replacement. As there were no rhythm problems, amiodarone was discontinued on day 45. Five days afterward, the patient noticed scotoma in the visual field of her left eye. After a couple of days, the patient was experiencing bilateral visual symptoms and the left eye felt foggy. A relative afferent pupillary defect was detected in the left eye and the optic nerve heads were swollen. Moreover, bilateral macular oedema was noted. Within 4 weeks of the first visual symptoms the patient had become blind. No improvement occurred during 8 months of follow-up. Other possible diagnoses were ruled out. Amiodarone-related optic neuropathy was the most likely reason for the profound visual loss [14]. 

A review of certain chemicals is essential. Ethylene glycol is an antifreeze used for gasoline engines and may produce somnolence, imreactive pupils, disc swelling, and kidney failure. Systemic lead poisoning produces headaches, coma, cranial nerve palsies, and papilledema. Wood alcohol, or methanol, may produce severe toxic neuropathy and disc edema. Drugs known to produce toxic optic neuropathy include amiodarone (an antiar-rhythmic), quinine, aminoquinolines, ibuprofen, ethambutol, isoniazid, and chloramphenicol. 

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