Acute onset of halos and glare: bilateral corneal epithelial edema with cystic eruptions--atypical presentation of amiodarone keratopathy.
BACKGROUND
Amiodarone (Cordarone; Wyeth, Ayerst, New York) is a potassium channel blocking antiarrythmal medication indicated for recurrent ventricular fibrillation and recurrent hemodynamically unstable ventricular tachycardia. Chemically, it is classified as an iodinated benzofuran derivate antiarrythmal drug not chemically related to any other available antiarrhythmic drug. Documented side effects of amiodarone include neurologic, gastrointestinal, dermatologic, cardiovascular, and ophthalmic. The ophthalmic abnormalities include optic neuropathy, optic neuritis, papilledema, corneal deposits, photosensitivity, lens opacities, and macular degeneration. Corneal microdeposits are seen in virtually all patients who receive amiodarone for more than 6 months. Corneal microdeposits result secondary to the secretion of amiodarone by the lacrimal gland with accumulation on, and absorption by, the corneal epithelium. Approximately 10% of these patients become symptomatic with glare and halos; however, that alone is usually not enough to precipitate intervention.


METHODS
A 69-year-old woman presented to our office with a 2-week history of halos and glare in both eyes (OU). Her ocular history was significant for occasional contact lens wear. Her systemic history was significant for atrial fibrillation, for which she was taking amiodarone daily for the last 6 years. Six weeks before the onset of her chief complaint, her daily amiodarone dosage was increased from 100 mg to 300 mg. Ophthalmic examination found decreased visual acuities OU, amiodarone keratopathy (subepithelial verticillata), and diffuse corneal epithelial edema with diffuse sodium fluorescein staining OU. The corneal compromise was treated in 2 ways: the source medication was discontinued, and the ocular signs were medicated with a prophylactic topical antibiotic along with supportive preparations (tears/lubricants) and monitored over 2 weeks until full elimination of the pathologic signs and their symptoms. Even after complete resolution of the acute keratitis, the infiltrative keratopathy persisted along with the initial complaints of halos and glare. The supportive treatments were maintained over the course of 2 months until full recovery.


CONCLUSIONS
By exclusion, it was determined that the subepithelial depositions and cystic formations were secondary to an acute amiodarone dosage increase by a new practitioner. Prompt communication resulted in the physician discontinuing that medicine.
Dovie
John M
JM
Wythe Eye Associates, Wytheville, Virginia 24382, USA. jmdovie@gmail.com
Gurwood
Andrew S
AS
D000368:Aged; D000638:Amiodarone / Q000009:adverse effects* / Q000627:therapeutic use; D000889:Anti-Arrhythmia Agents / Q000009:adverse effects* / Q000627:therapeutic use; D001281:Atrial Fibrillation / Q000188:drug therapy; D015715:Corneal Edema / Q000139:chemically induced* / Q000473:pathology; D003560:Cysts / Q000139:chemically induced* / Q000473:pathology; D019573:Epithelium, Corneal / Q000187:drug effects / Q000473:pathology*; D005260:Female; D005500:Follow-Up Studies; D007839:Functional Laterality; D019466:Glare; D006801:Humans; D014792:Visual Acuity
D000889:Anti-Arrhythmia Agents; D000638:Amiodarone