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May 1966

Treatment of Experimental Siderosis Bulbi, Vitreous Hemorrhage, and Corneal Bloodstaining With Deferoxamine

Author Affiliations

From the Wilmer Institute of Ophthalmology, Johns Hopkins Hospital and Johns Hopkins University, Baltimore.

Arch Ophthalmol. 1966;75(5):698-707. doi:10.1001/archopht.1966.00970050700023

The retention of an iron foreign body within an eye almost always results in progressive iron deposition throughout the eye, cataract formation, glaucoma, and eventually atrophy of all the intraocular tissues. This condition is known as siderosis bulbi.1 To prevent it, any intraocular iron particle must be removed surgically, if possible, even if the surgery itself may result in loss of the eye. Once siderosis is established, surgery seldom helps.2 Furthermore, as in two patients seen at the Wilmer Clinic recently, small iron particles may oxidize to nonmagnetic rust which cannot be localized or surgically extracted.

Medical therapy of siderosis has been attempted using galvanic deactivation,3 intravenous edetic acid,4,5 and subconjunctival edetic acid or adenosine triphosphate.6,7 Edetic acid (formerly known as edathamil), the principal agent studied, has shown a number of toxic effects in humans receiving chronic systemic therapy.8,9

In 1960, Bickel et al

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