From EyeWiki

Siderosis is a complication due to a magnetic intraocular or intraorbital foreign body. Generally metals with a low redox potential, such as Fe++and Cu++, have the greatest potential for metallosis. Siderosis may develop within weeks, but the course is variable depending on the iron content in the foreign body and its location. Virtually all ocular structures are involved in the siderotic process—Glaucoma, Cataract, iris color changes, mydriasis, retinal function destruction, and optic nerve atrophy.


Bivalent iron (ferrous) is more toxic to ocular tissue than the trivalent ion (ferric). The toxicity is caused by interference with the essential enzyme system. Studies of the pathologic features of eyes with siderosis have revealed iron deposits accumulated in the regions of ocular pumps i.e., corneal endothelium and Descemet's membrane, trabecular meshwork, pupillary constrictor muscles, dilator muscle, non-pigmented ciliary epithelium, lens epithelium, retinal pigment epithelium, and internal limiting membrane. Histologically, Prussian blue stains the iron blue and shows it to be present in all ocular epithelial structures and in areas of trabecular meshwork scarring and retinal gliosis. By electron microscopy, intracellular sideromes are present in the lens epithelium and in corneal keratocytes.

Clinical Manifestations

Earliest symptom is failure of accommodation and iris heterochromia. Late and end stage symptoms are progressive loss of visual field and nyctalopia.


Iron usually remains within the epithelial cells that take it up, rather than appearing in the basement membrane. Iron granules may deposit in any layer of the cornea but are usually more prominent in the deeper cornea.

Trabecular Meshwork

Siderosis from retained iron IOFB can cause open-angle glaucoma. Breakdown products and iron can accumulate in the trabecular meshwork, producing increased intraocular pressure. The unilaterality may be confusing, particularly when the previous ocular history is unknown and the foreign body is occult. The iron may be seen clinically in the anterior chamber angle as irregular, scattered, black blotches that may resemble malignant melanoma.

Iris & Pupil

Acquired hyperchromic heterochromia of iris can result from the stromal deposition of iron in siderosis. With siderosis, irides become more brown or rusty, developing after weeks or years (Rusty Green Iris). Anisocoria and Abnormal Pupillary Reaction may be present. Tonic or Adies pupil has been reported.


In siderosis or hemosiderosis the lens epithelium takes on a yellow-brown or rusty appearance from minute dots of intracellular iron, identifiable by Perls' or other iron stains. Focal rusty-brown nodules of subcapsular cataract may develop. When the foreign body is in the lens there may be progression to a mature cataract, with diffusion of ionizable iron throughout the lens fibers. The iron appears to bind to enzymes within these cells and becomes insoluble and incorporated in phagolysosomes with eventual cellular degeneration.


The iron concentrates mainly in RPE and inner limiting membrane neurosensory retina. Necrosis of the photoreceptor cells occurs over large areas of the retina. Electron-dense material deposits between adjacent saccules in the outer segments of the photoreceptors. Functional damage to the retina occurs at a very early stage, before extensive siderosis is apparent, and before stainable iron is detected in retinal tissues. Accumulation of intracellular iron leads to inner retinal and RPE degeneration followed by full-thickness retinal degeneration and secondary gliosis. Vitreous degeneration in association with retinal degeneration may lead to rhegmatogenous retinal detachment. Optic atrophy ensues after longstanding disruption of retinal function.


ERG and electrooculogram (EOG) testing is used to study the degree of ocular injury from metallosis and to monitor ocular recovery after metallic foreign body removal. Initially hypernormal a- and b-waves, followed by a steady decrease in a- and b-wave amplitudes, is seen with iron-containing intraocular foreign bodies in humans. The transient increase in a- and b-wave amplitudes in the first week after injury has been attributed to recovery from the ocular trauma before the onset of severe metallic ion injury to the retina and Müller cell responses to ionic changes in the outer retina. Progressive diminution of b wave occurs over 1- 2 year period if monitored serially. EOG changes may not occur in eyes with metallic intraocular foreign bodies presumably because of sparing of the outer segments of the rod and the retinal pigment epithelium. EOG abnormalities indicate severe metallosis and poor visual prognosis. The ERG is a sensitive way of monitoring intraocular injury from metallic ion poisoning.

Removal of the foreign body is indicated if there is recurrent uveitis or evidence of progressive retinal damage by serial ERG. The foreign metallic body may be detected by ophthalmic B-scan ultrasonography and/or ultrasound biomicroscopy (UBM) to examine the cornea, anterior chamber and angle, iris, lens, sulcus, vitreous, retina, RPE, choroid, and related anterior and posterior structures to identify a hyperechoic foreign body with posterior shadowing. CT scans of the orbit with thin cuts (ideally 1 to 3 mm) and coronal reconstruction may also detect metallic foreign bodies as well-defined, hyperdense foreign bodies producing streak artifacts with near 100% sensitivity.[1] Plain films of the skull and orbits have also historically been used to detect intraocular or orbital metallic foreign bodies as radio-opaque and well defined entities. Cataract may be managed by conventional ECCE or phacoemulsification with PCIOL. Ciliary body iron IOFB may be removed after accurate localization.


  1. Albert & Jakobiec's Principles & Practice of Ophthalmology, 3rd Edition
  2. System of Ophthalmology - Duke-Elder
  3. Ocular siderosis. Diagnosis and management. Retina. 1997;17(2):105-8.
    1. Sensitivity of spiral computed tomography scanning for detecting intraocular foreign bodies. Dass AB, Ferrone PJ, Chu YR, Esposito M, Gray L Ophthalmology. 2001 Dec; 108(12):2326-8.