Siderotic cataract after intraocular foreign body removal

Watane, Arjun BS; Quan, Ann MD; Koo, Eubee MD; Patel, Nish BA; Dubovy, Sander MD; Sridhar, Jayanth MD

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doi: 10.1097/j.jcro.0000000000000026
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Ocular siderosis, also known as siderosis bulbi, was first described in 1894 by von Hippel.1 It can develop due to an iron-containing intraocular foreign body (IOFB), causing a degenerative process induced by chemical reactions between iron particles and ocular tissues.2 The ferrous particles dissociate from the IOFB and can deposit in the intraocular epithelial structures, such as the lens epithelium, iris, ciliary body epithelium, and the sensory retina, where it can exert toxic effects on cellular enzyme systems.3

Ocular siderosis may present with a yellow cataract with brown deposits on the anterior capsule, pigmentary retinal degeneration, and optic disk hyperemia, leading to attenuated vessels and visual field loss. The resulting retinopathy can be confirmed by characteristic electroretinogram (ERG) changes. Initially, the a-wave increases, and a progressive reduction in the b-wave subsequently follows.3

Here, we describe a unique presentation of a siderotic cataract and ocular siderosis in a patient who underwent vitrectomy and IOFB removal 4 months after the initial eye trauma.


A 39-year-old male mechanic presented to the emergency department 4 months after trauma to the right eye while hammering metal. He complained of difficulty focusing and light flashes in the right eye since the injury. On initial examination, the visual acuity was 20/20, and slitlamp examination revealed traumatic mydriasis, iritis, and pigment on the conjunctiva 3.0 mm posterior to the limbus at 5 o'clock, indicating an entry wound. A metallic IOFB was found floating in the vitreous humor at 6 o'clock (Figure 1). ERG demonstrated an increased a-wave and decreased b-wave, consistent with siderosis (Figure 2).

Figure 1.
Figure 1.:
B scan shows a metallic intraocular foreign body floating in the vitreous.
Figure 2.
Figure 2.:
Electroretinogram demonstrates an increased a-wave and decreased b-wave.

The patient underwent vitrectomy and IOFB removal without complications the following week. The IOFB was removed from the inferior vitreous, and laser was applied to the areas of pigmentation at the entry sign in the inferior pars plana. Finally, a fluid–air exchange was performed.

Five months later, the patient presented to the clinic with a reduced visual acuity of 20/30, black floaters, and visible deposits in the right eye in a clock face pattern (Figure 3). Slitlamp examination demonstrated metal deposits on the anterior capsule in a symmetric, circular configuration and a posterior subcapsular cataract, as seen in Figure 2. Ganglion cell optical coherence tomography showed retinal thinning and atrophy with a normal foveal contour (Figure 4), and the retina was attached.

Figure 3.
Figure 3.:
Visible iron deposits and cataract.
Figure 4.
Figure 4.:
Retinal thinning is seen in the right eye.

The patient underwent uneventful cataract surgery of the right eye (Video 1, available at, 1_m9sy8mk4). On pathology, the Perls' Prussian blue stain was positive within the lens epithelium, demonstrating iron deposition and siderosis (Figure 5). At the most recent follow-up visit 1 year after the initial diagnosis of ocular siderosis, corrected distance visual acuity was 20/20.

Figure 5.
Figure 5.:
Lens capsule and lens epithelium: Iron deposition is present within the lens epithelium (Perls' Prussian blue; original magnification ×200)


Ocular siderosis is a chemical manifestation caused by an IOFB that contains iron. Iron reacts with carbon dioxide to form ferrous carbonate, which diffuses into surrounding tissues. Iron converts to iron oxide and causes lysosomal breakdown and enzyme disruption. In addition, iron oxide fuses with proteins and deposits as yellow-brown particles.3,4 The iron deposition may lead to iris heterochromia, pupillary mydriasis, cataract formation, secondary glaucoma, and retinal pigmentary degeneration.3,5,6 Our patient presented with rust-colored iron deposits on the anterior capsule. Although ocular siderosis is a known but unique complication of IOFBs, interestingly, the pattern of deposition was a near symmetric clock face distribution, which to our knowledge has not been reported in the literature (Figure 3). The features of the IOFB that lead to a certain cataract pattern are unknown, but it may represent an underlying chemical and pathological process.

In addition to the pigmentation that can be visualized, ERG changes can be characteristic of ocular siderosis. Specifically, an increased a-wave followed by a progressive decline of the b-wave is usually seen.7 The toxic effects of iron on the retina cause dysfunction in all retinal layers, with a greater effect on the inner retina than on the outer retina in later stages.8 The ERG changes indicate that rods are more sensitive to the toxic chemical sequelae than the cones. Over time, the responses of the rod cells diminish in amplitude.9 Our patient's ERG displayed the common changes that occur with ocular siderosis.

Patients presenting with siderosis normally present with a history of ocular trauma yet may remain asymptomatic until later when visual acuity decreases.10,11 In addition, the timing of the development of siderotic cataract is variable: from as early as a few days to several years after the injury, and before or after IOFB removal.3 In one case series of nine patients who sustained an IOFB, siderotic cataracts developed between 3 months and 12 years (mean: 2.9 years) after the initial trauma and IOFB removal.9 Another patient with a missed IOFB developed siderotic changes 1 year after trauma.12 Lens siderosis was proven histopathologically in another patient with a history of trauma, but there were no signs of a retained IOFB.13 Our patient presented with iron deposits 5 months after IOFB removal. Taken together, our case along with previous cases suggests that the timing of clinical manifestations of ocular siderosis is unpredictable, and that it may occur even if the IOFB is removed. Despite this uncertainty, if the IOFB is removed in a timely manner, the visual acuity may improve, and the visible siderotic and ERG signal changes are reversible.14–16 Finally, the symmetrical pattern of the cataract appearance may highlight the possibility of an underlying chemical process that influences the pattern of siderotic deposition.

This case illustrates a unique complication that can arise due to an iron-containing IOFB. It highlights the clinical manifestations that arise with ocular siderosis and also demonstrates the importance of close monitoring of all patients with a history of ocular trauma with and without an IOFB. The timeline of siderotic changes is variable, as is the visual appearance of the cataract, which may be due to an unknown underlying process. Even if the IOFB is removed in a timely manner, a siderotic cataract and damage to the retina may develop. With careful follow-up, the changes due to ocular siderosis may be prevented or reversed.


  • Ocular siderosis may develop from intraocular foreign objects through a degenerative chemical process between iron particles and ocular tissue.
  • The timing of a siderotic cataract and the pattern of deposition is variable.


  • The visual appearance of the siderotic cataract in our case was a near symmetric, circular configuration. Therefore, we hypothesize a siderotic cataract may be due to an underlying chemical process.


1. Ballantyne JF. Siderosis bulbi. Br J Ophthalmol 1954;38:727–733
2. Schechner R, Miller B, Merksamer E, Perlman I. A long term follow up of ocular siderosis: quantitative assessment of the electroretinogram. Doc Ophthalmol 1990;76:231–240
3. Ferenc Kuhn VM, Morris R. Intraocular foreign bodies. In: Kuhn F, Pieramici DJ, ed. Ocular Trauma Principles and Practice. New York, NY: Thieme; 2002:235–263
4. Tawara A. Transformation and cytotoxicity of iron in siderosis bulbi. Invest Ophthalmol Vis Sci 1986;27:226–236
5. Taylor WL Jr. MRI for metallic foreign bodies? Ophthalmology 2000;107:410–411
6. Kita M, Negi A, Kawano S, Honda Y. Photothermal, cryogenic, and diathermic effects of retinal adhesive force in vivo. Retina (Philadelphia, Pa) 1991;11:441–444
7. Loporchio D, Mukkamala L, Gorukanti K, Zarbin M, Langer P, Bhagat N. Intraocular foreign bodies: a review. Surv Ophthalmol 2016;61:582–596
8. Imaizumi M, Matsumoto CS, Yamada K, Nanba Y, Takaki Y, Nakatsuka K. Electroretinographic assessment of early changes in ocular siderosis. Ophthalmologica 2000;214:354–359
9. Kannan NB, Adenuga OO, Rajan RP, Ramasamy K. Management of ocular siderosis: visual outcome and electroretinographic changes. J Ophthalmol 2016;2016:7272465
10. O'Duffy D, Salmon JF. Siderosis bulbi resulting from an intralenticular foreign body. Am J Ophthalmol 1999;127:218–219
11. Wu TT, Kung YH, Sheu SJ, Yang CA. Lens siderosis resulting from a tiny missed intralenticular foreign body. J Chin Med Assoc 2009;72:42–44
12. Lapira M, Karl D, Murgatroyd H. Siderosis bulbi as a consequence of a missed intraocular foreign body. BMJ Case Rep. 2014;bcr2013202904
13. Zhang KK, He WW, Lu Y, Zhu XJ. Siderotic cataract with no signs of intraocular foreign body. BMC Ophthalmol 2017;17:26
14. Sneed SR, Weingeist TA. Management of siderosis bulbi due to a retained iron-containing intraocular foreign body. Ophthalmology 1990;97:375–379
15. Peyman GA, Raichand M, Goldberg MF, Brown S. Vitrectomy in the management of intraocular foreign bodies and their complications. Br J Ophthalmol 1980;64:476–482
16. Kuhn F, Witherspoon CD, Skalka H, Morris R. Improvement of siderotic ERG. Eur J Ophthalmol 1992;2:44–45
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