Siderosis Bulbi

1. Siderosis Bulbi Zamzam Al-baker,MD Consultant Opthalmology Ophthalmology depart./Hamad Medical Corporation-Qatar

2. Ocular History • 10 year old boy . • January /2005: OS: recurrentredness and photophobia for 9 months , improved after topical steroids • gradual decreased vision since 3 months • he remembered a trivial non-specific ocular trauma 12 months back.

3. OcularHistory • Systemic review and medical check up: unremarkable • Laboratory blood investigations and systemic uveitis work-up : normal

4. December 2005- First Presentation • VA: OD 20/20, OS 20/400 . • IOP:OD 14 mmHg, OS 6 mmHg. • OD: anterior and posterior segmentnocells • OS: • Conjunctiva: mild cilary injection . • Cornea : diffuse stromal haze and brown discoloration with white large keratic precipitates inferior

5. First Presentation • A/C: deep, 3 + cells. • Pupil: 6mm, round with multiple areas of posterior synechia, on dilatation with multiple brown-rusty deposits on anterior lens capsule. • Lens: 3+ nuclear & PSCC cataract • Vitreous: 2+ Vitreous haze • Fundus: hazy view, scattered RPE clumping, pigmented shadow at inferior temporal quadrant

6. Rusty brown deposits on anterior lens capsule

7. First Presentation - Ultrasound Vitreous opacities with small foreign body on the retina with posterior shadow effect

8. Further Investigations ERG: patient was not cooperative CT scan orbit: no foreign body seen

9. Diagnosis Siderosis Bulbi Masquerading as Panuveitis

10. Treatment – Follow up • December- 2006 • anteriorgranulomatous reaction was controlled with topicalsteroidsdrops • January-2006 • OD phacoemulsification + parsplana vitrectomy + removal of intraocular foreign body +intraocular lens implant + silicon oiltamponade

11. Follow-up – June 2006 • VA: 20/400 • cornea: stromal haze and browndeposits • A/C: clear • pale opticdisc • generalized RPE clumbing, flat retina centrally under siliconeoil • inferior tractional detachment with subretinal fibrosis • Patient did not attend for further follow up

12. Conclusion Metallic FB are electrolytically dissociated or react with the tissue-fluid to form decomposition product, usually by oxidation and cause specific toxic reaction such as siderosis or chalosis. The clinical manifestations of ocular siderosis result from a chronic degenerative process presumably induced by the oxidation of reduced forms of elemental iron that result in the libration of toxic oxidants canmimic multiple otheruveitisdisorders

13. Clinical Manifestations of ocular Siderosis Rust-colored corneal stroma Iris heterochromia (affected side is darker) Pupillary mydriasis Chronic uveitis rust-colored anterior subcapsular deposits Cataract Lens sub-luxation Secondary glaucoma Retinal pigmentary changes.

14. Diagnosis of Ocular Siderosis • suspicion • detailed history • complete ocular examination • gonioscopy • X-ray , CT scan • US, ERG, EOG

15. Comments • In this case the presence of unilateral granulomatous panuveitis in such age alerted us to the possibility of masquerade. • There were other anterior segment signs typical for ocular siderosis, like the rusty corneal stromal haze, and the brown rustic anterior subcapsular deposits .

16. Conclusion • Siderosis seems to be more advanced when the foreign body is located in the posterior segment. • Foreign bodies tend to be better tolerated when located in the anterior chamber or imbedded in the lens.

17. Conclusion • The natural course of a retained IOFB varies • small IOFBs may be completely resorbed, the FB may become encapsulated • the siderotic changes may stabilize or regress • the FB may lose its magnetic properties or become radiolucent to X-rays • or progressive siderotic changes may occur.

18. Conclusion Siderotic changes have been reported to occur from 18 days to 8 years after the injury The VA at presentation is an indicator for the final VA in severe forms of siderosis Hypotony and retinal pigment changes are signs of advanced severe cases of ocular siderosis