Siderosis Bulbi Zamzam Al-baker,MD Consultant Opthalmology Ophthalmology depart./Hamad Medical Corporation-Qatar Ocular History 10 year old boy . January /2005: OS: recurrent redness 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. Ocular History Systemic review and medical check up: unremarkable Laboratory blood investigations and systemic uveitis work-up : normal December 2005 - First Presentation VA: OD 20/20, OS 20/400 . IOP:OD 14 mmHg, OS 6 mmHg. OD: anterior and posterior segment no cells OS: Conjunctiva: mild cilary injection . Cornea : diffuse stromal haze and brown discoloration with white large keratic precipitates inferior 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 Rusty brown deposits on anterior lens capsule First Presentation - Ultrasound Vitreous opacities with small foreign body on the retina with posterior shadow effect Further Investigations ERG: patient was not cooperative CT scan orbit: no foreign body seen Diagnosis Siderosis Bulbi Masquerading as Panuveitis Treatment – Follow up December- 2006 anterior granulomatous reaction was controlled with topical steroids drops January-2006 OD phacoemulsification + parsplana vitrectomy + removal of intraocular foreign body +intraocular lens implant + silicon oil tamponade Follow-up – June 2006 VA: 20/400 cornea: stromal haze and brown deposits A/C: clear pale optic disc generalized RPE clumbing, flat retina centrally under silicone oil inferior tractional detachment with subretinal fibrosis Patient did not attend for further follow up 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 can mimic multiple other uveitis disorders 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. Diagnosis of Ocular Siderosis suspicion detailed history complete ocular examination gonioscopy X-ray , CT scan US, ERG, EOG 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 . 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. 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. 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