Siderosis bulbi

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siderosis bulbi intraocular iron foreign body

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Siderosis Bulbi

Definition

Siderosis bulbi (also called siderosis oculi) is a progressive degenerative condition of the eye caused by the retention of an iron-containing (ferrous) intraocular foreign body (IOFB). The iron undergoes electrolytic dissociation and deposits throughout the intraocular epithelial structures, where it exerts direct toxic effects on cellular enzyme systems, causing progressive cell death.

Etiology and Mechanism

  • Cause: A retained ferrous IOFB - most commonly a steel fragment projected during hammering or power tool use
  • Mechanism: The ferrous IOFB undergoes spontaneous dissociation in the ocular environment. Free iron ions deposit into epithelial structures and generate reactive oxygen species (Fenton reaction), disrupting cellular enzyme systems and leading to progressive cell death
  • Structures affected: Lens epithelium, iris epithelium, ciliary body epithelium, and sensory retina (particularly the photoreceptors and RPE)

Clinical Features (Signs)

StructureSign
LensAnterior capsular cataract with radially distributed iron deposits on the anterior lens capsule ("iron lines" or rust-colored deposits)
IrisReddish-brown staining of the iris → heterochromia iridis (the affected eye becomes darker/rust-colored)
PupilDilated (iron mydriasis) - a classic and notable sign
Trabecular meshworkTrabecular damage → secondary open-angle glaucoma
Retina/RPEPigmentary retinopathy → atrophy of the retina and RPE, potentially leading to profound, irreversible visual loss
ERGProgressive attenuation of the b-wave on electroretinography (photoreceptor toxicity) - an early and sensitive marker
The iris heterochromia and iron mydriasis may be subtle or missed in cases of an occult (unrecognized) IOFB.
Siderosis oculi - (A) anterior capsular lenticular iron deposits and (B) retinal and RPE atrophy with an impacted ferrous foreign body
Fig. 22.30 - Siderosis oculi. (A) Lenticular deposits on the anterior capsule; (B) atrophy of the retina and RPE associated with an impacted ferrous IOFB. (Kanski's Clinical Ophthalmology, 10th ed.)

Symptoms

  • Gradual, painless deterioration of vision (often delayed - weeks to years after the original injury)
  • Night blindness (early, due to rod photoreceptor toxicity)
  • Constriction of visual fields
  • History of ocular trauma is often present but may be forgotten

Investigations

  1. Slit-lamp examination - iris discoloration, anterior capsular deposits, pupil dilation
  2. Electroretinography (ERG) - progressive b-wave attenuation is the most sensitive early marker of retinal toxicity; used to monitor progression
  3. Plain X-ray - initial screening for radiopaque IOFB
  4. CT scan (axial + coronal) - gold standard for detecting and localizing a metallic IOFB; superior sensitivity and specificity compared to X-ray or ultrasound
  5. B-scan ultrasonography - useful when CT is unavailable or for posterior segment assessment
  6. MRI - CONTRAINDICATED when a ferrous metallic IOFB is suspected (risk of movement of the IOFB)
  7. Gonioscopy - assess trabecular iron deposition and glaucoma risk

Differential Diagnosis of the Heterochromia

  • Fuchs heterochromic iridocyclitis
  • Congenital iris heterochromia
  • Iris nevus / melanoma
  • Hemosiderosis (from old hyphema or vitreous hemorrhage)
  • Pigment dispersion syndrome

Treatment

  1. Prompt surgical removal of the IOFB - the definitive treatment; prevents further iron dissociation
    • Magnetic removal: Sclerotomy adjacent to the FB + application of a magnet, followed by cryotherapy to the retinal break
    • Forceps removal (pars plana vitrectomy): For non-magnetic or poorly positioned FB, or those that cannot be safely extracted with a magnet
  2. Treat secondary glaucoma - topical IOP-lowering therapy or surgical intervention as needed
  3. Antibiotics - prophylaxis for endophthalmitis (open globe): ciprofloxacin 750 mg BD or moxifloxacin 400 mg OD, plus topical antibiotics and cycloplegia
  4. Serial ERG monitoring - if IOFB removal is delayed or not feasible, to track progressive retinal toxicity

Prognosis

  • If the IOFB is removed early (before significant retinal damage), vision may be preserved or improved
  • Delayed diagnosis leads to irreversible photoreceptor and RPE loss
  • A missed ferrous IOFB is a common medicolegal pitfall - any patient with ocular trauma and unexplained progressive visual loss must be investigated

Siderosis vs. Chalcosis - Key Comparison

FeatureSiderosis (Iron IOFB)Chalcosis (Copper IOFB)
Foreign bodyIron/steelCopper alloy (brass, bronze)
IrisRust-brown discoloration, heterochromiaKayser-Fleischer ring
LensAnterior capsular rust deposits"Sunflower" cataract
RetinaPigmentary retinopathy, atrophyGolden plaques; retina relatively spared
Visual outcomeProgressive, severe lossBetter preserved (copper less retinotoxic)
ERGProgressive b-wave attenuationLess severely affected
Endophthalmitis riskLowerHigh copper content → violent endophthalmitis → phthisis bulbi

Source: Kanski's Clinical Ophthalmology - A Systematic Approach, 10th ed., pp. 942-943; Wills Eye Manual, 7th ed.; Localization in Clinical Neurology, 8th ed.
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