Intraocular Foreign Body (IOFB) Management

Overview

Presentation

• Clinically visible entry wound (corneal or scleral perforation), iris hole, focal lens opacity, or visible IOFB
• Irregular/teardrop-shaped pupil, hyphema, shallow/flat AC
• Microcystic corneal edema in the peripheral cornea (clue to AC angle foreign body)
• 360° subconjunctival hemorrhage, prolapse of uveal tissue

Fig. 3.15.1 — IOFB visible on fundoscopy (Wills Eye Manual)

Classification of Foreign Bodies by Reactivity

Brass/bronze (copper alloy with low copper content) → chalcosis rather than violent endophthalmitis. Most BBs and gunshot pellets contain 80–90% lead + 10–20% iron.

Workup

History

• Nature and composition of the foreign body
• Mechanism (hammering, grinding, blast)
• Time of last meal (surgical planning)

Examination

1. Visual acuity
2. Slit lamp: Entry sites, iris TID (transillumination defects), pupil shape, lens disruption, hyphema, AC depth, IOP
3. Gonioscopy if no wound leak and globe appears intact (to locate AC angle FB)
4. Dilated indirect ophthalmoscopy — deferred if risk of extrusion of intraocular contents
5. CT orbits (axial + coronal + parasagittal, ≤1-mm sections) — preferred imaging; sensitivity superior to plain X-ray and ultrasound for metallic IOFBs
6. B-scan ultrasound / UBM — useful for non-metallic foreign bodies and when CT is equivocal; intraocular air can mimic a foreign body
7. MRI is contraindicated in the setting of any metallic (especially ferrous) IOFB

Immediate Emergency Management

1. NPO — no food or drink until surgical repair
2. Rigid protective shield over the eye (do not patch)
3. Tetanus prophylaxis (see tetanus schedule)
4. Systemic broad-spectrum antibiotics covering gram-positive and gram-negative organisms:
   • Vancomycin 1 g IV q12h + ceftazidime 1 g IV q12h
   • OR ciprofloxacin 400 mg IV q12h
   • OR moxifloxacin 400 mg IV daily
   • (Fluoroquinolones contraindicated in children and pregnant women)
5. Cycloplegia (e.g., atropine 1% b.i.d.) for posterior-segment IOFBs
6. Emergent ophthalmology consultation — any further examination to be performed only in the OR

Surgical Removal

Magnetic (Ferrous) IOFBs

• Magnetic extraction via sclerotomy adjacent to the foreign body, using an intraocular magnet, followed by cryotherapy to seal any retinal break created
• This is the preferred approach for ferro-magnetic bodies that can be safely reached

Non-Magnetic (or Inaccessible Magnetic) IOFBs

• Pars plana vitrectomy (PPV) with forceps extraction — the IOFB is removed either through the pars plana or the limbus depending on location and size

Special Situations

• Copper/contaminated foreign bodies require especially urgent removal
• Chronic IOFB may be observed if inert, but requires removal if associated with severe recurrent inflammation, location in the visual axis, or evidence of siderosis
• Inert foreign bodies (glass, gold, etc.) are often well tolerated; surgical removal risk must be weighed against the risk of delayed complications

Complications

Siderosis Bulbi (Iron/Steel)

• Anterior subcapsular cataract (radial iron deposits on anterior lens capsule)
• Reddish-brown iris staining → heterochromia iridis
• Pigmentary retinopathy → RPE atrophy → profound visual loss
• Trabecular damage → secondary glaucoma
• Anisocoria, lens dislocation, optic atrophy
• ERG: Progressive attenuation of the b-wave — a key monitoring tool

Chalcosis (Copper Alloy)

• Copper alloy (brass/bronze) → electrolytic dissociation → copper deposition
• Kayser–Fleischer ring, anterior sunflower cataract, retinal golden plaques
• Less retinotoxic than iron — degenerative retinopathy usually does not develop

Fig. 22.30 — Siderosis oculi (Kanski's Clinical Ophthalmology, 10th ed.)

Endophthalmitis

• Develops in ~1 in 10 cases of penetrating trauma with retained IOFB
• Risk factors: Delay in primary repair, retained IOFB, wound position/extent
• Pathogens: Staphylococcus spp. and Bacillus spp. account for ~90% of culture-positive cases
• Management: Prompt IOFB removal + prophylactic intravitreal antibiotics (especially for high-risk cases such as agricultural injuries); treat established endophthalmitis as for acute postoperative endophthalmitis
• Culture the removed IOFB

Proliferative Vitreoretinopathy (PVR)

Sympathetic Ophthalmia

• Vision-threatening autoimmune response to the fellow (uninjured) eye
• Triggered by exposure of the immune system to intraocular contents from the perforated eye
• Rare but devastating; another argument for prompt primary repair

Follow-Up

• Observe closely for signs of inflammation or infection post-repair
• If uncertain whether FB was fully removed, perform post-op CT/B-scan/UBM
• Serial ERGs to monitor for toxic retinopathy when an IOFB is retained — retinopathy often reverses if the FB is removed before severe damage
• Long-term periodic follow-up for years (watch for delayed inflammatory reactions in both the traumatized and fellow eye)

Recent Evidence

Fundus Fluorescein Angiography (FFA / FA)

Principle

• Excitation peak: ~465–490 nm (blue light)
• Emission peak: ~520–530 nm (yellow-green light)

Blood–Retinal Barrier Anatomy (Critical to FA Interpretation)

Camera Setup & Filters

• Cobalt blue excitation filter: Passes only blue light into the eye (~490 nm) to excite fluorescein
• Yellow-green barrier filter: Blocks reflected blue light, allowing only emitted yellow-green fluorescence to reach the sensor
• Modern digital CCD cameras allow immediate image availability, lower fluorescein doses, and enhanced image manipulation — with correspondingly lower adverse effect rates

Technique

1. Adequate pharmacological mydriasis is essential
2. Baseline colour photographs + red-free images (green incident light to enhance red detail) + autofluorescence images taken first
3. IV cannula inserted (standard cannula preferred over butterfly); flush with normal saline to confirm patency
4. 5 ml of 10% sodium fluorescein injected over 5–10 seconds
5. Photography begins 5–10 seconds after injection at 1–2 second intervals to capture the critical early transit phases
6. Images continue into the late phase (10–20 minutes)
7. Oral alternative (if IV access not possible): 30 mg/kg, images taken 20–60 minutes after ingestion
8. Stereo images may demonstrate elevation (e.g., neovascular membranes)

Phases of FA

Normal intravenous fluorescein angiogram (Wills Eye Manual)

Interpreting the Abnormal Study

HYPERFLUORESCENCE (Increased signal)

Key differentiator: Leakage = grows in size AND brightness. Pooling = grows in brightness only (fixed border). Window defect = fades in late phase, does not grow.

HYPOFLUORESCENCE (Reduced signal)

Clinical Indications

1. Retinal vascular disease — diabetic retinopathy (capillary non-perfusion, neovascularization), CRVO, BRVO, CRAO
2. Choroidal neovascularization (CNV) — AMD (classic vs occult), pathologic myopia, angioid streaks
3. Macular disease — CSCR, CME, macular degeneration, macular hole
4. Optic disc evaluation — disc swelling, drusen, ischemic optic neuropathy
5. Iris vasculature — rubeosis iridis
6. Transit time analysis — arm-to-retina time, arteriovenous transit time; useful in ocular ischemic syndrome
7. Treatment planning — identify targets for laser photocoagulation or anti-VEGF therapy

FA should only be performed if the findings are likely to influence management. — Kanski's

Adverse Effects

Contraindications

Comparison with ICG Angiography (ICGA)