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Siderosis Bulbi
Introduction
Siderosis bulbi refers to the pigmentary, degenerative process of the eye following chronic retention of an iron-containing intra-ocular foreign body (IOFB). It can also occur due to iron derived from the blood.[1] First described by Bunge in 1890, siderosis bulbi has an affinity for ocular structures of epithelial origin such as the cornea, iris, lens, trabecular meshwork, and retina. Iron deposition at these sites leads to the altered morphology of the tissues.[2] A comprehensive clinical evaluation is thus vital to timely detect the development of ocular siderosis and effectively manage these patients without delay.
Etiology
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Etiology
Siderosis bulbi occurs due to intra-ocular retention of an iron-containing foreign body. The most common mechanism is a hammer and chisel injury, seen in about 41.7% to 59% of cases. Other less frequent mechanisms include gunshot injuries, electric welding, injury due to nail gun, explosion injuries, and road traffic accidents.[3][4][5][6]
Epidemiology
Metallic foreign bodies account for 78% to 86% of cases of all intra-ocular foreign bodies (IOFBs), with iron being the most common, followed by lead.[4][7][8] The majority of these patients are middle-aged males. The most common site of entry of an IOFB is the cornea (82.9%) followed by the sclera (11.4%), and the limbus (5.7%).[8] The most common location of an intraocular foreign body lodged in the posterior segment is intravitreal (61%), followed by intra-retinal (14%) and sub-retinal(5%).[9][10][11][6]
Pathophysiology
Oxidative stress, excitotoxicity, and calcium influx play an important role in the pathogenesis of iron-induced retinal toxicity.[12] Two mechanisms of siderosis bulbi have been postulated in the literature, namely, ‘Direct’ and ‘Indirect’ siderosis bulbi.
“Direct siderosis’’ primarily occurs due to the hydroxyl radical formation following Fenton’s reaction (Fe + HO → Fe + HO• + OH).[13] This results in excessive glutamate accumulation due to inhibition of the reuptake of glutamate by oxygen free radicals. Glutamate leads to activation and opening of the ligand-gated calcium ion channels and triggers calcium ion influx within the cells with resultant activation of calcium-dependent enzymes. Ultimately, this leads to irreversible retinal damage involving the degeneration of photoreceptors and retinal pigment epithelium (RPE). Bruch’s membrane and the choroid are spared in the early phase.[14]
“Indirect siderosis” is due to tissue destruction occurring at sites distal to the IOFB. It involves the retinal vasculature causing toxic microvasculopathy, also termed as the ‘‘vascular siderosis’’. This happens due to the affinity of iron for acid mucopolysaccharides that can result in subsequent degeneration of inner retinal layers, supplied by capillaries of the central retinal artery. Additionally, damage to RPE cells can occur indirectly by the migration of iron ions via vitreous to aqueous through the trabecular meshwork into the suprachoroidal space. Ultimately, from here, the ions diffuse across the choroid and Bruch’s membrane to reach RPE.[15][13] Eventually, all retinal layers get involved in chronic ocular siderosis with the involvement of photoreceptors and RPE in the early direct phase and the inner retinal layers in the indirect form of siderosis.[16]
History and Physical
A detailed history and meticulous evaluation play a vital role in ruling out IOFB in ocular trauma. Initial presenting features of siderosis bulbi include gradually progressive diminution of vision and night blindness.[1] The patient may also present with dyschromatopsia or progressive scotomas. [13]
A seidel’s test must be performed in all cases of suspected open-globe injuries to detect the entry wound. In cases of a negative seidel’s test, signs such as corneal edema, subconjunctival hemorrhage, or an iris hole may be suggestive of an entry wound. Apart from the clinical features usually seen in a case of suspected IOFB following penetrating trauma, there are certain signs specific to siderosis bulbi.
A slit-lamp examination may reveal rust-colored or yellowish pigment deposits within the corneal stroma or endothelium.[2]
Iron deposition within the layers of iris, particularly stroma and epithelium, results in greenish-brown discoloration, which is reversible in eliminating the foreign body (FB). It is an early sign of ocular siderosis. [17][18]
The pupillary examination may reveal a fixed, dilated pupil which may be the earliest sign of siderosis bulbi. An exaggerated pupillary constriction to 0.1% (low-dose) concentration of pilocarpine is seen owing to denervation hypersensitivity.[19] Evidence of iron deposits within the sphincter and dilator muscles of the iris is seen on histopathology. Both iris discoloration and “iron mydriasis” are reversible phenomena.[19][20][21]
Secondary open-angle glaucoma may develop due to iron deposition in the trabecular meshwork. Eventually, trabecular fibrosclerosis may result due to iron toxicity, resulting in medically uncontrollable glaucoma. The incidence of glaucoma is, however, uncommon in siderosis bulbi (5%).[1][11][22] It is critical to perform gonioscopy in every case of suspected IOFB to rule out a foreign body at the iridocorneal angle.[22]
Intra-lenticular foreign bodies constitute 10% of all IOFBs and are mostly associated with cataract formation.[23] Classical dark-brown anterior subcapsular deposits may be noted. The mechanism of cataract development is either due to iron deposition or direct trauma to the lens. Progression of ocular siderosis in a case of a localized intra-lenticular foreign body is slower when compared to a posterior-segment foreign body.[24][25]
Siderosis bulbi classically affects the RPE resulting in pigmentary degeneration of the retina. Iron toxicity may also lead to optic disc edema, though it may resolve after the removal of IOFB.[23] IOFB within the posterior segment may result in vitreous hemorrhage (46%), retinal detachment (RD) (27%), Proliferative vitreoretinopathy (PVR) changes (21% to 89%), the formation of epiretinal membrane, and macular edema. The occurrence of subretinal hemorrhage may further damage the choroid and the inner surface of the sclera.[26][27][28][29][28][27] Infrequently, ocular siderosis may manifest as anterior uveitis, posterior uveitis, or even pan-uveitis.[30][31][28][31]
Evaluation
Radiological evaluation to detect an IOFB plays a key role in the management of ocular trauma. Several useful imaging modalities include X-ray, computed tomography (CT), magnetic resonance imaging (MRI), ultrasonography (USG), ultrasound biomicroscopy (UBM), and Optic coherence tomography (OCT). Electrophysiological tests like Electroretinography (ERG) play an essential role in assessing retinal damage in ocular siderosis. Ancillary tests, including electrooculogram, fluorescein angiography (FA), and visual field tests, help in assessing further damage.[32]
Metallic IOFBs are recognized on plain X-ray films as radio-opaque bodies. However, it poses a great challenge in localizing and predicting the nature of FB, and therefore, has a limited role as a diagnostic modality.[33]
USG, a popular imaging modality, can detect both metallic as well as for non-metallic IOFBs. On B-scan, IOFB appears as a hyperechoic lesion with acoustic back-shadowing.[13] It is a highly sensitive and specific investigation to identify associated ocular injuries, such as lens dislocation, vitreous hemorrhage, RD, choroidal detachment, even in the presence of media opacities owing to trauma.[34] However, USG has certain limitations of its own. Firstly, it tends to overestimate the size of the foreign body.[35] Secondly, a FB lying in the posterior third of the orbit or within the peri-orbital soft tissues may be missed on USG.[34][36] Thirdly, USG requires expertise and is largely operator-dependent. Lastly, it should always be used with great caution in cases of open-globe injuries.[37]
Non-contrast CT (NCCT) is the gold standard investigation for identifying metallic foreign bodies. It is highly accurate in predicting the nature, location (intraocular, extraocular, or retro-bulbar), and size of the FB. Thin scans (1.0 to 1.5 mm) are preferred as they provide higher resolution. It has a high sensitivity for detecting IOFBs (45% to 65% ≤ 0.06 mm and 100% >0.06 mm size), which may otherwise be missed on the orbital X-ray.[33][38][39][40]
MRI has better sensitivity (95%) than CT scan to detect non-metallic IOFBs and visualize optic nerve, orbital apex, and soft tissue details without radiation exposure.[41] However, MRI is contraindicated in suspected ferromagnetic foreign bodies since these tend to move within the electromagnetic field, causing more ocular damage.[42]
Ultrasound biomicroscopy (UBM) is the preferred imaging for foreign bodies located anteriorly (subconjunctival space, corneal layers, angle, anterior iris surface, ciliary body, pars plana, 100um from the retina). Since UBM requires contact, it should be avoided in cases of an open-globe injury due to an increased risk of intraocular infection.[43][44][45]
Anterior segment OCT (AS-OCT), a non-contact, non-invasive imaging investigation, facilitates the visualization of the anterior segment FBs. Unlike UBM, it ensures greater patient comfort and better compliance. It can also be used as an effective prognosticating tool in ocular siderosis. Owing to its poor penetration across the posterior pigmented layer of the iris, FBs lying behind this plane may often be missed.[46][47]
Posterior segment OCT is a useful tool in detecting the accurate location of an IOFB lying in the posterior segment (epiretinal, intraretinal, or subretinal) and for quantifying cystoid macular edema. It can also identify the encapsulation of the foreign body, a factor that helps in deciding the timing of surgical intervention.[48]
Full-field ERG (ffERG) is the gold standard electrophysiological test for identifying subclinical siderosis bulbi. It is an efficient diagnostic and prognosticating tool in ocular siderosis.[49] In the early phase of the disease, both a- and b-wave amplitude increases (also called the supernormal response).[50][51] The b-wave amplitude subsequently decreases with a reduction in the b /a-wave ratio to less than 1. In advanced cases, an extinguished response is seen on ERG with absent a- and b-waves.[52][11] Early predictors of siderosis bulbi on ERG include the increased amplitude of b-wave (Supernormal response), reduction in the amplitude of Oscillatory potentials, decrease in amplitude of P1 and N1 waves along with a delay in P1-implicit time on mfERG even in the presence of a normal ffERG.[53][54][55] Early removal of the foreign body leads to recovery of ERG amplitudes as iron toxicity is reversible in the early phase of the disease.[51][56]
Fluorescein angiography (FA) in ocular siderosis may reveal hyperfluorescent window defects owing to RPE changes, capillary non-perfusion areas, and ischemic maculopathy.[32][16] Progressive visual field constriction has also been reported in cases of ocular siderosis. Although there may be associated glaucomatous damage, the underlying postulated mechanism involves the insufficiency of retinal circulation in advanced cases.[32][22]
Treatment / Management
Acute presentation following trauma with a metallic foreign body mandates evaluating the patient’s vaccination status and administering the tetanus booster dose accordingly. Systemic and topical broad-spectrum antibiotics should be instituted against the commonest organisms, such as gram-positive cocci (streptococcus, coagulase-negative staphylococcus), anaerobic bacteria (clostridium species), and gram-negative bacilli (Escherichia coli, Klebsiella pneumoniae).[57] Once the metallic FB has been identified on imaging, it is strongly recommended to promptly remove the foreign body to avoid the occurrence of siderosis bulbi (in case of an iron IOFB) and endophthalmitis. A single-setting surgical procedure is usually associated with better visual outcomes when compared to multiple surgeries.[58](B2)
The indications for immediate removal include FB localized in the anterior chamber, vitreous cavity and a non-encapsulated FB in the retina.[59][52] Once the FB located in the posterior segment encapsulates, surgical removal becomes cumbersome.[52] It is also important to emphasize that delayed surgery (for more than 14 days) is associated with an increased risk of tractional RD and PVR changes.[60] Intra-lenticular iron FBs may be removed simultaneously with cataractous lens extraction as the iron particles tend to leak out, especially when located in the periphery, further predisposing to siderosis bulbi.[59](B3)
Immediate wound closure must be performed in all cases of open-globe injuries. However, the surgical removal of IOFBs can be delayed due to the non-availability of the vitreoretinal setup or in cases where corneal edema precludes Pars Plana Vitrectomy (PPV).[57] The ultimate decision to remove an IOFB must be weighed against the risk-benefit ratio.(B3)
In cases of delayed surgical intervention, it is critical to perform serial assessments with ERG testing every 2 to 3 months. If the ERG remains stable, the patient can be observed further with gradually increasing intervals between subsequent follow-ups. On every follow-up, evaluation of best-corrected visual acuity, ophthalmoscopy, appropriate imaging, along with serial ERG should be performed. If the patient appears non-compliant to follow-up or a diminishing response on ERG is noted, immediate removal is warranted.[52](B3)
Surgical Management
Posterior segment metallic IOFB may be removed via the traditional external approach using an external electromagnet (EEM) or an internal approach using forceps or intra-ocular magnets (IOMs).[11] In the external approach, a sclerotomy is made at 4.5mm from the limbus, and extraction is initiated using EEM under visualization of the indirect ophthalmoscope.[61] This approach is associated with a higher incidence of iatrogenic ocular injuries, such as hyphema, vitreous hemorrhage, retinal laceration, RD, vitreous prolapse, trauma to the iris, lens, and zonules. Thus, the use of EEM is now obsolete and is only reserved for the removal of IOFB remnants.[62][61](B2)
In the internal approach, 23G or 25G (sutureless) PPV is done using forceps or an IOM.[63] 20-gauge vitrectomy may be indicated in cases of large foreign bodies.[57] Forceps are advisable over IOMs as it may be difficult to remove the metallic foreign body once the IOMs or the IOFBs lose their magnetic properties.[11] This approach is comparatively less traumatic than the external approach. Surgical removal of IOFB and the resultant intra-operative complications can be concurrently managed using this approach.[62] It is recommended to use perfluorocarbon liquid (PFCL) before lifting the IOFB to prevent macular damage.[61] (B2)
A new surgical procedure, known as the ‘‘handshake technique’’ has been recently described wherein two IOMs are introduced through the PPV sclerotomies followed by safe delivery of the IOFB through the corneoscleral tunnel. This technique is especially preferred for large foreign bodies as it doesn’t require enlargement of the pre-existing sclerotomy.[64]
For foreign bodies located in the anterior segment, removal is initiated through the limbal approach in cases of FBs larger than 6mm, or through the sclera for smaller FBs.[65] Removal through the entry wound is usually not advocated, except in cases of a large foreign body or a gaping corneal wound, due to the risk of scarring and endothelial damage.[39] Balanced salt solution or ophthalmic viscoelastic devices may be used to dislodge FB located in the anterior chamber. Gonioscopy-assisted removal is warranted for foreign bodies located in the irideocorneal angle.[39] IOFBs within the iris may be removed by iridotomy or iridectomy.[66] (B3)
Role of Deferoxamine
Deferoxamine is a chelating agent with a high affinity for free iron ions. It is used in thalassaemic patients undergoing multiple blood transfusions to avoid siderosis due to iron overload.[67] Subconjunctival use of deferoxamine (10 to 100 mg) has been shown to prevent the development of ocular siderosis. In advanced siderosis, where cells are already damaged, deferoxamine cannot reverse the toxic effects of iron as it cannot remove the bound iron ions from the tissue.[68] Deferoxamine-related toxicity, such as bone dysplasia, sensorineural hearing loss, nyctalopia, color vision impairment, RPE alteration, and reduction in ERG amplitudes, limits its use in the management of ocular siderosis.[69](B2)
Differential Diagnosis
Since retinal arteriolar narrowing and sheathing with pigmentary retinal degeneration can be seen in siderosis bulbi, it closely resembles retinitis pigmentosa (RP). In rare cases of suspected unilateral RP, the diagnosis clinches more towards ocular siderosis when associated with a typical history of trauma with iron FB.[70][13][70]
Mydriasis, with a hypersensitive response to 0.1% pilocarpine in ocular siderosis, mimics Adie’s tonic pupil and must be considered as one of the differential diagnoses. The pathophysiology of Adie’s tonic pupil involves damage to the ciliary ganglion, as opposed to the local parasympathetic neuropathy in siderosis bulbi.[20][23][71]
Prognosis
Factors such as young age, large IOFBs (mean length= 5.7mm) with high kinetic energy, best-corrected visual acuity < 20/200 at presentation, prolonged retention of FB, posterior segment IOFBs, and associated hyphema, vitreous hemorrhage, RD or endophthalmitis at presentation are associated with a poorer prognosis.[72][73][74][75]
Multiple surgeries are associated with enhanced morbidity. Ocular trauma score (OTS), developed by Kuhn et al., can be used to prognosticate ocular siderosis and predict visual outcomes in penetrating ocular injuries.[76][6] The length of the entry wound also determines the risk of retinal damage. Less energy dissipation occurs in shorter wounds allowing deeper penetration into the eye, resulting in significant retinal damage.[66] Blunt IOFBs tend to cause more damage to the globe than the sharper ones of the same size, owing to significant energy transfer at the time of impact.[77]
Complications
IOFB can lead to several complications, such as those associated with an open-globe injury. Endophthalmitis is the most dreaded complication following ocular trauma. Post-traumatic endophthalmitis has been reported to develop in 2.1% to 11.9% of patients with open-globe injury in the absence of IOFB. In contrast, endophthalmitis associated with an IOFB accounts for 3.8% to 48.1% of cases.[78][79][80] Poor prognosticating factors include increased occurrence of virulent organisms, associated tissue damage, and delay in management.[81]
Another sight-threatening complication of an open-globe injury is Sympathetic Ophthalmia (SO). It is a bilateral granulomatous pan-uveitis usually following penetrating ocular trauma or surgery. The incidence of SO is reported as 0.28-1.9% in penetrating ocular trauma.[82][83][84]
IOFB can also be associated with several anterior segment complications such as hyphema, traumatic cataract, capsular rupture, subluxation or dislocation, and secondary open-angle glaucoma.[75][6][1][25]
Siderosis bulbi can also lead to optic atrophy and cystoid macular edema.[85][32] There is also an increased risk of epiretinal membrane formation leading to macular puckering, PVR, and retinal detachment.[26][27]
Deterrence and Patient Education
Public awareness regarding workplace-related ocular trauma should be strengthened as prevention is the key to avoid the dreaded complications of penetrating ocular injuries and siderosis bulbi. A better understanding of the detrimental consequences of ocular siderosis will encourage people to take appropriate measures for eye protection at workplaces, such as safety glasses, eye goggles, and face shields. Patients must be warned about the complications of open-globe trauma and siderosis bulbi. They must be counseled regarding the final prognosis and the importance of regular follow-up visits.
Pearls and Other Issues
A thorough history and meticulous examination are recommended in every case of ocular trauma to rule out the intraocular foreign body. Radiological investigations play an instrumental role in timely detection and appropriate management. Serial monitoring and regular follow-up are advocated in all cases of suspected ocular siderosis.
Enhancing Healthcare Team Outcomes
A general ophthalmologist must be well-trained in dealing with cases of ocular trauma. A high index of suspicion for the presence of an intraocular foreign body must be maintained in all cases of ocular injuries, especially in young children who may present without any apparent history of trauma. In cases where a vitreoretinal facility is not available, a proficient specialist must be consulted immediately.
Media
(Click Image to Enlarge)
Subconjunctival hemorrhage with evidence of entry wound (blue arrow) in a 29 year old male following hammer and chisel injury
Contributed by Isha Acharya, MBBS
(Click Image to Enlarge)
NCCT, sagittal view, showing hyperdense lesion suggestive of an IOFB following a penetrating injury
Contributed by Ayushi Agarwal, MBBS
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