摘要
Siderosis bulbi is a spectrum of toxicity complications resulting from intraocular iron, commonly introduced during trauma.1Ballantyne J.F. Siderosis bulbi.Br J Ophthalmol. 1954; 38: 727-733Crossref PubMed Scopus (11) Google Scholar Within ocular structures, iron generates powerful oxidants that inactivate enzymes and damage cell membranes,1Ballantyne J.F. Siderosis bulbi.Br J Ophthalmol. 1954; 38: 727-733Crossref PubMed Scopus (11) Google Scholar culminating in vision loss. Therefore, timely surgical removal is preferred when possible. Plain-film, computed tomography, ultrasonography, and gonioscopy can help locate the intraocular foreign body (IOFB), but diagnosis may still hinge on clinical manifestations: decreased visual acuity (VA), nyctalopia, constricted visual fields, iris heterochromia, tonic pupil, cataract, changes in retinal pigmentary epithelium (RPE), retinal detachment, optic nerve atrophy, and secondary open-angle glaucoma.1Ballantyne J.F. Siderosis bulbi.Br J Ophthalmol. 1954; 38: 727-733Crossref PubMed Scopus (11) Google Scholar, 2Xie H. Chen S. Ocular siderosis.Eye Sci. 2013; 28: 108-112PubMed Google Scholar, 3Kuhn F, Mester V, Morris R. Intraocular foreign bodies. In: Kuhn F, Pieramici D, eds. Ocular Trauma: Principles and Practice. New York: Thieme Medical Publishers; 2002:237-263Google Scholar, 4Parke 3rd, D.W. Flynn Jr, H.W. Fisher Y.L. Management of intraocular foreign bodies: a clinical flight plan.Can J Ophthalmol. 2013; 48: 8-12Abstract Full Text Full Text PDF PubMed Scopus (27) Google Scholar, 5Bhagat N. Nagori S. Zarbin M. Post-traumatic Infectious Endophthalmitis.Surv Ophthalmol. 2011; 56: 214-251Abstract Full Text Full Text PDF PubMed Scopus (150) Google Scholar, 6Weiss M.J. Hofeldt A.J. Behrens M. Fisher K. Ocular siderosis. Diagnosis and management.Retina. 1997; 17: 105-108Crossref PubMed Scopus (47) Google Scholar, 7Luo Z. Gardiner M. The incidence of intraocular foreign bodies and other intraocular findings in patients with corneal metal foreign bodies.Ophthalmology. 2010; 117: 2218-2221Abstract Full Text Full Text PDF PubMed Scopus (16) Google Scholar Serial electroretinograms can track progression of siderotic retinal and RPE injury.2Xie H. Chen S. Ocular siderosis.Eye Sci. 2013; 28: 108-112PubMed Google Scholar, 3Kuhn F, Mester V, Morris R. Intraocular foreign bodies. In: Kuhn F, Pieramici D, eds. Ocular Trauma: Principles and Practice. New York: Thieme Medical Publishers; 2002:237-263Google Scholar, 4Parke 3rd, D.W. Flynn Jr, H.W. Fisher Y.L. Management of intraocular foreign bodies: a clinical flight plan.Can J Ophthalmol. 2013; 48: 8-12Abstract Full Text Full Text PDF PubMed Scopus (27) Google Scholar, 5Bhagat N. Nagori S. Zarbin M. Post-traumatic Infectious Endophthalmitis.Surv Ophthalmol. 2011; 56: 214-251Abstract Full Text Full Text PDF PubMed Scopus (150) Google Scholar, 6Weiss M.J. Hofeldt A.J. Behrens M. Fisher K. Ocular siderosis. Diagnosis and management.Retina. 1997; 17: 105-108Crossref PubMed Scopus (47) Google Scholar, 7Luo Z. Gardiner M. The incidence of intraocular foreign bodies and other intraocular findings in patients with corneal metal foreign bodies.Ophthalmology. 2010; 117: 2218-2221Abstract Full Text Full Text PDF PubMed Scopus (16) Google Scholar Siderosis bulbi can induce marked intraocular pressure (IOP) rise and glaucomatous damage.1Ballantyne J.F. Siderosis bulbi.Br J Ophthalmol. 1954; 38: 727-733Crossref PubMed Scopus (11) Google Scholar, 8Broendstrup P. Two cases of temporary siderosis bulbi with spontaneous resorption and without impairment of function.Acta Ophthalmol. 1944; 22: 311-316Crossref Scopus (2) Google Scholar, 9Sangermani C. Mora P. Mancini C. Vecchi M. Gandolfi S.A. Ultrasound biomicroscopy in two cases of ocular siderosis with secondary glaucoma.Acta Ophthalmol. 2010; 88: e1-e2Crossref PubMed Scopus (11) Google Scholar, 10Bai H.Q. Yao L. Wang D.B. Jin R. Wang Y.X. Causes and treatments of traumatic secondary glaucoma.Eur J Ophthalmol. 2009; 19: 201-206PubMed Google Scholar Sangermani et al.9Sangermani C. Mora P. Mancini C. Vecchi M. Gandolfi S.A. Ultrasound biomicroscopy in two cases of ocular siderosis with secondary glaucoma.Acta Ophthalmol. 2010; 88: e1-e2Crossref PubMed Scopus (11) Google Scholar presented 2 cases of siderosis glaucoma, both persistent after primary IOFB removal and requiring filtering surgery. Bai et al.10Bai H.Q. Yao L. Wang D.B. Jin R. Wang Y.X. Causes and treatments of traumatic secondary glaucoma.Eur J Ophthalmol. 2009; 19: 201-206PubMed Google Scholar published a case of siderotic glaucoma successfully treated with combination trabeculectomy, lensectomy, and vitrectomy. We report a unique case of siderosis glaucoma with late presentation more than 30 years after trauma that resolved after IOFB extraction without further glaucomatous intervention. Our case is a 43-year-old female who experienced a remote drill-bit accident in 1979 and retained metallic IOFB OS. At the time of the accident, traumatic cataract was removed with lens implant and pars plana vitrectomy was attempted for IOFB extraction. However, the IOFB was too deeply embedded in the posterior pole for complete removal; thus, barrier laser was applied around the remnant. The patient underwent strabismus surgery in 1983 and reported long-term poor vision OS. Her full medical records were unavailable; however, the patient stated she had no pain or major symptomatic changes for the next several decades. In 2013, she began experiencing discomfort OS and 3 months later presented to a local ophthalmologist with IOP measured at 40 mm Hg. Brimonidine 0.2%-timolol 0.5% bid, brinzolamide 1% tid, and bimatoprost 0.01% at bedtime were promptly initiated OS, and the patient was transferred to the Ross Eye Institute. On referral, VA was 20/20 OD and counting fingers OS. Applanation tonometry measured 12 mm Hg OD and 48 mm Hg OS. Patient had positive relative afferent pupillary defect OS and iris heterochromia (Fig. 1A). Left cornea was thickened and hazy with intrastromal rust-coloured deposits (Fig. 1B). Gonioscopy showed heavy rusty brown pigmentation throughout the entire angle, particularly in the trabecular meshwork (TM), but was otherwise open (Shaffer grade III) without synechiae or neovascularization. There was no anterior chamber (AC) or vitreous inflammation. Dilated examination revealed prominent arteriolar attenuation OS and marked cup/disc asymmetry of 0.45 OD and 0.85 OS. A large IOFB was lodged in the retina inferior to the optic nerve with surrounding elevated, pigmented fibrotic tissue and laser scars (Fig. 2A). The fellow eye was unremarkable beyond incipient cataract.Fig. 2A, Colour fundus photo OD with normal cup/disc ratio, healthy optic nerve and retina, and normal vasculature. B, Preoperative colour fundus photo OS with increased optic disc cupping, marked arteriolar attenuation, and a large, pigmented intraocular foreign body (IOFB) with surrounding fibrous scar and barrier laser. C, Heidelberg ocular coherence tomography image of OS through the IOFB and scar tissue inferior to optic nerve (yellow arrowhead) showed irregular elevation. D, Sample piece of the IOFB extracted with magnetic forceps during vitrectomy surgery. The largest piece measured 7 × 2 × 2 mm.View Large Image Figure ViewerDownload (PPT) Despite maximum topical regimen, IOP OS remained elevated above 40 mm Hg. Systemic carbonic anhydrase inhibitor was deferred because of the patient’s sulfa allergy. Decision was made for staged intervention with initial removal of IOFB and later glaucoma surgery if initial steps inadequately decreased IOP. One month after presentation to the Ross Eye Institute, 23-gauge vitrectomy was performed. Curved scissors, vitrector, and forceps were used to transect necrotic and fibrotic tissue partially encapsulating the IOFB. Forcible dislodging of the IOFB with 20-gauge forceps was required under wide-field BIOM viewing. The large, rectangular piece was then manoeuvred to the pars plana. On anterior visualization, handshake technique with serrated jaw and Maxgrip forceps was used to withdraw the IOFB through a 4-mm circumferential pars plana wound. Lewicky cannula maintained AC pressure while a 20-mL syringe was used to irrigate the AC and the angles 360 degrees with 100 mL balanced salt solution. Multiple air–fluid exchanges were performed to suction any residual particles. Additional barrier laser was completed around the trough left behind after IOFB removal. Postoperatively, the patient’s VA remained unchanged. This was attributed to extensive siderotic retinal and RPE damage, corroborated by nearly extinguished electroretinogram signals (Fig. 3A–D). Also, her prominent arteriolar attenuation corresponded with significant vascular occlusion and retinal ischemia that in previously reported siderotic degeneration was confirmed by fluorescein angiography.11Shaikh S. Blumenkranz M.S. Fluorescein angiographic findings in ocular siderosis.Am J Ophthalmol. 2001; 131: 136-138Abstract Full Text Full Text PDF PubMed Scopus (16) Google Scholar Most importantly, IOP OS after surgery decreased to 23 and 25 mm Hg at 1 day and 1 week, respectively. From postoperative weeks 2 to 11, the patient remained normotensive without medications at maximum IOP of 19 mm Hg. Her last known IOP was 17 mm Hg. The patient has been lost to follow-up. This case of extremely late-presentation glaucoma secondary to siderotic injury is distinct in several ways. First, a large, metallic, retained IOFB was tolerated for more than 30 years without symptomatic IOP issues. Fibrous encapsulation of the IOFB likely protected against or slowed siderotic damage.1Ballantyne J.F. Siderosis bulbi.Br J Ophthalmol. 1954; 38: 727-733Crossref PubMed Scopus (11) Google Scholar, 3Kuhn F, Mester V, Morris R. Intraocular foreign bodies. In: Kuhn F, Pieramici D, eds. Ocular Trauma: Principles and Practice. New York: Thieme Medical Publishers; 2002:237-263Google Scholar, 12McGimpsey S.J. Rankin S.J. Presentation of intraocular foreign body 25 years after the event.Clin Experiment Ophthalmol. 2005; 33: 665-666Crossref PubMed Scopus (6) Google Scholar, 13Lim L.T. Shankar V. Blum R.A. Hammer H.M. Long-standing iron-containing intraocular foreign body without siderosis.Clin Exp Optom. 2011; 94: 387-388Crossref PubMed Scopus (7) Google Scholar On our evaluation, the fibrotic layers appeared eroded. Prior lensectomy and vitrectomy facilitated anterior migration of microscopic iron released from the newly exposed IOFB. Subsequently, the patient experienced pain caused by IOP elevation rather acutely. Most notably, removal of residual IOFB normalized IOP without additional glaucoma medication or surgery. Theories on the pathogenesis of secondary glaucoma in ocular siderosis include physical obstruction of the TM with metallic particles, ciliary body changes, and trabecular fibrosclerosis.1Ballantyne J.F. Siderosis bulbi.Br J Ophthalmol. 1954; 38: 727-733Crossref PubMed Scopus (11) Google Scholar, 6Weiss M.J. Hofeldt A.J. Behrens M. Fisher K. Ocular siderosis. Diagnosis and management.Retina. 1997; 17: 105-108Crossref PubMed Scopus (47) Google Scholar, 9Sangermani C. Mora P. Mancini C. Vecchi M. Gandolfi S.A. Ultrasound biomicroscopy in two cases of ocular siderosis with secondary glaucoma.Acta Ophthalmol. 2010; 88: e1-e2Crossref PubMed Scopus (11) Google Scholar We believe that heavy TM clogging caused by new exposure of the embedded IOFB accounted for the acute IOP spike and pain in this case. Thus, removing the metallic source in conjunction with meticulous washout, giving particular attention to the angle, has produced the IOP normalization known to date. Despite this initial success of dramatic IOP decrease with vitrectomy surgery alone, there is likely pre-existing trabecular fibrosclerosis that may necessitate a glaucoma-filtering procedure in the future. Nevertheless, IOFB removal and IOP normalization have alleviated discomfort and the danger of blindness for now. Siderosis bulbi resulting from IOFB can manifest with widely varying timeline and clinical findings. Our report has described a unique case of secondary glaucoma presenting more than 30 years after original injury. Furthermore, IOFB extraction with thorough intraocular washout alone has adequately controlled IOP known to date without additional antihypertensive medication or surgery as previously reported. Thus, when heavy TM clogging is present in ocular siderosis, we offer this management method as an option to delay and/or preclude further glaucoma surgery.