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 Table of Contents  
CASE REPORT
Year : 2022  |  Volume : 2  |  Issue : 3  |  Page : 739-743

Optic neuropathy and retinopathy due to advanced cobalt toxicity


1 Division of Ophthalmology, Department of Surgery, Lahey Hospital and Medical Center, Beth Israel Lahey Health, Burlington; Department of Ophthalmology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States
2 Department of Ophthalmology, Tufts University School of Medicine, Boston, MA, United States
3 Division of Ophthalmology, Department of Surgery, Lahey Hospital and Medical Center, Beth Israel Lahey Health, Burlington; Department of Ophthalmology, Tufts University School of Medicine, Boston, MA, United States

Date of Submission06-Dec-2021
Date of Acceptance18-Apr-2022
Date of Web Publication16-Jul-2022

Correspondence Address:
Dr. Geetha K Athappilly
Lahey Medical Center, 1 Essex Center Drive, Peabody, MA - 01960
United States
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijo.IJO_3047_21

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  Abstract 


We report a rare case of cobalt toxicity resulting in a combined optic neuropathy and retinopathy. A 58-year-old woman with a recent revision of a hip implant presented with profound loss of vision. Although her initial exam was structurally unremarkable, she developed progressive outer retinal atrophy and optic nerve pallor. Abnormalities were also demonstrated in the full-field electroretinogram and optic nerve sheath on magnetic resonance imaging (MRI). Cobalt levels in the serum were severely elevated (734 μg/L) from the dysfunctional metal-on-metal (MoM) hip implant. Removal of the implant led to a rapid reduction in cobalt levels and stabilization of her declining vision.

Keywords: Cobalt toxicity, electroretinography, toxic optic neuropathy, toxic retinopathy


How to cite this article:
Shaikh N, Mills HM, Konstantinou EK, Ramsey DJ, Athappilly GK. Optic neuropathy and retinopathy due to advanced cobalt toxicity. Indian J Ophthalmol Case Rep 2022;2:739-43

How to cite this URL:
Shaikh N, Mills HM, Konstantinou EK, Ramsey DJ, Athappilly GK. Optic neuropathy and retinopathy due to advanced cobalt toxicity. Indian J Ophthalmol Case Rep [serial online] 2022 [cited 2022 Dec 3];2:739-43. Available from: https://www.ijoreports.in/text.asp?2022/2/3/739/351167



Cobalt functions as an important cofactor for many enzymes and regulates the production and function of red blood cells and platelets.[1] Normal plasma concentrations are less than 0.2 μg/L.[1] Systemic toxicity occurs when cobalt accumulates above 7 μg/L.[1] Cobalt exposures have resulted from the release of metal from implants in dentistry[2] and metal-on-metal (MoM) protheses in orthopedics.[2],[3],[4],[5],[6],[7] Ophthalmic complications include toxic optic neuropathy and retinopathy.[1],[8],[9] This case tracks the course of a patient with advanced cobalt toxicity.


  Case Report Top


A 58-year-old woman with a history of amblyopia in her right eye was referred for evaluation of 6 months of progressive, painless vision loss. Baseline vision in the right eye was count fingers (CF) and 20/30 in the left eye. Her past medical history was significant for 2 months of bilateral hearing loss with tinnitus, a 30-pound unintentional weight loss, and thyroid dysfunction. The patient also had a history of a hip fracture repaired 13 years ago with a revision 18 months before her presentation.

Examination revealed an anxious, cachectic woman with CF vision in both eyes. She was unable to identify any color plates. Pupils remained reactive without an afferent pupillary defect. Dilated examination revealed myopic degeneration and posterior staphyloma in the right eye and a normal fundus in the left eye. Anterior segment exam and efferent pathways were normal.

Optical coherence tomography (OCT) of the retinal nerve fiber layer (RNFL), and ganglion cell layer/inner plexiform layer (GCL/IPL) were obtained in both eyes [Figure 1]a and [Figure 1]b. The left eye showed mild segmental loss of the GCL/IPL with full RNFL. Humphrey visual field (HVF) testing revealed a central scotoma in both eyes in addition to generalized depression in the left eye [Figure 1]c. An MRI of the brain and orbits was ordered along with blood tests of thiamine, vitamin B12, and folate levels to evaluate for a toxic/nutritional optic neuropathy.
Figure 1: Imaging studies at presentation. (a) RNFL OCT of both eyes. Anomalous, tilted disc on the right, consistent with myopic degeneration with posterior staphyloma; the nerve fiber layer in the left eye has normal thickness. (b) OCT segmenting the GCL/IPL of both eyes is uninterpretable in the right eye, whereas the left eye shows mild-to-moderate segmental thinning. (c) HVF 30-2 of the right eye shows generalized depression consistent with dense amblyopia with a central scotoma (mean deviation [MD]: −22.06 dB), whereas the left eye demonstrates a paracentral scotoma (MD: −7.41 dB)

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Unfortunately, the patient was lost to follow-up for 8 months due to worsening of her neurocognitive status and physical state. Upon return evaluation, she reported declining vision and increasing difficulty with ambulation because of right hip pain and lower extremity tremor. Vision remained CF in both eyes. Her fundus examination now revealed pallor of both optic nerves with patchy areas of retinal depigmentation [Figure 2]a. OCT revealed new areas of outer retinal atrophy with retinal pigment epithelium (RPE) loss [Figure 2]b and thinning of the RNFL [Figure 2]c and GCL/IPL [Figure 2]d, consistent with progressive optic nerve injury. HVF of the left eye showed expansion of her central scotoma [Figure 2]e.
Figure 2: Imaging studies at follow-up. (a) Color fundus images show a posterior staphyloma in the right eye and patchy depigmentation and optic nerve pallor in the left eye. (b) Macular OCT scans of both eyes show areas of outer retinal atrophy. (c) RNFL OCT scans show extensive thinning on the left (right is unchanged). (d) OCT segmentation of the GCL/IPL shows diffuse loss on the left (right is unchanged). (e) HVF 30-2 of the right eye remains unchanged (MD: −23.60 dB), whereas the left eye shows an expanding central scotoma with inferior and superonasal defects (MD: −15.78 dB)

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MRI of the brain and orbits revealed perineural abnormalities of both optic nerves [Figure 3]a and enhancement of the right cochlea. She underwent auditory testing that confirmed bilateral sensorineural hearing loss. The history of two earlier hip replacements and constellation of systemic symptoms raised a suspicion for cobalt-associated toxicity. A serum cobalt level was drawn and found to be elevated at 734 ug/L (normal <1 μg/L). Blood work for demyelinating, infectious, inflammatory causes, and vitamin deficiencies was not remarkable.
Figure 3: Radiology studies. (a) Coronal T1 fat-saturated MRI orbits with gadolinium demonstrating perineural enhancement of the optic nerve sheaths, especially of the left optic nerve (arrows). (b) Pelvic computed tomography scan demonstrating radio-opaque debris surrounding the right metallic hip implant

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The patient was urgently admitted for orthopedic evaluation to remove the failed hip implant. A computerized tomography (CT) scan of her right hip revealed radio-opaque material surrounding the implant [Figure 3]b; aspiration of the hip joint by orthopedics revealed a dark gray–black sludge. Low voltage was noted in precordial leads of her electrocardiogram, and cardiac echocardiogram revealed a small pericardial effusion with preserved ejection fraction. The patient was taken to the operating room for an urgent washout and repeat total right hip arthroplasty. The patient's cobalt levels dramatically declined following the removal of the MoM prosthesis to 99 μg/L by 6 weeks. Full-field electroretinogram obtained 4 weeks after surgery confirmed cobalt-associated retinopathy [Figure 4].
Figure 4: Full-field ERG of the left eye showed a normal rod b-wave and mixed a-wave and b-wave amplitudes. The photopic b-wave was depressed with a tendency toward a smaller photopic a-wave. The flicker ERG was also depressed but without significant delay. The dark-adapted 0.01 ERG (rod response) b-wave amplitude, 219.7 μV; dark-adapted 3.0 (rod–cone response) a-wave amplitude, -143.4 μV, and b-wave amplitude, 275.6 μV; light-adapted 3.0 ERG (cone response) a-wave amplitude, -26.9 μV, and b-wave amplitude, 56.1 μV; light-adapted 3.0 flicker (30 Hz flicker) amplitude, 46.9 μV (appearing at approximately 29 ms)

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Postoperatively, the patient reported a significant improvement in her general health with resolution of her hip pain, reversal of her hearing and hair loss, weight gain, and improved cognition. Her central vision remained CF, but her visual fields and color vision both improved.


  Discussion Top


Total hip arthroplasty is one of the most common orthopedic procedures worldwide.[5] Over a million MoM implants have been implanted since the 1960s.[10] Despite the sharp decline in MoM implants because of recognized toxicityfrom cobalt particles liberated as protheses fail, a large number of patientshave aging joint replacement hardware; early recognition and removal offailed hardware is key to stopping progressive and irreversible toxicity.[6],[7]

Cobalt toxicity can present with local and/or systemic toxicity, including cardiac, renal, and endocrine abnormalities, as well as neurologic deficits such as hearing loss, visual disturbances, and cognitive decline.[5],[6],[7] The incidence of ocular complications from cobalt are rare, comprising only 12 documented cases in the literature.[1] In addition to advanced cobalt-associated optic nerve and retinal degeneration, our patient also had signs of multisystem cobalt toxicity, including hearing loss, thyroid and cardiac dysfunction, which can lead to potentially fatal arrhythmias or heart failure if left untreated.[3]


  Conclusion Top


Critical to halting disease progression is the early recognition of heavy metal poisoning by checking serum cobalt levels, followed by prompt removal the offending hardware. Ophthalmologists can play a valuable role in preventing potentially fatal systemic complications by detecting ocular signs of cobalt toxicity, which themselves can lead to irreversible vision loss or blindness.

Ethics approval and consent to participate

The research followed the tenets of the Declaration of Helsinki and did not require institutional review board approval by virtue of being a single reported case. Information was gathered and secured in compliance with the Health Insurance Portability and Accountability Act.

Consent for publication

Informed consent for publication of clinical details and images was obtained from the patient.

Authors' statement

All authors have read and approved the manuscript.

Acknowledgments

The authors thank the patient for her cooperation and acknowledge the help of many physicians involved in caring for the patient. The authors thank Dr. Jeffrey L. Marx, Dr. Shiyoung Roh, Timothy Tivnan, Amy Swan, Miranda Prosniewski, David H. Pfennighaus, and Carol Spencer, Lahey Hospital Librarian, for research support. D.J. Ramsey is the Harry N. Lee Family Chair in Innovation at the Lahey Hospital & Medical Center, Beth Israel Lahey Health.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

D.J.R.: Supported by the Harry N. Lee Family Chair in Innovation, Lahey Hospital & Medical Center, Beth Israel Lahey Health, Peabody, Massachusetts.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Garcia MD, Hur M, Chen JJ, Bhatti MT. Cobalt toxic optic neuropathy and retinopathy: Case report and review of the literature. Am J Ophthalmol Case Rep 2020;17:100606. doi: 10.1016/j.ajoc.2020.100606.  Back to cited text no. 1
    
2.
Wataha JC. Biocompatibility of dental casting alloys: A review. J Prosthet Dent 2000;83:223-34.  Back to cited text no. 2
    
3.
Packer M. Cobalt cardiomyopathy: A critical reappraisal in light of a recent resurgence. Circ Heart Fail 2016;9:e003604. doi: 10.1161/CIRCHEARTFAILURE.116.003604.  Back to cited text no. 3
    
4.
Hu CY, Yoon TR. Recent updates for biomaterials used in total hip arthroplasty. Biomater Res 2018;22:33.  Back to cited text no. 4
    
5.
Bijukumar DR, Segu A, Souza JCM, Li X, Barba M, Mercuri LG, et al. Systemic and local toxicity of metal debris released from hip prostheses: A review of experimental approaches. Nanomedicine 2018;14:951-63.  Back to cited text no. 5
    
6.
Liao Y, Hoffman E, Wimmer M, Fischer A, Jacobs J, Marks L. CoCrMo metal-on-metal hip replacements. Phys Chem Phys 2013;15:746-56.  Back to cited text no. 6
    
7.
Bradberry SM, Wilkinson JM, Ferner RE. Systemic toxicity related to metal hip prostheses. Clin Toxicol 2014;52:837-47.  Back to cited text no. 7
    
8.
Ng SK, Ebneter A, Gilhotra JS. Hip-implant related chorio-retinal cobalt toxicity. Indian J Ophthalmol 2013;61:35-7.  Back to cited text no. 8
[PUBMED]  [Full text]  
9.
Grillo LM, Nguyen HV, Tsang SH, Hood DC, Odel JG. Cobalt-chromium metallosis with normal electroretinogram. J Neuroophthalmol 2016;36:383-8.  Back to cited text no. 9
    
10.
Pilania K, Jankharia B. Longitudinal followup of incidentally detected pseudotumors in patients with metal on metal implants: A retrospective study. Indian J Orthop 2017;51:440-6.  Back to cited text no. 10
[PUBMED]  [Full text]  


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