Cobalt Toxicity Presenting as Bilateral Optic Neuropathy

Cobalt, a ferromagnetic metal with a wide range of uses, has been known to cause systemic toxicity in humans that results in thyroid dysfunction, cardiomyopathy, hematologic abnormalities, and neuropathy. Arthroprosthetic cobaltism is a term used to describe systemic cobalt toxicity originating from cobalt-containing prosthetic joints. Ocular toxicity from elevated serum levels of cobalt is a rare phenomenon.

We describe a case of bilateral toxic optic neuropathy resulting from a damaged cobalt-containing shoulder prosthesis in a 76-year-old female. The patient exhibited classic clinical findings of toxic optic neuropathy, with painless insidious vision loss, dyschromatopsia, and bilateral central scotomas. Clinical testing showed a progressive reduction in the thickness of the peripapillary retinal nerve fiber layer and ganglion cell complex on optical coherence tomography. Magnetic resonance imaging of the brain and orbits without contrast were unrevealing. Extensive laboratory testing ruled out infectious, inflammatory, demyelinating, and nutritional causes of optic neuropathy. However, slightly elevated levels of serum cobalt were found. Considering the possibility of arthroprosthetic cobaltism, arthrocentesis from the patient's shoulder prosthesis was performed and revealed that the cobalt levels in her synovial fluid were 35 times higher than the normal limit. Replacement of the damaged prosthetic joint resulted in a decrease in the patient's serum cobalt levels and improvement of her vision.

While arthroprosthetic cobaltism from hip joints has been reported, to our knowledge, ours is the first case to prove a damaged shoulder prosthesis was the etiology. The patient's relatively low levels of serum cobalt and the lack of systemic features are also intriguing.