Sunday, July 13, 2014

Arthroprosthetic Cobaltism

Orthopedic Principles

 

Discussion

 

Cobalt poisoning by hip replacement: Arthroprosthetic-Cobaltism

Stephen Tower, MD, University of Alaska, Alaska, USA

  • Cobalt, in excess, has the potential to block oxidative metabolism at the mitochondrial level.
  • The peripheral and central nervous systems, the heart, and the thyroid gland are variably compromised whether the means of cobalt exposure is iatrogenic (use of cobalt chloride as a hematemic), industrial (exhalation or ingestion of cobalt powders or ores), from the ingestion of cobalt laced beer (beer drinkers cardiomyopathy), or arthroprosthetic (wear of chrome-cobalt articular surfaces or corrosion and fretting of modular chrome-cobalt femoral necks and heads).
  • The toxicity of cobalt has been known since 1948.(1 2)
  • The first case report of arthroprosthetic-cobaltism was in Italian in 2001. The mechanism was wear or a revision chrome-cobalt femoral head by ceramic bits from the primary fractured ceramic component embedded in the revision plastic socket liner.
  • The degree of hypercobaltemia was unreported; symptoms of peripheral neuropathy were first noted 9 months after the first revision operation. Diagnosis was serendipitous.
  • A metal laden pericardial effusion was found on CT scan, prompting a radiograph of the asymptomatic hip revealing an aspherical femoral head. Resection arthroplasty was not performed until 16 months after the first revision operation, by then the patient’s pathology had progressed to severe motor and sensory neuropathy, pericardial tamponade, and hypothyroidism(.3)
  • Reports of 8 additional extreme cases of cobaltism from the ceramic-on-metal wear have followed. Blood cobalt levels in mcg/L ([BCo]) have ranged from 400 to 1000, latency to symptoms ranged from 3-48 months, and latency to diagnosis or revision surgery from 9 to 72 months.
  • All patients had neurologic pathology, most were hypothyroid, and all but three were noted to have cardiomyopathies. One patient died of heart failure, those patients followed > 6 months post second revision improved as their [BCo] declined.
  • The typical presentation of cobaltism was fatigue and anorexia, followed by numbness and weakness, hypothyroidism, deafness and blindness, and finally and sometimes fatally, heart failure or arrhythmias. Hypothyroidism was diagnosed in most cases before the diagnosis of cobaltism was made and some clinical improvement noted with onset of thyroid replacement therapy. None of the patients had notable sentinel hip symptoms before onset of overt systemic pathology.(4-11)
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