TTE demonstrated dilated cardiomyopathy with severe biventricular impairment (Figures 5 and 6). Mr BH presented back to hospital in November 2019 with an acute decompensation of his cardiomyopathy with paroxysmal atrial tachycardia. He was subsequently referred for an implantable cardiac defibrillator in May 2019 due to his risk of malignant ventricular arrhythmias. Myocarditis or sarcoidosis was felt to have been less likely.Īs amyloidosis was felt to have been clinically unlikely, Mr BH continued with optimal medical therapy for his heart failure. The possibility of amyloidosis was raised due to the persistent nature of the findings. This revealed progressive deterioration of his left ventricular function with ongoing features suggestive of an infiltrate condition.
#Cobalt toxicity symptoms serial
A chest x-ray revealed cardiomegaly (Figure 1).įigure 1: Chest x-ray showing mild cardiomegaly.ĭue to his persistently elevated serial TnT levels, a repeat cMRI was performed in 2019. His brain natriuretic peptide was 512ng/L (normal<40ng/L), with elevated serial troponin T (TnT) levels. His history included bilateral BHR (right side 2006, left side 2012). Mr BH initially presented to Timaru Hospital in 2015 with progressively worsening dyspnoea and associated bilateral peripheral oedema, with preceding flu like symptoms. It also requires normalisation of both structure and function of cardiac tissue once the insult has been removed (explantation of prosthesis or reduction of sCo levels).4 Case report Cobalt-toxicity induced cardiomyopathy is defined as both biventricular dilatation with systolic dysfunction in the presence of raised sCo levels. One in every three diagnosed cases of cardiomyopathy in general have been found to be non-ischaemic in origin.4 Given the established cardio-toxic effects of cobalt and its prevalent use in joint replacements, more robust systems of monitoring should be considered, especially for those at risk. This makes fulfilling the Bradford Hill criteria difficult, thereby delaying the diagnosis of this potentially life threatening, yet easily preventable situation. Revision rates of BHR occurred in 8% of cases,1 and the commonest cause of failure is adverse reaction to metal debris (ARMD).1 Despite several cases confirming cobalt-toxicity induced cardiomyopathy, there remains a paucity of high-quality research linking the cause with the effect. In MoM constructs, cobalt and chromium form the basis of the bearing surface, as opposed to a traditional arthroplasty construct where both femoral and/or acetabular components involve ceramic or polyethylene as part of their bearing surfaces. Last year in New Zealand, over 9,000 hip arthroplasties were performed.2 The Birmingham Hip Resurfacing (BHR) (Smith and Nephew, Memphis, TN) is manufactured using as-cast cobalt chrome and is classified as the world’s most successful metal-on-metal (MoM) hip resurfacing system, with over 140,000 people globally having received this implant.3 Prevalent use of these elements in MoM hip arthroplasty accounted for <1% of cases in 2018.
Total joint arthroplasty is a commonly performed orthopaedic procedure with the aims of relieving pain, restoring joint function and improving quality of life for patients. Despite successful chelating therapy and heart failure treatment, he passed away secondary to cobalt-toxicity induced cardiomyopathy (CTCM). In 2015, Mr BH was diagnosed with dilated cardiomyopathy, presumed secondary to viral myocarditis. Unfortunately, Mr BH moved to a different health district and was subsequently lost to follow-up. Although there has been no direct correlation between sCo levels and toxicity, levels above 119nmol/L are concerning. In 2013, these levels rose to 1981nmol/L. As part of routine metal-on-metal arthroplasty follow-up, Mr BH had sCo level checks. He had previous bilateral total hip arthroplasties using the Birmingham Hip Resurfacing (right side 2006, left side 2012). His serum cobalt (sCo) levels were 5244nmol/L (normal<12nmol/L). Clinically, he had concurrent decompensated cardiomyopathy requiring dopamine and furosemide infusions. Imaging of his hip demonstrated radiographic evidence of bony changes, suggestive of an adverse reaction to metal debris (ARMD), along with a non-traumatic left peri-prosthetic neck-of-femur fracture.
Mr BH was a 53-year-old gentleman who presented to hospital in November 2019 with decompensated heart failure, new-onset paroxysmal atrial tachycardia and increasing left hip pain.
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