Fatal Cobalt-Induced Cardiomyopathy After Revision of a Failed Total Hip Arthroplasty with Metallosis
Presenter
Priya Nair, MD, The University of Chicago Medical Center, Darien, IL
Priya Nair, MD1, Meghan Whitmarsh-Brown, MD1, Christopher Fernandez2, Tyler Gunn, MD3, Jonathan Lattell, MD, FSCAI4, Kunjan Udani, MD2, Atman P. Shah, M.D., FSCAI2 and Sandeep Nathan, M.D., FSCAI2, (1)The University of Chicago Medical Center, Darien, IL, (2)The University of Chicago, Chicago, IL, (3)University of Chicago, Chicago, IL, (4)The University of Chicago Medical Center, Chicago, IL
Title:
Fatal Cobalt-Induced Cardiomyopathy After Revision of a Failed Total Hip Arthroplasty with Metallosis Introduction:
Cobalt cardiomyopathy is a rare, rapidly progressive dilated cardiomyopathy caused by systemic heavy metal release from worn or corroded metal-on-metal hip prostheses. Cobalt ions impair myocardial function by disrupting calcium transport and mitochondrial oxidative phosphorylation. Although overt heart failure occurs in only about 1.2 per 100 person-years among implant recipients, subclinical myocardial dysfunction correlates with circulating cobalt concentrations. Clinically, cobalt cardiotoxicity often mimics acute coronary syndrome with chest pain, elevated cardiac biomarkers, and new wall motion abnormalities. While implant removal is the definitive treatment, patients with acute decompensated heart failure face a 9.3% 30-day postoperative mortality risk. When revision surgery precipitates hemodynamic collapse, temporary mechanical circulatory support may provide a bridge to myocardial recovery. Clinical Case:
An 87-year-old female with hyperlipidemia, minor arrhythmia, and multiple joint arthroplasties presented with acute left hip pain and inability to ambulate after a popping sensation. Radiographs demonstrated failure of her 15-year-old left total hip arthroplasty. Preoperative evaluation classified her as low cardiac risk (6.36 METs). During emergency revision arthroplasty, she developed profound hypotension and narrow pulse pressure despite minimal blood loss, requiring vasoactive support. Postoperatively in the surgical intensive care unit, she reported pressure-like chest pain. Bedside echocardiography demonstrated a plethoric inferior vena cava, severely reduced left ventricular ejection fraction (LVEF), and new regional wall motion abnormalities. Electrocardiography showed sinus bradycardia with new lateral T-wave inversions. High-sensitivity troponin exceeded 500 ng/L, and lactate was 3.1 mmol/L. Emergent coronary angiography demonstrated nonischemic cardiomyopathy without obstructive coronary artery disease. On postoperative day one, the patient experienced pulseless electrical activity arrest following aspiration. After transient return of spontaneous circulation, she deteriorated into unstable narrow-complex tachycardia and ventricular fibrillation. Following advanced cardiac life support and defibrillation, return of spontaneous circulation was achieved, but echocardiography demonstrated severe global biventricular dysfunction. She underwent emergent Impella CP placement and venoarterial extracorporeal membrane oxygenation (VA-ECMO) cannulation. Extensive metallosis observed during revision prompted heavy metal testing. Serum cobalt concentration was markedly elevated at 13.8 ng/mL. Following mechanical circulatory support, her hemodynamics improved, allowing decannulation from VA-ECMO and Impella on postoperative day six. Cobalt levels decreased to 12.0 ng/mL, and LVEF recovered to 55–60% by postoperative day seven. Her course was complicated by severe acute kidney injury. After multidisciplinary discussions, the family elected comfort-focused care, and she died on postoperative day fourteen. Discussion:
This case demonstrates fulminant cobalt cardiomyopathy precipitated by metallosis and unmasked by the physiologic stress of revision arthroplasty. Cobalt toxicity impairs mitochondrial respiration, producing rapidly progressive biventricular failure, lactic acidosis, and elevated cardiac biomarkers that closely resemble acute coronary syndrome. Although removal of the offending prosthesis is definitive therapy, patients presenting with cardiogenic shock have prohibitive operative risk. In this case, VA-ECMO and Impella successfully reversed refractory shock and allowed myocardial recovery despite the patient's eventual death from noncardiac multiorgan failure. Clinicians should maintain a high index of suspicion for cobalt toxicity in patients with failing cobalt-chromium hip prostheses who present with unexplained, rapidly progressive cardiomyopathy.