A Patient Who Suffers From Refractory Cardiogenic Shock Due to Cobalt Toxicity
A 63-year-old male was admitted with decompensated systolic heart failure four months after initial onset of symptoms. An echocardiogram showed normal wall thickness, left ventricular end diastolic diameter (LVEDd) 60 mm, left ventricular ejection fraction (LVEF) 10-15%, and a dilated RV with reduced systolic function. Right heart catheterization showed biventricular elevation of filling pressures and a cardiac index of 1.85 L/min/m2. Endomyocardial biopsy did not show an infiltrative process. Left heart catheterization showed normal coronary arteries.
The patient’s only significant past medical history was degenerative arthritis of the left hip, for which he had undergone total hip arthroplasty with a metal-on-metal prosthesis approximately three years earlier. Following surgery, while the patient regained typical levels of activity, he consistently experienced a clicking sensation in the left hip. Imaging of the left hip suggested premature wear of the prosthesis.
One year prior to presentation, testing by the patient’s primary care physician had revealed a serum cobalt level of 85 mcg/L (normal 0.1-0.4 mcg/L). The patient’s initial serum cobalt level during hospitalization was 202.4 mcg/L and chelation therapy with succimer 10 mg/kg every eight hours was started. Serum cobalt levels subsequently decreased to 11.9 mcg/L over a period of two weeks.
During the course of the hospitalization, his heart failure deteriorated rapidly into cardiogenic shock. He was started on and was refractory to IV milrinone. He developed line-associated methicillin-sensitive S. aureus (MSSA) bacteremia. His deterioration continued, requiring veno-arterial extracorporeal membrane oxygenation (ECMO). This was complicated by a distal left leg occlusion needing embolectomy and fasciotomy. On hospital day 19, the patient had left and right ventricular HeartWare HVADs implanted. Despite biventricular support, his shock state worsened. He subsequently developed alveolar hemorrhage with acute respiratory distress syndrome (ARDS) and was placed on veno-venous ECMO for oxygenation. By hospital day 34, his situation became futile and support was withdrawn. Transmission electron microscopy of the left ventricular apical core showed severe loss of myofibers associated with myofiber degeneration and fragmentation. There was significant mitochondrial degeneration with clumps of electron dense material within many of the mitochondria.
Which of the following factors most likely resulted in the patient’s refractory cardiogenic shock and poor outcome?