![]() The subset of alcoholics most susceptible to development of the cardiomyopathy was those with liver disease, protein malnutrition, and hypoalbuminemia. In the 1960s, a cobalt-induced cardiomyopathy was described in alcoholics who consumed large quantities of beer (15-30 per day) containing a cobalt-derived foam stabilizer. In human cobalt-exposed cohorts, the dose-response relationship varies as well, indicating the importance of biological factors beyond the serum cobalt level. While several regulatory agencies have threshold serum cobalt concentrations, animal studies differ in the serum concentrations necessary for developing clinical signs and symptoms of toxicity, in part due to the route and duration of exposure. Elevated serum cobalt levels have been associated with polycythemia, impaired thyroid function, visual and hearing deficits, a variety of dermatologic conditions, and rarely, cardiomyopathy. Cobalt is principally excreted in the urine. 1 In healthy individuals, 90-95% of blood cobalt is bound to serum albumin, rendering it biologically inactive. Serum cobalt levels in the general population are estimated to be in the range of 0.1-0.4 mcg/L. Impaired protein binding of cobalt II ion in the setting of severe systemic illness.Ĭobalt is a component of cyanocobalamin (B12) only trace amounts are needed in the diet. Delayed initiation of chelation therapy once LV systolic dysfunction was present. Use of a metal-on-metal (MoM) hip prosthesis rather than a metal-on-ceramic (MoC) prosthesis. Impaired protein binding of cobalt II ion in the setting of severe systemic illness. Serum cobalt level >0.6 mcg/L as defined by the UK Supra-Reginal Assay Service (SAS). Which of the following factors most likely resulted in the patient’s refractory cardiogenic shock and poor outcome? There was significant mitochondrial degeneration with clumps of electron dense material within many of the mitochondria. Transmission electron microscopy of the left ventricular apical core showed severe loss of myofibers associated with myofiber degeneration and fragmentation. ![]() By hospital day 34, his situation became futile and support was withdrawn. He subsequently developed alveolar hemorrhage with acute respiratory distress syndrome (ARDS) and was placed on veno-venous ECMO for oxygenation. Despite biventricular support, his shock state worsened. On hospital day 19, the patient had left and right ventricular HeartWare HVADs implanted. This was complicated by a distal left leg occlusion needing embolectomy and fasciotomy. His deterioration continued, requiring veno-arterial extracorporeal membrane oxygenation (ECMO). He developed line-associated methicillin-sensitive S. ![]() He was started on and was refractory to IV milrinone. ![]() Serum cobalt levels subsequently decreased to 11.9 mcg/L over a period of two weeks.ĭuring the course of the hospitalization, his heart failure deteriorated rapidly into cardiogenic shock. 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. 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). Imaging of the left hip suggested premature wear of the prosthesis. Following surgery, while the patient regained typical levels of activity, he consistently experienced a clicking sensation in the left hip. 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. Endomyocardial biopsy did not show an infiltrative process. Left heart catheterization showed normal coronary arteries. Right heart catheterization showed biventricular elevation of filling pressures and a cardiac index of 1.85 L/min/m 2. 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. A 63-year-old male was admitted with decompensated systolic heart failure four months after initial onset of symptoms.
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |