Abstract Introduction Selenium is an essential trace element involved in myocardial oxidative stress regulation via selenoprotein activity. Deficiency can lead to rapidly progressive and potentially reversible dilated cardiomyopathy. However, diagnosis is frequently delayed in critically ill patients due to overlapping etiologies of shock and cardiac dysfunction. Case Presentation A 68-year-old woman with a history of bariatric surgery, chronic right groin wound infections, and multiple recent hospitalizations presented with hypotension, diarrhea, and lethargy from a skilled nursing facility. She was admitted to the medical ICU for septic shock, requiring norepinephrine and vasopressin. Echocardiography revealed an ejection fraction of 29% with severe global hypokinesis (previously 35-40% two months prior). She received broad-spectrum antibiotics and wound management; infectious disease and cardiology were involved. Given her history of malabsorption and persistent cardiac dysfunction, micronutrient studies were sent. Thiamine (B1) was normal at 249 nmol/L, zinc was 32 µg/dL, and copper was 68 µg/dL. The patient’s clinical course progressed to multi-organ dysfunction, and after discussion, she elected for comfort-focused care. After the patient passed away, Selenium returned at 39 µg/L (severe deficiency; reference range ∼70-150 µg/L). Discussion This case highlights that selenium deficiency remains an under-recognized contributor to cardiomyopathy in patients with prior gastrointestinal surgery, chronic inflammation, and prolonged critical illness. Importantly, selenium-associated cardiomyopathy is reversible, and delayed testing in critical care settings may miss an opportunity for recovery. Early evaluation for micronutrient deficiencies should be considered when cardiac dysfunction is disproportionate to septic physiology. This abstract is funded by: None
Ghishan et al. (Fri,) studied this question.