INTRODUCTION: Selenium deficiency is known to cause cardiomyopathy. There have been several cases of selenium deficiency reported in total parenteral nutrition (TPN) users. The following case presents a young female with selenium deficiency and cardiomyopathy that corrected after selenium supplementation.
CASE PRESENTATION: The patient is a 34 year old African American female with past medical history of gastric bypass for weight loss 9 years ago, deep vein thrombosis and pulmonary embolism 2 years ago. Her clinical course was complicated by small bowel obstruction which required exploratory laporatomy, small bowel resection and ligation of intraabdominal adhesion. A percutaneous gastrostomy tube was placed for malnutrition secondary to major depression and anorexia. She was bed bound for several months prior to this admission and developed a sacral decubitus ulcer. She presented with back pain and hypotension secondary to an infected stage IV decubitus ulcer. The patient was admitted to ICU for treatment of septic shock with antibiotics and pressors, then subsequently developed respiratory failure and required mechanical ventilation. Chest radiograph revealed bilateral opacities with small bilateral pleural effusions. A transthoracic echocardiogram showed normal left ventricular size with reduced ejection fraction (EF) of 15%, which decreased from 25% on the previous echocardiogram 2 months ago. The differential diagnosis of her cardiomyopathy included nutritional cardiomyopathy. Laboratory data revealed a selenium level 54 mcg/L (Normal range: 110–160 mcg/L), total carnitine level 47 αmol/L (Normal range: 25–55 μmol/L), and vitamin B1 97 nmol/L (Normal range: 87–280 nmol/L). Selenium 200 αcg per day was started intravenously. The patient was successfully extubated. Remeron was started for her depression. After 20 days of selenium supplementation her selenium level improved to 90 mcg/L. Repeat echocardiogram showed normal left ventricular size and function. The patient improved and no longer required blood pressure support medications, and eventually she was discharged to a rehabilitation facility.
DISCUSSIONS: Selenium deficiency induced cardiomyopathy is well known as Keshan disease in areas of low selenium intakes, such as China. Cardiomyopathy due to acquired selenium deficiency in nonendemic area has been reported among patients on TPN. Although our patient has never been on TPN, nutritional cardiomyopathy was considered as a possible diagnosis because of her poor nutritional status. The diagnosis of selenium deficiency was made based on low selenium level. Her echocardiogram showed severely reduced LV function but no dilation, which is usually seen in selenium deficiency induced cardiomyopathy. Since LV function recovered to normal after selenium supplementation, selenium deficiency was the likely cause of her cardiomyopathy.
CONCLUSION: Even without a history of TPN use selenium deficiency should be considered in the differential diagnosis when patients with malnutrition have cardiomyopathy. Patients status post rouex-en Y gastric bypass who exhibit depression, anorexia, and otherwise unexplained cardiomyopathy should be evaluated for selenium deficiency.
DISCLOSURE: Mayuko Fukunaga, None.