Date of Presentation
5-4-2023 12:00 AM
College
School of Osteopathic Medicine
Poster Abstract
Background: Severe anemia and thiamine deficiency can independently result in high output heart failure (HOHF) through different mechanisms. Data on the threshold and timeframe at which these etiologies may precipitate HOHF is unclear.
Case: A 63-year-old male with alcohol use disorder consuming 18 drinks/week presented with progressive shortness of breath and lower extremity edema for a few months. Physical exam revealed tachycardia, anasarca, jugular venous distension, Lancisi’s sign, and a midsystolic murmur. Echocardiogram demonstrated EF of 30-35%, dilated left ventricle, and cardiac index of 4.2L/min/m2.
Decision-Making: Heart failure can independently precipitate anemia while severe alcoholism can induce myelosuppression and promote risk for bleeding. Thus, iron studies and endoscopy are crucial to elucidating the underlying pathophysiology to further direct therapy. Labs demonstrated hemoglobin 3.0 g/dL (baseline 11 g/dL 7 months prior), ferritin 5 ng/mL, thiamine 26 nmol/L, and hemoccult positive stool while colonoscopy revealed bleeding diverticulosis and hemorrhoids, thereby confirming critical iron deficiency anemia from lower GI bleed and thiamine deficiency. Cardiac catheterization ruled out ischemic cause of his new onset cardiomyopathy, supporting the diagnosis of HOHF in the setting of severe anemia and concomitant cardiac Beri Beri. Our patient was treated with parental thiamine infusions, intravenous iron sucrose, blood transfusions, and gradually diuresed with bumetanide. Repeat evaluation of his left ventricular function 3 months later showed recovery of EF to 50-55%.
Conclusion: HOHF can generally be reversed with etiology-directed treatments. In chronic alcoholic patients, we advocate for routine testing of whole blood thiamine to assess for occult vitamin deficiency to determine whether supplementation may assist in therapy. The relative independent contributions or synergistic effects of iron deficiency and thiamine deficiency on HOHF remains unknown, but thorough investigations are essential to ensure recovery of cardiac function.
Keywords
Anemia, Thiamine Deficiency, Heart Failure, Beriberi, Case Reports
Disciplines
Cardiology | Cardiovascular Diseases | Diagnosis | Emergency Medicine | Internal Medicine | Medicine and Health Sciences | Nutritional and Metabolic Diseases | Pathological Conditions, Signs and Symptoms | Therapeutics
Document Type
Poster
Included in
Cardiology Commons, Cardiovascular Diseases Commons, Diagnosis Commons, Emergency Medicine Commons, Internal Medicine Commons, Nutritional and Metabolic Diseases Commons, Pathological Conditions, Signs and Symptoms Commons, Therapeutics Commons
Mixed Beri’s: High Output Heart Failure from Severe Anemia and Thiamine Deficiency
Background: Severe anemia and thiamine deficiency can independently result in high output heart failure (HOHF) through different mechanisms. Data on the threshold and timeframe at which these etiologies may precipitate HOHF is unclear.
Case: A 63-year-old male with alcohol use disorder consuming 18 drinks/week presented with progressive shortness of breath and lower extremity edema for a few months. Physical exam revealed tachycardia, anasarca, jugular venous distension, Lancisi’s sign, and a midsystolic murmur. Echocardiogram demonstrated EF of 30-35%, dilated left ventricle, and cardiac index of 4.2L/min/m2.
Decision-Making: Heart failure can independently precipitate anemia while severe alcoholism can induce myelosuppression and promote risk for bleeding. Thus, iron studies and endoscopy are crucial to elucidating the underlying pathophysiology to further direct therapy. Labs demonstrated hemoglobin 3.0 g/dL (baseline 11 g/dL 7 months prior), ferritin 5 ng/mL, thiamine 26 nmol/L, and hemoccult positive stool while colonoscopy revealed bleeding diverticulosis and hemorrhoids, thereby confirming critical iron deficiency anemia from lower GI bleed and thiamine deficiency. Cardiac catheterization ruled out ischemic cause of his new onset cardiomyopathy, supporting the diagnosis of HOHF in the setting of severe anemia and concomitant cardiac Beri Beri. Our patient was treated with parental thiamine infusions, intravenous iron sucrose, blood transfusions, and gradually diuresed with bumetanide. Repeat evaluation of his left ventricular function 3 months later showed recovery of EF to 50-55%.
Conclusion: HOHF can generally be reversed with etiology-directed treatments. In chronic alcoholic patients, we advocate for routine testing of whole blood thiamine to assess for occult vitamin deficiency to determine whether supplementation may assist in therapy. The relative independent contributions or synergistic effects of iron deficiency and thiamine deficiency on HOHF remains unknown, but thorough investigations are essential to ensure recovery of cardiac function.