Presentations

Abstract

Introduction: Lactic acidosis is a potentially life-threatening type of anion gap metabolic acidosis caused by lactic acid build, either due to excessive production or decreased excretion. In this case report, we discuss a unique case of lactic acidosis and its management.

Case Information: The patient was a 61-year-old female with a medical history of hypertension, type II diabetes mellitus, and uterine carcinosarcoma with peritoneal carcinomatosis, and ascites who presented with abdominal pain and shortness of breath. Admission labs were significant for leukocytosis and an elevated lactic acid level of 2.6 nmol/L. A sepsis workup was initiated, and she was started on broad-spectrum antibiotics. Abdominal and Pelvic imaging did not reveal any definitive source of infection. Despite adequate fluid resuscitation and broad-spectrum antibiotics, her lactic acid levels remained elevated. Due to her hemodynamic stability and negative blood cultures, antibiotics were discontinued. Liver function tests were normal, suggesting that lactic acidosis was possibly secondary to malignancy and the Warburg effect. Her thiamine level was normal but her Riboflavin level was found to be <5 nmol/L (normal range: 6.2-39 nmol/L). She was diagnosed with Riboflavin deficiency due to poor oral intake and started on daily Riboflavin supplementation, which ultimately resolved her lactic acidosis.

Discussion/Clinical Findings: Lactic acidosis is broadly divided into 2 major types: type A caused by tissue ischemia leading to anaerobic metabolism and excessive lactic acid production, and type B caused by impaired cellular metabolism and lactic acid buildup without tissue hypoperfusion. There are also some less common types of Lactic Acidosis such as type D lactic Acidosis caused by intestinal overproduction. Type A lactic acidosis is the most common and dangerous type due to its association with hypoxemia and shock. Type B lactic acidosis is less common but can indicate serious underlying issues such as hematologic and solid organ malignancies with or without the Warburg effect, or liver failure. The Warburg effect is due to increased rates of lactate production by the neoplastic cells that shift to primarily anaerobic glycolysis. Other causes of type B lactic acidosis include thiamine or riboflavin deficiency, alcoholism, toxic alcohol ingestion/poisoning, and medication side effects from metformin, linezolid, propofol, or IV epinephrine. Riboflavin, a water-soluble vitamin, is essential for the coenzymes flavin mononucleotide and flavin adenine dinucleotide. The impaired function of those enzymes disrupts cellular metabolism and mitochondrial energy production, resulting in impaired pyruvate metabolism and lactic acid accumulation. Riboflavin deficiency is seen in patients with anorexia nervosa, malabsorptive syndromes, prolonged use of barbiturates, and HIV patients on HAART therapy. Overt Riboflavin deficiency is rare as it is found in many commonly consumed foods, including milk, meat, eggs, cereal, and green leafy vegetables. Treatment with oral or intramuscular supplementation typically resolves symptoms quickly. If deficient, then the recommended daily riboflavin replacement is 1.7 mg/day, found in most multivitamin preparations.

Conclusion: Riboflavin deficiency is an important cause of type B lactic acidosis to remember, as its diagnosis can avoid unnecessary testing and therapeutics.