Case Presentation: We present a case of a 63-year-old male with a past medical history of hypertension and alcohol use disorder (multiple beers per day) who presented with a two-week history of black stools. On arrival, he was hypothermic, tachycardic, and hypotensive, likely due to hemorrhagic shock. Physical examination revealed melena and anasarca. Labs were most notable for a hemoglobin of 7.1 (14.0-17.0 g/dL), creatinine of 2.6 (0.6-1.3 mg/dL), lactate of 2.8 (0.4-2.0 mmol/L), and albumin of 2 (3.4-5.0 g/dL). He was started on antibiotics and vasopressors. He underwent an endoscopy and colonoscopy, which revealed severe friability of the colon, suggestive of Scurvy. The vitamin C level was 0.1 (0.4-2.0 mg/dL), and he was subsequently started on Vitamin C. Push enteroscopy showed a Dieulafoy’s lesion, which was cauterized. The patient did not have further episodes of hypotension or bleeding. However, his lactate remained elevated. After causes of Type A lactic acidosis were ruled out, causes for Type B lactic acidosis were explored. On admission, AST was mildly elevated at 50 (15-37 U/L). ALT was normal, and imaging of the liver did not show cirrhosis. The patient had an extensive, unrevealing malignancy workup. He had no history of diabetes mellitus. He was not receiving medications known to cause lactic acidosis. The patient’s thiamine level was 64 (70-180 nmol/L). After administering intravenous thiamine 200mg every 8 hours, the patient’s lactate went from 2.4 to 1.6 overnight. He received thiamine 200mg IV every 8 hours for three days and was then transitioned to 100mg oral daily. The patient had no other signs of thiamine deficiency, including peripheral neuropathy, high-output heart failure, ataxia, nystagmus, or memory impairment.
Discussion: Lactic acidosis can be subdivided into Type A or Type B lactic acidosis. Type A lactic acidosis is secondary to hypoperfusion and hypoxia. It is commonly seen in states of shock, such as septic, cardiogenic, hypovolemic, and obstructive shock. It is also widely seen with seizures or ischemia, such as limb or mesenteric [1]. Type B lactic acidosis can be secondary to underlying liver dysfunction, malignancy, medications, congenital mitochondrial dysfunctions, excessive exercise, ethanol intoxication, and diabetic ketoacidosis. Less commonly remembered, lactic acidosis can be attributed to thiamine deficiency [2]. Thiamine, also known as Vitamin B1, is a vital cofactor for enzymes of glycolysis, the Krebs cycle, and the pentose phosphate pathway [3]. When thiamine is deficient, pyruvate cannot enter the Krebs cycle. It accumulates and is metabolized to lactate [2]. In the setting of poor oral intake, thiamine stores may be depleted in 18-20 days. Patients with alcohol use disorder are prone to poor eating habits. Furthermore, alcohol damages the lining of the intestine, resulting in poor thiamine absorption. Therefore, it is not uncommon to see thiamine deficiency in these patients [4].
Conclusions: This case highlights the importance of investigating uncommon causes of persistent lactic acidosis. Initially, we had an explanation for lactic acidosis in the setting of hypoperfusion. However, as the hypoperfusion resolved, the lactate remained elevated, prompting further investigation. Thiamine deficiency is an uncommon cause of lactic acidosis that should be evaluated. If left untreated, thiamine deficiency can cause severe complications.