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Abstract: PO1489

Persistent Lactic Acidosis due to Thiamine Deficiency

Session Information

Category: Trainee Case Report

  • 902 Fluid, Electrolyte, and Acid-Base Disorders: Clinical


  • Co, Mita Zahra Estrada, Loma Linda University Medical Center, Loma Linda, California, United States
  • Zhang, Zhiwei, VA Loma Linda Healthcare System, Loma Linda, California, United States

Lactic acidosis is one of the most common causes of metabolic acidosis in hospitalized patients. Clinically it is usually associated with obviously impaired tissue oxygenation, but also occurs in situation where systemic impairment in oxygenation does not exist or is not readily apparent. Here we present a case of persistent lactic acidosis found to be due to thiamine deficiency and resolved rapidly after thiamine supplementation.

Case Description

A 38-year old woman presented with 4-day history of abdominal pain, vomiting, diarrhea, and not able to eat. She has a history of alcoholism in remission, vitamin B12 deficiency, PTSD and bipolar disorder. Her medications included cyanocobalamin, disulfiram, lithium, trazodone, and ziprasidone. Vital signs were normal except for mild sinus tachycardia, and the rest of her examination was unremarkable. Laboratory results indicated normal CBC, glucose, BUN, Cr, LFT, and urine analysis. Serum Na, K, Mg, Ca, and PO4 were all low. Serum ethanol and salicylate were not detected, and urine drug screen was negative. Serum HCO3 was low at 14 mmol/L with anion gap of 26. Serum ketone was negative, but serum lactic acid was severely elevated at 9 mmol/L. ABG was consistent with compensated metabolic acidosis.

Cardiac echo and other imaging studies did not reveal significant abnormalities. The patient received intravenous fluid replacement and supplementation for various electrolyte abnormalities. While her symptoms of gastroenteritis had improved, the serum lactic acid continued to remain high (7-9s).

Since most of the apparent causes of lactic acidosis were excluded in this patient, thiamine deficiency was suspected and thiamine level was confirmed to be low at 59 nmol/L (normal 78-185). Supplementation was initiated with rapid normalization of lactic acidosis.


Thiamine is essential for normal aerobic metabolism, and its deficiency may lead to accumulation of pyruvate and conversion to lactic acid. Because thiamine is water soluble, its stores are limited. Thiamine deficiency can occur readily if intake is suboptimal in people who have risk factors, such as long-term heavy alcohol ingestion in this patient.

Teaching points
Thiamine deficiency is a potential cause of lactic acidosis that is reversible with supplementation. A high index of suspicion is necessary for diagnosis in patients with risk factors but no other apparent cause of lactic acidosis.