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Abstract: PO1177

Mysterious Case of Recurrent Life-Threatening Lactic Acidosis

Session Information

Category: Fluid, Electrolyte, and Acid-Base Disorders

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


  • Shaik, Zakir, Temple University Health System Inc, Philadelphia, Pennsylvania, United States
  • Khan, Waqas Ahmad, Temple University Health System Inc, Philadelphia, Pennsylvania, United States
  • Rao, Ajay D., Temple University Health System Inc, Philadelphia, Pennsylvania, United States
  • Lee, Jean, Temple University Health System Inc, Philadelphia, Pennsylvania, United States

Group or Team Name

  • Temple University Hospital

Patients living with diabetes are prone to type-B lactic acidosis, often presenting with profound acid-base derangements. The reason for lactate production is not obvious hence management can be challenging. We present a case of life-threatening recurrent lactic acidosis in a diabetic patient.

Case Description

A 67-year-old man with type 2 diabetes, hypertension, presented to the hospital with malaise for 2 days. He had been on metformin in the past but had recently switched to insulin. There was no history of alcohol ingestion nor use of herbal supplements. The lactic acid level was 24.2 mmol/L with Ph of 6.82, PCO2 of 27 mmHg, serum bicarb of 7 mEq/L, anion gap of 28, and serum Cr of 1.4 mg/dL with baseline of 1 mg/dL. No evidence of infection or ischemia found. Toxicology screen was negative and serum metformin level was undetectable. Lactic acidosis resolved with continuous renal replacement (CRRT) for 24 hours. A month later he returned with similar complaints and his lactate level was 14.8 mmol/L. This was treated with supportive care alone. Six months later he returned again with lactate of 13.5 mmol/L, worsening to 18.6 mmol/L. He improved after treatment with CRRT and supportive care. Alcohol levels, liver function tests, pyruvate, glutamate, metformin levels were all negative or normal. The thiamine level was not checked during his first admission. During the second visit, the value was normal but this was drawn after thiamine had been given. During the third visit, the thiamine level was noted to be less than 6 nmol/L. The patient was started on thiamine and has not had further episodes of lactic acidosis.


Patients with diabetes are prone to excess lactic acid generation due to the derangement in mitochondrial oxidative phosphorylation with relative hypoxia at the microvascular level. In addition, it has been noted that many diabetics are thiamine deficient. In the absence of thiamine, pyruvate cannot enter the Krebs cycle and is converted to lactic acid predisposing diabetics to type-B lactic acidosis. Thiamine is filtered in the glomerulus and is reabsorbed in the proximal tubule through the thiamine/H+ antiporter. Long term use of diuretics has been associated with thiamine deficiency. However our patient was not taking any nor did he have chronic kidney disease or any evidence of malnutrition.