Abstract Introduction Diabetic ketoacidosis (DKA) typically resolves with insulin therapy and fluid resuscitation, leading to normalization of metabolic parameters and closure of the anion gap. Persistent lactic acidosis beyond DKA resolution is uncommon and often triggers extensive evaluation for sepsis, hypoperfusion, or tissue ischemia. Thiamine (vitamin B1) deficiency, a reversible cause of Type B lactic acidosis, may complicate DKA through osmotic diuresis, impaired renal reabsorption, and increased metabolic demand. Recognition of this mechanism is crucial, as timely supplementation can rapidly correct metabolic derangements. Case Presentation A patient with poorly controlled type 2 diabetes mellitus presented with DKA requiring hospitalization. Initial laboratory values demonstrated an anion gap of 26, β-hydroxybutyrate 8.14 mmol/L, glucose 538 mg/dL, and lactate 9.9 mmol/L. Standard management with intravenous insulin and isotonic fluids led to resolution of hyperglycemia and closure of the anion gap, yet serum lactate levels remained persistently elevated ( 6 mmol/L). The patient remained hemodynamically stable with no evidence of sepsis, hypoxia, hepatic dysfunction, or toxin exposure. Nutritional history revealed inconsistent dietary intake and recent weight loss. Given the absence of Type A causes of lactic acidosis, empiric intravenous thiamine (200-500 mg daily) was initiated. Over the subsequent 48 hours, lactate concentrations declined to 2 mmol/L, accompanied by improved acid-base status and resolution of metabolic acidosis. The patient was transitioned to oral thiamine and discharged in stable condition. Discussion This case highlights the diagnostic challenge of persistent hyperlactatemia following resolution of DKA. Thiamine deficiency is biochemically plausible in this context, as thiamine serves as a cofactor for the pyruvate dehydrogenase complex, deficiency diverts pyruvate toward anaerobic metabolism and lactate accumulation. In DKA, osmotic diuresis, glycosuria, and metabolic stress exacerbate thiamine depletion. Although mild thiamine deficiency is common in patients with diabetes, clinically significant Type B lactic acidosis remains underrecognized. Empiric thiamine therapy is safe, inexpensive, and may hasten metabolic recovery while preventing unnecessary diagnostic testing or escalation of care. Conclusion Persistent lactic acidosis after apparent resolution of DKA should prompt consideration of thiamine deficiency as a reversible metabolic complication. Early empiric supplementation represents a low-risk, high-yield intervention that may accelerate recovery and reduce diagnostic uncertainty in patients with unexplained hyperlactatemia. This abstract is funded by: None
Fuesser et al. (Fri,) studied this question.