What is the role of intravenous (IV) thiamine in patients with lactic acidosis, particularly those with a history of alcohol abuse or malnutrition?

IV Thiamine in Lactic Acidosis

Administer IV thiamine 100-300 mg immediately in any patient with unexplained lactic acidosis, particularly those with malnutrition, alcohol use disorder, or recent parenteral nutrition without vitamin supplementation, as thiamine deficiency is a reversible cause of severe lactic acidosis that responds rapidly to treatment. 1, 2, 3

Clinical Rationale for Thiamine in Lactic Acidosis

Thiamine (vitamin B1) is an essential cofactor for pyruvate dehydrogenase and α-ketoglutarate dehydrogenase, enzymes critical for aerobic glucose metabolism. 1 Without adequate thiamine, pyruvate cannot be converted to acetyl-CoA, leading to accumulation of lactate and pyruvate, resulting in type B lactic acidosis. 4, 5

The FDA explicitly indicates IV thiamine when giving IV dextrose to individuals with marginal thiamine status to avoid precipitation of heart failure, and for cardiovascular disease due to thiamine deficiency. 2 This includes patients presenting with unexplained metabolic lactic acidosis. 1

High-Risk Populations Requiring Immediate Treatment

Suspect thiamine deficiency-induced lactic acidosis in patients with:

• Parenteral nutrition without vitamin supplementation - this is the most commonly reported scenario in case series, with lactic acidosis developing within 4 weeks of inadequate supplementation 3, 4, 6
• Chronic alcohol use disorder - 30-80% show clinical or biological signs of thiamine deficiency 7
• Severe malnutrition or prolonged inadequate oral intake - thiamine reserves deplete within 20 days 1, 7
• Critical illness - deficiency found in >90% of critically ill patients with sepsis, major trauma, or severe burns 7
• Post-bariatric surgery with prolonged vomiting 7
• Chronic diuretic therapy - increases renal thiamine losses 1, 7

Diagnostic Clues for Thiamine-Deficient Lactic Acidosis

Look for this clinical pattern:

• Severe lactic acidosis (lactate ≥10.9 mmol/L) with elevated lactate/pyruvate ratio (≥0.029) 4
• Metabolic acidosis with pH ≤7.13 and base excess ≤-17.5 mmol/L 4
• Hemodynamic instability (hypotension ≤80/60 mmHg) despite fluid resuscitation 3, 4
• Neurological symptoms - confusion, lethargy, impaired consciousness, or signs of Wernicke encephalopathy 3, 4
• Failure to respond to sodium bicarbonate or conventional shock treatments 4, 5
• No other identifiable cause - normal hepatic, renal, and pancreatic function on routine labs 4

Critical pitfall: Do not wait for thiamine levels before treating - serum thiamine measurement takes days to return, and treatment must not be delayed. 1, 7 Red blood cell thiamine diphosphate (ThDP) is the preferred test if confirmation is needed, but empiric treatment should begin immediately. 1

Dosing Protocol for Lactic Acidosis

Administer 100 mg IV thiamine every 12 hours (total 200 mg/day) as the initial regimen. 4 This dose has been shown to rapidly reverse severe lactic acidosis in multiple case series. 3, 4, 5

Alternative high-dose regimens supported by guidelines:

• 100-300 mg IV daily for 3-4 days for high-risk/acute situations 7
• 200 mg IV three times daily for high suspicion or proven deficiency 7
• 500 mg IV three times daily if Wernicke encephalopathy is suspected or confirmed 7, 8

Always administer thiamine BEFORE any glucose-containing IV fluids to prevent precipitating acute Wernicke encephalopathy, as thiamine is required for glucose metabolism. 7, 8, 2

Expected Clinical Response

The response to thiamine in deficiency-induced lactic acidosis is dramatic and rapid:

• Lactate normalization within hours - documented cases show lactate dropping from 10.9-11.8 mmol/L to 2.0-2.4 mmol/L within hours of thiamine administration 3, 5
• Acid-base correction - pH improvement from 7.11-7.24 to 7.30-7.46 within hours 5
• Hemodynamic stabilization - resolution of hypotension and circulatory instability 3, 5
• Neurological improvement - disappearance of confusion, lethargy, or encephalopathy 3
• Cardiovascular improvement - reversal of right ventricular heart failure if present 5

If lactic acidosis does not improve within 12-24 hours of thiamine administration, other causes must be aggressively pursued. 4

Adjunctive Treatment

Correct magnesium deficiency concurrently - magnesium is necessary for adequate function of thiamine-dependent enzymes. 7 Administer magnesium sulfate if levels are low or borderline. 3

Monitor and correct other electrolyte abnormalities (potassium, phosphate) that commonly coexist in malnourished patients. 7

Safety Profile

Thiamine has an excellent safety profile with no established upper limit for toxicity - excess is excreted in urine. 7, 8 High IV doses rarely cause anaphylaxis, and doses >400 mg may only induce mild nausea, anorexia, or mild ataxia. 7, 8 The benefit-risk ratio strongly favors empiric treatment in any patient with unexplained lactic acidosis and risk factors. 7

Prevention in High-Risk Patients

All patients receiving parenteral nutrition must receive adequate vitamin supplementation from day one - standard PN formulations should contain at least 2-6 mg thiamine daily. 1, 7 The inadvertent non-administration of thiamine during PN is a preventable condition that has led to documented deaths from lactic acidosis. 6

For patients with alcohol use disorder, malnutrition, or critical illness, prophylactic thiamine 100-300 mg IV daily should be administered routinely. 7