From the Guidelines
Thiamine deficiency is a significant cause of lactic acidosis that requires prompt treatment with thiamine supplementation, as emphasized in the 2022 espen micronutrient guideline 1. For patients with suspected thiamine deficiency lactic acidosis, administer thiamine 100 mg intravenously three times daily for 2-3 days, followed by 100 mg daily until clinical improvement occurs, then transition to oral thiamine 100 mg daily for at least several weeks. This condition occurs because thiamine is an essential cofactor for pyruvate dehydrogenase, which converts pyruvate to acetyl-CoA. Without adequate thiamine, pyruvate accumulates and is converted to lactate, resulting in lactic acidosis. Some key points to consider in the management of thiamine deficiency lactic acidosis include:
- Clinical manifestations may include neurological symptoms (confusion, ataxia, ophthalmoplegia), cardiovascular abnormalities (high-output heart failure), and metabolic acidosis with an elevated anion gap, as noted in the espen micronutrient guideline 1.
- Laboratory findings typically show elevated lactate levels despite normal tissue perfusion.
- Treatment should not be delayed for laboratory confirmation, as thiamine replacement is safe and potentially life-saving, especially considering that thiamine reserves are depleted as early as 20 days of inadequate oral intake 1.
- Additionally, glucose administration without concurrent thiamine in deficient patients can precipitate or worsen lactic acidosis by increasing pyruvate production, so thiamine should always be given before glucose in at-risk patients. Common settings for thiamine deficiency include:
- Alcoholism
- Malnutrition
- Prolonged vomiting
- Bariatric surgery
- Refeeding syndrome, which is of particular concern in inpatients and is associated with increased mortality, as highlighted in the espen micronutrient guideline 1.
From the FDA Drug Label
Clinical Pharmacology ... Its role in carbohydrate metabolism is the decarboxylation of pyruvic acid in the blood and -ketoacids to acetaldehyde and carbon dioxide. Increased levels of pyruvic acid in the blood indicate vitamin B1 deficiency.
- Thiamine deficiency can lead to increased levels of pyruvic acid in the blood, which can contribute to lactic acidosis.
- The decarboxylation of pyruvic acid is a critical step in carbohydrate metabolism, and thiamine plays a key role in this process as a coenzyme.
- Vitamin B1 deficiency can occur after approximately three weeks of total absence of thiamine in the diet, leading to body depletion of thiamine 2.
From the Research
Thiamine Deficiency and Lactic Acidosis
- Thiamine plays a critical role in energy metabolism, and its deficiency can lead to lactic acidosis, a potentially life-threatening condition 3, 4, 5, 6.
- Studies have shown that thiamine deficiency can cause lactic acidosis in both adults and children, and that prompt treatment with thiamine can rapidly reverse the condition 3, 4, 5, 6, 7.
- The symptoms of thiamine deficiency-associated lactic acidosis can include severe lactic acidosis, unstable circulatory state, and neurological disorders such as lethargy, impaired consciousness, and Wernicke encephalopathy 3, 4, 5, 6.
Diagnosis and Treatment
- Thiamine deficiency should be included in the differential diagnosis of lactic acidosis, particularly in patients with poor nutrition or those receiving parenteral nutrition without vitamin supplementation 3, 4, 5, 6.
- The treatment of thiamine deficiency-associated lactic acidosis typically involves the administration of intravenous thiamine, with dosing regimens ranging from 25 to 1000 mg as a single dose or multiple daily doses for several days 7.
- Prompt diagnosis and treatment of thiamine deficiency are crucial to prevent severe cardiac and neurological impairment, and to improve patient outcomes 3, 4, 5, 6, 7.
Prevention
- Thiamine deficiency can be prevented by ensuring that patients receiving parenteral nutrition also receive adequate vitamin supplementation, including thiamine 3, 5.
- Clinicians should be aware of the importance of thiamine in normal glucose metabolism and the potential consequences of thiamine deficiency, including lactic acidosis 3, 4, 5, 6, 7.