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Journal Scan

April 2015

A rare cause of metabolic (lactic) acidosis highlighted

Summarized from Giacalone M, Martinelli R, Abramo A et al. Rapid reversal of severe lactic acidosis after thiamine administration in critically ill adults: a report of three cases. Nutrition in Clinical Practice 2015; 30: 104-10 Salvatori G, Mondi V, Piersigelli F et al. Thiamine deficiency in a developed country: acute lactic acidosis in two neonates due to unsupplemented parenteral nutrition. J Parenter Enteral Nutr 2015. Published online Jan 2015 ahead of print publication. Available at: http://pen.sagepub.com/content/early/2015/01/13/0148607114568316.full.pdf

Lactic acidosis, the most common kind of metabolic acidosis, is characterized by reduced blood pH (usually <7.25) in association with marked increase in blood lactate (usually >5.0 mmol/L). Lactic acidosis has many possible causes but two broad etiological classes have been defined: type A (hypoxic) lactic acidosis and type B (non-hypoxic) lactic acidosis.

Of the two, type A lactic acidosis, i.e. lactic acidosis arising from reduced tissue perfusion and/or severe hypoxemia, is the more common. In the absence of an adequate oxygen supply, tissue cells must depend on less efficient anaerobic metabolism of glucose for its energy production, and this alternative metabolic pathway results in accumulation of lactic acid. 

Type B lactic acidosis (i.e. lactic acidosis in the presence of adequate tissue perfusion and normal blood oxygenation) has many possible causes, including a range of medicinal drugs, liver failure, renal disease, diabetic ketoacidosis, hematological malignancy, and some inherited defects of metabolism.

Deficiency of vitamin B1 (thiamine) is a very rare cause of type B lactic acidosis that is highlighted in two recently published papers. The mechanism of lactic acidosis in vitamin B1 deficiency is explained by the fact that thiamine is an essential co-factor for the enzyme pyruvate dehydrogenase that allows oxidation of pyruvate to acetyl CoA. 

This is a key step in the process that allows energy production, in the form of ATP, from glucose oxidation. In the absence of thiamine this reaction cannot proceed and instead, pyruvate is converted to lactate. The resulting accumulation of lactate causes lactic acidosis.

Lactic acidosis due to thiamine deficiency is rare because thiamine deficiency is rare. A diet containing a normal amount of carbohydrates provides more than the daily requirement and in any case the body stores sufficient thiamine for a 2-3 week period on a diet entirely devoid of thiamine. 

In the developed world a deficiency of thiamine due purely to a deficient diet is rare indeed. But as the two papers clearly demonstrate it can occur in the context of prolonged parenteral nutrition without vitamin supplementation.

The first of the two papers describes three cases of lactic acidosis due to thiamine deficiency occurring in adult patients. In all three cases patients required parenteral feeding for an underlying condition (the first had undergone major bowel surgery, the second was recovering from acute pancreatitis and the third had chronic bowel inflammation with associated malabsorption) and in all three cases vitamin supplementation was not included in the parenteral feed. 

Some weeks or months (in one case) after starting this therapy they suddenly became critically ill with severe hypotension, renal failure and rapidly deteriorating neurological state. Blood gases at this time revealed severe metabolic acidosis in association with markedly raised lactate, allowing the diagnosis of lactic acidosis. 

Without any other explanation for the sudden and catastrophic decline in the patient’s condition, the possibility of thiamine deficiency was entertained and 100 mg of thiamine was administered intravenously. 

In all three cases this had a remarkably rapid effect. Within 2-4 hours there was marked improvement in blood gas and lactate results and by 12 hours after the injection these parameters were within reference range and the patients’ acute cardiovascular and neurological symptoms had resolved.

A second paper describes a similar course of events occurring in two premature neonates with respiratory distress. Parenteral nutrition without vitamin supplementation had been given for 40 days and 45 days respectively, when their condition suddenly deteriorated catastrophically. 

Blood gas analysis at this time revealed severe lactic acidosis. As in the adult cases administration of thiamine (150 mg IV for these neonates) resulted in a rapid recovery. Within 24 hours normal blood gases and clinical condition were restored in both cases.

In discussion of both adult and neonatal case histories the respective authors provide much detail of the pathogenesis of thiamine deficiency and the link with lactic acidosis. 

Both sets of authors make the point that the medical emergencies described were, with hindsight, entirely avoidable with vitamin supplementation. They advise that sudden deterioration with development of lactic acidosis among patients receiving parenteral nutrition should raise suspicion of thiamine deficiency.

 

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Chris Higgins

has a master's degree in medical biochemistry and he has twenty years experience of work in clinical laboratories.

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