Anion gap/lactic acidosis caused

Normally, the sum of the cations exceeds the sum of the anions by no more than 12-16 mEq/L (or 8-12 mEq/L if the formula used for estimating the anion gap omits the potassium level). A larger-than expected anion gap is caused by the presence of unmeasured anions (lactate, etc) accompanying metabolic acidosis. This may occur with numerous conditions, such as diabetic ketoacidosis, renal failure, or shock-induced lactic acidosis. Drugs that may induce an elevated anion gap metabolic acidosis (Table 58-1) include aspirin, metformin, methanol, ethylene glycol, isoniazid, and iron. 

Tissue ischemia may result from many causes in general, hypoperfusion leads to hypoxia of cells, which results in anaerobic metabolism with the attendant accumulation of organic (mainly lactic) acids. The kidneys (and brain) are especially sensitive to hypoperfusion, such that acute renal failure often is a contributing factor m the high anion gap metabolic acidosis associated with global tissue ischemia (as may occur in major trauma). 

Kidney damage results from precipitation of oxalate crystals in the convoluted tubules. The elevated anion-gap metabolic acidosis is caused by glycolic acid and lactic acid. The latter is formed from pyruvate due to a shift in the redox potential favoring the production of lactate. The treatment is the same as that for methanol intoxication. 

Although there is a long list of causes of metabolic acidosis with an increased anion gap (286,287), clinical clues can help diagnosis. A case report has illustrated the acute metabolic and hemodynamic effects of ingestion of a massive load of oral citric acid. The principal findings included a metabolic acidosis accompanied by an increase in the plasma anion gap, not due to lactic acidosis, hyperkalemia, and the abrupt onset of hypotension (288). 

The diagnosis of D-lactic acidosis is suspected in patients with disorders of the small intestine causing malabsorption and when the serum anion gap (Chapter 39) is elevated in the presence of normal serum levels of L-lactate and other organic acids. Measurement of serum D-lactate requires special enzymatic procedures utilizing D-lactate dehydrogenase and NADH. As D-lactate is converted to pyruvate, NADH is oxidized to NAD+ which is detected spectrophotometrically (Chapter 8). 

The commonest causes of metabolic acidosis are renal disease, diabetic ketoacidosis and lactic acidosis. Consideration of fhe anion gap may sometime be helpful in esfablishing the cause of a metabolic acidosis. 

Type 1 lactic acidosis occurs in hypoxic subjects and is due to an excessive production of lactate by peripheral tissues. Hypoxia is not a feature of type II lactic acidosis which is probably caused by the impaired metabolism of lactate in the liver. Both are chtuacterized by an extreme metabolic acidosis ((H above 100 nmol/1). There is a high anion gap with low or absent ketones, and high blood lactate concentrations. 

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