Lactoacidosis

Lactic acidosis develops as a result of increased production or decreased metabolism of lactate, as well as a combination of both.

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Causes lactoacidosis

Lactate is a normal byproduct of glucose and amino acid metabolism. The most severe form, type A lactic acidosis, occurs when lactic acid is overproduced in ischemic tissue to form ATP when O2 is deficient. Overproduction is usually seen in tissue hypoperfusion due to hypovolemic, cardiac, or septic shock and is exacerbated by decreased lactate metabolism in the poorly perfused liver. It may also occur in primary hypoxia associated with pulmonary disease or hemoglobinopathies.

Type B lactic acidosis occurs with normal tissue perfusion (and hence ATP production) and is less ominous. Lactic acid production may be increased by excessive muscle stress (eg, exercise, cramps, cold shivering), alcohol ingestion, cancer, drugs such as biguanides (eg, phenformin and to a lesser extent metformin), reverse transcriptase inhibitors, or exposure to various toxins. Metabolism may be decreased by liver failure or thiamine deficiency.

D-lactic acidosis is an unusual form of lactic acidosis in which the D-isomer of lactic acid, a product of bacterial carbohydrate metabolism in the intestines of patients with jejunoileal anastomosis or intestinal resection, is absorbed. The isomer persists in the circulation because lactate dehydrogenase metabolizes only the L-form of lactic acid.

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Diagnostics lactoacidosis

The diagnosis is similar to other metabolic acidoses, with the exception of D-lactic acidosis. In D-lactic acidosis, the anion gap is lower than expected from the decrease in HCO3, and a urinary osmolar gap (the difference between calculated and measured urine osmolarity) may be observed.

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Treatment lactoacidosis

Lactic acidosis is treated with intravenous fluids, carbohydrate restriction, and sometimes antibiotics (eg, metronidazole).