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Lactic acidosis
Last reviewed: 23.04.2024
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[Causes of the lactic acidosis
Lactate is a normal by-product of the metabolism of glucose and amino acids. The most severe form is lactoacidosis of type A, which develops during the hyperproduction of lactic acid in ischemic tissue for the formation of ATP in the presence of O2 deficiency. Hyperproduction is usually observed with tissue hypoperfusion in hypovolemic, cardiac or septic shock and aggravated by a decrease in lactate metabolism in poorly blood-supplying liver. It can also be observed with primary hypoxia associated with lung diseases or hemoglobinopathies.
Lactoacidosis type B is observed with normal tissue perfusion (and, therefore, ATP formation) and is less threatening. The formation of lactic acid can be increased with excessive muscle tension (for example, physical activity, convulsions, cold muscle tremor), alcohol intake, cancer, drugs such as biguanides (eg, phenformin and to a lesser extent metformin), reverse transcriptase inhibitors or exposure to various toxins. Metabolism can be reduced with hepatic insufficiency or thiamine deficiency.
D-lactic acidosis is an unusual form of lactic acidosis, in which the D-isomer of lactic acid, which is the product of the bacterial metabolism of carbohydrates in the intestines of patients with ejaculatory anastomosis or intestinal resection, is absorbed. The isomer persists in the bloodstream, since lactate dehydrogenase only metabolizes L-forms of lactic acid.
Diagnostics of the lactic acidosis
Diagnosis is similar to other metabolic acidosis, with the exception of D-lactic acidosis. In D-lactic acidosis, the anion gap is lower than the expected decrease in HCO3, a urinary osmolar gap (the difference between the calculated and measured urinary osmolality) can be observed.
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Treatment of the lactic acidosis
Lactic acidosis is treated with intravenous fluids, restriction of carbohydrates and sometimes the administration of antibiotics (eg, metronidazole).