Lactate is a normal byproduct of glucose and amino acid metabolism. There are 2 main types of lactic acidosis:
D-Lactic acidosis (D-lactate encephalopathy) is an unusual form of lactic acidosis.
Type A lactic acidosis, the most serious form, occurs when lactic acid is overproduced in ischemic tissue—as a byproduct of anaerobic generation of ATP ( adenosine triphosphate) during oxygen deficit. Overproduction typically occurs during global tissue hypoperfusion in hypovolemic, cardiogenic, or septic shock and is worsened by decreased lactate metabolism in the poorly perfused liver. It may also occur with primary hypoxia due to lung disease and with various hemoglobinopathies.
Type B lactic acidosis occurs in states of normal global tissue perfusion (and hence ATP production) and is less ominous.
Causes include local tissue hypoxia (eg, as with vigorous muscle use during exertion, seizures, hypothermic shivering), certain systemic and congenital conditions, cancer, and ingestion of certain drugs or toxins (see table Causes of Metabolic Acidosis). Drugs include the nucleoside reverse transcriptase inhibitors and the biguanides phenformin and, less so, metformin; although phenformin has been removed from the market in most of the world, it is still available from China (including as a component of some Chinese proprietary medicines). Metabolism may be decreased due to hepatic insufficiency or thiamin deficiency.
D-Lactic acidosis is an unusual form of lactic acidosis in which D-lactic acid, the product of bacterial carbohydrate metabolism in the colon of patients with jejunoileal bypass or intestinal resection, is systemically absorbed. It persists in circulation because human lactate dehydrogenase can metabolize only L-lactate.
ABG values in types A and B lactic acidosis are as for other metabolic acidoses. Diagnosis requires blood pH < 7.35 and lactate > 45 to 54 mg/dL (> 5 to 6 mmol/L). Less extreme lactate and pH changes are referred to as hyperlacticemia.
In D-lactic acidosis, the anion gap is lower than expected for the decrease in bicarbonate (HCO3−), and there may be a urinary osmolar gap (difference between calculated and measured urine osmolarity). Typical laboratory lactate assays are not sensitive to D-lactate. Specific D-lactate levels are available and sometimes needed to clarify the cause of acidosis in patients with multiple potential causes including bowel problems.
Treatment of types A and B lactic acidosis is similar to treatment of other metabolic acidoses.
Treatment of the cause is paramount. In treating inadequate tissue perfusion, pressors should be omitted when possible because they may worsen tissue ischemia. Bicarbonate is potentially dangerous in high anion gap acidosis but may be considered when pH is < 7.00, with a target pH of ≤ 7.10.
In D-lactic acidosis, treatment is IV fluids, restriction of carbohydrates, and sometimes oral antibiotics (eg, metronidazole) for short bowel syndrome and bicarbonate for severe acidosis.
There are 2 main types of lactic acidosis, type A and type B; type A is more serious because it is caused by ischemia.
Diagnosis requires blood pH < 7.35 and serum lactate levels > 45 to 54 mg/dL (> 5 to 6 mmol/L).
Avoid pressors when possible for types A and B lactic acidosis because they worsen tissue ischemia.
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