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Diagnosing and monitoring patients with lactic acidosis
Lactate is the end product of anaerobic carbohydrate metabolism. Major sites of production are skeletal muscle, brain, and erythrocytes. Lactate is metabolized by the liver. The concentration of lactate depends on the rate of production and the rate of liver clearance. The liver can adequately clear lactate until the concentration reaches approximately 2 mmol/L. When this level is exceeded, lactate begins to accumulate rapidly. For example, while resting lactate levels are usually <1 mmol/L, during strenuous exercise levels can rise >20 mmol/L within a few seconds.
Lactic acidosis signals the deterioration of the cellular oxidative process and is associated with hyperpnea, weakness, fatigue, stupor, and finally coma. These conditions may be irreversible, even after treatment is administered. Lactate acidosis may be associated with hypoxic conditions (eg, shock, hypovolemia, heart failure, pulmonary insufficiency), metabolic disorders (eg, diabetic ketoacidosis, malignancies), and toxin exposures (eg, ethanol, methanol, salicylates).
< or =2 years: 0.6-3.2 mmol/L
>2 years: 0.6-2.3 mmol/L
While no definitive concentration of lactate has been established for the diagnosis of lactic acidosis, lactate concentrations exceeding 5 mmol/L and pH <7.25 are generally considered indicative of significant lactic acidosis.
Proper specimen collection and processing techniques are critical for reliable results.
This test does not measure D-lactate, an uncommon, often undiagnosed cause of lactic acidosis. See DLAC / D-Lactate, Plasma.
1. Mizock BA: The hepatosplanchnic area and hyperlactatemia: A tale of two lactates. Crit Care Med 2001;29(2):447-449
2. Duke T: Dysoxia and lactate. Arch Dis Child 1999;81(4):343-350