L-lactate is the end product of anaerobic glycolysis. It is derived predominantly from white skeletal muscle, brain, skin, renal medulla and erythrocytes. Lactate dehydrogenase catalyses the reduction of pyruvate to lactate.
There are two major clinical settings in which lactic acidosis occurs, conditions associated with hypoxia (e.g. shock, congestive heart failure, myocardial infarction, blood loss and pulmonary oedema) and metabolic or drug/toxin related disorders. Examples of metabolic disorders include diabetes mellitus, hepatic disease and neoplasia. Congenital metabolic disorders include type I glycogen storage disease.
Examples of drugs/toxins which give rise to elevated lactate are methanol, ethanol, epinephrine and acetaminophen. Lactate levels in CSF will generally mirror those in blood/plasma. However, increased lactate levels in CSF in the absence of increased blood/plasma lactate concentration have been reported in cases of bacterial meningitis, cerebral hypoxia, ischemia and in certain inborn errors of metabolism e.g pyruvate dehydrogenase deficiency, mitochondrial myopathies and biotinidase deficiency.
Plasma: 0.5 – 2.2 mmol/L
- CSF and Plasma from blood collected into Sodium Fluoride-Potassium Oxalate Tubes is the specimen of choice due to fluoride’s ability to inhibit glycolysis, which provides a more stable lactate level in the plasma.
- EDTA and Lithium Heparin Plasma can also be used.
- Glycolysis resulting from physical exercise gives rise to an increased lactate concentration in the bloodstream. Therefore, the patient should be at rest before taking the sample. In particular, movement of the hand or arm should be avoided.
- It is not important if the blood is venous or arterial provided that care is taken to avoid stasis at the site of collection. Stasis will lead to falsely elevated results.
- Three patient identifiers from
- N.H.S. number
- Unit Number