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1 - 3 days
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
0.5 mL (Note: This volume does not allow for repeat testing.)
Gray-top (sodium fluoride/potassium oxalate or sodium fluoride/sodium heparin) tube
Keep gray-top tube on ice. Draw blood in gray-top tube. Mix well by gentle inversion at least six times. Return to ice bath to cool. Avoid hand-clenching and, if possible, avoid use of a tourniquet. A tourniquet with patient clenching and unclenching hand will lead to high potassium and lactic acid buildup from the hand muscles, and pH will decrease. It is best to avoid a tourniquet for electrolytes and lactic acid or to release it after blood begins to flow into the tube. If the tourniquet is released before blood is drawn, wait about a minute before drawing. Within 15 minutes of draw, separate the plasma from blood by centrifugation for 10 minutes. Immediately transfer the plasma portion of the sample to a labeled plastic transport tube. Avoid excessive forces that contribute to hemolysis.
Patient should not be on any intravenous infusion that would affect the acid-base balance. Patient should be in a fasting and resting state (should not exercise).
Specimen not separated from cells within 15 minutes of draw; marked hemolysis; slight or moderate turbidity; perchloric acid supernatant; serum specimen
Hypoperfusion is the most common cause of lactic acidosis and hyperlactacidemia may be the only marker of tissue hypoperfusion.1 Suspect lactic acidosis when unexplained anion gap metabolic acidosis is encountered, especially if azotemia or ketoacidosis are not present. Evaluate metabolic acidosis, regional or diffuse tissue hypoperfusion, hypoxia, shock,2 congestive heart failure, dehydration, complicated postoperative state, ketoacidosis or nonketotic acidosis in diabetes mellitus, patients with infections, inflammatory states, postictal state, certain myopathies, acute leukemia and other neoplasia, enzyme defects, glycogen storage disease (type I), thiamine deficiency, and hepatic failure. A spontaneous form of lactic acidosis occurs. It is a prognostic index in particular clinical settings, especially in critically ill patients in shock.3 A relationship to renal disease also exists. With skin rash, seizures, alopecia, ataxia, keratoconjunctivitis, and lactic acidosis in children, consider defective biotin metabolism.4 Phenformin, ethanol, methanol, and salicylate poisoning and ethylene glycol may cause lactic acidosis. Acetaminophen toxicity causes lactic acidosis, sometimes with hypoglycemia. Cyanide, isoniazid, and propylene glycol are among the causes of lactic acidosis.1 Lactic acidosis may be due to inborn errors of metabolism.
Gross hemolysis elevates plasma results. Intravenous injections, or infusions which modify acid-base balance, may cause alterations in lactate levels. Epinephrine and exercise elevate lactate, as may IV sodium bicarbonate, glucose, or hyperventilation. False-low values may be found with a high LD (LDH) value.
0 to 7 d
8 to 30 d
1 to 6 m
7 m to 5 y
Phosphorus is sometimes significantly abnormal in lactic acidosis. Creatinine is higher in ketoacidosis than in lactic acidosis, by interference produced by acetoacetic acid on creatinine. Causes of lactic acidosis (usually <45 mg/dL) include carbohydrate infusions, exercise, diabetic ketosis, alcohol. Causes of lactic acidosis (>45 mg/dL) include shock (in which lactic acidosis may occur early, before fall in blood pressure, decrease in urine output), hypoxia (including congestive failure, severe anemia, hypotension) and malignancies. Severe lactic acidosis can develop in minutes. Lactic acidosis can accompany dehydration. Blood lactate concentration correlates negatively with survival in patients with acute myocardial infarction, with persistent elevation, >36 mg/dL for more than 12 hours, being associated with poor prognosis.5 At a given bicarbonate level, the average pCO2 is lower in lactic acidosis than in diabetic ketoacidosis. Lactic acid determination is generally indicated if anion gap is <20 and if pH is >7.25 and the pCO2 is not elevated. (Mizock uses pH 7.35 as a diagnostic criterion.1) The measurement of lactate levels may be indicated in the clinical setting of metabolic acidosis. Serum salicylate, ethanol level, and osmolality may be helpful. Spontaneous lactic acidosis may be fatal. High CSF lactate levels suggest the meningitis is bacterial while low values suggest a viral cause.6
|Order Code||Order Code Name||Order Loinc||Result Code||Result Code Name||UofM||Result LOINC|
|004770||Lactic Acid, Plasma||14118-4||004770||Lactic Acid, Plasma||mg/dL||14118-4|
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