Lactic Acid, Plasma

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.

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

1. Mizock BA. Lactic acidosis. Dis Mon. 1989; 35(4):233-300. PubMed 2656163

2. Anderson CT Jr, Westgard JO, Schlimgen K, et al. Contribution of arterial blood lactate measurement to the care of critically ill patients. Am J Clin Pathol. 1977; 68(1):63-67. PubMed 17295

3. Schuster HP. Prognostic value of blood lactate in critically ill patients. Resuscitation. 1984; 11(3-4):141-146 (review). PubMed 6326218

4. Thoene J, Baker H, Yoshino M, et al. Biotin-responsive carboxylase deficiency associated with subnormal plasma and urinary biotin. N Engl J Med. 1981; 304(14):817-820. PubMed 6782477

5. Henning RJ, Weil MH, Weiner F. Blood lactate as a prognostic indicator of survival in patients with acute myocardial infarction. Circ Shock. 1982; 9(3):307-315. PubMed 7094222

6. Bailey EM, Domenico P, Cunha BA. Bacterial or viral meningitis? Measuring lactate in CSF can help you know quickly. Postgrad Med. 1990; 88(5):217-219, 223 (review). PubMed 2216980

Bishop PA, May M, Smith, JF, et al. Influence of blood handling techniques on lactic acid concentrations. Int J Sport Med. 1991; 13(1):56-59. PubMed 1544734