Lactic acidosis is a high anion gap metabolic acidosis due to elevated blood lactate. Lactic acidosis results from overproduction of lactate, decreased metabolism of lactate, or both.
(See also Metabolic Acidosis, Acid-Base Regulation, and Acid-Base Disorders.)
Lactate is a normal byproduct of glucose and amino acid metabolism. There are 2 main types of lactic acidosis:
Type A lactic acidosis
Type B lactic acidosis
A third type, D-lactic acidosis (D-lactate encephalopathy) is an unusual form of lactic acidosis.
Type A 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 shock, cardiogenic shock, 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
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 medications or toxins (see table Causes of Metabolic Acidosis). Medications include the nucleoside reverse transcriptase inhibitors and the biguanides metformin and phenformin (although phenformin is no longer available). Metabolism may be decreased due to hepatic insufficiency or thiamin deficiency.
D-Lactic acidosis
D-Lactic acidosis is an unusual form of lactic acidosis in which excess D-lactic acid is produced. D-lactic acid is normally produced in small quantities as the product of carbohydrate metabolism by bacteria in the colon. In patients with jejunoileal bypass or intestinal resection and resultant short bowel syndrome, excess D-lactic acid is produced and is systemically absorbed. It persists in circulation because human lactate dehydrogenase can metabolize only L-lactate, but it is otherwise chemically similar to L-lactate and has similar effects on acid-base balance.
Symptoms and Signs of Lactic Acidosis
Symptoms and signs of lactic acidosis are dominated by those of the underlying disorder (eg, shock in Type A, toxin ingestion in Type B).
Neurologic symptoms, including confusion, ataxia, and slurred speech, occur after a high-carbohydrate ingestion and are characteristic of D-lactic acidosis.
Diagnosis of Lactic Acidosis
Arterial blood gas (ABG) and serum electrolyte measurements
Anion gap and delta gap calculated
Blood lactate level
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 are sometimes needed to clarify the cause of acidosis in patients with multiple potential causes, including bowel problems.
Treatment of Lactic Acidosis
Treatment of cause
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.
Key Points
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.
