Lactate is a substance constantly produced by the body’s cells as a byproduct of metabolism, primarily during the conversion of glucose into energy. When oxygen is adequate, lactate is efficiently processed further for energy or cleared by the liver and kidneys. High lactate levels, known as hyperlactatemia, signify an imbalance where production exceeds clearance. If the blood lactate concentration rises high enough to cause a significant drop in blood pH, the condition is termed lactic acidosis. Lactate measurement is frequently used in intensive care for infants as a sensitive marker for poor tissue oxygenation or underlying metabolic distress.
Acute Causes Related to Low Oxygen
The most immediate cause of high lactate levels is a lack of oxygen delivery to the tissues, classified as Type A Lactic Acidosis. When cells are deprived of oxygen, they switch from efficient aerobic energy production to anaerobic glycolysis. This less efficient emergency pathway rapidly produces energy, but its end product, pyruvate, is quickly converted into lactate, causing a sharp rise in blood concentration.
Conditions that impair blood flow or oxygen saturation trigger this shift, leading to tissue hypoperfusion. Sepsis is a frequent offender, as septic shock causes widespread dilation of blood vessels and poor microcirculation, preventing oxygen from reaching the cells. Birth asphyxia, a lack of oxygen during delivery, also immediately floods the newborn’s system with lactate.
Severe respiratory distress syndrome (RDS) or pneumonia impair the lungs’ ability to transfer oxygen into the blood. Heart conditions like congenital heart disease or cardiogenic shock cause poor circulation and low oxygen delivery. In these scenarios, elevated lactate signals that the body’s cells are relying on a temporary, unsustainable method of energy production.
Systemic Stress and Clearance Issues
Type B Lactic Acidosis occurs when the primary problem is not oxygen deprivation but a failure in the body’s ability to clear or process lactate. The liver is the main organ responsible for metabolizing lactate, converting approximately 60% of it back into glucose through the Cori cycle. Impaired liver function, such as in acute liver failure, drastically reduces this clearance mechanism, allowing lactate to accumulate even if production is normal.
The kidneys also play a role, clearing about 30% of the circulating load; thus, significant kidney dysfunction contributes to lactate buildup. Type B elevation can also result from non-hypoxic systemic stresses and environmental factors. Specific medications, such as nucleoside reverse transcriptase inhibitors used in HIV treatment, can directly interfere with mitochondrial function and increase lactate production.
Severe dehydration can impair circulation, leading to localized hypoperfusion and reduced clearance. Thiamine deficiency is another cause, as thiamine is a required cofactor for the enzyme that converts pyruvate to acetyl-CoA, creating a metabolic block that shunts pyruvate toward lactate.
Genetic and Metabolic Conditions
Persistently high lactate levels in infants may indicate an underlying inborn error of metabolism (IEM). These are rare, inherited disorders where a specific enzyme or protein required for a metabolic pathway is faulty or missing. This creates a metabolic bottleneck, forcing energy precursors to accumulate and convert into lactate, regardless of oxygen supply.
Many of these disorders involve defects in the utilization of pyruvate, the molecule linking glycolysis to the main energy-producing cycle. Pyruvate Dehydrogenase Deficiency (PDHC) is a prime example; a defect in the PDHC enzyme complex prevents pyruvate from entering the tricarboxylic acid (TCA) cycle. Since the cell cannot use pyruvate for aerobic energy, the molecule is shunted to lactate, causing chronic or episodic lactic acidosis.
Mitochondrial disorders also frequently present with elevated lactate. These conditions affect the organelles responsible for the final steps of energy production, the electron transport chain (ETC). When the ETC is dysfunctional, the aerobic process backs up, forcing reliance on the lactate-producing anaerobic pathway.
Diagnosis and Management
Detecting high lactate triggers a rapid process of diagnosis and intervention. Initial management focuses on immediate stabilization, ensuring adequate respiratory support and circulatory function to restore oxygen delivery. Frequent lactate measurements monitor treatment effectiveness, as a quickly clearing level often indicates a reversible cause like shock or respiratory failure.
The diagnostic process requires thorough investigation to differentiate between acute problems and underlying metabolic disorders. This involves comprehensive blood gas analysis to assess acidosis and specialized metabolic screening. If a genetic cause is suspected, the ratio of lactate to pyruvate may be analyzed to help identify the location of the metabolic block.
Management focuses on reversing the underlying disease state, not treating lactate as a symptom. For example, sepsis requires antibiotics and fluid resuscitation, while severe respiratory failure requires mechanical ventilation. Management for inborn errors of metabolism may involve:
- Specialized dietary modifications.
- Cofactor supplementation with vitamins like thiamine or carnitine.
- Medications to help neutralize the excessive acid load.