Treatment of Elevated Lactate (Hyperlactatemia)
The primary treatment for elevated lactate levels is identifying and addressing the underlying cause, with particular focus on improving tissue perfusion in cases of shock or hypoperfusion, which is the most common etiology of hyperlactatemia. 1
Causes of Hyperlactatemia
- Tissue hypoperfusion and hypoxia is the most common cause, resulting from inadequate oxygen delivery to tissues causing anaerobic metabolism 1
- Sepsis and septic shock is a major cause due to both tissue hypoperfusion and inflammatory mediators affecting cellular metabolism 1
- Shock states (hypovolemic, cardiogenic, distributive) all lead to impaired tissue perfusion 1
- Medication-induced elevations can occur with drugs like epinephrine through beta-2-adrenergic receptor stimulation 1
- Metabolic causes include accelerated aerobic glycolysis driven by excess beta-adrenergic stimulation 1
Treatment Approach Based on Etiology
Sepsis-Induced Hyperlactatemia
- Implement protocolized, quantitative resuscitation with the following goals during the first 6 hours 2:
- Central venous pressure 8-12 mmHg
- Mean arterial pressure (MAP) ≥65 mmHg
- Urine output ≥0.5 mL/kg/h
- Central venous oxygen saturation 70% or mixed venous oxygen saturation 65%
- Target resuscitation to normalize lactate as rapidly as possible 2
- Administer IV antibiotics within the first hour of recognition of septic shock 2
- Provide fluid resuscitation with 30 cc/kg within 3 hours for septic shock 2
Shock States
- Restore adequate tissue perfusion through fluid resuscitation 1
- If hypotension persists after fluid administration or initial lactate ≥4 mmol/L, reassess volume status and tissue perfusion 2
- If SBP or MAP remains low after fluids, start vasopressors (norepinephrine is preferred) to maintain MAP at 65 mmHg 2
- Consider adding vasopressin (0.04 units/min) if MAP remains inadequate despite moderate doses of norepinephrine 2
- For cardiac dysfunction with persistent hypoperfusion, consider adding epinephrine 2
Severe Metabolic Acidosis with Lactic Acidosis
- For severe primary lactic acidosis, sodium bicarbonate IV is indicated 3
- In cardiac arrest with lactic acidosis, rapid IV dose of 44.6 to 100 mEq sodium bicarbonate may be given initially 3
- For less urgent forms of metabolic acidosis, administer approximately 2-5 mEq/kg of sodium bicarbonate over 4-8 hours 3
- Caution: Avoid full correction of low total CO2 content during first 24 hours to prevent rebound alkalosis 3
Monitoring Response to Treatment
- Serial lactate measurements provide an objective evaluation of response to therapy 1
- Lactate clearance is a significant predictor of survival, with decreased survival if lactate levels remain elevated >24-48 hours 1
- Normalization of lactate within 24 hours is associated with improved survival 1
- Monitor blood gases, plasma osmolarity, arterial blood lactate, hemodynamics, and cardiac rhythm during treatment 3
Special Considerations
- Patients developing severe hyperlactatemia (>10 mmol/L) after 24 hours of ICU treatment have significantly higher mortality (89.1%) than those developing it within 24 hours (69.9%) 4
- A 12-hour lactate clearance of less than 32.8% is associated with extremely high ICU mortality (96.6%) 4
- Simultaneously elevated lactate-to-pyruvate ratio (>18) with hyperlactatemia is associated with higher mortality and suggests inadequate tissue perfusion 5
Important Pitfalls to Avoid
- Don't ignore elevated lactate in seemingly stable patients, as it may indicate occult tissue hypoperfusion 1
- Avoid attempting full correction of acidosis too quickly, as this may lead to rebound alkalosis 3
- Remember that sodium bicarbonate can increase lactate production, so use judiciously 6
- Consider that certain medications can cause elevated lactate levels independent of tissue perfusion 1
By systematically addressing the underlying cause of hyperlactatemia while monitoring response to therapy through serial lactate measurements, clinicians can optimize outcomes in patients with elevated lactate levels.