What is the treatment for hyperlactatemia?

Treatment of Hyperlactatemia

The treatment of hyperlactatemia depends fundamentally on identifying and treating the underlying cause rather than targeting lactate itself—prioritize resuscitation for tissue hypoperfusion when present, while recognizing that lactate elevation may reflect impaired clearance or non-hypoperfusion mechanisms that do not benefit from aggressive fluid resuscitation. 1, 2

Initial Assessment and Context Recognition

The first critical step is determining whether hyperlactatemia reflects tissue hypoperfusion or alternative mechanisms:

• Assess for hypoperfusion context by evaluating ScvO2 (<70%), P(cv-a)CO2 (≥6 mmHg), capillary refill time (≥4 seconds), and clinical markers of organ dysfunction 1, 3
• In sepsis, hyperlactatemia more frequently results from impaired tissue oxygen utilization rather than inadequate oxygen delivery—ScvO2 is <70% in only 35% of hyperlactatemic septic patients 2
• Hyperlactatemia without hypoperfusion context (normal ScvO2, normal P(cv-a)CO2, normal CRT) carries significantly lower mortality (5% vs 16%) and may not benefit from aggressive resuscitation 3

Sepsis-Specific Management

For septic shock with elevated lactate:

• Initiate fluid resuscitation with 30 mL/kg crystalloid within the first 3 hours as part of initial stabilization 1
• Guide subsequent resuscitation to normalize lactate as a marker of tissue hypoperfusion (weak recommendation, low quality evidence) 1
• Target mean arterial pressure of 65 mm Hg with vasopressors after appropriate fluid resuscitation 1
• Use lactate clearance as a therapeutic target—lactate-guided resuscitation has been consistently shown to be effective 1
• Monitor serial lactate measurements along with other perfusion markers (urine output, mental status, skin perfusion, renal/liver function) 1

Critical Lactate Thresholds in Sepsis

• Lactate >10 mmol/L represents severe hyperlactatemia with 78-79% ICU mortality 4, 5
• 12-hour lactate clearance <32.8% predicts 96.6% ICU mortality—this represents a critical decision point for evaluating benefit of continued aggressive therapy 4
• Patients developing severe hyperlactatemia >24 hours after ICU admission have significantly higher mortality (89.1%) than those with early severe hyperlactatemia (69.9%) 4

Shock States Requiring Delayed Enteral Nutrition

Delay enteral nutrition if shock is uncontrolled and hemodynamic/tissue perfusion goals are not reached, but start low-dose EN as soon as shock is controlled 1

• Particular concern exists when very high vasopressor doses (e.g., norepinephrine >1 μg/kg/min) are required with persistent hyperlactatemia or other signs of end-organ hypoperfusion 1

NRTI-Associated Hyperlactatemia (HIV Patients)

For nucleoside reverse transcriptase inhibitor (NRTI)-related hyperlactatemia:

• Lactate 2-5 mmol/L: Close monitoring is advised; no intervention necessary for levels <2 mmol/L 1
• Lactate >5 mmol/L: Abnormal and requires action 1
• Lactate >10 mmol/L: Indicates serious, possibly life-threatening situation 1
• Discontinue NRTIs for symptomatic hyperlactatemia with unexplained gastrointestinal symptoms, hepatomegaly, or elevated anion gap 1
• Consider thiamine and riboflavin supplementation based on mitochondrial dysfunction pathophysiology, though efficacy requires clinical validation 1
• For severe lactic acidosis: intensive support including bicarbonate infusions and hemodialysis may be necessary 1

Sodium Bicarbonate Considerations

Bicarbonate therapy should be used cautiously and only for severe metabolic acidosis:

• In cardiac arrest: 1-2 vials (44.6-100 mEq) initially, then 50 mL every 5-10 minutes as indicated by arterial pH and blood gas monitoring 6
• For less urgent metabolic acidosis: 2-5 mEq/kg over 4-8 hours, guided by blood gases, plasma osmolarity, arterial lactate, and hemodynamics 6
• Avoid attempting full correction in first 24 hours—this may produce unrecognized alkalosis due to delayed ventilatory readjustment 6
• Target total CO2 of approximately 20 mEq/L at end of first day, which typically associates with normal blood pH 6
• Monitor for complications: metabolic alkalosis, hypernatremia, and tissue necrosis from extravasation 6

Special Populations

Diabetes Mellitus Patients

• Patients with diabetes have higher baseline lactate levels (mean 6.3 vs 5.1 mmol/L in non-diabetics) 7
• Lactate >4 mmol/L may not have equal prognostic significance in diabetic vs non-diabetic patients—it was an independent predictor of mortality in non-diabetic patients but not in diabetic patients 7
• Consider metformin accumulation with renal impairment as a contributor to severe hyperlactatemia in diabetic patients 7

Pediatric Patients

• Rapid injection (>10 mL/min) of hypertonic bicarbonate in neonates and children <2 years may cause hypernatremia, decreased CSF pressure, and intracranial hemorrhage 6
• Limit bicarbonate administration rate to ≤8 mEq/kg/day in young children; 4.2% solution preferred 6

Smoke Inhalation/Cyanide Poisoning

• Plasma lactate >8 mmol/L correlates with cyanide poisoning (83% of cases) 1
• Hydroxocobalamin 5-10 g in adults with suspected severe cyanide poisoning and cardiac/respiratory arrest, shock, or coma 1
• In children: 70 mg/kg (maximum 5 g) for moderate-to-severe cyanide poisoning signs 1

Key Clinical Pitfalls

• Avoid over-resuscitation in hyperlactatemia without hypoperfusion context—this risks fluid overload and vasoactive drug toxicity 3
• Do not rely solely on lactate normalization—complement with multiple perfusion markers and clinical assessment 1
• Recognize that persistent severe hyperlactatemia (>10 mmol/L) with negative delta lactate at 24 hours carries 92% mortality and should prompt discussion of treatment limitations 4, 5
• In sepsis, hyperlactatemia often reflects impaired oxygen utilization rather than delivery—aggressive fluid resuscitation may not be beneficial in all cases 2