Treatment of Lactic Acidosis
The primary treatment of lactic acidosis is identifying and aggressively treating the underlying cause—restoration of tissue perfusion through fluid resuscitation is the cornerstone, while sodium bicarbonate should NOT be used in most cases as it does not improve outcomes and may cause harm. 1, 2
Immediate Management Priorities
Identify and Treat the Underlying Cause
- Restore tissue perfusion first if shock is present with fluid resuscitation using 15-20 mL/kg/h isotonic saline initially, or at least 30 mL/kg IV crystalloid within the first 3 hours for sepsis-induced hypoperfusion 1, 2
- Target mean arterial pressure ≥65 mmHg as your hemodynamic goal 2
- Aim for urine output ≥0.5 mL/kg/hr as a marker of adequate perfusion 2
- Remeasure lactate within 2-6 hours to assess trajectory and response to therapy 2
Treat Sepsis Aggressively
- Administer antibiotics within 3 hours if infection is suspected 1, 2
- Obtain blood cultures before antibiotics 1
- Provide aggressive source control 1, 2
- Follow hemodynamic support per Surviving Sepsis Campaign protocols 1
Discontinue Offending Medications Immediately
- Stop metformin immediately in patients with lactic acidosis, particularly those with renal impairment—hemodialysis is the definitive treatment for metformin-associated lactic acidosis and often reverses symptoms 1
- Discontinue NRTIs (stavudine, didanosine) immediately in HIV patients with lactic acidosis, as mortality is high without intervention 1
The Bicarbonate Controversy: When NOT to Use It
Sodium bicarbonate should NOT be used to improve hemodynamics or reduce vasopressor requirements in hypoperfusion-induced lactic acidemia with pH ≥7.15. 1
Why Bicarbonate Fails
- Does not improve hemodynamics or cardiovascular function 1
- May increase lactate production 1, 3
- Causes hypernatremia and volume overload 1, 4
- Generates CO₂ which can worsen intracellular acidosis 1
- Has never been shown to improve survival 1, 3
When Bicarbonate May Be Considered (FDA-Approved Indications)
- Severe primary lactic acidosis with pH <7.15 where rapid increase in plasma CO₂ content is crucial 4
- Cardiac arrest situations where risks from acidosis exceed those of hypernatremia 4
- Dosing: 1-2 vials (44.6-100 mEq) initially in cardiac arrest, continued at 50 mL every 5-10 minutes as indicated by arterial pH monitoring 4
- For less urgent metabolic acidosis: 2-5 mEq/kg over 4-8 hours, with stepwise titration based on response 4
Critical caveat: It is unwise to attempt full correction of low total CO₂ content during the first 24 hours, as this may cause unrecognized alkalosis due to delayed ventilatory readjustment 4
Special Clinical Scenarios
D-Lactic Acidosis (Short Bowel Syndrome)
- Restrict mono/oligosaccharides 1, 2
- Encourage polysaccharides (starch) 1, 2
- Administer thiamine supplements 1
- Provide broad-spectrum antibiotics 1
Mesenteric Ischemia
- Consider CT angiography immediately if lactate >2 mmol/L with abdominal pain and elevated BUN—do NOT delay, as diagnostic delay is the dominant factor in mortality (30-70%) 1, 2
- Consider urgent laparotomy if signs of intestinal perforation are present 1
Renal Replacement Therapy Considerations
- Continuous renal replacement therapy (CRRT) with bicarbonate-based dialysate can provide alkali without hypernatremia or hypervolemia 5, 6
- Bicarbonate is preferred over lactate as buffer in patients with lactic acidosis and/or liver failure 5
- However, kinetic studies suggest lactate removal cannot meaningfully counteract lactate production 3
Supportive Care Measures
- Consider thiamine supplementation to address potential pyruvate dehydrogenase dysfunction 1
- Monitor electrolytes closely, particularly in patients on CRRT 1
- Avoid volume overload, especially in patients with acute lung injury 5
Prognostic Considerations
- Lactate >5 mmol/L is abnormal and >10 mmol/L represents severe, life-threatening hyperlactatemia 2
- Consider goals of care discussions within 72 hours of ICU admission when 12-hour lactate clearance is inadequate, as mortality risk approaches 95% 2
- Despite improvement in lactic acidemia with treatments like dichloroacetate, ultimate prognosis depends on the underlying disease 7
Common Pitfalls to Avoid
- DO NOT ignore mesenteric ischemia when lactate is elevated with abdominal pain and elevated urea—88% of patients with acute mesenteric ischemia present with metabolic acidosis and elevated lactate 1
- DO NOT rely on bicarbonate therapy alone—treating the underlying cause is the only warranted intervention 8
- DO NOT continue metformin in patients with sepsis, acute kidney injury, or hemodynamic instability 1
- DO NOT use aggressive bicarbonate without considering the serious complications of hypernatremia, volume overload, and paradoxical worsening of intracellular acidosis 1, 6