What is the best approach to manage severe lactate acidosis in a critically ill adult patient with a history of sepsis or diabetic ketoacidosis and impaired renal function, considering dialysis as a treatment option?

Management of Severe Lactate Acidosis with Dialysis

Primary Recommendation

Do not use dialysis or continuous renal replacement therapy (CRRT) for severe lactic acidosis unless there are other definitive indications for renal replacement therapy (such as severe hyperkalemia, uremia, or fluid overload refractory to diuretics). 1

The Surviving Sepsis Campaign explicitly recommends against initiating RRT in patients with sepsis and acute kidney injury solely for increase in creatinine or oliguria without other definitive indications for dialysis. 1 This recommendation is based on two large randomized controlled trials from 2016 showing either no benefit or potential harm (including increased central line infections and increased dialysis dependence) with early RRT. 1

Treatment Algorithm for Severe Lactic Acidosis

Step 1: Identify and Aggressively Treat the Underlying Cause

The cornerstone of management is correcting the underlying etiology, not dialysis. 1, 2

For sepsis-induced lactic acidosis:

• Administer effective IV antimicrobials within the first hour of recognition 1
• Begin immediate fluid resuscitation with 30 mL/kg IV crystalloid within first 3 hours 1
• Target MAP ≥65 mmHg using norepinephrine as first-line vasopressor 1
• Achieve urine output ≥0.5 mL/kg/hr 1
• Target central venous oxygen saturation ≥70% (ScvO2) or ≥65% (SvO2) 1

For diabetic ketoacidosis:

• Continuous intravenous insulin is the standard of care 1
• Administer basal insulin 2-4 hours prior to stopping IV insulin to prevent rebound 1
• Provide adequate fluid replacement 1

Step 2: Bicarbonate Therapy - Use Only in Specific Circumstances

The Surviving Sepsis Campaign recommends AGAINST sodium bicarbonate therapy for hypoperfusion-induced lactic acidemia with pH ≥7.15. 1 Two blinded, crossover RCTs showed no difference in hemodynamic variables or vasopressor requirements, and bicarbonate administration causes sodium and fluid overload, increased lactate and PaCO2, and decreased serum ionized calcium. 1

However, the FDA label for sodium bicarbonate indicates it is approved for "severe primary lactic acidosis" when rapid increase in plasma CO2 content is crucial. 3 This creates a clinical dilemma that should be resolved as follows:

Bicarbonate may be considered only when:

• pH <7.15 (the guideline threshold where evidence is insufficient) 1
• Severe acidosis is causing life-threatening cardiovascular instability 3
• Used as a temporizing measure while definitive treatment of underlying cause takes effect 3

Step 3: Monitor Lactate Clearance as Primary Endpoint

Serial lactate measurements every 2-6 hours during acute resuscitation provide objective evaluation of response to therapy. 4 Target normalization within 24 hours, as this is associated with 100% survival in trauma patients. 4 Lactate clearance of at least 10% every 2 hours during the first 8 hours is the goal. 4

Why Dialysis is Ineffective for Lactic Acidosis

The evidence against dialysis for lactic acidosis is compelling:

• A case report of high-volume hemofiltration at 7 L/h (58 mL/kg/h) achieved lactate clearance of only 79 mL/min, which is quite small compared to rates of lactate overproduction in septic shock. 5 The authors concluded that CRRT with high-volume hemofiltration is not effective for severe lactic acidosis and that lactic acidosis alone should not be considered a nonrenal indication for CRRT. 5

• The Surviving Sepsis Campaign reviewed two large multicenter RCTs comparing doses of RRT and found no benefit of more aggressive renal replacement dosing on mortality. 1 A meta-analysis of sepsis patients in all relevant RCTs showed no significant relationship between RRT dose and mortality. 1

• The physiologic rationale is clear: lactate production rates in severe septic shock far exceed the clearance capacity of even high-volume CRRT. 5 The liver's capacity to metabolize lactate through the Cori cycle is approximately 100-200 mmol/hr, while CRRT removes only a fraction of this. 5

When Dialysis IS Indicated in Patients with Lactic Acidosis

Dialysis should be initiated for standard renal indications only, not for lactate removal: 1

• Severe hyperkalemia (K+ >6.5 mEq/L) refractory to medical management
• Uremic complications (pericarditis, encephalopathy, bleeding)
• Severe fluid overload refractory to diuretics causing pulmonary edema
• Severe acid-base disturbances from renal failure (not from lactate itself)
• Toxic ingestions requiring removal (e.g., metformin overdose with concurrent severe acidosis) 6

Special Case: Metformin-Associated Lactic Acidosis

This represents the one exception where dialysis may have a role, but not for lactate removal per se. 6 In metformin overdose with severe lactic acidosis (pH <7.1, lactate >20 mmol/L), high-volume venovenous hemofiltration combined with aggressive alkalinization has been reported successful. 6 The rationale is removal of the drug (metformin) rather than lactate itself, as metformin has a small volume of distribution and is dialyzable. 6

Critical Pitfalls to Avoid

• Do not delay definitive treatment of the underlying cause (source control in sepsis, hemorrhage control in trauma, insulin in DKA) while considering dialysis. 1, 2

• Do not use bicarbonate reflexively for pH ≥7.15, as it does not improve outcomes and may cause harm through sodium/fluid overload, increased PaCO2, and decreased ionized calcium. 1

• Do not assume lactate elevation always means tissue hypoxia - epinephrine can cause elevated lactate through beta-2-adrenergic receptor stimulation independent of tissue perfusion. 4, 7

• Do not use CVP alone as a marker of adequate resuscitation - it has significant limitations and should be interpreted alongside MAP, urine output, lactate clearance, and ScvO2. 1

Monitoring Parameters During Management

Assess these parameters together, not in isolation: 1, 4

• Lactate levels every 2 hours initially, targeting 10% clearance every 2 hours 4
• MAP ≥65 mmHg 1
• Urine output ≥0.5 mL/kg/hr 1
• ScvO2 ≥70% or SvO2 ≥65% 1
• Base deficit from arterial blood gas (provides independent information from lactate) 4
• Clinical perfusion markers: capillary refill ≤2 seconds, warm extremities, normal mental status 4