From the Guidelines
Management of lactic acidosis in acute liver failure requires a multifaceted approach targeting both the underlying liver dysfunction and the metabolic derangement, with the primary goal of improving morbidity, mortality, and quality of life.
Key Considerations
- Ensure adequate tissue perfusion by maintaining hemodynamic stability with intravenous fluids like normal saline or balanced crystalloids, targeting a mean arterial pressure above 65 mmHg 1.
- If fluid resuscitation is insufficient, vasopressors such as norepinephrine (starting at 0.05-0.1 mcg/kg/min) may be necessary.
- Correct any contributing factors like sepsis with appropriate antibiotics.
- Avoid medications metabolized by the liver that may worsen acidosis, such as metformin or certain antiretrovirals.
- Consider continuous renal replacement therapy (CRRT) when acidosis is severe (pH < 7.2) or refractory to other measures, as it can help remove lactate and correct acid-base disturbances.
- Thiamine supplementation (100 mg IV daily for 3-5 days) is important as deficiency can contribute to lactic acidosis.
- Sodium bicarbonate administration (1-2 mEq/kg IV) may be considered for severe acidosis (pH < 7.1) but should be used cautiously as it can worsen intracellular acidosis and cause volume overload, and its use is generally not recommended for patients with hypoperfusion-induced lactic acidemia with pH ≥ 7.15 1.
Nutrition Support
- Early involvement of nutrition support teams is recommended among hospitalized patients with acute-on-chronic liver failure (ACLF) 1.
- An objective assessment of nutrition status and risk should be performed at ICU admission for patients with cirrhosis and/or ACLF.
- Energy and protein requirements should be measured by indirect calorimetry if available or, if not available, calculated using predictive equations.
Ultimate Treatment
- The ultimate treatment is addressing the underlying liver failure through supportive care and, in appropriate cases, liver transplantation evaluation.
- Lactic acidosis occurs in liver failure because the liver normally clears lactate from the bloodstream, and impaired hepatic function leads to lactate accumulation, while tissue hypoxia from hypoperfusion further increases lactate production.
From the Research
Management of Lactic Acidosis in Acute Liver Failure
- The management of lactic acidosis in acute liver failure is a complex clinical problem, associated with increased morbidity and mortality 2.
- Treatment involves correcting the underlying cause, ensuring adequate oxygen delivery to tissues, and reducing oxygen demand through sedation and mechanical ventilation 3.
- The use of sodium bicarbonate to alkalinize the blood is controversial, with some studies suggesting it has no salutary effects and may even have negative side effects 3, 4.
- Continuous renal replacement therapy (CRRT) and dialysis have been advocated as treatments for lactic acidosis, but evidence is lacking, and their effectiveness is unclear 5, 6.
- Bicarbonate-buffered solutions may be preferred over lactate-buffered solutions in patients with severe liver failure or lactic acidosis, as lactate can exacerbate metabolic and hemodynamic parameters 6.
Treatment Options
- Correcting the underlying cause of lactic acidosis is crucial, and treatment should be focused on optimizing adequate oxygen delivery to tissues 3, 4.
- Sedation and mechanical ventilation may be used to reduce oxygen demand 3.
- CRRT with high-volume hemofiltration may not be effective for severe lactic acidosis, and its use should be carefully considered 5.
- Bicarbonate therapy may be considered in severe acidemia, but its use should be cautious and carefully monitored 3, 4.
Key Considerations
- The management of lactic acidosis in acute liver failure requires a multidisciplinary approach, involving anesthesia, post-operative, and critical care teams 2.
- The choice of buffer solution in CRRT should be carefully considered, with bicarbonate-buffered solutions preferred in patients with severe liver failure or lactic acidosis 6.
- Effective therapy of lactic acidosis due to shock is to reverse the cause, rather than relying on bicarbonate therapy or other treatments 4.